Edited by The Japanese Societyof Periodontology

Foreword to the“2022 Guidelines for Periodontal Therapy”
In Japan, elderly people accounted for more than 23% of the population in 2010, resulting in asuper-aged society. In 1989, when the “80-20 Campaign” started, less than 10% of people aged 75
years or older achieved the 80-20 goal (age over 80 with 20 teeth). Achievement of this goal has
increased year by year and the 2016 Survey of Dental Diseases showed that 51% of people aged
75 to 84 years accomplished the 80-20 goal. However, there is an increasing number of elderly
patients with periodontal disease and other diseases. Periodontal therapy is important to maintainoral health care and control general health because periodontal disease is a risk factor for systemic
health. Therefore, guidelines for periodontal therapy including prevention of periodontal disease
are required.
The 2015 Guidelines for Periodontal Therapy were revised more than 6 years after publication
based on changes in social conditions, leading to publication of the 2022 Guidelines for Periodontal Therapy. Since guidelines proposed by major academic societies have a great influence on medical care, the JSP discussed future periodontal therapy strategies in detail.
These guidelines were compiled based on the following concepts.
1. The guidelines are integrated with the 2007 Guidelines for Diagnosis and Treatment of Periodontal Disease, which was the first general statement of periodontal therapy published by the
JSP, and the detailed exposition 2008 Guidelines for Examination, Diagnosis and Treatment
Planning for Periodontal Disease.
2. JSP Clinical Practice Guidelines for Periodontal Treatment, 2015 combined and revised theabove two guidelines. The JSP Clinical Practice Guidelines for Periodontal Treatment, 2022 ispublished as a further revised version.
3. The guidelines were developed based on evidence and classification of periodontal disease,consideration of systemic diseases, examination, diagnosis, treatment planning, oral biofilm
infection, peri-implant disease, and continued management.
4. We focused on issues such as, cooperation with medical staff in performing periodontal treatment for the elderly, sick or home care patients, perioperative patients, and disabled people.
5. The aim of the guidelines is to provide objective criteria for periodontal treatment that can beused by many dentists, including clinical dental residents.
6. The guidelines refer to lectures and clinical teaching on periodontology and periodontal therapeutics at educational institutions and questions in the national dentist examination.
We expect that the guidelines will contribute to maintenance and promotion of oral and systemic health by providing a correct understanding of periodontal disease, periodontal therapeutics
and delivery of appropriate treatment and high-quality periodontal treatment to the public,
including elderly persons, sick persons, perioperative patients and disabled persons.
We gratefully acknowledge the chairperson, Dr. Kazuhiro Gomi, and members of the Guidelines Development Subcommittee (JSP Medicine Committee), the JSP Board members, and Ishiyaku Publishers, Inc.
March 2022

Yorimasa Ogata
President of the Japanese Society of Periodontology

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Edited by the Japanese Society of Periodontology“2022 Guidelines for Periodontal Therapy”
Members of the Guidelines Development Subcommittee (JSP Medicine Committee)(April 2021 to March 2023)
Chairperson:

Kazuhiro Gomi (Professor, School of Dental Medicine, Tsurumi University, Chief Director of JSP)

Members:

Taneaki Nakagawa (Professor, Keio University, Director of JSP)
Kazuhisa Yamazaki (Visiting Senior Researcher, RIKEN IMS, JSP member)
Nobuo Yoshinari (Professor, Matsumoto Dental University, Chief Director of JSP)
Akira Aoki (Professor, Tokyo Medical and Dental University, JSP member)
Hiroyuki Kawaguchi (Professor, Hiroshima University, Chief Director of JSP)
Sachiyo Tomita (Associate Professor, Tokyo Dental College, JSP member)
Tsuyoshi Fujita (Chairman, Fujita Dental Clinic, Visiting Professor, Hiroshima University, JSP member)
Toshiya Morozumi (Associate Professor, Kanagawa Dental University, JSP member)
Hideki Takai (Associate Professor, Nihon University School of Dentistry at Matsudo, JSP member)
Takatoshi Nagano (Associate Professor, School of Dental Medicine, Tsurumi University, JSP member)

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CONTENTS

1 What is periodontal disease? ・・・・・・・・・・・・・・・・・・ 9❶C urrentstatusofperiodontaldiseaseinJapan／9
1 Definition of periodontal disease ／9
2 Morbidity of periodontal disease ／9
3 Trend in the rate of patients receiving periodontal therapy ／9❷ Typeofperiodontaldisease ／10
1 Gingival lesions ／10⑴ Plaque-induced gingivitis ／10⑵ Non-plaque-induced gingival lesions ／10⑶ Gingival hyperplasia ／10a）Drug-induced gingival hyperplasia b) Hereditary gingival fibromatosis⑷ HIV infection-related gingival lesions ／10
2 Periodontitis (classified into localized and generalized types) ／10⑴ Chronic periodontitis ／11⑵ Aggressive periodontitis ／11⑶ Periodontitis associated with genetic disorders／11
3 Necrotizing periodontal diseases ／12⑴ Necrotizing ulcerative gingivitis ／12⑵ Necrotizing ulcerative periodontitis ／12
4 Abscesses of the periodontium ／12⑴ Gingival abscess ／12⑵ Periodontal abscess ／12
5 Combined periodontic-endodontic lesions ／12
6 Gingival recession ／13
7 Occlusal trauma ／13❸N ewclassificationofperiodontaldisease(2018
AmericanAcademyofPeriodontology/EuropeanFederationofPeriodontology) ／13<Periodontal health, gingival diseases/conditions>／13
1 Periodontal health and gingival health ／13⑴ Clinical gingival health on an intact periodontium ／13⑵ Clinical gingival health on a reduced periodontium ／13a）Stable periodontitis patient b）Non-periodontitis patient

2 Gingivitis - dental biofilm-induced ／13⑴ Associated with dental biofilm alone ／13⑵ Mediated by systemic or local risk factors ／13⑶ Drug-influenced gingival enlargement ／13
3 Gingival diseases - non-dental biofilm-induced／13⑴ Genetic/developmental disorders ／13⑵ Specific infections ／13⑶ Inflammatory and immune conditions ／14⑷ Reactive processes ／14⑸ Neoplasms ／14⑹ Endocrine, nutritional & metabolic diseases ／14⑺ Traumatic lesions ／14⑻ Gingival pigmentation ／14<Forms of periodontitis> ／14
1 Necrotizing periodontal diseases ／14⑴ Necrotizing gingivitis ／14⑵ Necrotizing periodontitis ／14⑶ Necrotizing stomatitis ／14
2 Periodontitis as a manifestation of systemic
diseases ／14
3 Periodontitis ／14⑴ Stage: Based on severity and complexity ofmanagement ／14⑵ Extent and distribution: Localized; generalized;
molar-incisor distribution ／14⑶ Grade: Evidence or risk of rapid progression,
anticipated treatment response ／14<Periodontal manifestations of systemic diseases
and developmental and acquired conditions> ／14
1 Systemic diseases or conditions affecting periodontal supporting tissues ／14
2 Other periodontal conditions ／14⑴ Periodontal abscesses ／14⑵ Endodontic-periodontal lesions ／14
3 Mucogingival deformities and conditions aroundteeth ／14
⑴ Gingival phenotype ／14⑵ Gingival/soft tissue recession ／14⑶ Lack of gingiva ／14⑷ Decreased vestibular depth ／14⑸ Aberrant frenum/muscle position ／14⑹ Gingival excess ／14⑺ Abnormal color ／14⑻ Condition of the exposed root surface ／14
4 Traumatic occlusal forces ／15⑴ Primary occlusal trauma ／15⑵ Secondary occlusal trauma ／15⑶ Orthodontic forces ／15
5 Prostheses and tooth-related factors that modify
or predispose to plaque-induced gingival diseases/periodontitis ／16⑴ Localized tooth-related factors ／16⑵ Localized dental prostheses-related factors ／16* Correspondence of the JSP with the new classifi-

5cation ／16❹C haracteristicsofgingivallesions(plaque-inducedgingivitis) ／16⑴ Bacterial plaque is pathogenic ／16⑵ Inflammation is localized to the gingiva ／16⑶ Gingival pockets are formed with no periodontal attachment loss ／16⑷ Gingival lesions are exacerbated by plaqueretention factors ／16⑸ Gingival lesions are improved by plaque control／16⑹ Gingival lesions are considered to be the precursor of periodontitis ／16❺ Characteristicsofperiodontitis ／16
1 Characteristics of onset of periodontitis ／17⑴ Plaque-induced gingivitis progresses to periodontitis, resulting in defects of the cementum,
periodontal ligament and alveolar bone ／17⑵ Development of attachment loss leads to periodontal pocket formation ／17⑶ The number of periodontopathic bacteria are
increased in deep periodontal pockets andinflammation is sustained ／17
2 Characteristics of progression of periodontitis ／17⑴ Gingival lesions are exacerbated by plaqueretention factors ／17⑵ Complication with traumatic occlusion induces
the progression of periodontitis ／17⑶ Region-specificity in progression rate ／17⑷ Resting and active stage ／17⑸ Advanced periodontitis produces a vicious
cycle and is likely to progress rapidly ／18
3 Characteristics of periodontal therapy ／18⑴ Cause elimination improves the system or suppresses the progression of periodontitis ／18⑵ Lifelong follow-up [supportive periodontal
therapy (SPT), maintenance and preventive
periodontal therapy (PPT)] is a prerequisite for
periodontal health ／18❻ Characteristicsofocclusaltrauma ／18⑴ Primary occlusal trauma ／18⑵ Secondary occlusal trauma ／18❼S ystemicconditionsandperiodontaldisease ／19

1 Factors affecting periodontal disease ／19⑴ Congenital factors ／19a）Genetic risk factors b）Age and sex c）Racial/ethnic difference⑵ Environmental and acquired risk factors ／19a）Smoking b）Stress c）Diabetes d）Obesitye）Routine medicines f）HIV infection

2 Diseases influenced by periodontal disease ／20⑴ Angiopathic disorder ／20⑵ Aspiration pneumonia ／20⑶ Preterm low weight birth ／20⑷ Diabetes ／20⑸ Rheumatoid arthritis ／20⑹ Other diseases ／20

2 Process of periodontal therapy ・・・・・・・・・・・・・・ 21❶ Systemicdisease ／21
1 Affected individuals ／21
2 Diabetic patients ／21
3 Elderly patients ／21❷E xamination-baseddiagnosis,therapeuticstrategyandinformedconsent ／21❸ Initialperiodontaltherapy ／22
1 Proactive participation of patients in treatment／22
2 Establishment of plaque control ／23
3 Elimination of plaque retention factors ／23
4 Recovery of masticatory function ／23
5 Abstention from symptomatic treatment ／23❹ Periodontalsurgery ／23❺ Oralrehabilitation ／23❻C ure,preventionofprogression,andstabilizationofperiodontaldisease ／23
1 Plaque-induced gingivitis ／24
2 Periodontitis ／24
3 Progression prevention ／24
4 Stable lesion ／24
5 Pathological progression ／24
6 Treatment after healing ／24

3 Medical interview, patient referral, andliaison with medicine ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 25❶ Medicalinterview ／25❷R eferralofpatientstoperiodontalspecialistsandadvancedcarefacilities ／25❸ Liaisonwithmedicine ／25
1 Disease state and drugs administered ／25
2 Precautions for invasive treatment in the oralcavity ／26

4 Examination, diagnosis and therapeuticstrategy for periodontal disease ・・・・・・・・・・・・ 27❶ Periodontalexamination ／27
1 Periodontal examination ／27⑴ Gingival inflammation ／27⑵ Probing depth ／27⑶ Attachment level (AL) ／27

6⑷ Periodontal epithelial surface area (PESA) andPeriodontal inflamed surface area (PISA) ／27⑸ Oral hygiene conditions (O’Leary plaque control
record) ／27⑹ Tooth mobility ／27⑺ Radiograph ／27⑻ Occlusion ／27⑼ Furcation involvement ／28a）Lindhe & Nyman’s furcation classificationb）Glickman’s furcation classification⑽ Plaque retention factors ／28⑾ Oral photography ／28⑿ Study model ／28
2 Microbiological assays ／28⑴ Bacterial test ／28⑵ Serum bacteria-specific antibody titer test ／28⑶ Quantitative measurements of oral bacteria ／28

3 Other examinations ／29⑴ Gingival crevicular fluid (GCF) test (fluid fromperiodontal pockets) ／29⑵ Saliva test ／29⑶ Blood test ／29
4 Psychological, social and behavioral assessment／29❷ Diagnosisofperiodontaldisease ／29
1 Diagnostic procedure for plaque-induced gingivitis and periodontitis ／29⑴ Diagnosis by tooth unit ／29a）Periodontitis classification by degree of tissue

disruption b）Periodontitis classification by inflam-mation severity c）Diagnosis of periodontitis by
tooth unit

⑵ Diagnosis at individual levels ／29a）Diagnosis by disease type b）Progression of

periodontitis c）Periodontitis severity of the wholeoral cavity

2 Diagnostic procedure for occlusal trauma ／31❸ Therapeuticstrategyplanning ／31
1 Initial periodontal therapy (cause elimination) ／31

2 Reassessment after initial periodontal therapy ／31

3 Periodontal surgery ／32
4 Reassessment after periodontal surgery ／32
5 Oral rehabilitation ／32
6 Reassessment before follow-up ／32
7 Supportive periodontal therapy (SPT) ／32
8 Preventive periodontal therapy ／32
9 Maintenance ／33

5 Periodontal therapy and oral biofilm infec-

tion in home care, perioperative patientsand disabled persons ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 34❶ Homecareandperiodontaltherapy ／34
1 Self-care ／34
2 Partial support for oral care ／34
3 Full support for oral care ／34❷P erioperativepatientsandperiodontaltherapy／34
1 Oral function control before surgery (treatment)／35
2 Oral function control during and after surgery(treatment) ／35
3 Aspiration and infection in oral hygiene control／35❸ Disabledpersonsandperiodontaltherapy ／35
1 Therapeutic strategy planning ／36
2 Initial periodontal therapy ／36
3 Periodontal surgery ／36
4 Oral rehabilitation ／36
5 Maintenance, preventive periodontal therapy
and supportive periodontal therapy (SPT) ／36❹ Oralbiofilminfection ／37

6 Emergency procedures ・・・・・・・・・・・・・・・・・・・・・・・・・・ 38❶ Identificationofcauseofpain ／38❷ Treatmentofacuteinflammation ／38

7 Preventive treatment ・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 39❶P reventionoftransitionfromplaque-induced
gingivitistoperiodontitis ／39❷ Preventivetreatmentforpregnantwomen ／39

8 Initial periodontal therapy ・・・・・・・・・・・・・・・・・・・・・ 40❶ Conceptsofinitialperiodontaltherapy ／40❷S trategyforinitialperiodontaltherapy ／40
1 Therapeutic strategy and process of initial periodontal therapy ／40
2 Therapeutic strategy focusing on bacterial infection and inflammation ／40❸ Treatmentofbacterialinfection ／40
1 Plaque control is a high priority in all therapies／40⑴ Motivation ／43⑵ Self-care (supragingival plaque control) ／43⑶ Instructions for brushing ／43⑷ Professional care (supragingival and subgingival
plaque control) ／43
2 Scaling and root planing ／43⑴ Significance and objective of scaling and root7

planing (SRP) ／44⑵ Precautions for SRP ／44⑶ Importance of sharpening ／44⑷ Ultrasonic scalers ／44⑸ Dentin hypersensitivity after SRP ／44
3 Improved plaque retention factors ／44
4 Extraction of teeth that cannot be saved ／44❹ Currenttreatmentofbacterialinfection ／45
1 Mechanical supragingival plaque control ／45
2 Mechanical subgingival plaque control ／45
3 Chemical supragingival plaque control ／45
4 Chemical subgingival plaque control ／46⑴ Subgingival pocket irrigation ／46⑵ Interpocket application of antimicrobial drug
／46⑶ Oral administration of antimicrobial agents／47
5 Patient’s choice of antibiotic therapy ／47❺ Treatmentofocclusaltrauma ／47
1 Relationship of occlusal trauma with progressionof periodontitis ／48
2 Occlusal adjustment and occlusal reshaping／48
3 Temporary splint ／48
4 Devices for periodontal therapy (provisional
restoration) ／49
5 Treatment of bruxism ／49
6 Orthodontic treatment ／50❻ Supportforsmokingcessation ／50

9 Risk factors for periodontal disease andrisk control during treatment ・・・・・・・・・・・・・・・・ 51

1 Systemic risk factors ／51
2 Environmental risk factors ／51❶ Periodontaltherapyfortheelderly ／51❷P eriodontaltherapyforpatientswithotherdiseases ／52
1 Metabolic syndrome ／52
2 Obesity ／52
3 Diabetes ／53⑴ Type 1 diabetes ／53⑵ Type 2 diabetes ／53
4 Hypertensive patients ／53
5 Patients with cardiovascular disease (particularly
those taking antithrombotic agents) ／53
6 Dialysis ／53
7 Respiratory disease ／53❸ Female-specificperiodontaldisease ／54
1 General precautions ／54
2 Periodontal therapy for pregnant women ／54

3 Patients with osteoporosis (particularly thosetaking BP products and anti-RANKL antibodies)／54❹ Periodontaltherapyforsmokers ／54⓾ Periodontal surgery ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 55❶ Tissueattachmenttherapy ／55
1 Periodontal curettage ／56
2 Excisional new attachment procedure (ENAP) ／57

3 Flap surgery ／57⑴ Flap curettage ／57⑵ Modified Widman flap surgery ／57❷ Resectivetherapy ／58
1 Gingivectomy ／58
2 Apically positioned flap surgery ／58❸ Periodontalregenerativetherapy ／59
1 Bone graft ／59
2 Guided tissue regeneration (GTR) ／59
3 Enamel matrix derivative-applied surgery ／59
4 Surgical procedure using basic fibroblast growth
factor (FGF-2) ／60
5 Surgical procedures using other biologically
active substances ／60❹P eriodontalplasticsurgery(includinggingival/
alveolarmucosaplasty) ／60
1 Frenectomy ／60
2 Laterally positioned flap surgery ／60
3 Coronally advanced flap surgery ／61
4 Apically positioned flap surgery ／61
5 Free gingival graft ／61
6 Connective tissue graft ／61
7 Other periodontal plastic surgery ／61❺ Laserapplicationinperiodontalsurgery ／62⓫ Treatment of furcation involvement ・・・・・・ 63❶ Examination ／63❷ Treatment ／63⓬ Treatment of combined periodontic-end-odontic lesions・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 65❶C lassificationofcombinedperiodontic-endodonticlesions ／65⑴ Class I (endodontic lesion-derived) ／65⑵ Class II (periodontic lesion-derived) ／65⑶ Class III (combined periodontal-endodontic
lesion-derived) ／65❷ Examination ／65❸ Treatment ／65

8⓭ Oral rehabilitation: Choice of splint, bridge,

denture and implant ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 67❶ Choiceoftherapeuticprocedures ／67
1 Test items ／67
2 Treatment of mobile teeth ／67
3 Temporary splint and splint with provisional
restoration ／68❷C hoiceofproceduresforprosthesisandprecautions ／68
1 Crown restoration (permanent splint) ／68
2 Treatment of partially edentulous arch ／68⑴ Bridge ／68⑵ Removal of partial denture ／69⑶ Implant ／69⑷ Tooth transplantation ／69❸ Orthodontictreatment ／70
1 Malalignment ／70
2 Remodeling of the periodontal tissue by orthodontic treatment ／70⓮ Implant therapy ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 71❶B enefitofimplanttherapyfororalfunctional
restorationinpatientswithperiodontaldisease／71❷ Peri-implanttissuestructure ／71❸ I mplanttherapyinpatientswithperiodontal
disease ／71
1 Importance of periodontal therapy prior to implant therapy ／71
2 Precautions for peri-implant mucositis andperi-implantitis ／71
3 Precautions for implant trauma ／72❹ I mplanttherapyandmaintenanceandsupportivetherapy(ST)afterimplantation ／72⓯ Treatment of peri-implant disease ・・・・・・・・ 73
1 Definition and classification of peri-implant disease ／73
2 Causes of peri-implant mucositis and peri-implantitis ／73
3 Clinical examination of peri-implant tissues ／74⑴ Assessment of plaque (biofilm) control ／74⑵ Probing depth (PD) in peri-implant tissues ／74⑶ Bleeding on probing (BOP) ／74⑷ Pus discharge ／74⑸ Radiographic assessment (bone resorption) ／74⑹ Implant deflection ／74⑺ Peri-implant keratinized mucosa ／74⑻ Occlusal relation ／74⑼ Microbiological tests ／74
4 Treatment of peri-implant mucositis and peri-implantitis ／75⑴ Non-surgical treatment ／75⑵ Surgical treatment ／75⑶ Cumulative interceptive supportive therapy(CIST) ／75⓰ Follow-up ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 78❶ Termdefinitions ／78
1 Maintenance ／78
2 Preventive periodontal therapy (PPT) ／78
3 Supportive periodontal therapy (SPT) ／78
4 Healing ／78
5 Suppression of progression (a new concept inhealth insurance) ／79
6 Stable lesion ／79
7 Professional tooth cleaning (PTC) ／79
8 Professional mechanical tooth cleaning (PMTC)／79❷ Examinationanddiagnosis ／79
1 Time of assessment ／79⑴ Plaque-induced gingivitis ／79⑵ Periodontitis ／80
2 Items of clinical examination ／81⑴ Periodontal examination ／81⑵ Bacterial tests ／81⑶ Other examinations ／81⑷ Risk assessment in SPT ／81❸ Therapeuticplannning ／82
1 Maintenance ／82
2 Suppressive therapy for periodontal diseaseprogression (new follow-up in health Insurance)／82
3 Supportive periodontal therapy (SPT) ／82
References ／84

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1 What is periodontal disease?
❶ Current status of periodontal disease in Japan
Two major dental diseases, periodontal disease and caries, develop and proceed to tooth loss, resulting in oral dysfunction that has adverse effects on both dental and oral health and general health. Maintenance of dental andoral health is the basis for living a productive life through enjoyment of a meal and conversation, as well as to ingest and chew foods. Elderly people with loss of 10 teeth or less have no serious problems in dietary habits; therefore, the “80-20 Campaign”, which supports people aged 80 years to have at least 20 teeth, was proposed and promoted to allow people to eat what they want and maintain their conversation and smile1).
Owing to improved attitudes of people toward oral hygiene and efforts of dental professionals (dentists anddental hygienists), 80-year-old people with 20 teeth or more (80-20 keepers) exceeded 20% in 20052), and accounted for 38.3% in 20113) and 51.2% in 20164). The mean number of remaining teeth was 15.3. The goal of
the National Health Promotion Movement in the 21st century (Health Japan 21) was to reach at least 20% of
people in the 80-20 keeper category and at least 50% of people as 60-24 keepers. This goal has been achieved, but
the number of elderly people with periodontal pockets ≥4 mm is increasing.
Japan is among countries with the highest longevity, but Japanese people aged around 80 years have few remaining teeth. As shown in the data of “number of existing teeth by age group” and “Survey of Dental Diseases”,
middle-aged and older people are likely to lose teeth rapidly1). Furthermore, the prevalence of periodontal diseasein Japan is much higher than that of other diseases and prevention and treatment of periodontal disease are criticalissues.

1）Definition of periodontal disease
Periodontal disease is roughly classified into gingival lesions and periodontitis. Periodontal disease, except for nonplaque-induced gingival lesions, is an inflammatory and infectious disorder caused by periodontopathic bacteriathat develop in the periodontium, which consists of the gingiva, cementum, periodontal ligament and alveolarbone. Periodontal disease also includes necrotizing periodontal disease, periodontal abscess, combined periodontic-endodontic lesions, gingival recession and occlusal trauma caused by a powerful bite force or abnormal force(Table 1). Herein, periodontal disease does not include apical periodontitis due to dental pulp disease or neoplasms (e.g. malignant tumors) that destroy the periodontium5). Recently, periodontal disease has also been viewed
as a lifestyle disease involved with eating and tooth brushing habits, smoking and systemic diseases including diabetes (periodontal disease has systemic health effects: periodontal medicine), showing the importance of healthguidance by dental professionals. It is necessary for patients to improve their lifestyle by themselves and to be supported in this goal by healthcare professionals (systemic disease).

2）Morbidity of periodontal disease
The 2016 Survey of Dental Diseases showed that the population with periodontal pockets ≥4 mm increased withage and accounted for 50% of persons aged 45-49 years and 57% of those aged 65-74 years4). The more remaining teeth elderly people have, the more periodontal pockets ≥4 mm they have. Those with gingival bleeding accounted for >30% in the age group of 15 to 29 years, and >40% in that of 30 years or older. Therefore, further
prevention of periodontal disease and severe conditions is required in younger patients.

3）Trend in the rate of patients receiving periodontal therapy
The municipal screening rate for periodontal disease was 4.3% in 2015 based on the Report on Regional Public
Health Services and Health Promotion Services6) and the Basic Resident Register7) and there is a need for increased

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screening rates. The 2016 Survey of Dental Diseases estimated that 3.983 million patients had gingivitis and periodontitis disease (under treatment), which was higher than patients in the 2011 survey by 660,000. The 2016
Survey of Dental Diseases also estimated that approximately 70 million patients had periodontal disease. However, approximately 4 million patients are actually treated at dental clinics, which is many fewer patients than the estimated total cases. This difference suggests that there are many people who are not aware of periodontal disease
and those who are aware of it are often not treated. It is preferable for these patients to undergo screening and tovisit clinics and hospitals.

❷ Types of periodontal disease
The JPS classification system of periodontal disease (2006)8) is shown in Table 1.

1）Gingival lesions（1）Plaque-induced gingivitis
Plaque-induced gingivitis is gingival inflammation caused by bacteria around the gingival margin. Clinical findings are gingival redness, edema, bleeding, pain and swelling. However, there is no radiographic finding or attachment loss of supporting tissues. Histopathological findings reveal junctional epidermal growth to the periapical orlateral region, telangiectasia surrounding the junctional epiderma, destruction of collagen fibers, and inflammatory cell infiltration. A classification of plaque-induced gingivitis by virulence factor is shown in Table 2.

（2）Non-plaque-induced gingival lesions

Non-plaque-induced gingival lesions are caused by reasons other than bacterial plaque. A classification is shown in
Table 3.

（3）Gingival hyperplasia
Gingival hyperplasia is gingival hypertrophy caused by hyperplasia of fibrillar collagen in gingival tissues. Onset
and recurrence can be partially prevented by thorough plaque control.
a）Drug-induced gingival hyperplasia

The responsible agents include phenytoin (antiepileptic drug, hydantoin product), nifedipine (antihypertensive,
calcium blocker) and cyclosporine A (immunosuppressant, calcineurin inhibitor).
b）Hereditary gingival fibromatosis

Hereditary gingival fibromatosis is a rare idiopathic disease that results in proliferative gingival swelling at the gingival margin, interdental papilla and attached gingiva. This disease develops in infants and swelling is found in the
buccolingual side of the maxillary and mandibular teeth, but disappears after extraction. Clinical cases with inheritable traits have been reported both in forms of autosomal-dominant and -recessive inheritance.

（4）HIV infection-related gingival lesions

The JPS classification system of periodontal disease (2006) does not describe this type of gingivitis; however,HIV-infected patients may develop gingivitis, including linear gingival erythema and necrotizing ulcerative gingivitis. Linear gingival erythema, which is rarely found in people without HIV infection, is characterized by linear
redness with a width of 1-2 mm along the gingival margin of multiple teeth. These two characteristic lesions arecaused by reduced immune function (low CD4 lymphocyte counts); therefore, abnormal gingival findings lead toearly detection of HIV infection.

2）Periodontitis (classified into localized and generalized types)
Periodontitis is an inflammatory destructive disease caused by bacteria in periodontal tissues. Inflammation
spreads from the gingival margin to deep periodontal tissues. Traumatic occlusion accelerates local lesion progression, but the progression rate is relatively slow. In the specific type, progression is acute and rapid and depends on
the host defense mechanism. A classification of periodontitis by risk factor is shown in Table 4.

11

Table 1. Classification system of periodontal disease by the JPS (2006)
Classification by pathology
I. Gingival lesions †1. Plaque-induced gingivitis ‡2. Non plaque-induced gingival lesions

3. Gingival overgrowth

II. Periodontitis †1. Chronic periodontitis ‡2. Aggressive periodontitis ‡Classification by virulence factor (risk factor)
1）Gingivitis induced by dental plaque only ‡2）Gingivitis modified by systemic conditions ‡3）Gingivitis modified by malnutrition ‡1）Gingival lesions induced by other infections2）Mucocutaneous disorders ‡3）Allergic reactions ‡4）Traumatic lesions of gingiva ‡Note
Table 2

Table 3

1）Drug-induced gingival overgrowth2）Hereditary gingival fibromatosis
1）Periodontitis associated with systemic diseases
2）Periodontitis associated with smoking3）Periodontitis associated with other risk factors

3. Periodontitis associated with genetic disorders ‡Table 4

Table 5

III. Necrotizing periodontal diseases †, ‡1. Necrotizing ulcerative gingivitis ‡2. Necrotizing ulcerative periodontitis ‡IV. Abscesses of periodontium ‡1. Gingival abscess ‡2. Periodontal abscess ‡V. Combined periodontic-endodontic lesions ‡VI. Gingival recession
VII. Occlusal trauma ‡1. Primary occlusal trauma ‡2. Secondary occlusal trauma ‡† Classified into localized and generalized types.
‡ Same disease name as that described in the Periodontal Disease Classification System of the American Academy of Periodontology(1999). Other diseases are defined by the JSP.

（1）Chronic periodontitis
Chronic periodontitis is a chronic inflammatory disease associated with attachment loss caused by periodontopathic bacteria and alveolar bone resorption. This disease was originally called adult periodontitis and onset isgenerally at ≥35 years old. Symptoms include periodontal pocket formation, drainage, bleeding, alveolar bone resorption, and tooth movement. This disease has a chronic course, but results in acute symptoms due to compromised host defense mechanisms.

（2）Aggressive periodontitis
Aggressive periodontitis is characterized by acute periodontal lesions (alveolar bone resorption, attachment loss)
and intrafamilial clustering in systemically healthy individuals. Attachment of bacterial plaque is generally small
and the age of patients ranges from 10 to the 30s. Some patients have large colonies of Aggregatibacter actinomycetemcomitans, and secondary characteristics are an abnormal defense mechanism and immune response. The prevalence of aggressive periodontitis in Japan is 0.05% to 0.1% in the 2012 report of the Japan Intractable Diseases
Information Center9).

（3）Periodontitis associated with genetic disorders
This is rapidly progressive periodontitis that develops as an oral symptom of genetic disorders associated with systemic abnormality. The genetic disorders include familial and cyclic neutropenia, Down syndrome, Papillon-Lefèvre syndrome, and Chédiak-Higashi syndrome (Table 5).

12

Table 2. Classification of plaque-induced gingivitis

Table 3. Classification of non-plaque-induced gingival lesions

1) Gingivitis induced by plaque only
2) Gingivitis modified by systemic conditions[1] Puberty-associated gingivitis[2] Menstrual cycle-associated gingivitis[3] Pregnancy-associated gingivitis[4] Diabetes-associated gingivitis[5] Leukemia-associated gingivitis[6] Other
3) Gingivitis modified by malnutrition[1] Ascorbic acid-deficiency gingivitis[2] Other

1) Gingival lesions induced by other infections[1] Gingival lesions of specific bacterial origin[2] Gingival lesions of viral origin[3] Gingival lesions of fungal origin2) Mucocutaneous disorders[1] Lichen planus[2] Pemphigoid[3] Pemphigus vulgaris[4] Lupus erythematosus[5] Others3) Allergic reactions
4) Traumatic lesions of gingiva

Table 4. Classification of periodontitis by risk factor

Table 5. Genetic disorders associated with periodontitis

1) Periodontitis associated with systemic diseases[1] Leukemia[2] Diabetes[3] Osteoporosis/osteopenia[4] Acquired immunodeficiency syndrome (AIDS)[5] Acquired neutropenia[6] Others
2) Periodontitis associated with smoking
3) Periodontitis associated with other risk factors

1) Familial and cyclic neutropenia
2) Down syndrome3) Leukocyte adhesion deficiency syndrome4) Papillon-Lefèvre syndrome5) Chédiak-Higashi syndrome6) Histiocytosis syndrome7) Infantile genetic agranulocytosis
8) Glycogen storage disease9) Cohen syndrome10) Ehlers-Danlos syndrome (Type IV and VIII)
11) Hypophosphatasia12) Other

3）Necrotizing periodontal diseases
These disorders are characterized by gingival necrosis and ulceration. The diseases are classified into gingivitis andperiodontitis.

（1）Necrotizing ulcerative gingivitis（2）Necrotizing ulcerative periodontitis
These diseases are distinguished as acute or chronic at diagnosis. Symptoms include gingival pseudomembrane
formation, bleeding, pain, fever, lymphadenopathy, and foul smell. The disorders are associated with Fusobacterium, spirochaetes and Prevotella intermedia. The pathogenesis includes poor oral hygiene, stress, smoking, and immunodeficiency. The disorders are also oral findings in HIV-infected patients.

4）Abscesses of the periodontium（1）Gingival abscessGingival abscess develops in gingival connective tissues and is caused by bacterial infection from adjacent periodontal pockets, external stimulation of the gingiva, and gingival trauma and infection. Localized redness andswelling are found in the gingiva near the causal site and pain is a frequent complication. Abscess develops regardless of periodontal pockets.

（2）Periodontal abscess
Periodontal abscess is the state of pus pooling in local tissue destruction by localized pyogenic inflammation in the
periodontium. Abscess develops in patients with deep periodontal pockets, localized pyogenic inflammation in
deep tissues with closed inlet of periodontal pockets, occlusal trauma, and poor resistance to infection in diabetic
patients.

5）Combined periodontic-endodontic lesions
Lesions in periodontal and endodontic regions affect each other. Marginal periodontal and periapical tissues are13

anatomically close, and lesions are likely to affect each other. Specifically, abnormality in marginal periodontal tissues affects the dental pulp via the accessory canal (lateral canal) and apical foramen, whereas lesions in pulp cavities have effects on periodontal tissues via the lateral canal, medullary tube and apical foramen.

6）Gingival recession
Gingival recession is the state in which marginal gingiva transfers from the cement-enamel junction (CEJ) toward
the periapical direction and the root surface is exposed. Recession is also caused by aging, mechanical processes
due to incorrect brushing, inflammation in the marginal gingiva, and disuse atrophy with pairing tooth loss. Afterthe root surface is exposed, caries, abrasion and dentin hypersensitivity sometimes develop.

7）Occlusal trauma
Occlusal trauma is a bite force-induced injury in deep periodontal tissues (cementum, periodontal ligament andalveolar bone). When no inflammation develops in the gingiva, attachment loss does not occur and X-ray findings
indicate radiolucency surrounding the tooth root. Disruption of the periodontium is expanded by excessive occlusal force to tissues with periodontitis (see Page 18, “ ❻ Characteristics of occlusal trauma”).

❸ New classification of periodontal disease(2018 American Academy of Periodontology/European Federation of Periodontology)
The World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions was held in
Chicago in November 2017 jointly by the American Academy of Periodontology (AAP) and the European Federation of Periodontology (EFP) to discuss a new classification of periodontal diseases. The results were compiled
into a consensus report and the new classification of periodontal diseases was published by the AAP and EFP
during EuroPerio9 in Amsterdam in June 2018 (Table 6 and 7). The new classification markedly revised thetypes of periodontitis. In the 1999 classification, periodontitis was categorized into two groups: aggressive periodontitis and chronic periodontitis. On the other hand, in the new classification, periodontitis is grouped under asingle category and is further characterized based on a multi-dimensional staging and grading system. Severity andcomplexity have 4 stages (Stage I: mild, Stage IV: severe) and progression risks have 3 grades (Grade A: lowest risk,
Grade C: highest risk). Risk factors including smoking and diabetes are considered in the grade determination10).

<Periodontal health, gingival diseases/conditions>
1）Periodontal health and gingival health（1）Clinical gingival health on an intact periodontium（2）Clinical gingival health on a reduced periodontiuma）Stable periodontitis patientb）Non-periodontitis patient2）Gingivitis - dental biofilm-induced（1）Associated with dental biofilm alone（2）Mediated by systemic or local risk factors（3）Drug-influenced gingival enlargement

3）Gingival diseases - non-dental biofilm-induced（1）Genetic/developmental disorders（2）Specific infections（3）Inflammatory and immune conditions

14（4）Reactive processes（5）Neoplasms（6）Endocrine, nutritional & metabolic diseases（7）Traumatic lesions（8）Gingival pigmentation<Forms of periodontitis>

1）Necrotizing periodontal diseases（1）Necrotizing gingivitis（2）Necrotizing periodontitis（3）Necrotizing stomatitis

2）Periodontitis as a manifestation of systemic diseases
3）Periodontitis（1）Stage: Based on severity and complexity of management (Table 6)
Stage I: Initial peiodontitis
Stage II: Moderate periodontitis
Stage III: Severe periodontitis with potential for additional tooth loss
Stage IV: Severe periodontitis with potential for loss of dentition（2）Extent and distribution: Localized; generalized; molar-incisor distribution（3）Grade: Evidence or risk of rapid progression, anticipated treatment response (Table 7)
Grade A: Slow progression
Grade B: Moderate progression
Grade C: Rapid progression<Periodontal manifestations of systemic diseases and developmental
and acquired conditions>1）Systemic diseases or conditions affecting periodontal supporting tissues
2）Other periodontal conditions（1）Periodontal abscesses（2）Endodontic-periodontal lesions3）Mucogingival deformities and conditions around teeth（1）Gingival phenotype（2）Gingival/soft tissue recession（3）Lack of gingiva（4）Decreased vestibular depth（5）Aberrant frenum/muscle position（6）Gingival excess（7）Abnormal color（8）Condition of the exposed root surface

15

Table 6. Periodontitis stage
Periodontitis stage

Severity

Stage I

Stage II

Stage III

Stage IVInterdental
CAL at site ofgreatest loss

1 to 2 mm

3 to 4 mm

≥5 mm

≥5 mm

Radiographic
bone loss

Coronal third (<15%)

Coronal third (15 to33%)

Extending to middle or apicalthird of the root

Extending to middle or apicalthird of the root

Tooth loss due to periodontitisof ≤4 teeth

Tooth loss due to periodontitisof ≥5 teeth

Tooth loss

No tooth loss due to periodontitis

In addition to Stage II complex- In addition to Stage III
ity:complexity:

Complexity

Local

Maximum probing
depth ≤4 mm
Mostly horizontalbone loss

Maximum probing
depth ≤5 mm
Mostly horizontalbone loss

Need for complex rehabilitation
due to:Probing depth ≥6 mm

Masticatory dysfunction
Secondary occlusal trauma(tooth mobility degree ≥2)
Severe ridge defectBite collapse, drifting, flaring
Less than 20 remaining teeth(10 opposing pairs)

Vertical bone loss ≥3 mm
Furcation involvement Class II
or III
Moderate ridge defect

Extent anddistribution

Add to stage as
descriptor

For each stage, describe extent as localized (<30% of teeth involved), generalized, or molar/incisor pattern
CAL: clinical attachment loss

Table 7. Grade of periodontitis
Periodontitis grade
Direct evidence ofprogression

Grade A:
Slow rate ofprogression

Grade B:
Moderate rate ofprogression

Longitudinal data
Evidence of no loss over(radiographic bone loss
<2 mm over 5 years
5 yearor CAL)≥2 mm over 5 years% bone loss/age

0.25 to 1.0

>1.0

<0.25

Case phenotype

Heavy biofilm deposits
with low levels ofdestruction

Destruction commensurate with biofilm
deposits

Destruction exceeds expectation
given biofilm deposits; specificclinical patterns suggestive of
periods of rapid progression
and/or early onset disease (e.g.,
molar/incisor pattern; lack of
expected response to standard
bacterial control therapies)

Smoking

Non-smoker

Smoker <10 cigarettes/
day

Smoker ≥10 cigarettes/day

Diabetes

Normoglycemic / nodiagnosis of diabetes

HbA1c <7.0% inpatients with diabetes

HbA1c ≥7.0% in patients withdiabetesPrimary criteria
Indirect evidenceof progression

Grade modifiers

Grade C:
Rapid rate of progression

Risk factor

Risk of systemic
impact ofperiodontitis

InflammatoryburdenHigh sensitivity CRP(hsCRP)<1 mg/L

1 to 3 mg/L

>3 mg/L

Biomarkers

Indicators of
CAL/bone loss

Saliva, gingival
crevicular fluid, serum?

?

?
CAL: clinical attachment loss4）Traumatic occlusal forces（1）Primary occlusal trauma（2）Secondary occlusal trauma（3）Orthodontic forces

165）Prostheses and tooth-related factors that modify or predispose toplaque-induced gingival diseases/periodontitis（1）Localized tooth-related factors（2）Localized dental prostheses-related factors* Correspondence of the JSP with the new classification
The JSP uses the conventional classification describing the new classification collectively as a temporary basis forcontinued use of clinical and research findings accumulated over the years. That is, the definition “localized or
generalized” is described first, and “chronic or aggressive” periodontitis second, followed by the stages and grades.

❹ Characteristics of gingival lesions (plaque-induced gingivitis)
Gingival lesions are inflammation only in the gingiva; the cementum, periodontal ligament and alveolar bone are
not disrupted. Among various gingival lesions, plaque-induced gingivitis is clinically important and its characteristics are described below.

（1）Bacterial plaque is pathogenic
Bacteria attached to teeth grow due to poor oral hygiene control and bacterial plaque is developed, resulting in
gingival inflammation. The inflammation grade depends on factors such as host resistance. Bacterial plaque is constructed with numerous bacteria on teeth, gingiva, and restorative and prosthesis products and their metabolites.
As a result of plaque maturation, there is coaggregation of different bacterial species and coverage with extracellular polymeric substances (EPS) including glycocalyx.

（2）Inflammation is localized to the gingiva
No inflammation affects the cementum, periodontal ligament or alveolar bone.

（3）Gingival pockets are formed with no periodontal attachment loss
The gingival swelling and edema to the crown-side direction due to inflammation results in formation of a gingival pocket (pseudopocket). Clinically, the bottom of the periodontal pocket is positioned at the CEJ. Since the attachment level does not change, there is no attachment or alveolar bone loss.

（4）Gingival lesions are exacerbated by plaque retention factors
Plaque retention factors (factors that make plaque control difficult and accelerate bacterial plaque retention: see

Page 28 （“ 10）Plaque retention factors” and Figure 6-2) cause bacterial plaque accumulation and progression to periodontitis.

（5）Gingival lesions are improved by plaque control
Gingival lesions are markedly improved by intensive oral hygiene control, including brushing and elimination or
reduction in bacterial plaque, which is the major cause of gingivitis. Gingival inflammation is further improved byremoval or revision of plaque retention factors.

（6）Gingival lesions are considered to be the precursor of periodontitis
In general, untreated plaque-induced gingivitis makes inflammation expand to the cementum, periodontal ligament and alveolar bone, resulting in periodontitis. Plaque-induced gingivitis may remain unchanged, but untreated gingivitis is the cause of subsequent of periodontitis.

❺ Characteristics of periodontitis
Periodontitis is inflammation that initially develops in the gingiva and spreads to deep periodontal tissues, including the cementum, periodontal ligament and alveolar bone. Long-term continuous stimulation of bacterial
plaque, the major cause, is required for progression of plaque-induced gingivitis to periodontitis. Such progression
is strongly associated with lifestyle and plaque retention factors that induce accumulation of bacterial plaque and17make it difficult to remove this plaque. The progression rate of periodontitis is relatively slow and takes several
years. However, sustained traumatic occlusion rapidly destroys the periodontal tissue. Furthermore, the host defense response has effects on the initiation and progression of periodontitis. For example, severe diabetes-reduced
resistance of periodontal tissues (e.g. leukocyte dysfunction, wound repair delay) and lifestyle factors, including
smoking, are involved in progression of periodontitis. Chronic periodontitis is the major type. Its characteristics
are shown below.

1）Characteristics of onset of periodontitis（1）Plaque-induced gingivitis progresses to periodontitis, resulting in defects of the cementum, periodontal ligament and alveolar bone

Enzymes produced by periodontopathic bacteria and their metabolites enhance the defense mechanism, i.e., immune function; consequently, gingival inflammatory destruction expands to the cementum, periodontal ligamentand alveolar bone.

（2）Development of attachment loss leads to periodontal pocket formation
Destruction of the attachment between teeth and periodontal tissues leads to attachment loss. The site of gingival
junctional epithelium (attached epithelium) and connective tissue attachment extend from the CEJ to root apex
and the gingiva detaches from the root. Consequently, a periodontal pocket (true pocket) is formed.

（3）The number of periodontopathic bacteria are increased in deep periodontal pockets andinflammation is sustained

The inside of the periodontal pocket is under anaerobic conditions, in which periodontopathic bacteria are likely
to grow. Consequently, bacteria and metabolites invade the gingiva through the epithelium of a periodontal pocket. In patients with chronic periodontitis, Porphyromonas gingivalis (P. gingivalis), Tannerella forsythia, A. actinomycetemcomitans, Fusobacterium nucleatum and Treponema denticola (T. denticola) are frequently detected in active lesions of periodontitis.

2）Characteristics of progression of periodontitis（1）Gingival lesions are exacerbated by plaque retention factors
Similarly to plaque-induced gingivitis, periodontitis progresses rapidly when plaque retention factors that makeplaque control difficult (e.g. calculus, malalignment, abnormal gingiva and alveolar mucosa, incompatible restoration and prosthetic devices, dental morphological defects, food impaction, mouth breathing, abnormal oral vestibule, caries in the tooth cervix, periodontal pocket) are present. After periodontal pocket formation, the insidesof pockets cannot be controlled by the patient; consequently, bacterial plaque increases and periodontitis progresses.

（2）Complication with traumatic occlusion induces the progression of periodontitis
Traumatic occlusion, including early contact, strong lateral pressure and bruxism, exacerbates inflammation inperiodontal tissues and tissue disruption rapidly progresses, resulting in vertical bone resorption and infrabony
pocket formation. Therefore, traumatic occlusion is a significant local modifier for aggravating periodontitis.

（3）Region-specificity in progression rate

Distinctions in the quality (type) and mass of infected periodontopathic bacteria and local modifiers cause significant differences in progression of periodontitis between regions in the oral cavity of the same patient.

（4）Resting and active stage

Periodontitis is generally considered to be a chronic disorder; however, disruption of the periodontium does notalways proceed at a constant rate, but rapidly progresses in active stages. There is no diagnostic procedure for
identifying the resting and active stages in a single test. Increased BOP ratio, rapid progression of attachment loss
and alveolar bone resorption are assessed as the active stage and their region of occurrence is referred to as the active region.

18（5）Advanced periodontitis produces a vicious cycle and is likely to progress rapidly
Periodontopathic bacteria increase in a deep periodontal pocket. Attachment loss is likely to occur in this kind of
pocket in comparison with that in a shallow pocket. Furthermore, reduced periodontal support due to alveolarbone resorption induces secondary occlusal trauma, which is complicated by bacterial infection, and disruption of
periodontal tissues proceeds.

3）Characteristics of periodontal therapy（1）Cause elimination improves the system or suppresses the progression of periodontitis
Initial periodontal therapy mainly as cause elimination leads to periodontal health in mild periodontitis and stops
progression. However, periodontal surgery and oral rehabilitation are frequently needed in moderate or severe
periodontitis, and more complicated periodontal therapy is required. In general, it is difficult to regenerate lost
periodontal tissues completely using current periodontal therapy, including periodontal tissue regenerative therapy.

（2）Lifelong follow-up [supportive periodontal therapy (SPT), maintenance and preventive
periodontal therapy (PPT)] is a prerequisite for periodontal health

Periodontitis has a high risk for recurrence because bacterial plaque (the major cause) and traumatic factors are always present in the oral cavity; deep periodontal pockets and furcation involvement often remain even after completion of appropriate periodontal therapy; and periodontitis is affected by systemic factors for a long time. Therefore, SPT, PPT and maintenance as healthcare are prerequisites as a part of periodontal therapy to maintain
periodontal tissues that are “healing” due to basic periodontal therapy, periodontal surgery and oral rehabilitation,or are in a “stable state of disease” or “preventive stage” due to gingival inflammation, although the probing depth
is <4 mm. SPT and PPT mainly comprise plaque control, scaling, root planing and occlusal adjustment by dental
professionals, whereas maintenance consists of self-care (home care) by patients themselves and professional care
(specialist care) by specialists. Since periodontal disease is likely to recur due to insufficient plaque control, SPT
and maintenance are essential. Teeth can be preserved by SPT and maintenance for appropriate intervals and canfunction for a long time.

❻ Characteristics of occlusal trauma
Occlusal trauma is injury in deep periodontal tissues (i.e., the cementum, periodontal ligament and alveolar bone)caused by traumatic occlusion (excessive bite force and abnormal lateral force) and is classified into primary andsecondary occlusal trauma. Histopathological findings include degenerative necrosis in the pressed region of theperiodontal ligament and alveolar bone resorption, and primary findings include tooth movement, enhanced cavity of the periodontal ligament and vertical (wedge-shaped) bone resorption in X-ray findings. Occlusal trauma is afactor in increasing disruption of the periodontium in periodontitis.

（1）Primary occlusal trauma

Primary occlusal trauma is trauma in the periodontal tissues caused by excessive bite force to teeth.

（2）Secondary occlusal trauma

Secondary occlusal trauma is trauma that occurs in teeth with reduced capacity of bite force due to reduction of
the supporting alveolar bone by progression of periodontitis, and is caused by physiological bite force. Occlusionthat causes occlusal trauma is called traumatic occlusion. Causes include malalignment, premature contact, cuspal
interference, bruxism, excessive bite force, lateral pressure, abnormal habits in the tongue and lips, and food impaction.

19

Congenital factors

Antibody
Polymorpho
nuclear leukocyte
Bacterial
invasion

AntigenHost
immunity/
Inflammatory
response

Cytokine
Prostaglandin

Matrix
metalloprotease

LPS
Other virulence
factors

Connective
tissue/Bonemetabolism

Clinicalfindings
ofperiodontal
development
andprogression

Environmental and acquired factors
Figure 1. Etiology of periodontal disease (ref 11, revised)❼ Systemic conditions and periodontal disease
Patients with periodontal disease who have or are suspected to have systemic disease should undergo a medical interview before the start of periodontal therapy, with immediate referral to attending physicians for symptoms. Patients are treated with periodontal therapy together with sufficient control of systemic disease. Some patients havedifficulty undergoing both periodontal and dental therapy, depending on the type and symptoms of systemic disease. In such a case, communication with advanced care facilities for systemic disease is recommended, with therequest that they provide the information necessary for treatment and control of systemic disease. Close attention
should also be given to patients in whom systemic conditions are sufficiently controlled.

1）Factors affecting periodontal disease (figure 1)（1）Congenital factorsa）Genetic risk factors

Genetic risk factors are associated with metabolic gene defects, and polymorphism in inflammatory immune related genes and gene expression. Patients with Down syndrome, Papillon-Lefèvre syndrome and Chédiak-Higashi
syndrome are known to have severe periodontal disease.
b）Age and sex

Periodontal disease with disruption of the periodontium in youth or with rapid progression has a poor prognosis(e.g. aggressive periodontitis). Increased sex hormones induces P. intermedia, resulting in pregnancy-associated/pubertal gingivitis. On the other hand, postmenopausal women with reduced estrogen secretion have increased production of inflammatory cytokines, which sometimes results in alveolar bone resorption and deeper periodontal
pockets12).

c）Racial/ethnic difference

Racial/ethnic differences are not important in Japan. In comparison of Caucasian, Mexican and African-Americans, attachment loss, probing values and prevalence of periodontitis are lowest in Caucasians. Racial/ethnic differences depend on oral bacterial flora, differences in host response, food habits, socioeconomic factors, and understanding of dental therapy.

（2）Environmental and acquired factorsa）SmokingSmoking is the strongest risk factor among environmental factors. Smokers are likely to have periodontal disease20

at a rate of 2-8 times higher than non-smokers. In addition, smoking decreases the response of periodontal disease
to curative therapy.
b）Stress

Stress is related to aggravation of periodontal disease and stress-induced mental tension (stress response) has effects
on the immune response.
c）Diabetes

Periodontitis complicated with diabetes is not induced by diabetes, but by immune system disorder, peripheral
circulatory disturbance and wound repair delay due to diabetes, which modulate the pathology of periodontitis.
d）Obesity

Obese individuals are likely to have periodontal disease and the causes are thought to be related to tumor necrosis
factor alpha (TNF-α) produced from visceral adipose tissues.
e）Routine medicines

Periodontal disease is an inflammatory disease induced by bacterial infection, resulting in bone metabolism, including disruption of the alveolar bone (Figure 1). Therefore, immunosuppressants, inflammatory cytokine-targeted agents, bone metabolism-related agents and corticosteroids have effects on the pathology of periodontal disease. For example, phenytoin (antiepileptic drug, hydantoin group), nifedipine (antihypertensive, calcium blocker)
and cyclosporine (immunosuppressant, calcineurin inhibitor) are routine medications that cause drug-induced
gingival hyperplasia.

f）HIV infection

HIV infection sometimes causes necrotizing ulcerative gingivitis (periodontitis)-like symptoms that require attention.

2）Diseases influenced by periodontal disease（1）Angiopathic disorder

In arteriosclerosis and ischemic heart disease (angina, cardiac infarction), cytokines are suspected to be involved inthrombus formation.

（2）Aspiration pneumonia
Oral bacteria including periodontopathic bacteria pass through the trachea and invade the lung with the saliva, resulting in aspiration pneumonia.

（3）Preterm low weight birth
Mothers with moderate periodontitis have higher risks for delivering a low birth weight infant.

（4）Diabetes

TNF-α, a mediator of inflammation caused by periodontitis, increases insulin resistance and aggravates diabetes.

（5）Rheumatoid arthritis

Patients with rheumatoid arthritis have large attachment loss and dental loss. Periodontal disease has many causes
and pathological conditions similar to those in rheumatoid arthritis. Enhanced production of inflammatory cytokines and prostaglandin E2 (PGE2) is involved in tissue disruption.

（6）Other diseases

Periodontal disease has effects on onset and progression of bacteremia, chronic kidney disease and non-alcoholicsteatohepatitis (NASH).

21

2 Process of periodontal therapy (see Figure 2)❶ Systemic disease
Systemic factors are extremely important in onset and progression of periodontal disease and it is likely that periodontal disease induces systemic disorders. Regardless of susceptibility to infection and the progression rate ofperiodontal disease, sufficient removal of causative bacterial plaque improves periodontal disease. Patients withsystemic disease (including diabetes, obesity [metabolic syndrome] and hematologic disease) related to onset andprogression of periodontal disease require thorough elimination of local factors for periodontal disease and improvement of systemic disease by attending physicians1). Environmental factors including smoking and stress also
induce progression of periodontal disease; therefore, it is important to improve these factors.

1）Affected individuals
Affected individuals are frequently given many agents and a medical interview is required before the start of periodontal therapy, with referral to attending physicians for symptoms and development of appropriate team treatment. In elderly and affected individuals, prevention of complications is needed to determine resting blood pressure, heart rate and oxygen saturation before surgery and monitor vital signs during therapy, even if treatment has
no problems. Dental therapy can be difficult in some patients with certain systemic diseases and symptoms. In
such cases, it is necessary to communicate with advanced care facilities for systemic disease and request that they
provide the information necessary for treatment and control of systemic disease.

2）Diabetic patients
For immunocompromised patients with periodontitis who have a decreased host defense mechanism due to poorly-controlled diabetes and those who have endothelial dysfunction due to atherosclerotic disease, combination
with antimicrobial therapy is recommended to improve the response of periodontal therapy and reduce adverse effects on the body and organs2, 3).

3）Elderly patients
Elderly patients are likely to have decreased resistance to periodontal disease due to age-related impaired immune
functions and may develop aspiration pneumonia because of decreased oral functions. There are no specific procedures for periodontal therapy in the elderly; however, it is important to have sufficient information on past andcurrent medical history and medication, as well as to perform careful observation of patients because of physicaldysfunction and various systemic diseases. It is necessary to refer to physicians with regard to the patient’s systemic
conditions, as required. To prevent aspiration pneumonia, it is important to examine oral contamination using anoral biofilm test for diagnosis of biofilm infection and to keep the oral cavity clean.

❷ Examination-based diagnosis, therapeutic strategy and informed consent
For appropriate periodontal therapy, correct testing and diagnosis of the current symptoms of periodontal disease
are required (see Page 27 “❶ Periodontal disease examination”). The first step is to conduct a periodontal
tissue examination to confirm gingival inflammation and tissue disruption, and plan the therapeutic strategy basedon the systemic conditions in cooperation with physicians, as required. The next step is to obtain informed consent from the patient after giving a thorough explanation and then to start treatment in accordance with the therapeutic strategy. The standard procedures for periodontal therapy are shown in Table 2. If the test results in eachstep indicate no need for therapy, skip and go to the next test.

22

Medical interview (first medical examination)

Periodontal disease examination
Diagnosis of periodontal disease
Treatment planning

Initial periodontal therapy(Plaque control, scaling and root planing, revision of habit, extraction, occlusal adjustment,
caries treatment, temporal splint, periodontal therapy devices, smoking cessation support)

Re-evaluation

Periodontal surgery

Periodontal tissue examination (re-evaluation)

Oral rehabilitation(Restorative and prosthetic therapy, orthodontic treatment, implant therapy)

Re-evaluation

Healing

Stable lesion

Progression prevention

MaintenanceSupportive periodontal
therapy (SPT)Preventive periodontal
therapy (PPT)

Figure 2. Standard procedures for periodontal therapy* Therapy considered unnecessary in a test can be skipped.

A new concept in health insurance.

❸ Initial periodontal therapy
The principle of periodontal therapy is to elucidate causes and precipitating factors of periodontal disease and toeliminate these causes.

1）Proactive participation of patients in treatment

Daily plaque control (self-care) by patients is important in periodontal therapy4). This is necessary to prepare conditions in which patients proactively participate in treatment based on appropriate instructions for oral hygiene.

23

Therefore, dentists and dental hygienists should fully explain that periodontal disease is caused by bacterial infection and that systemic diseases are involved in periodontal disease, so that patients recognize the importance ofprevention and therapy.

2）Establishment of plaque control
Successful initial periodontal therapy depends on continuous plaque control in all therapeutic stages. Plaque control is roughly classified into self-care by patients and professional care by dental specialists. If basic plaque control
is not performed successfully, an effect of the following therapy cannot be obtained.

3）Elimination of plaque retention factors
It is important to eliminate plaque retention factors that are causes of accumulation of bacterial plaque and factorsthat make them difficult to eliminate to make it easier to control oral hygiene5).

4）Recovery of masticatory function
Traumatic factors that cause occlusal trauma in periodontal tissues and aggravate periodontitis must be eliminated. In patients who have extreme tooth movement due to periodontal disruption after traumatic factors are eliminated, it is important to splint and install devices for periodontal therapy temporarily for occlusal stabilization andrecovery of masticatory function6).

5）Abstention from symptomatic treatment
It is inappropriate to administer antibacterial and antiinflammatory agents alone, conduct incisional drainage forthe swollen gingiva, and just fix tooth movement in patients with gingival inflammation and gingival and periodontal abscess. Such procedures are referred to as symptomatic treatment, and do not remove bacterial plaquescausing periodontal disease. Bacterial plaques temporarily decrease and seem to be relieved by symptomatic treatment; however, plaques soon increase again, resulting in recurrence of periodontal disease. Therefore, periodontal
therapy should be conducted to eliminate causes.

❹ Periodontal surgery
After completion of initial periodontal therapy, appropriate surgery is conducted to repair and regenerate lost periodontal tissues in regions requiring this procedure, based on the patients' systemic conditions and the generalneed for surgery, with the goal of improvement of remaining deep periodontal pockets and morphological defects
in the oral mucosa.

❺ Oral rehabilitation
After completion of initial periodontal therapy and periodontal surgery, restorative and prosthetic therapy is performed and stable occlusion is established to restore oral functions (occlusion, mastication, dental esthetics, articulation function, etc.). Plaque retention factors and traumatic occlusion are improved and dental esthetics is restored by orthodontic treatment.

❻ Cure, prevention of progression, and stabilization of periodontal disease
Patients with a probing depth <4 mm without gingival inflammation are considered to be “healing” after initialperiodontal therapy and periodontal surgery or occlusal function restoration, and can undergo maintenance. Patients with a probing depth <4 mm, but with gingival inflammation are considered to be in the “preventive stage”.

24

In this stage, periodontal disease is likely to be in progression; therefore, routine PPT should be used for these patients. Patients with a periodontal pocket ≥4 mm, slight tooth movement and furcation involvement without gingival inflammation are considered to be clinically stable and to have a “stable lesion”. However, periodontal diseaseis likely to recur in this stage; therefore, patients with a “stable lesion” should be encouraged to visit a clinic at appropriate intervals and undergo SPT. It is important for patients in this stage to receive maintenance, PPT and
SPT and maintain oral health7). Determination of the “healing”, “preventive stage” or “stable lesion” stage depends
on the state of periodontal disease progression.

1）Plaque-induced gingivitis
Plaque-induced gingivitis is cured by initial periodontal therapy and diagnosed by re-evaluation after therapy in acase with “healing” or in the “preventive stage”. Periodontal therapy is not discontinued, but maintenance or PPT
is performed at appropriate intervals.

2）Periodontitis
Slight periodontitis is often determined as “healing” or in the “preventive stage” in basic periodontal therapy.
Moderate or severe periodontitis depends on lesions, and periodontal surgery is performed for lesions as required.
Furthermore, after completion of this surgery, re-evaluation (including partial re-evaluation) is conducted to evaluate the effect of periodontal therapy and the state of periodontal tissues. Patients who are determined to be in a
“preventive stage”, “stable lesion” or “healing” at the completion of oral rehabilitation can transfer to PPT, SPT or
maintenance.

3）Progression prevention“Progression prevention” is a new concept in health insurance that was introduced in the 2020 revision of medical
service fees. When re-evaluation shows that a patient has gingival inflammation in some regions, but recovery in
all regions with probing depth <4 mm, PPT is used due to the high possibility of periodontal disease progression.
Risks should be assessed in the patient, and re-evaluation and PPT should be performed.

4）Stable lesion
Patients who have healthy periodontal conditions, but a periodontal pocket ≥4 mm, slight tooth movement andfurcation involvement without gingival inflammation in a re-evaluation are considered to be have a “stable lesion”.
These patients undergo SPT. Some of these patients who cannot undergo periodontal surgery due to systemic disease or other risk factors should frequently undergo a re-evaluation and SPT. Patients who have bruxism and abnormal habit, decrease tooth-supporting volume due to severe alveolar bone resorption resulting in occlusal trauma even with physiological bite force, or have systemic disease (e.g. diabetes), should also frequently undergo a
re-evaluation and SPT.

5）Pathological progression
Patients who have a periodontal pocket >4 mm and BOP during follow-up (maintenance, SPT and PPT) are considered to be in a state of progression of periodontal disease and are assessed as in a “preventive stage”. Patients
who have attachment loss >2 mm, continuous BOP, X-ray findings of progressive bone resorption, and increased
tooth movement should undergo periodontal therapy again.

6）Treatment after healing
Patients with a probing depth <4 mm, but gingival recession and exposed furcation are sometimes determined tobe “healing”. However, these patients with an exposed root who were determined to be “healing” are likely to develop root caries and require careful maintenance.

25

3 Medical interview, patient referral, and liaison withmedicine❶ Medical interview
The major reason (chief complaint) for the patient’s visit, and particularly their wish for periodontal therapy,
should be determined by asking the patient. This is important for good communication with patients and performance of treatment without problems. Patients with a chief complaint of periodontal disease visit a clinic with astrong wish for treatment, and it is important to assess anxiety, discomfort and subjective symptoms of periodontal disease. For patients with a chief complaint other than periodontal disease, treatment of their chief complaintand direction for them to recognize the periodontal pathology are recommended. For patients with systemic disease to be considered for dental treatment, interview and inspection are necessary to determine systemic healthconditions. Furthermore, it is important to obtain information on periodontal disease-related systemic disease, including diabetes mellitus, obesity, ischemic heart disease, aspiration pneumonia, preterm low weight birth, osteoporosis, and immune/allergic disease, as well as environmental factors (smoking, stress, etc.) and genetic factors.

❷ Referral of patients to periodontal specialists and advanced care facilities
Patients with severe periodontal disease should be referred to periodontists and advanced facilities with therapeutic
information, including medical history and treatment record.

❸ Liaison with medicine
Aging patients with periodontal disease complicated with different systemic diseases have begun to visit dental
clinics. If a patient has a medical history of systemic disease or is currently under treatment, it is necessary to ask
an attending physician to provide medical records. A patient who is suspected to have systemic disease in the interview before periodontal therapy should be referred to a hospital with provision of the available symptoms.
Dentists are required to have the information and knowledge about the type and symptoms of systemic diseases
and prescription drugs, and should refer patients to appropriate facilities with appropriate timing. With regard todiseases including diabetes mellitus that are deeply involved in onset and progression of periodontal disease (seePage 52 “❷ Periodontal therapy for patients with other diseases”), it is preferable to interact with attending physicians to share respective symptoms and treat patients.

1）Disease state and drugs administered
If a patient is suspected to have drug-induced gingival hyperplasia due to phenytoin (antiepileptic drug, hydantoin), nifedipine (antihypertensive, calcium antagonist) or cyclosporine (immunosuppressant, calcineurin inhibitor),
the patient is informed of this possibility and the effect of the prescription drugs is communicated to the attending physician. Close coordination with the attending physician is important to allow a decision on possible drug
replacement based on a mutual understanding of the patient. Bisphosphonate (BP) drugs and anti-receptor activator of nuclear factor kappa-B ligand (RANKL) antibody products are used for treatment of osteoporosis and bonemetastasis (bone modifying agents: BMA). Osteonecrosis of the jaw (ONJ) is an adverse event caused by theseagents. Appropriate oral control decreases onset of ONJ during BMA treatment1, 2), and it is recommended that all
patients undergo dental examination before BMA treatment and preventive dental procedures3). Therefore, physicians ask dentists about these agents and an appropriate therapeutic strategy should be designed in cooperation
with each other.

262）Precautions for invasive treatment in the oral cavity
Dentists provide information on diagnosis of periodontal disease and treatment details, and particularly invasive
procedures including extraction, subgingival scaling and root planing (SRP), in initial periodontal therapy. The
type and dose of local anesthetics scheduled, use of adrenaline and surgical time are added. Invasive dental procedures including extraction are performed without withdrawal of antiplatelet agents and anticoagulants when possible.

27

4 Examination, diagnosis and therapeutic strategy forperiodontal disease❶ Periodontal disease examination
The objectives of this examination are to find the progression stage and causes of periodontal disease and obtain
information to make a correct diagnosis and plan an appropriate therapeutic strategy. It is important to conduct
examinations systematically for patients, analyze the results, and plan or revise the therapeutic strategy based onthese results. Examinations are also necessary to evaluate the conditions of periodontal tissues in SPT and maintenance. Examination results should always be described in medical records to facilitate planning of the therapeuticstrategy and compare with re-evaluated results.

1）Periodontal tissue examination
A periodontal tissue examination includes the following items.

（1）Gingival inflammation

Gingival inflammation is evaluated with the gingival index (GI)1) and bleeding on probing (BOP)2,3).

（2）Probing depth

The standard method is to measure one tooth at 6 measurement points (6 points method), with the number ofmeasurement points increased or decreased as required.

（3）Attachment level (AL)The attachment level is the distance from the baseline such as the cement enamel junction (CEJ) to the pocketbase and is measured using a periodontal probe as an indicator of the status of progression and improvement of
periodontal disease. The standard approach is to use the 6 points method, with the number of measurement
points increased or decreased as required.

（4）Periodontal epithelial surface area (PESA) and periodontal inflamed surface area (PISA)
Quantitative evaluation of the periodontal epithelial surface area (PESA) and periodontal inflamed surface area
(PISA) gives values for the severity of periodontal disease and inflammatory expansion. The clinical attachmentlevel (CAL) of periodontal pockets, gingival recession volume and BOP are used for estimation (http://www.perio.
jp/member/news/file/info_200210_pisa_format.xls). These values are effective as indicators to investigate relationships between periodontal and systemic diseases.

（5）Oral hygiene conditions (O’Leary plaque control record)
Bacterial plaque-attachment conditions are recorded and evaluated using plaque charts. A tooth is divided into
four regions, mesial, distal, labiobuccal and lingopalatal sides, and a plaque-sensing agent is used to determine ifbacterial plaque is present in the tooth cervix of each side4).

（6）Tooth mobility

Tooth mobility is measured using the Miller classification of tooth mobility: Grade 0 (physiological movement<0.2 mm), Grade 1 (slight: labiolingual 0.2-1 mm), Grade 2 (moderate: labiolingual/mesiodistal 1-2 mm), andGrade 3 (high: labiolingual/mesiodistal >2 mm or vertically choreatic movement).

（7）X-ray images

Digital dental X-ray images or panoramic X-ray images are normally used and a combination of these images canalso be used, as required. The number of radiographs is variable. Cone-beam computed tomography (CBCT) provides a three-dimensional structure of periodontal tissues. CBCT is an excellent procedure for finding the bone
defect type and the relationship with periapical lesions.

（8）Occlusion

The occlusal relation in whole tooth alignment (e.g. malocclusion) and traumatic occlusion due to premature con-

28

tact and cuspal interference are examined (see Page 29 “ ❷ Diagnosis of periodontal disease”).

（9）Furcation involvement

Furcation involvement in multi-(double-) rooted teeth is examined using a furcation probe and a roentgenogram,with progression classified into 3 grades (Lindhe & Nyman’s furcation classification) or 4 grades (Glickman’s furcation classification).

a）Lindhe & Nyman’s furcation classification5)

This is a procedure for examining the degree of horizontal destruction of periodontal tissues in furcation. Degree I:
Horizontal destruction of periodontal tissues not exceeding one-third of the width of the tooth. Degree II: Horizontal destruction of periodontal tissues exceeding one-third of the width of the tooth, but not encompassing thetotal width of the furcation area. Degree III: Horizontal through-and-through destruction of the attachment in
the furcation, and buccolingual or mesiodistal penetration of the periodontal probe.
b）Glickman’s furcation classification6)

Grade I: Early bone resorption in the furcation area. Grade II: Disruption and resorption of the alveolar bone in
the partial furcation area, but no penetration of the periodontal probe through the furcation area. Grade III: Resorption of bone beneath the furcation area and buccolingual or mesiodistal penetration of the periodontal probe,
but the furcation area covers the gingiva. Grade IV: Exposed furcation area in the oral cavity and complete penetration of the periodontal probe.

（10）Plaque retention factors
Factors accumulating and increasing plaques to be examined include calculus, faulty dental restoration, caries,
wedge-shaped defect, tooth malalignment, abnormal gingiva and alveolar mucosa, abnormality of frenulum, abnormal oral vestibule, mouth breathing, dental morphological abnormality, food impaction, and periodontal
pocket.

（11）Oral photography
Oral photography provides a record of the oral status that is difficult to record in words or as a figure. Photography is performed at 5 points: frontal, right and left molars, and maxillary and mandibular occlusions. Four lingopalatal sides of the molar are sometimes added, giving 9 points in total.

（12）Study model

Tooth malalignment, attrition and soft tissue morphological abnormalities are examined in a study model.

2）Microbiological assays（1）Bacterial test

Subgingival plaque or saliva samples are collected to examine periodontopathic bacteria such as P. gingivalis and A.
actinomycetemcomitans. Polymerase chain reaction (PCR) analysis and the PCR invader method are used in bacterial tests. The procedure for determining bacterial enzymes, a chair-side test, does not identify bacterial species,
but is used as a convenient method. Bacterial test kits using a monoclonal antibody for P. gingivalis are also underdevelopment.

（2）Serum bacteria-specific antibody titer test
An enzyme-linked immunoassay (ELISA) is used to determine serum antibodies against periodontopathic bacteria
and shows sensitivity to bacteria. Increased serum antibody titers against these bacteria show the history of bacterial infection or infection on testing7).

（3）Quantitative measurements of oral bacteria
Samples collected from the saliva or upper tongue are used to count oral bacteria to understand contamination of
the entire oral cavity, using a chair-side instrument.

293）Other examinations（1）Gingival crevicular fluid (GCF) test (fluid from periodontal pockets)
Periodontal disease activity at sampling sites is examined by testing the fluid volume or free hemoglobin, aspartate
aminotransferase (AST), elastase, bacteria-derived enzymes, and cytokines.

（2）Saliva test

Periodontal disease activity in the whole oval cavity is examined by testing salivary occult blood, free hemoglobin,
lactate dehydrogenase (LDH), AST, and alkaline phosphatase (ALP).

（3）Blood test

If a patient with aggressive periodontitis is suspected to have leukocyte dysfunction, blood tests including blood
cell morphology and blood biochemistry are conducted.

4）Psychological, social and behavioral assessment
In addition to surgeon-driven examination of the above-mentioned biomedical parameters, patient-centered psychological, social and behavioral assessments are introduced to evaluate periodontal therapy. For example, oral-related quality of life (QOL) scales are used8-10).

❷ Diagnosis of periodontal disease1）Diagnostic procedure for plaque-induced gingivitis and periodontitis
Plaque-induced gingivitis and periodontitis are diagnosed using the classification of periodontal disease (see Page
10). First, the cause of periodontal disease is roughly identified: [1] systemic factors, [2] traumatic occlusion, and[3] lifestyle. Next, each tooth unit is diagnosed with plaque-induced gingivitis or periodontitis. Based on these diagnoses, a patient is identified as having plaque-induced gingivitis or periodontitis. Periodontitis is further diagnosed as slowly progressive chronic periodontitis, rapidly progressive aggressive periodontitis, or periodontitis associated with a genetic disorder (Figure 4). The disease is also identified as localized or generalized, and slight,
moderate or severe.

（1）Diagnosis by tooth unit (Figure 3)
Gingival inflammation without and with attachment loss is diagnosed as plaque-induced gingivitis and periodontitis, respectively. The degree of tissue disruption and inflammation is also considered in diagnosis.
a）Periodontitis classification by degree of tissue disruption• Slight periodontitis has a bone resorption level (bone level: BL) <15% or an attachment level (AL) <3 mmand no furcation involvement (Stage I).
• Moderate periodontitis has BL ≥15% or AL ≥3 mm to <5 mm and furcation involvement (Stage II).
• Severe periodontitis has BL ≥33% or AL >5 mm and furcation of grade 2 (Stage III, IV).
b）Periodontitis classification by inflammation severity• Slight periodontitis has a probing depth <4 mm (Stage I)• Moderate periodontitis has a probing depth ≥4 mm to <6 mm (Stage II)• Severe periodontitis has a probing depth ≥6 mm (Stage III, IV)c）Diagnosis of periodontitis by tooth unit

The diagnostic classification is based on the degree of tissue disruption and inflammation severity.

（2）Diagnosis at individual levels (Figure 4)a）Diagnosis by disease type

• A patient with teeth with plaque-induced gingivitis and periodontitis is diagnosed with periodontitis.
• The effect on periodontal disease is assessed based on the presence of systemic disease, familial onset, smoking
and stress.
• Disruption of periodontal tissues that is slower than that in the same age group is diagnosed as chronic peri-

30

Bacterial plaque attachment to the tooth surface

No

No

Yes

Yes
p
BL: <15%or
AL: <3 mm%/DQG
or$/PPDQGPP%/
or$/PP

PD:
<4 mm

PD:
PPDQGPP

Yes

Patient
atient with periodonti
periodontiti
periodontit
periodontitiss
associated withge et
ge
genetice c ddisorders
so de sPD:
PP

Figure 3. Diagnosis of plaque, induced gingivitis and periodontitis by tooth unit
PD: probing depth; BL: bone level; AL: attachment level

Healthy person

Patient
atient with plaqueplaque-induced gingivitis
g g

Confirmation of systemic factors
Periodontal tissue examination

Plaque-induced gingivitis:no affected tooth
Periodontitis: noaffected tooth

Periodontitis:
DIIHFWHGWRRWK

Diagnostic result
by tooth unit

Patient withperiodontitis

Plaque-induced gingivitis:
DIIHFWHGWRRWKNo

Disruption rate ofperiodontal tissues in comparison
with age

RapidpCharacteristics•0RVWSDWLHQWVDJHGVWRV•Bacterial plaque and calculus:
relatively small•Familial clustering: Yes

Slow
Characteristics•Aged 35 years and older•Bacterial plaque and calculus: many
Patient withchronic periodontitispPatient withaggressive
ggressive periodonti
periodontiti
periodontit
periodontitis

Attachment loss in thefirst molar or incisors of
2 teeth or more

Affected site

Systemic disease ĺ Periodontitis associatedwith systemic diseases
Smoking ĺ Periodontitis associated with smoking
Periodontitis associated with other risk factors

Range
R
g off
moderate/severepperiodontitis

Attachment loss in thefirst molar and 3 teethor more, other thanincisors<30% ofall sitesRI
all sites<30% ofall sitesRI
all sites

Localized

Generalized
Generalized

Localized

Generalized

Diagnostic result
by tooth unit
Most advanced toothas reference

Mild

Figure 4. Diagnosis of plaque-induced gingivitis and periodontitis at individual levels

Moderate

Severity

31

odontitis and that with a more rapid rate is diagnosed as aggressive periodontitis.

b）Progression of periodontitis• A patient with slight, moderate and severe periodontitis is diagnosed with severe periodontitis, which may bedescribed as “generally moderate and partially severe”.
• In diagnosis of chronic periodontitis by tooth unit, classifications of localized and generalized periodontitis areused if the number of teeth with moderate and severe periodontitis is <30% and ≥30%, respectively.
• Similarly, in diagnosis of aggressive periodontitis, classifications of localized and generalized periodontitis areused if the number of teeth involved is <30% and ≥30%, respectively. However, the AAP Consensus Report11)
indicates that a patient with attachment loss in the first molar or 2 incisors or more (at least one tooth is thefirst molar) has localized periodontitis and a patient with attachment loss in at least 3 teeth other than the firstmolar and incisors has generalized periodontitis. It is important to classify patients based on consideration ofthese definitions.

c）Periodontitis severity of the whole oral cavity• Periodontitis severity by individual is estimated based on progression by tooth unit and the number of affected teeth because the severity is identified by diagnosis of the oral cavity unit.

2）Diagnostic procedure for occlusal trauma
Occlusal trauma is injury in the deep periodontal tissues (cementum, periodontal ligament and alveolar bone) andis classified into primary occlusal trauma caused by excessive bite force to healthy periodontal tissues and secondary occlusal trauma caused by decreased supporting alveolar bone due to periodontal-induced periodontal disruption. Occlusal trauma is a diagnostic term used for each tooth unit. A tooth with occlusal trauma of tooth mobility Grade 1 or higher and enhanced cavity of the periodontal ligament and bone resorption on intraoral X-ray isdiagnosed with occlusal trauma. Other findings include [1] excessive attrition, [2] pathological tooth migration,[3] tooth fracture, [4] lamina dura defect and hyperplasia, and [5] root resorption on X-ray.

❸ Therapeutic strategy planning (see Figure 2)
The therapeutic strategy uses the best approach for the required treatment and outcomes based on diagnostic results, combined with the patient’s chief complaint and the surgeon’s technical capability. After planning this strategy, it is necessary to give a clear and detailed explanation to the patient, including disease and treatment details.
The therapeutic strategy depends on the severity of periodontal disease. The basic periodontal therapy approach isshown below.

1）Basic periodontal therapy (cause elimination)
Basic periodontal therapy consists of plaque control, scaling, root planing, elimination of plaque retention factors,
occlusal adjustment, and temporary splint. This is cause-related therapy and is performed in all patients with periodontal disease.

2）Reassessment after basic periodontal therapy
Reassessment uses the same items as the first dental examination, in principle. Comparison of the results of these
examinations provides feedback to the patient and an understanding of the correct pathology and helps to judge
the outcomes and revise the therapeutic strategy. In particular, it is important to examine gingival inflammation,
depth of periodontal pocket, oral hygiene conditions, tooth mobility, and furcation involvement. These results
may show that basic periodontal therapy cannot cure the periodontal disease, and the next steps of periodontal
surgery and procedures for furcation lesions can be planned as a revised therapeutic strategy, with informed consent from the patient after an explanation. For periodontal surgery, maintenance of at least 20% of O’Leary32

plaque control, no inflammation including gingival redness, and no smoking are recommended.

3）Periodontal surgery
If an active periodontal pocket ≥4 mm remains after basic periodontal therapy or periodontal tissues disrupted byperiodontal disease are to be regenerated, periodontal surgery is considered. This surgery is roughly classified into
tissue attachment therapy, resective therapy, periodontal regenerative therapy, and periodontal plastic surgery. If
tissue regeneration is needed, periodontal regenerative therapy is considered, whereas gingival recession and oral
vestibule are treated by periodontal plastic surgery. It is preferable to refer a patient to a periodontal specialist if
difficulties are encountered with dental surgery.

4）Reassessment after periodontal surgery
After periodontal surgery, necessary examinations are conducted again to assess healing status. It takes about 4
weeks (depending on surgical type) for wound healing and an examination about 4 weeks after surgery is recommended. If occlusal function needs to be restored earlier, partial reassessment of operative sites is conducted about
4 weeks after surgery. The items in partial reassessment are gingival inflammation, periodontal pocket depth, attachment level and furcation involvement. If the therapeutic effect after reassessment is insufficient, the causes areanalyzed and repeated basic periodontal therapy and periodontal surgery are considered.

5）Oral rehabilitation
Restorative and prosthetic therapy is required to restore oral functions (e.g., occlusion, mastication, dental esthetics, articulation function) after basic and periodontal surgery. Decreased periodontal supporting tissues requires
fixation. The main devices (crown, bridge, denture and implant) are designed to avoid development of occlusal
trauma or bacterial plaque. Orthodontic treatment improves malalignment, plaque retention factors and traumatic occlusion, increases the effect of periodontal therapy, and restores esthetic outcomes.

6）Reassessment before follow-up
This examination is performed as in the first dental examination, in principle. Based on these results, the need for
repeated basic periodontal therapy and periodontal surgery is determined. If this is not necessary, the patient is assessed to be in a “stable state”, “preventive stage” or “healing” and transferred to SPT, PPT or maintenance therapy.

7）Supportive periodontal therapy (SPT)In a case in which basic periodontal therapy, periodontal surgery and oral rehabilitation are complete, and mostperiodontal tissues are cured, but periodontal pockets in the progression-resting stage remain, SPT is performed
for long-term stabilization of the disease stage of periodontal tissues. The main therapy includes plaque control,
scaling, root planing and occlusal adjustment to eliminate causal factors, and instructions on oral hygiene and remotivation are added.

8）Preventive periodontal therapy
Preventive periodontal therapy (PPT) is treatment to suppress progression of periodontal disease because patientswith a probing depth <4 mm but slight gingival inflammation in reassessment after completion of periodontal
therapy are likely to be under progression. PPT includes maintenance of motivation, enhanced plaque control,
scaling, root planing and professional mechanical tooth cleaning.

339）Maintenance
Periodontal disease is likely to recur and routine maintenance, including plaque control, scaling, root planing andocclusal adjustment, is necessary, even in patients with “healing”. Maintenance consists of self-care (home care) by
patients to maintain clinically restored healthy periodontal tissues, motivation to encourage patients to undergo
therapy, and professional care by dental specialists.

34

5 Periodontal therapy and oral biofilm infection in homecare, perioperative patients and disabled persons❶ Home care and periodontal therapy
Many bedridden patients at home, who cannot visit a dental clinic or hospital, have functional impairments suchas cerebral infarction sequelae, heart disease and lower hemiparesis. A long-term bed-ridden status causes joint
contracture, muscular atrophy and dementia, often resulting in reduced mental and physical performance. Therefore, it is important for patients with normal mastication function to perform oral care to maintain oral healthand QOL, including mental activity. Patients with swallowing hypofunction require oral care, including feeding
and swallowing training, to prevent aspiration pneumonia, and instructions to caregivers are also necessary1). Since
these home care patients have difficulty undergoing periodontal tissue examination and radiography, inquiry andinspection play a role in planning the therapeutic strategy. Oral contamination level is assessed by bacterial countwith quantitative measurements of oral bacteria or tongue coating index (TCI). Periodontal tissue examination
includes inspection of gingival inflammation and soft tissues, tooth mobility and probing depth, if possible. In allcases, dentists need to coordinate with physicians, nurses, dental hygienists, care workers and caregivers for improvement of the oral environment2). Treatment depends on the environment at home and the mobility of thefingers of patients.

1）Self-care
In addition to self-care, patients should receive oral hygiene instructions by dental hygienists, nurses, care workers
and caregivers under a dentist’s instructions, and control oral hygiene with scaling supragingival plaques, mouth
washing with agents and oral care devices (e.g. sponge). Patients can also improve their oral environment with atemporary splint and occlusal adjustment, as required.

2）Partial support for oral care

If a clean environment can be maintained, the procedures are almost consistent with those described in 1）. If aclean environment cannot be maintained and patients cannot stay in a sitting position, oral hygiene control using
a toothbrush, etc. is routinely performed by nurses, dental hygienists, care workers and caregivers (patient’s family)
under a dentist’s instructions. Initial periodontal therapy is also performed, depending on the circumstances.
Much attention should be paid to aspiration during oral hygiene control (narrow-sense oral care).

3）Full support for oral care
Regardless of the oral hygiene environment, oral hygiene control using a toothbrush, etc. is routinely performedby nurses, dental hygienists and care workers under a dentist’s instructions. Local administration of agents to periodontal pockets is also considered, as required. Oral hygiene control is instructed to daily caregivers to maintainclean oral conditions as much as possible. In this situation, much attention should be paid to aspiration during
oral hygiene control (narrow-sense oral care).

❷ Perioperative patients and periodontal therapy
For patients who undergo cancer therapy and major surgery, treatment of periodontal disease and chronic infectious disease probably reduces postoperative complications. Therefore, perioperative (preoperative, intraoperative,
postoperative) intraoral control is important. In addition to surgical therapy, radiotherapy and pharmacotherapy

35

are used in cancer therapy. Intraoperative and postoperative complications are likely to occur, and maintenance ofthe oral environment is required. Information sharing and cooperation between physicians and dentists are essential for cancer therapy.

1）Oral function control before surgery (treatment)
Periodontal disease with inflammatory conditions often causes bacteremia, resulting in oral bacteria including
periodontopathic bacteria spreading to the whole body. This is a particular risk for infective endocarditis after
heart valve replacement. Before any major surgery, antibiotics combined with appropriate oral hygiene procedures
are necessary as measures against oral bacterial infection. In radiotherapy for craniocervical regions, it is necessary
to apply fluoride before radiotherapy to prevent dental caries, and is also necessary to remove restoration overhangs or dental calculus that may irritate soft tissue. Cancer-related osteonecrosis of the jaw (ONJ) after radiotherapy in the craniocervical region, and ONJ related to Bone-Modifying Agent (BMA) administration is a severe
adverse event. It is important to perform periodontal therapy before treatment and reduce as many inflammatory
risk factors as possible. Patients who undergo hematopoietic stem cell transplantation sometimes develop bacteremia caused by oral bacteria. Dental disease control including periodontal therapy before surgery reduces severe
oral mucositis and decreases the disease duration of febrile neutropenia.

2）Oral function control during and after surgery (treatment)
Oral hygiene conditions in the perioperative period of major surgery are always exacerbated. Oral hygiene control
before surgery is significant and leads to reduced risks for intraoperative and postoperative aspiration pneumonia
and postoperative complications after oral and pharyngoesophageal surgery. In radiotherapy for the craniocervicalregion, worsening of periodontal disease is a concern, as well as salivation disorder, oral mucositis and trismus. In
chemotherapy, invasive procedures should be performed with consideration of thrombocytopenia and leukopenia
induced by myelosuppression. In cancer radiotherapy and pharmacotherapy, it is important to perform continuous oral hygiene control during and after therapy and prevent oral adverse events and progression of periodontal
disease after therapy.

3）Aspiration and infection in oral hygiene control
Perioperative oral function control (herein oral hygiene control is referred to as narrow-sense oral care) reducesrisks for aspiration pneumonia and improves the postoperative course in the oral cavity and ascending regions. In
contrast, patients who undergo oral care are frequently compromised hosts after invasive surgery, before and after
chemotherapy or radiotherapy, or are immunosuppressed and elderly. Therefore, inappropriate procedures for oral
care and hygiene control with oral care devices induce aspiration pneumonia. To prevent aspiration during oralcare, it is important to evaluate oral contamination conditions using quantitative measurements of oral bacteria(bacterial count) and tongue coating index and to assess patients in cooperation with other healthcare professionals and choose appropriate surgical procedures. Cross infection via oral care has risks for causing nosocomial infection. Studies have shown outbreak of nosocomial infection by multidrug-resistant strains via oral care. Cross infection can be prevented by appropriate hygiene control (cleaning disinfection, sterilization) of devices used fororal care, and introduction and appropriate use of disposable devices (particularly vacuum hoses and tips).

❸ Disabled persons and periodontal therapy
The Japanese Basic Act for Persons with Disabilities defines the term “persons with disabilities” in this Law tomean individuals whose daily life or social life is substantially and continuously limited due to physical, intellectual or mental disability (hereinafter referred to as “disability”) in Section 2. Disabled persons often have difficultywith oral care and their morbidity rates are high because they have various risk factors for periodontal disease, in-36cluding the influence of systemic disease and oral drugs. Furthermore, they have little interest in or understandingof oral care and are sometimes not willing to receive this care. Treatment and care should be performed based on
the disability level and the needs of the patients. Basic periodontal therapy including plaque control and scaling is
performed similarly to that for general patients with periodontal disease. If periodontal tissue examination is difficult, oral care is planned based on the results of quantitative measurements of oral bacteria for oral biofilm infection. If normal treatment is difficult, there may be a need for behavior adjustment procedures (behavior modification, body movement control, sedation, general anesthesia). Disabled persons have limitations of self-care due tocharacteristics of their disabilities and physical handicaps. Professional care by dentists and dental hygienists andoral care by caregivers including their family are important to treat periodontal disease. Periodontal therapy facilitates behavior modification and emotional stability, leading to improved QOL3). The details of each step of periodontal therapy are described below.

1）Therapeutic strategy planning
It is important for disabled persons themselves and caregivers to plan a reasonable therapeutic strategy. A feasible
strategy should be planned from the viewpoint of “prevention of exacerbation” rather than “complete remission”
considering the characteristics of the disabled person.

2）Initial periodontal therapy
Brushing instructions and initial periodontal therapy should be appropriately performed after analyzing and assessing the patient’s level of disabilities (cognitive, motor and affective functions required for tooth brushing).
However, self-care alone is insufficient and it is important to control inflammation by supragingival/subgingival
plaque control by professionals and brushing by a caregiver. A combination of full-mouth scaling, root planingand oral antibiotic therapy has been reported to give clinical and bacteriological improvement in patients with intellectual disabilities and severe periodontitis4). These patients may have systemic disease, which depends on the
disability level, and adverse reactions of oral drugs and infection should be considered.

3）Periodontal surgery
Periodontal surgery requires good oral hygiene conditions; therefore, a patient without sufficient oral cleansing
cannot undergo surgery due to recurrence. Periodontal surgery should be carefully conducted because plaque control can sometimes become more difficult with this surgery.

4）Oral rehabilitation
Although treatment depends on the disability level, easy-to-clean fixed prosthetic devices are preferable because
denture is difficult to manage by oneself.

5）Maintenance, preventive periodontal therapy (PPT) andsupportive periodontal therapy (SPT)
Bacterial flora in pockets return to previous conditions for 1-2 months if plaque control is poor. Therefore, a shortinterval is preferable to restart maintenance, PPT and SPT. Professional care should be performed continuously toprevent progression or recurrence of periodontal disease. It is important to make patients and their caregivers understand the necessity of continuous oral care.

37❹ Oral biofilm infection
Patients in home care, perioperative patients, disabled persons and elderly people described above require control
of oral function and hygiene, but some have difficulties with periodontal tissue examination. These patients areevaluated by quantitative measurements of oral bacteria (count of oral bacteria using a chair-side instrument) or
assessment of oral contamination using the tongue coating index5) for oral biofilm infection. These results are used
for diagnosis of oral biofilm infection (general term for disease caused by biofilms in the oral cavity and influencing the oral cavity or whole body) and to prevent severe oral biofilm infection and onset of systemic disease6) (Table 8).
Table 8. Assessment criteria for oral biofilm infection
Tongue coating: TCI(%)

Count of oral bacteria Gingival inflammation(CFU/mL)
statusRisk

Oral biofilm infection

≥50%

≥108

+++

Critical region

Poor

≥40%

≥107

++

Attention region

Stable

<40%

<107

±

Normal range

38

6 Emergency procedures❶ Identification of cause of pain
Improvement of pain is the highest priority in patients with a chief complaint of pain induced by periodontal disease. Local factors are acute attack of gingival abscess and periodontal abscess and combined periodontic-endodontic lesions. Abnormal bleeding and pain not related to local factors are considered to be systemic factors.
Leukemia-associated gingivitis, necrotizing ulcerative gingivitis, periodontitis, aphthous stomatitis and hemorrhagic desquamative gingivitis with lichen planus in the marginal gingiva are particularly involved in decreased
systemic resistance. Treatment requires cooperation with physicians.

❷ Treatment of acute inflammation (see Page 42, Figure 6 [3])Patients who visit a clinic with a chief complaint of pain, frequently have localized acute inflammation. A subgingival mechanical approach alone does not always have a sufficient effect on acute inflammation. Antibiotic use iseffective for suppressing inflammation and facilitating periodontitis healing. In an acute attack of gingival abscessand periodontal abscess, occlusal conditions are confirmed and occlusion is adjusted as required. Furthermore,
periodontal pockets, which are possible causes, are thoroughly cleaned and an abscess with marked fluctuation isincised. A local drug delivery system (LDDS) using slow-release drug can be combined with periodontal pocket
cleaning1). A LDDS is convenient due to its prompt effect and easy-to-use procedures. Refer to “Guidelines forappropriate use of antibiotics in patients with periodontal disease 2020” (edited by the JSP). If an abscess withfluctuation is in a combined periodontic-endodontic lesion, the abscess is incised for drainage. Antibiotics are administered and endodontic treatment is performed early as required. Early non-chronic combined periodontic-endodontic lesions are likely to be improved, while prolonged periodontal-endodontic lesions with remaining
periodontal pockets are treated by subgingival SRP. Patients with marked tooth mobility are treated with a temporary splint.

39

7 Preventive treatment❶ Prevention of transition from plaque-induced gingivitis to periodontitis
The 2016 Dental Disease Survey showed that the number of 15- to 25-year-old patients with periodontal pockets≥4 mm has rapidly increased1). Since plaque-induced gingivitis is transferred to periodontitis in these patients, appropriate preventive procedures for periodontal disease inhibits transfer from gingivitis to periodontitis. Persons
aged 40 years or more often have periodontal disease. Therefore, appropriate preventive care from age 15 to 25
years is significant for substantial reduction of patients with periodontal disease. Periodontal disease is a bacterial
infection; therefore, both self and professional care are important. Furthermore, it is lifestyle-related disease andcommunity care for local groups, students and personnel is also important. Preventive procedures during this period include periodontal tissue examination, oral hygiene instruction, mechanical tooth cleaning and scaling. Prevention of periodontal disease is closely related to treatment; therefore, routine primary and secondary prevention
is necessary to prevent progression to periodontitis.

❷ Preventive treatment for pregnant women(see Page 54 “2）Periodontal therapy for pregnant women”)

Pregnant women are likely to have poor oral hygiene control due to the changed oral environment caused by hormone imbalance and hyperemesis gravidarum, resulting in pregnancy-associated gingivitis and onset or deterioration of periodontitis. Chronic inflammatory conditions in the oral cavity may result in release of various chemical
mediators in blood, leading to increased preterm delivery and low birth weight infants. At present, municipalities
conduct dental examinations for pregnant women and those who are found to have periodontal disease are advised to visit a dental clinic. Early detection and treatment are important, but preventive procedures are more important. Routine preventive procedures for pregnant women include periodontal tissue examination, oral hygiene
instructions, mechanical tooth cleaning, scaling, scaling root planing and occlusal adjustment, and health guidance. These procedures are also recommended for women planning pregnancy. Refer to pages 28-37 of “Periodontal disease and general health” (edited by the JSP).

40

8 Initial periodontal therapy❶ Concepts of initial periodontal therapy (Figure 5)
Initial periodontal therapy is treatment to eliminate etiological and risk factors for periodontal disease, improveinflammation in periodontal tissues, and enhance the effect of periodontal therapy, leading to successful therapy.
Therefore, etiological and risk factors for periodontal disease require clarification, and systemic problems and patient background and lifestyle should be considered. A medical interview and cooperation with physicians are important and medical test data should be fully understood. Based on these results, the pathology is diagnosed and atherapeutic strategy to eliminate causes is planned. Sensitivity to periodontal disease affects the duration of periodontal therapy, and understanding systemic conditions is important to predict the reaction to periodontal therapy and the effects of periodontal disease on the whole body.

❷ Strategy for initial periodontal therapy1）Therapeutic strategy and process of initial periodontal therapy
It is important to plan a comprehensive therapeutic strategy based on patient background and systemic conditions. The severity of etiological and risk factors should be identified and the major items in initial periodontal
therapy determined. Generally, disruption of periodontal tissues and plaque control conditions are the focus; consequently,
y brushing instructions and SRP take priority. However, efficient initial periodontal therapy can be performed by prioritizing etiologic and risk factors.

2）Therapeutic strategy focusing on bacterial infection and inﬂammation

Detailed treatment contents (Figure 6) include [1] bacterial plaque-attached conditions; [2] plaque retention factors; [3] acute inflammation and probing depth; and [4] periodontopathic bacteria tests and antibody titer tests.

❸ Treatment of bacterial infection

1）Plaque control is a high priority in all therapies
The major causes of plaque-induced gingivitis and periodontitis are supragingival and subgingival bacterial
plaques1). Elimination of bacterial plaques, the main causes of plaque-induced gingivitis and periodontitis, is thegFigure 5. Concept of initial periodontal therapy

41

Figure 6 [1]. Initial periodontal therapy for bacterial plaque-attached conditions

Malalignment

Supragingival Subgingival

Figure 6 [2]. Initial periodontal therapy for plaque retention factors

basis of treatment and prevention of periodontal disease. Insufficient plaque control in periodontal therapy substantially decreases the effects of dental therapy, including SRP, temporary splint and periodontal surgery, resulting
in failure of periodontal therapy itself. Good plaque control is useful for healing after periodontal surgery and prevention of tissue inflammation2), and desirable clinical results are obtained in tissue regenerative therapy3). On theother hand, self-care of oral hygiene control (not including routine control) does not frequently include cause-related therapy, which cannot be considered to be an effective approach to periodontal therapyy4,5).
Periodontal therapy maintains good oral hygiene conditions and inhibits progression of periodontitis6,7). There-

42

Yes

No

Figure 6 [�]. Initial periodontal therapy considering acute in�a��ation and probing depth(LDDS: local drug delivery system, TBI: tooth brushing instruction, SC: scaling; SRP: scaling and root planing)

(+)
(++)

(-)

(-)or(+)

Figure 6 [4]. Initial periodontal therapy using a periodontopathic bacteria test and antibody titer test
(SRP: scaling and root planing; LDDS: local drug delivery system)

fore, periodontal therapy depends on plaque control and instructions are given throughout periodontal therapy(from the beginning to SPT). Plaque control is successfully completed by cooperation among dental staff and patients. Plaque control is roughly classified into self-care by patients and professional care by dental specialists. Bacterial plaque is likely to attach in the current dietary environment; therefore, health guidance including improvement in dietary habit is needed. If a patient has difficult sites for elimination of bacterial plaque (e.g., inside aperiodontal pocket) or cannot eliminate plaque, dental staff take the initiative to eliminate supragingival and subgingival bacterial plaques. If plaque retention factors including supragingival and subgingival calculus and faulty
dental restoration are found, they should be improved.

43（1）Motivation
Motivation is essential to make patients complete plaque control and for periodontal therapy to be successful.
Therefore, credibility with patients is necessary to promote understanding of the importance of oral health and theeffect of periodontal disease on the whole body. It is necessary for patients to understand that plaque removal isindispensable for recovery and maintenance of oral health. Specifically, it is important to inform patients of theiroral conditions (pathology) based on the results of periodontal tissue examinations, bacteria tests and others, explain the relationship between bacterial plaque and periodontal disease, and show them that bacterial plaque is a
microorganism using a phase-contrast microscope. In addition, patients should be shown the effect of plaque control on changes in gingival inflammation and periodontal pockets visually. Motivation generally decreases overtime; therefore, repeated motivation sessions are necessary and effective.

（2）Self-care (supragingival plaque control)

Plaque control is classified into mechanical and chemical control. The basic procedures are mechanical plaquecontrol using a toothbrush and supportive cleaning devices (interdental brush and dental floss), and a combination of mainly mechanical plaque control with chemical control is effective. Chemical plaque control is used forregions in which mechanical control cannot be used immediately after periodontal surgery, and is useful for regions in which mechanical procedures cannot be used. Instructions for improving lifestyle are given as required todecrease soft food that increases bacterial plaque and to eat self-cleaning high-fiber foods. Patient education, oral
hygiene and health instructions are required to make such plaque control procedures successful. Specifically, it isnecessary to make patients understand the importance of plaque control by themselves (motivation) and givethem practical cleaning procedures (brushing). Self-care by patients is the basis of periodontal therapy, and has agreat effect on the success of this therapy and is important for maintaining stable periodontal tissues after therapy.

（3）Instructions for brushing

Instructions for brushing should be repeated, similarly to motivation, and these are combined for most patients.
Toothbrushes suitable for a patient’s oral conditions (e.g. dentition size, teeth alignment, gingival condition, regions difficult to clean, defects, type and form of restoration and prosthetic device) and technical level are chosen
and instructions on effective brushing are given. Technicians must fully understand the characteristics of various
brushing methods, understand a patient’s conventional brushing method and oral conditions, and give brushing
instructions. Technicians choose an appropriate and effective cleaning instrument (interdental brush, dental floss,
electric, sonic and ultrasonic toothbrush). Instructions are given gradually in order and changed according to thepatient’s motivation and technical level. Instructions should not be stereotypical and should be patient-oriented.
The effect of instructions is improved by showing and explaining changes in a plaque chart and improved gingival
conditions to patients. For patients with periodontal disease, oral hygiene control using a cleaning instrument including an interdental brush and dental floss are effective; therefore, it is important to give instructions for appropriate use8).

（4）Professional care (supragingival and subgingival plaque control)
Self-care is most important, but when patients have regions with insufficient oral hygiene control due to oral conditions and technical brushing problems, technicians eliminate bacterial plaque on the tooth surface and prostheses and simultaneously remotivate and reinstruct for oral hygiene control at the patient’s visit9). Professional care isreferred to as professional tooth cleaning (PTC) or professional mechanical tooth cleaning (PMTC).

2）Scaling and root planing
Scaling and root planing are extremely important procedures, in addition to plaque control, for periodontal therapy, and are performed during initial periodontal therapy and periodontal surgery and SPT. Scaling mechanicallyeliminates supragingival and subgingival bacterial plaque attached to teeth, calculus and other prostheses using
various scalers. Calculus is calcified bacterial plaque. It has a crude surface and is attached to many bacterial
plaques. Therefore, calculus is the most important local plaque retention factor. The objectives of scaling are to44eliminate factors attached to bacterial plaques and build an environment in which bacterial plaque is easily eliminated by technicians and patients. Root planing eliminates pathologic tooth substances (mainly cementum) including bacteria on root surfaces and other metabolites using various scalers, produces lubricant tooth roots without biological hazard, and enhances attachment between the gingiva and roots. Scaling and root planing are
performed in series as SRP.

（1）Significance and objective of scaling and root planing (SRP)
SRP decreases bacteria and their metabolites. Subgingival SRP using a curette type scaler is performed for the
tooth surface facing periodontal pockets. The deeper the periodontal pocket, the more complicated the process,requiring appropriate techniques, time and effort. Root planing is unnecessary for gingival lesions because lesions
do not reach the tooth root.

（2）Precautions for SRP
Before starting SRP, bacterial plaque attached to teeth and suspended in periodontal pockets should be eliminated.
Although less than preparation for periodontal surgery, infection control including thorough sterilization and disinfection of instruments is necessary with consideration of systemic pain and past history because SRP involves
invasive procedures. Patients with systemic disease are given antibiotics and antiinflammatory agents, as requiredby bacteremia. After SRP, debridement* including calculus and residual contaminants are cleaned out. There arestudies showing that excessive cementum elimination is not desirable for periodontal therapy10-12).

（3）Importance of sharpening

Use of the blunt edge of a hand scaler is difficult for effective SRP. Such scalers make it difficult to eliminate calculus sufficiently and also cause technician fatigue, resulting in poor efficiency. Therefore, sharpening (grinding) of
the hand scaler is important for successful SRP.

（4）Ultrasonic scalers

Bacterial plaque, calculus and other deposits can be mechanically eliminated using ultrasonic scalers. These scalers
are effective for elimination of supragingival calculus, and improved scaler tips are also available for subgingival
scaling, with high elimination effects for certain regions13). Studies have shown clinical effects similar to those ofhand scalers14,15).

（5）Dentin hypersensitivity after SRP
Elimination of calculus, deposits and infected tooth substances sometimes causes transient dentin hypersensitivity
after SRP. This should be explained to patients in advance. Patients with dentin hyperesthesia should be appropriately treated.

3）Improved plaque retention factors (see Figure 6 [2])Plaque retention factors that are improved by initial periodontal therapy include calculus, faulty dental restoration, caries, wedge shape defects, and mouth breathing. Tooth malalignment, abnormal gingiva and alveolar
mucosa, abnormal frenulum, and a narrow oral vestibule are treated after initial periodontal therapy.

4）Extraction of teeth that can not be saved
Teeth that cannot be saved are extracted in initial periodontal therapy. However, such a tooth that maintains an
occlusal relationship or plays an important role in oral function may be extracted after teeth in other regions aretreated to maintain the occlusal relationship and oral function. If a tooth cannot be evaluated in the initial examination, it is not extracted in initial periodontal therapy and is re-evaluated after completion of this therapy. In
particular, teeth with acute inflammation are likely to have increased movement as periodontal pockets become
deeper. Therefore, these teeth are evaluated after elimination of acute inflammation to diagnose the condition cor* Debridement: procedure for elimination of foreign stimuli and denatured tissues. In periodontal therapy, eliminationof bacterial plaque, calculus, contaminated roots, and inflammatory granulation tissue.

45

rectly. When extraction is performed or scheduled, but teeth in other regions are treated before extraction in initialperiodontal therapy, or extraction is indicated in re-evaluation, it is important to explain to patients and obtain
informed consent because most patients who undergo periodontal therapy want to keep as many teeth as possible.
Even for teeth that clearly require extraction after dentomedical assessment, informed consent is required for extraction.

❹ Current treatment of bacterial infection (Table 9)
1）Mechanical supragingival plaque control

The major oral hygiene control is brushing by patients using a toothbrush. Use of a cleaning instrument including
an interdental brush, dental floss, and electric, sonic and ultrasonic toothbrushes is necessary considering the periodontal severity, treatment period, and the patient’s technique and lifestyle. Scaling and professional mechanicaltooth cleaning are likely to help plaque control and enhance and maintain a patient’s motivation 1). Adjustment
and removal of an incompatible restoration and prosthetic device disturbing supragingival plaque control and occlusion reshaping are performed as required. Subgingival plaque control is combined for periodontal pockets ≥4mm. Supragingival plaque control is essential to maintain the effect of subgingival procedures2).

2）Mechanical subgingival plaque control
SRP is standard treatment for periodontal therapy, but has less therapeutic effect on advanced furcation involvement and complicated or deep infrabony pockets. SRP also has risks of causing attachment loss in periodontal
pockets <3 mm. It is more difficult to eliminate subgingival plaque and calculus as periodontal pockets become
deeper3). Periodontal pockets of depth 5-7 mm have decreases of 1-2 mm and attachment gain of 0.5-1 mm2).

3）Chemical supragingival plaque control
After mechanical plaque control, chemical plaque control is performed using a mouthwash. Effective mouthwashes includes low-concentration chlorhexidine solution, which has inhibitory action on bacterial plaque formation
Table 9. Initial periodontal therapy chosen by diagnostic classification
Mechanical plaque control

Chemical plaque control
Supragingival

Diagnostic
classification

Systemic
control*(medical cooperation)

Subgingival

Application of antimicrobial
and antiseptic agentsSupragingival(brushing,scaling)

Subgingival(scaling androot planing)

Mouthwash

Subgingival
pocket irrigation

Antibiotic therapy
Interpocket
application of
antimicrobial
drug(Local drugdelivery system: LDDS)

Oral
administration

Plaque-induced
gingivitis

▲

●

▲

▲

▲

Chronic
periodontitis(slight)

▲

●

●

▲

▲

▲

Chronic
periodontitis(severe)

●

●

●

●

●

▲

▲

Aggressive
periodontitis

●

●

●

●

●

▲

▲

● : Necessary or recommended treatment▲ : Treatment as required* Control of systemic disease, improved psychosocial stress, dietary modification, instruction for smoking cessation

46

Table 10. Major drugs used for chemical plaque control
Upper limit of theReference
concentration in
Presentation type/the Japan
analysis method/
pharmaceutical
Reference
selected RCTs
affairs guidelines(study period)(as a quasi-drug)

Antibiotics

Product
type

Concentrations ofantibiotics used inEurope and theUnited States

Chlorhexidine
gluconate

Mouthwash

0.12-0.20%−0.67
in QHI

−0.32
in GI

0.05%

systematic review
Meta-analysis 30
RCTs (≥ 4W)

J Clin Periodontol,
39: 1042-1055,
2012.

Essential oil

Mouthwash

0.063% Thymol
0.091% Eucalyptol
0.042% Menthol
0.055% Methyl
salicylate−0.83
in QHI

−0.32
in GI

1% Menthol
0.1% Methyl
salicylate
No other criteria

systematic review
Meta-analysis
7 RCTs (≥ 6W)

J Periodontol, 78:
1218-1228, 2007.

Triclosan/
copolymer

Dentifrice

0.3%/2%−0.48
in QHI

−0.26
in GI

0.1%/NL

systematic review
Meta-analysis
15 RCTs (≥6W)

J Clin Periodontol,
31: 1029-1033,
2004.

Triclosan/
Zinc citrate

Dentifrice

0.2-0.3%/
0.5-1.0%+6- −37%
in QHI+4- −52%
in GI

0.1%/NL

systematic review
6 RCTs (≥6W)

Periodontol 2000,
48: 23-30, 2008.

Triclosan/
Sulfuric acid
pyrophosphate

Dentifrice

0.28-0.3%/
5.0%+2.5−14%+4−24%

0.1%/NL

systematic review
5 RCTs (≥6W)

Periodontol 2000,
48: 23-30, 2008.

Cetylpyridinium chloride

Mouthwash/
Dentifrice

0.05-0.1%−0.42
in QHI

−0.15
in GI

0.01%

systematic review
Meta-analysis
4 RCTs (≥6W)

Int J Dent Hyg,
6: 290-303, 2008.

Tin fluoride

Dentifrice

0.45%−3−33%+1−40%

NL

systematic review
10 RCTs (≥6W)

Int J Dent Hyg,
3: 162-78, 2005.

Amine fluoride/
Tin fluoride

Dentifrice

1,400 PPMF-/
250 PPMF-−3.5−11.8%−4.329.9%

1,000 PPMF-

systematic review
4 RCTs (≥6W)

Int J Dent Hyg,
3: 162-78, 2005.

Sanguinarine

Mouthwash

0.01%+4−33.9%+5−33.8%

NL

systematic review
6 RCTs (≥6W)

Int J Dent Hyg,3:162-78, 2005.

Delmopinol

Mouthwash

0.1-0.2%−9.3−35%+1−18%

NL

systematic review
3 RCTs (≥6W)

Int J Dent Hyg,
3: 162-78, 2005.

Inhibitory effectof the drug at thisconcentration onplaqueInhibitory effectof the drug at thisconcentration inperiodontitis

RCT: randomized controlled trial; QHI: Quigley & Hein Plaque Index, GI: Gingival Index; NL: not listed in the quasi drug additives list PFSB/MHLW
0327004, March 27, 2008.Cited from reference5)

and a depositing action on the tooth surface. Phenols, povidone-iodine, cetylpyridinium chloride, and essential
oils are also used4). In initial periodontal therapy, continuous use for 2-4 weeks after scaling prevents regrowth ofperiodontopathic bacteria (Table 10)5).

4）Chemical subgingival plaque control
Precautions for chemical subgingival plaque control are [1] complete supragingival plaque control in advance, [2]give priority to mechanical plaque control, and [3] an understanding that chemical plaque control is not neededin most cases of chronic periodontitis and in regions with a good response to SRP.

（1）Subgingival pocket irrigation

The subgingival pocket is irrigated with drug solution using a syringe. Drugs available for subgingival pocket irrigation are povidone-iodine, benzethonium chloride, oxydol and acrinol. A combination of these drugs with SRP
has clinical effects, whereas the effect of subgingival pocket irrigation alone is limited.

（2）Interpocket application of antimicrobial drug

Drugs for periodontal pockets include sustained-release tetracycline antibiotic ointment6-8), which is used for local
drug delivery. The indications and usage are once per 1-2 weeks, continuously 3-4 times for [1] periodontal abscess (acute symptom of periodontitis), [2] immunocompromised patients with periodontitis (including diabetes),[3] combination with SRP for moderate or severe periodontitis, and [4] periodontal pockets not improved by ini-

47

tial periodontal therapy. However, incorrect administration may induce microbial substitution and antimicrobial
resistance, and there has been no validation of repeated administration of antibiotics in SPT.

（3）Oral administration of antimicrobial agents

Oral administration of antibiotics is considered for patients with periodontitis that is not improved by initial therapy, patients who cannot undergo invasive treatment, immunocompromised patients with periodontitis, and patients with generalized aggressive periodontitis and severe generalized chronic periodontitis. Antibacterial therapy
must be performed after [1] thorough planning, [2] clarification of objectives, [3] reconfirmation of adverse reactions, and [4] a bacteria test9,10).

5）Patient’s choice of antibiotic therapy
Antibacterial therapy (intrapocket application and oral administration) may be indicated for the following patients.
[1] Patients with treatment-resistant/refractory periodontitis that was not clinically improved by mechanicalplaque control[2] Patients with severe generalized chronic periodontitis or generalized aggressive periodontitis[3] Immunocompromised patients with diabetes, etc.
[4] Patients with moderate/severe periodontitis complicated with atherosclerotic disease[5] Patients with periodontitis with a high risk for bacteremia caused by periodontal therapy (e.g. infectious endocarditis, aortic valve disease, cyanotic congenital disease, prosthetic valve/shunt).
The details of antibacterial therapy for patients with periodontal disease are described in the “Guidelines for
Appropriate use of Antibiotics in Patients with Periodontal Disease 2020” published by the JSP.

❺ Treatment of occlusal trauma
Occlusal trauma is injury in periodontal tissues caused by traumatic occlusion and is classified into primary andsecondary occlusal trauma (see Page 18 “❻ Characteristics of occlusal trauma”). Occlusal trauma is associated with degenerative necrosis in the pressed region of periodontal ligament and alveolar bone resorption (seeTable 11). Before treatment, occlusal trauma should be accurately diagnosed (see Page 31 “2）Diagnostic pro-cedure for occlusal trauma”) and the need of procedures for occlusal trauma confirmed. Therapy for occlusal
trauma is performed to eliminate vertical and horizontal traumatic occlusion1) and establish stable occlusion. The
treatment reduces injury in periodontal tissues aggravated by traumatic occlusion and recovers reduced periodontal tissues due to periodontitis. Findings of occlusal trauma are shown in Table 11: “tooth mobility” and “enhanced periodontal ligament space” are important2).

Table 11. Clinical findings and X-ray images of occlusal trauma (revised 1999 AAP New Periodontal Disease
Classification)
One or more clinical findings are included
1) Increased tooth movement
2) Early contact
3) Marked attrition
4) Deep periodontal pocket formation
5) Pathological tooth migration
6) Abfraction (wedge shape detect)7) Tooth fracture
Findings on X-ray images include one or more of the following items
1) Enhanced periodontal ligament space
2) Changed alveolar bone (loss, hyperplasia)
3) Bone loss (furcation, vertical, circumferential)
4) Root resorption5) Cementum hyperplasia

481）Relationship of occlusal trauma with progression of periodontitis
Traumatic occlusion is not an initial factor for periodontitis, but is an important modifier in progression of periodontitis3). Treatment for occlusal trauma eliminates traumatic occlusion, establishes stable occlusion, and reduces
damage in periodontal tissues aggravated by traumatic occlusion. Occlusal adjustment and splint are performed
for marked symptoms and manifestations of occlusal trauma found after completion of procedures for bacterial
infection. The specific procedures are as follows.
[1] Initial periodontal therapy for bacterial infection. If functional impairment is found, occlusal adjustment
may be a priority.
[2] Occlusal adjustment or splint when initial periodontal therapy for bacterial infection causes inflammation
to disappear and reduces tooth movement in partial regions; however, movement remains or increases insome teeth.
[3] Occlusal adjustment and splint for teeth without improved movement.
[4] Occlusal adjustment and splint for teeth with increasing movement.
For a patient with severe periodontitis and no therapeutic effect on occlusal adjustment limited to one to several
teeth, occlusal reshaping and temporary splint, it is necessary to plan a therapeutic strategy using temporary andpermanent splints with wide-ranging periodontal therapy devices.

2）Occlusal adjustment and occlusal reshaping
Occlusal adjustment is used to reduce the load bearing of bite force on periodontal tissues during dental occlusionand calm inflammation in periodontal tissues by correcting traumatic occlusion. Selective grinding makes bite
force distribute evenly in multiple teeth and transfers the tooth axis forward; consequently, more corrective tooth
contact is maintained and periodontal tissues are stabilized4), but premature contact is not necessary for all teeth
with premature contact if there are no findings, including movement. The objectives of occlusal adjustment are to
improve occlusal trauma in periodontal tissues as a priority, and improve temporomandibular joint disorder andbruxism, stabilize occlusion after tooth crown restoration and orthodontic treatment, revise food impaction, andeliminate premature contact interfering with orthodontic treatment. Occlusal reshaping5) is performed to revise
the ridge and buccolingual diameter of the crown or reshape crown morphology, including the cuspal angle andcusp, to eliminate and distribute traumatic occlusion caused by a poor crown shape. Occlusal reshaping is performed regardless of premature contact; however, bite force is reduced by preserving the contact site of the intercuspal position and grinding lateral pressure-induced regions and broad contact area. However, tooth grinding is
an irreversible process; therefore, it is necessary to examine the detailed occlusal status, and give patients a thorough explanation on the need to perform appropriate grinding after obtaining informed consent. Teeth with inflammatory periodontal tissues due to poor oral hygiene sometimes transfer, and these teeth are likely to return tothe original normal site due to improved inflammation. Therefore, if inflammation is found, severe traumatic occlusion alone is adjusted and then precise occlusal adjustment is performed after inflammation disappears due toplaque control.

3）Temporary splint
Temporary splint is performed when occlusal trauma cannot be improved by occlusal adjustment alone, strong
tooth movement is detected, or periodontal tissues are disrupted, resulting in secondary occlusal trauma6). Temporary splint is performed to distribute and stabilize occlusal pressure to periodontal tissues, improve occlusal trauma, and prevent destructive stress with connection of the relevant teeth with surrounding teeth. Temporary splint
is performed to observe changes in periodontal tissues after splinting for a certain period. If tooth movement is severe and occlusal and masticatory dysfunction is found, temporary splint should be performed earlier to improve
masticatory function. Temporary splint is generally performed when occlusion is not stabilized by improved gingival inflammation with plaque control and occlusal adjustment. If tooth movement is temporally increased by in-

49vasion after periodontal surgery and may affect healing, temporary splint is performed before surgery and thesplint is removed after periodontal tissues stabilize and movement is improved after surgery. As described above,the decision on timing, period and procedures for temporary splint should take into account the severity andrange of disruption in periodontal tissues, movement on the dental arch, and teeth position.
[Precautions for temporary splint][1] Perform occlusal adjustment fully before and after temporary splint.
[2] Do not let a temporary splint device inhibit oral hygiene control.
[3] C heck plaque control conditions, early contact and damage of the splint device because routine observationand management is necessary.
[4] Remove temporary splint if periodontal tissues are sufficiently stabilized and consider transfer to a permanent splint if possible.
Choose a temporary splint method that is sufficiently durable for the bite force on the splint site.

4）Devices for periodontal therapy (provisional restoration)
For patients with a tooth defect who require extraction or elimination of incompatible restoration and prosthetic
devices, temporary prosthetic treatment is performed to recover occlusal function and dental esthetics during periodontal therapy. These devices improve masticatory and esthetic dysfunction and reduce load bearing of the bite
force to remaining teeth, and are referred to as devices for periodontal therapy and denture base and crown typedevices7). If incompatible restoration and prosthetic devices are involved in onset of periodontal disease, periodontal tissues are stabilized by eliminating incompatible restoration and prosthetic devices for periodontal therapy
during initial periodontal therapy. In cases of masticatory dysfunction caused by a tooth defect or secondary occlusal trauma caused by decreased remaining teeth, periodontal tissues should be stabilized by installing devices
for periodontal therapy during initial periodontal therapy and improving mastication and occlusion. For patients
who are likely to undergo long-term periodontal therapy, it is particularly important to use devices for periodontal
therapy and to install these devices in advance of periodontal surgery8).

[Precautions for periodontal therapy devices][1] Design a structure for easy control of oral hygiene, as well as improvement of occlusion and esthetics. A
crown type device is preferable on the supragingival margin due to periodontal control. Prevention of overcontour of the tooth crown and maintenance of the size of the interdental embrasure are important for useof the interdental brush.
[2] Observe the periodontal tissue conditions during installation of devices for periodontal therapy, confirm theregions with possible recurrence, consider appropriate forms, and incorporate these results into design of the
final prosthetic device.
[3] Perform routine control (adjustment and repair) of devices for periodontal therapy and oral hygiene instructions.

5）Treatment of bruxism
Bruxism is a habit of grinding upper and lower teeth, clenching or continuously tapping by masticatory muscle
hypertonia, which is unrelated to normal function such as biting, swallowing and talking. Specifically, upper andlower teeth are connected without food and strong bite force, and lateral force is particularly applied to teeth,
leading to risks for inducing occlusal trauma in periodontal tissues. If periodontitis is complicated with occlusal
trauma due to bruxism, the disease is likely to progress rapidly to severe periodontitis. Basic treatment is performed to eliminate causes of bruxism, local factors (abnormal occlusal contact including premature contact) andsystemic factors (e.g., emotional stress)9). However, the causes and mechanism of bruxism are not fully understoodand individual differences are significant; consequently, it is currently difficult to treat bruxism. First, occlusion ofsmall ranges is adjusted by grinding the premature contact site alone, which is a cause, and an occlusal splint (oc-50

clusal base for bruxism) is installed, followed by observation. It is not recommended to adjust wide occlusion andmake an irreversible process including oral rehabilitation. Treatment for sleep bruxism is bedtime autosuggestion
to remind oneself not to grind the teeth; however, many factors are involved in sleep bruxism and there is no established therapy to improve sleep bruxism.

6）Orthodontic treatment
If an abnormal tooth position inhibits plaque control or occlusal trauma due to malalignment is found, the effectof periodontal therapy can be enhanced by orthodontic treatment10). However, this treatment may be difficult inpatients with extremely advanced alveolar bone resorption, which makes it necessary to choose indications. Orthodontic treatment should be performed after gingival inflammation is improved and periodontal tissues are stable, and it is preferable to conduct treatment after eliminating periodontal pockets. If orthodontic treatment starts
before periodontal therapy is sufficient, although malalignment is a cause of bacterial plaque accumulation, periodontal tissues result in disruption. Occlusal adjustment after orthodontic treatment is essential and it is important to obtain balanced occlusal conditions and continue to follow up. An improved dental arch by orthodontic
treatment makes oral hygiene control easier and stabilizes periodontal tissues.

❻ Support for smoking cessation
Smoking is a risk factor for periodontal disease. Therefore, support for smoking cessation of patients with periodontal disease based on an understanding of smoking history including tobacco products, physical/mental nicotine dependence, and preparation of smoking cessation is important to make periodontal therapy successful1-3).
Smokers who require periodontal therapy do not intend to quit smoking and many have risks for various diseases1-3). Therefore, patients with findings4) induced by self and passive smoking should be positively enlightened
about relationships between smoking and worsening of periodontal disease5), passive smoking and periodontal
disease, and systemic health problems, and should receive smoking cessation instructions as part of initial periodontal therapy.

51

9 Risk factors for periodontal disease and risk control
during treatment

Factors defining the onset and progression of periodontal disease and those useful for prediction are defined as risk
factors. The cause of periodontal disease is bacterial plaque, and plaque control is the most important treatment.
However, onset, progression and reaction to treatment are influenced by risk factors. In this chapter, risk factors
are classified as systemic and environmental, and an overview of risk factor control in periodontal disease is provided. For local plaque retention factors, see Page 28. In addition, the characteristics and procedures are describedfor elderly people, sick persons, women, and smokers at risk of treatment.

1）Systemic risk factors (see Page 19 “ ❼ Systemic conditions and periodontal disease”)
Systemic risk factors include age, sex, ethnic differences, genetics, systemic disease, and genetic factors such as individual sensitivity to periodontal disease. For patients with systemic risk factors, including systemic disease suchas metabolic syndrome (diabetes, hypertension), cardiovascular disease1) and medication, information on the effects of systemic factors on periodontal disease should be provided to allow an understanding of these factors. Instructions are given to allow patients to understand why higher level plaque control is necessary for them in comparison with people without systemic risk factors, and thorough plaque control should be performed. Following
positive periodontal therapy, routine control at appropriate intervals is necessary to maintain healthy periodontal
tissues.

2）Environmental risk factors
Environmental risk factors include social factors such as psychological and social stress and lifestyle factors such as
dietary habit, smoking and drinking. In particular, smoking is an important risk factor for progression of periodontal disease2). The necessity of smoking cessation for periodontal therapy should be explained to smokers andthey should be referred to a smoking cessation clinic. The effect of social stress on progression of periodontal disease is not fully understood; however, stress is strongly related to onset of necrotizing periodontal disease. Instructions are given to patients to have sufficient rest, sleep, and relaxation. Some patients unconsciously develop awake
bruxism due to stress. It is important to make patients understand that avoidance of bruxism prevents disruption
in periodontal tissues due to occlusal trauma.

❶ Periodontal therapy for the elderly
The elderly population in Japan has been increasing; however, individual differences in health are significant andhealth conditions depend on the quality of earlier healthcare. Elderly people generally have decreased cardiopulmonary and immune function and restorative performance, and have significantly less secondary memory andpsychological functions, in comparison with those in late middle age. Maintenance of masticatory function is extremely important for elderly people, both physically and mentally.
In periodontal therapy for elderly people, it is necessary to consider the general characteristics of old age, mental
and physical conditions, the level of finger function, swallowing hypofunction and limitation of secondary memory3). Elderly people have less residual function to maintain homeostasis in response to physical stress4) and are likely to develop water and electrolyte imbalance. If it is difficult to perform long-term periodontal therapy, including
flap surgery, in an elderly patient, and non-surgical treatment should be repeated. This should be mainly debridement in periodontal pockets including plaque control and SRP as required, and supplemental combined chemicalplaque control. Elderly people also often develop new systemic disease during maintenance, preventive treatment

52

for severe periodontal disease and SPT; consequently, medication has to be changed or increased. Therefore, there
is a need to ask about new disease or medication at every visit. Cognitive decline may also occur. If unprecedented
problems with a patient’s fingers or brushing actions decline during maintenance, preventive periodontal therapy
and SPT, and it is necessary to contact their family and provide assistance according to cognitive function andbrushing actions.
Patients with oral hypofunction associated with decreased swallowing function should undergo tongue coating
test and oral biofilm test to assess bacteria counts to examine contamination of the entire oral cavity and manage
the whole oral cavity, including the tongue and mucosa. Even for patients without oral hypofunction, it is usefulto understand oral conditions using an oral biofilm test and control the whole oral cavity for suppression of systemic disease, including aspiration pneumonia in elderly patients. More attention should be given to physical,
mental and environmental changes in periodontal therapy for elderly people, compared to therapy for those inlate middle age.

❷ Periodontal therapy for patients with other diseases
Patients with periodontal disease often also have diseases such as hypertension, cardiovascular disease, diabetes andosteoporosis5,6). Many kinds of systemic diseases are closely related to periodontal disease; therefore, periodontal
therapy is also important to control systemic diseases. Furthermore, these patients are frequently given many different drugs, and periodontal surgery is severely invasive in these cases, similarly to elderly patients. It is important
to conduct a lengthy interview before the start of periodontal therapy, refer to attending physicians for symptoms,
and establish appropriate medical cooperation. In elderly and diseased individuals, prevention of complications
requires determination of resting blood pressure, heart rate and arterial oxygen saturation before surgery and monitoring of vital signs during therapy, even if treatment has no problems. Periodontal and dental therapy may bedifficult in some patients, depending on the type and symptoms of systemic disease. In such a case, communication with advanced care facilities for systemic disease is recommended, with a request for information on risk factors for therapeutic strategies and control of systemic disease. Medical information on the effects of systemic risk
factors on periodontal disease should be provided to patients. Instructions are given to allow an understanding of
why higher level plaque control is necessary in comparison with people without systemic risk factors, with performance of thorough plaque control and improved recognition of the need for routine control of periodontal tissues. Patients should understand the effect of periodontal disease on the whole body (e.g. metabolic syndrome including diabetes, and hypertension, cardiovascular disease, osteoporosis) and should be given appropriate advice
from the periodontal perspective7). Patients who particularly require monitoring are described below.

1）Metabolic syndrome
Metabolic syndrome is a combined risk syndrome in which obesity increases the risk for atherosclerotic disease.
Diagnostic criteria are visceral fat accumulation and two or more of serum dyslipidemia, elevated blood pressureand hyperglycemia. In the United States, periodontal disease is a basic disease of metabolic syndrome, as well as
obesity, diabetes, hypertension and hyperlipidemia. In particular, obesity and diabetes have been shown to be related to periodontal disease in many studies, and procedures for preventing periodontal disease that include lifestyle factors are required.

2）Obesity
Obese individuals are likely to have periodontal disease and the causes are considered to be related to hyperlipidemia and insulin resistance.

533）Diabetes
Periodontitis complicated with diabetes is not induced by diabetes, but by immune system disorder and peripheral
circulatory disturbance due to diabetes modulating the pathology of periodontitis. See “2014 Guidelines for Periodontal Therapy in Diabetic Patients, Second Revision” (JSP).

（1）Type 1 diabetes

When undergoing tooth extraction or periodontal surgery, it is necessary to be careful not to develop hypoglycemia in patients who are restricted in eating and drinking for a long period of time.

（2）Type 2 diabetes

It is generally preferable not to perform SRP until patients achieve plaque control by themselves; however, periodontopathic bacteria in periodontal pockets are related to diabetes. Therefore, debridement in these pockets
should be conducted earlier than usual. For patients with generalized chronic periodontitis complicated with diabetes and those with severe diabetes-related periodontitis, combination with antibacterial therapy is recommended
to reduce adverse reactions in other organs.

4）Hypertensive patients
If blood pressure is not fully controlled, the priority is stabilization of blood pressure. Before treatment, the patient’s conditions are discussed with the attending physician and treatment is performed with cooperation between
the physician and dentist. Local anesthetics without epinephrine are used and vital signs are monitored during
periodontal surgery.

5）Patients with cardiovascular disease(particularly those taking antithrombotic agents)

A correlation between periodontal disease and onset of cardiovascular disease is found after known confounding
factors are adjusted. In addition, functional improvement in vascular endothelial cells occurs after improvement of
periodontal disease, which suggests that periodontal disease has an effect on the cardiovascular system. There are
two hypotheses for the mechanism connecting periodontal disease with cardiovascular disease: [1] bacteria directly
enhance onset and progression of cardiovascular disease; and [2] an inflammatory response evoked by periodontal
disease increases C-reactive protein in blood and periodontal disease is indirectly related to onset of cardiovasculardisease7). Antithrombotic agents (antiplatelet drugs, anticoagulants) affect cardiovascular disease and various underlying diseases, such as prevention of complications of diabetes. Periodontal therapy in a patient treated withantithrombotic agents should be performed after discussing underlying disease and current systemic conditions
with an attending physician and understanding these conditions. Invasive dental procedures, including extraction,
are commonly performed without withdrawal of antithrombotic agents when possible. To perform such invasive
procedures, it is important to pay attention to hemostasis and drug administration after completion of procedures.
For details of antibacterial therapy, refer to the “Guidelines for Appropriate use of Antibiotics in Patients with
Periodontal Disease 2020” published by the JSP.

6）Dialysis
Some antibiotics affect excretion rates from the body and consultation with an attending physician is necessary tochoose appropriate antibiotics for periodontal therapy. Since anticoagulants are often administered on dialysis day,invasive periodontal therapy should not be performed.

7）Respiratory disease
Oral bacteria, including periodontopathic bacteria, pass through the trachea and invade the lung with the saliva,
resulting in aspiration pneumonia.

54❸ Female-specific periodontal disease1）General precautions

Female hormones including estrogen and progesterone increase and decrease during menstruation and pregnancy.
These hormones are secreted into the gingival sulcus via blood and induce proliferation of periodontopathic bacteria (e.g., P. Intermedia) and induce gingival inflammation8). Thus, women are more susceptible to periodontal disease in comparison with men throughout life.

2）Periodontal therapy for pregnant womenDuring early pregnancy, brushing instructions are mainly given and therapy without stress is performed in as shorta time as possible. SRP is performed during stable pregnancy (4 to 5 months gestation)9). Administration during
pregnancy is avoided as much as possible and it is desirable to combine professional care, including mechanicaltooth cleaning, with self-care. If extraction is required due to periodontal disease during pregnancy, debridementin periodontal pockets is conducted and a tooth is extracted during stable pregnancy; however, invasive proceduresshould basically be performed after delivery. Periodontal disease is a risk factor for preterm and low birth weight
infant delivery; therefore, appropriate periodontal therapy is required for pregnant women. However, procedures

are limited during pregnancy and it is desirable to perform oral hygiene control daily. (See Page 39 “❷ Preventive treatment for pregnant women”).

3）Patients with osteoporosis(particularly those taking BP products and anti-RANKL antibodies)

Osteoporosis develops frequently in postmenopausal women and the elderly, and BP products are the first choicefor osteoporosis. Anti-RANKL antibodies inhibit bone resorption through a mechanism that differs from that of
BP products and are used as therapeutic agents for osteoporosis. BP products and anti-RANKL antibodies are also

administered to cancer patients. (See Page 25 “❸ Liaison with medicine”). Patients taking BP products andanti-RANKL antibodies can develop ONJ after invasive dental therapy, and this is suggested to be related to theseagents10-12). Treatment should be discussed and planned with cooperation between the physician and dentist.

❹ Periodontal therapy for smokers
Smoking is a cause of lung cancer and other diseases. Many epidemiologic studies have shown that smoking is thehighest risk factor for periodontal disease, regardless of race, and smokers develop periodontal disease at 2-8 times
higher a rate than non-smokers. Nicotine in blood constricts capillaries and the clinical characteristics of smokers
include less BOP and mild redness, which are unlikely to present as symptoms13). Since smoking delays healing of
periodontal disease, smokers are less responsive to periodontal therapy than non-smokers. However, patients who
were heavy smokers, but then abstained from smoking, have a decreased risk for periodontal disease14). Therefore,
it is necessary to explain to patients that smoking cessation is essential for periodontal therapy and to support theirabstention from smoking in cooperation with medical facilities.

55

10 Periodontal surgery
The JSP published a clinical path for a standardized periodontal surgical process as guidelines for periodontal surgery. The clinical path facilitates appropriate and safe periodontal surgery, and has been improved by revision,leading to improvement in the quality of healthcare. The JSP recommends use of this clinical path in periodontal
surgery. It is preferable to refer a patient to a JSP Board-Certified Periodontist in case of difficulties with periodontal surgery by oneself. The indications for periodontal surgery are [1] a deep periodontal pocket after initial periodontal therapy, [2] poor plaque control and relapse of periodontitis due to soft and/or hard tissue morphologicalabnormality, and [3] esthetic dysfunction and anatomical morphological abnormality preventing installation of
appropriate restoration and prosthetic devices1).
A patient should also meet the following conditions before periodontal surgery: [1] provision of informed consent after a full explanation, [2] good general conditions, [3] good oral hygiene, and [4] current non-smoker. Periodontal surgery is classified into four types: tissue attachment therapy, resective therapy, periodontal tissue regenerative therapy, and periodontal plastic surgery. The type of periodontal surgery is determined by comprehensive
consideration based on the bone defect type, oral hygiene conditions, probing depth, BOP, and radiographic findings (Table 12, Figure 7). The indications for periodontal surgery are probing depth ≥4 mm with BOP in
re-evaluation; however, surgery may be conducted to improve poor gingival forms in cases with a lower probing
depth and no BOP. Bone defect conditions are important criteria in the choice of the surgical procedure (Figure8)2).

Definition of flap surgery: Flap surgery is periodontal surgery to detach the gingiva using a full thickness orpartial thickness flap; curette plaque, calculus and inflammatory granulation tissues with clear visibility; and eliminate or decrease periodontal pockets. Flap surgery is classified into flap curettage and modified Widman flap surgery based on the incision and detachment procedures. Recently, less invasive flap surgery has been conducted using MIST (minimally invasive surgical technique) and M-MIST (modified minimally invasive surgical technique)for localized lesions, with consideration of flap design to avoid postoperative gingival recession and depression andto maintain clots obtained from tightly closed wounds3,4). These procedures apply to incision methods to conserve
interdental papilla using MPPT (modified papilla preservation technique) and SPPF (simplified papilla preservation flap)5,6). The procedures are also combined with periodontal regenerative therapy.

❶ Tissue attachment therapy
Tissue attachment therapy is a surgical procedure to eliminate bacteria and bacteria-derived contaminants on roots
Table 12. Bone defect type and periodontal surgical procedures
Tissue attachment therapy· Flap curettage (flap surgery)· Modified Widman flap surgery

Resective therapy· Apically-positioned flap surgery + osteoplasty or ostectomy

Periodontal tissue regenerative therapy· Bone graft· Guided tissue regeneration (GTR) method· Enamel matrix derivative (EMD) applied surgical procedure· Surgical procedure using basic fibroblast growth factor (FGF-2)· Surgical procedure using other biologically active substances

Tissue attachment therapy· Periodontal curettage· Excisional new attachment procedure (ENAP)· Flap curettage (flap surgery)· Modified Widman flap surgery

Resective therapy· Apically-positioned flap surgery (+ ostectomy)· Gingivectomy

Vertical bone loss

Horizontal bone loss

56

• General conditions are good?
• Oral hygiene conditions are good?
• 1RQVPRNHU"• ,QIRUPHGFRQVHQWREWDLQHGDIWHUDQ
explanation was given?

7RPRGLI\WKHIRUP
and obtain
esthetics
and function.

<Objectives>
7RPRGLI\WKHIRUPDQG
reduce gingival/periodontal
SRFNHWTo clean the tooth roots
and attach soft tissues
to the root

To regenerate periodontal
tissues and obtain
QHZDWWDFKPHQW

Figure 7. Selection criteria for periodontal surgery by purpose

Horizontal bone loss only

Vertical (wedge shape) bone loss

<4 mm

PP

 PP
<2 mm

 PP

<2 mm
1, 4 walls

2, 3 walls

Figure 8. Selection criteria for periodontal surgery by bone defect type� ��e �e��� ��� �i��� �� ��e ���e �e�e�� �re r��i�gr���i� ���i�g��

and inside periodontal pockets, and facilitate attachment of gingival soft tissues on roots7). Tissue attachment therapy does not include ostectomy, osteoplasty or apically positioned flap surgery, but includes periodontal curettage,excisional new attachment procedure (ENAP), flap curettage (access flap surgery), and modified Widman flap surgery. The major selection criteria, surgical characteristics and indications for tissue attachment therapy are shownin Figure 9. In patients with fully controlled oral hygiene, tissue attachment therapy results in better attachment
gain than resective therapyy7).

1）Periodontal curettage
Periodontal curettage treats roots (e.g., elimination of bacterial biofilm, calculus and pathological cementum) withsimultaneous curettage of inflammatory lesions (periodontal pocket epithelium, inflammatory granulation tissue)

57

Shallow probing depth or simple tooth root form

Deep probing depth or complex tooth root form

Small

Large

Figure 9. Selection criteria for tissue attachment therapy

on the inner walls of periodontal pockets using curette type scales. This is a procedure for promoting attachmentof the gingiva on root surfaces and decreasing periodontal pockets. This procedure is performed to attenuate inflammation in the tissues surrounding periodontal pockets and stabilize the pathology, even for deep periodontal
pockets that are difficult to eliminate.

Characteristics: Shorter operative time and less invasive than flap surgery, but clear visible surgery cannot be

performed on roots and curettage of inflammatory lesions is likely to be insufficient.

2）Excisional new attachment procedure (ENAP)
ENAP is a procedure for removing the periodontal epithelia and inflammatory tissues using a scalpel. Inner wallsof periodontal pockets are eliminated by internal bevel incision from the gingival margin to the bottom of a periodontal pocket, the root surface is treated with SRP, and the gingiva is pressed and attached to the root, followedby suturing.

Characteristics: Similarly to periodontal curettage, ENAP is less invasive and results in less gingival recession

than flap surgery. However, new attachment is seldom gained and outcomes result in cure with long epithelial attachment.

3）Flap surgery
Flap surgery is periodontal surgery to detach the gingiva from the alveolar bone, remove contaminants including
plaque and calculus on the tooth root with clear visibility, remove the periodontal epithelia and granulation tissues, and then return and suture the gingival flap to remove or decrease periodontal pockets.

Characteristics: The surgical procedure is also usable for vertical bone resorption. Cure condition is long epi-

thelial attachment8).

（1）Flap curettage
This surgery is conducted with almost similar objectives and procedures as those of modified Widman flap surgery
described below. The gingiva is incised from the gingival margin to alveolar crest to access the tooth root and detached to make the alveolar crest slightly exposed in the full thickness flap. The tooth root can be cleansed withclear visibility. Surgical invasion is reduced and postoperative gingival recession is minimal.

（2）Modiﬁed Widman ﬂap surgery

Modified Widman flap surgery was introduced by Ramförd4). The gingiva is incised from 1-2 mm outside of thegingival margin and detached 2-3 mm from the alveolar crest in the full thickness flap. This surgery ensures definite removal of periodontal pockets, but postoperative gingival recession and the exposed tooth root are large.

58

Yes

No

Yes

InsufficientInsufficientSufficientSufficientSufficientorFigure 10. Inclusion criteria for resective therapy� ���i�e �ur��er �u��i�e �� ��e gi�gi��� ��rgi��

❷ Resective therapy
Resective therapy includes gingivectomy, an apically positioned flap surgery, ostectomy and osteoplasty. Flap surgery is usually classified as tissue attachment therapy; however, a procedure using gingival collars rather than gingival margins in the incision process is close to resective therapy. Inclusion criteria for resective therapy, including
flap surgery, are shown in Figure 10. Since resective therapy causes gingival resection after surgery, detailed instructions and management for oral cleaning and dentin hyperesthesia are needed.

1）Gingivectomy
This is a procedure for gingivectomizing with external bevel incision to decrease or eliminate gingival (false) pockets, proliferative gingiva or shallow suprabony periodontal (true) pockets.

Characteristics: Gingivectomy is a simple procedure for definite elimination of gingival and periodontal

pockets, and outcomes after surgery are easily predictable. However, gingivectomy may cause postoperative bleeding, pain, decreased attached gingiva width, and esthetic dysfunction due to gingival resection. Vertical bone resorption inhibits visual confirmation of the root and bone during gingivectomy; consequently, such cases are excluded from the indication.

2）Apically positioned ﬂap surgery
The gingival flap over the mucogingival junction is removed, and then transferred to the apical side before suture.
This procedure is classified as resective therapy because it completely eliminates periodontal pockets, but is also included in periodontal plastic surgery because the attached gingiva width is allowed to increase. The gingival flap
over the mucogingival junction is removed and then transferred to the apical side before suture. However, the gingival flap of the maxillary palate cannot be transferred to the apical root and the gingival thickness and height are
adjusted using a scallop shaped incision. The gingival flap can be removed on the mucoperiosteal and mucosal

59

flaps, respectively. For removal on the mucoperiosteal flap, the gingival flap is tightly in contact with the alveolarbone after suture and a periodontal pack is used as required. For removal on the mucosal flap, a periosteal suture
is applied. In the longitudinal incision site, the gingival flap can be transferred to the apical root and sutured. In
apically positioned flap surgery, osteoplasty and ostectomy are usually combined to eliminate vertical osseous defects and bone torus or keep supracrestal tissue attachment and biologic width.

Characteristics: Periodontal pockets are reduced by the periapical flap procedure, but the root exposed area

increases; therefore, it is necessary to give instructions on careful oral hygiene management. This procedure is also
used as a clinical crown lengthening procedure.

❸ Periodontal regenerative therapy(see “2012 Guidelines for Regenerative Therapy in Patients with Periodontal Disease” (JSP9)))
Several periodontal regenerative therapies are based on recent studies of periodontal regeneration. There is a long
history of bone transplantation and guided tissue regeneration (GTR) as regenerative therapy. In the 21st century,
clinical applications include use of biologically active substances. The main procedures with these substances are
surgery using enamel matrix derivative (EMD) or basic fibroblast growth factor (FGF-2). This therapy is aimed atregenerating periodontal tissues, and it is important to assess the amount of regenerated bone and the attachmentlevel gain accurately for a certain period after surgery using standardized radiography measurements. Several othermaterials for regeneration have not been approved in Japan. These guidelines describe these materials to allow anunderstanding of the current conditions of periodontal regenerative therapy, but do not recommend surgical procedures using the materials. Many regenerative materials are approved in Japan and are currently used off-label;
therefore, particular attention including medical ethics is required in use of this therapy.

1）Bone transplantation
Bone transplantation is performed to stabilize periodontal tissues with regeneration of bone defects and maintaindental function and esthetics by supporting or enhancing teeth. Bone transplantation also includes heterogenous
bone grafts and xenografts, but mainly uses autogenous grafts and artificial bone grafts (e.g. hydroxyapatite, tricalcium phosphate and carbonate apatite) as bone graft materials for safety.

Characteristics: Indications are various bone defects and furcation. Good bone regeneration is expected whenmany bone walls support graft materials. Bone transplantation is clinically applied in combination with GTR and
EMD; however, there is no clear evidence of an additional effect. Therefore, careful consideration should be given
to application.

2）Guided tissue regeneration (GTR)
GTR is a surgical procedure for preventing extension and contact of gingival epithelia and connective tissues toroots during healing and regeneration of periodontal tissues with new connective tissue attachment on roots using
gingiva and a GTR membrane.

Characteristics: Indications are vertical osseous defect in 2 or 3 walls and class II furcation. In such cases,

GTR provides significant attachment gain and improved vertical osseous defect in comparison with flap surgery.
However, for class III furcation, there is no definite evidence for regeneration.

3）Enamel matrix derivative-applied surgery
This is a surgical procedure for introducing cementum and facilitating regeneration of periodontal tissues by applying EMD containing enamel matrix proteins extracted and purified from tooth germs of juvenile pigs to roots
with attachment loss.

Characteristics: The indications are vertical osseous defect in 2 or 3 walls, but some cases with osseous defectin 1 wall are also included. EMD is considered to have outcomes similar to those of GTR (nonabsorbable mem-60

brane) for probing depth and attachment gain one year after surgery. For furcation involvement, there are studies
showing that EMD provides significantly improved attachment gain and improved vertical osseous defect in comparison with flap surgery; however, furcation is not currently included in indications of EMD in Japan and its use
requires careful consideration. Use of EMD requires treatment of tooth roots (EDTA, etc.).

4）Surgical procedure using basic fibroblast growth factor (FGF-2)
This is a surgical procedure for inducing regeneration of periodontal tissues with topical application of FGF-2
products. FGF-2 is a cytokine that acts upstream of the wound healing cascade and facilitates healing. FGF-2 application promotes proliferation and migration of periodontal stem cells, induces angiogenesis, and prepares the
local environment for reconstruction of periodontal tissues, leading to regeneration of these tissues. In 2016, theworld’s first periodontal tissue regenerator was made in Japan (0.3% FGF-2; Product name: REGROTH®, dental
fluid kit, 600 µg/1,200 µg). This has achieved marketing approval and is commercially available in Japan.

Characteristics: The indication is vertical osseous defect with probe depth ≥4 mm and osseous defect depth≥3 mm. No treatment of tooth roots is needed and fluid is applied to tooth defect sites. The contraindications aremalignant tumors in the oral cavity or a past history of these tumors, and thorough examination is necessary before surgery.

5）Surgical procedures using other biologically active substances
Commercial regenerative materials combined with tricalcium phosphate (β-TCP), bone graft materials, and BB
isoforms of platelet-derived growth factor (PDGF-BB) are used for periodontal regenerative therapy in the UnitedStates. Platelet-rich plasma (PRP) therapy that uses isolated platelet-rich components from autologous blood toactivate biologically active substances including PDGF to induce periodontal regeneration is also applied clinically. The Law on Securing Safety of Regenerative Medicine was enforced on December 25, 2014 and PRP is classified as a Regenerative Medicine Class III. (The names of regenerative medicines and institutions performing regenerative medicine are shown on the website of the Ministry of Health, Labour and Welfare).

❹ Periodontal plastic surgery (including gingival/alveolar mucosaplasty)
Periodontal plastic surgery is a collective term for surgical procedures for improving anatomical problems, including those of the labial frenum and muscle attachment, which inhibit the marginal gingiva, lack and loss of attached gingiva, shallow oral vestibule and frenulum, and exposed tooth roots (gingival recession) to treat and prevent periodontal disease, confirm the oral environment to facilitate plaque control, and improve esthetics10).

1）Frenectomy
The objective of this surgery is to incise an abnormal frenulum, increase the width of attached gingiva, and stabilize periodontal teeth and tissues. The procedure incises the transfer site of the frenulum and gingiva, removes theattached frenulum from the bone, and resects the frenulum.

Characteristics: Abnormality in the frenulum is likely to cause periodontal pocket formation and deepening

due to traction of the marginal gingiva, and is also the cause of median and interdental diastema, leading to injury
in brushing. This surgery establishes an oral environment suitable for plaque control and may also stabilize dentures.

2）Laterally positioned flap surgery
In this procedure for localized gingival recession, keratinized gingiva in adjacent teeth is transferred laterally as apedicle flap to cover an exposed root. The supply regions are required to have sufficient thickness and width (approx. 1-2 teeth) of keratinized gingiva.

61

Characteristics: This is an effective procedure to cover a solitary exposed root of mild (≤4 mm) gingival recession or a severe case with a narrow width. A marked osseous defect in the region to be covered, a large area of the
exposed root, and a shallow oral vestibule are excluded from indications. The disadvantages are the complicatedoperation because a pedicle flap is produced through a combination of mucoperiosteal and mucosal flaps, and ahigh possibility that new gingival recession will develop in teeth adjacent to the transplanted marginal gingiva.

3）Coronally advanced flap surgery
This procedure is surgery to produce a pedicle flap by removing the gingiva beneath the gingival recession, transfer
the flap to the crown side, and cover an exposed root.

Characteristics: The indication is exposed roots of 1-2 teeth with sufficient attached gingiva width. This pro-cedure is also used to cover a bone graft and GTR membrane in dressing of connective tissue transplantation andperiodontal regenerative therapy. However, pressing on a gingival flap sometimes causes recurrence and necrosis,
leading to relaxing incision. Another procedure is semilunar coronally positioned flap surgery that covers an exposed root of 2-3 mm.

4）Apically positioned flap surgery
This is a surgical procedure for increasing the attached gingiva width and eliminating periodontal pockets in patients with a narrow attached gingiva width or a periodontal pocket bottom beyond the mucogingival junction(for details, see Page 58 “❷ Resective therapy”).

5）Free gingival graft
A free gingival graft is a procedure for transplanting grafts containing epithelium and connective tissues collectedfrom the supply site (e.g., palate) to the receptor. The objectives include covering of exposed roots, expanded oral
vestibules, and definite acquisition and increase of attached gingiva. Grafting is performed for regions with a narrow attached gingiva width due to a shallow oral vestibule that are difficult to clean.

Characteristics: A graft meeting the size of the receptor can be collected, but the graft requires two surgicalsites. Laterally-moved flap and periapical flap procedures are sometimes combined with the grafting. A disadvantage is that the grafted gingiva forms a keloid-like region (graft island).

6）Connective tissue graft
Connective tissue graft is a procedure for transplanting subepithelial connective tissues collected mainly from thepalate. This procedure is divided into subepithelial and free connective tissue grafts. The objectives of the former
include gingival recession and covering of exposed roots, and those of the latter include expanded oral vestibules,acquisition of attached gingiva, alveolar ridge augmentation in a region requiring esthetics, and protection of
GTR membranes and newly formed tissues on the GBR membrane.

Characteristics: Subepithelial connective tissue graft in the receptor is supplied with blood from the perioste-

al and epithelial sides; consequently, the graft is likely to engraft in comparison with a free gingival graft. This
grafting is superior to free gingival graft in esthetics and is currently the best method.

7）Other perioplasty
Besides the periodontal plastic surgery mentioned above, vestibuloplasty and a bilateral papilla flap procedure areincluded in periodontal plastic surgery.

62❺ Laser application in periodontal surgery
Debridement to the root in periodontal surgery is usually performed mechanically with a hand scaler and ultrasonic scaler. However, use of lasers for periodontal therapy has increased and an Erbium (Er):YAG laser and
Er,Cr:YSGG laser with high water-absorbability have particularly been used in debridement of pathologic roots,
including calculus elimination. The Er:YAG and Er,Cr:YSGG laser output is absorbed by water in calculus andthe internal pressure increases as vaporization is produced, with contaminants including calculus transpired by“micro-explosion”. The laser is likely to have bactericidal action on the irradiated area and effects on endotoxin
degradation and removal. However, a laser is light therapy with a non-contact action and is completely different
from a conventional mechanical instrument. Therefore, dentists must be familiar with laser procedures. A laser
beam has orientation and may cause mis-irradiation at untreated sites due to reflection from a mirror used fortreatment and a metal crown. The safety of patients is a concern and staff should wear protective goggles. A position paper on lasers for periodontal therapy “Calculus removal by laser” was developed by the Japanese Society of
Periodontology and Japanese Society for Laser Dentistry11).

63

11 Treatment of furcation involvement (Figure 11)
Furcation involvement occurs in a lesion of periodontal tissues in the interradicular septum of double-rootedteeth. The furcation is a region with complicated anatomical morphology and it is frequently difficult to performdefinitive debridement using common periodontal instruments. Consequently, a laser is currently used to treat the
furcation. Furcation involvement is caused by inflammation spreading from marginal periodontal tissues, traumatic occlusion and periodontal-endodontic lesions. A lesion spreading to the furcation and its severity dependon root form and divergence, root trunk length and local anatomical factors, including enamel projection in thetooth cervix. Therapeutic procedures and outcomes vary based on causes, severity and affected tooth conditions;however, periodontal lesions spreading from margins require more complicated therapeutic procedures and it isimportant to make an appropriate diagnosis in accordance with the Lindhe and Nyman furcation classification or
Glickman furcation classification1).

❶ Examination
In the examination of furcation involvement, the cause and lesion range should be identified; therefore, precise
probing using a furcation probe and examination with a dental X-ray are essential. This examination is conductedusing eccentric projection and an instrument with contrast media as required. CBCT is effective because it gives
three-dimensional images of the lesion range. Radiographic interpretation includes [1] conditions of the root
trunk, [2] crown root ratio, and [3] root conditions (length, form, curvature, separation, and divergence).

❷ Treatment
In determining the therapeutic strategy, it is necessary to carefully consider whether the teeth after removal of
periodontal pockets are ready to be maintained by the patient and appropriate restorative and prosthetic therapy
are performed. Therapy is generally decided using the Lindhe and Nyman furcation classification.

Class 1orClass 2orororClass 3

* Decision-making basedon root conditions andremaining alveolar bone
Figure 11. Inclusion criteria for therapy for furcation involvement

or

or

64

[1] Class I or mild Class II lesion: treated with basic periodontal therapy, selective grinding and removal ofenamel projection and pearl, furcation plasty, and a local drug delivery system (LDDS).
[2] Class II lesion: an indication for tissue attachment therapy and periodontal regenerative therapy.
[3] Class III lesion: an indication for tunnel preparation and root separation. A lesion localized in the surrounding area of a specific root is treated with root resection (maxillary), trisection (maxillary), and hemisection(mandibular).
In all cases, detailed instructions and management, including postoperative plaque control, are important.

65

12 Treatment of combined periodontic-endodontic lesions
The root canal and periodontal tissues communicate with each other via the apical pore, accessory root canal andcollateral (medullary canal), and infection in either can affect the other. Therefore, in advance of therapy, a definite diagnosis is required based on pulp viability, periodontal pocket depth and radiographic findings, and a decision is made to prioritize endodontic therapy or simultaneously perform endodontic and periodontal therapies. In
a case with deeper periodontal pockets due to progression of periodontitis, bacterial infection in a root adjacent to
the pockets can spread to the pulp via the dentinal tubule, accessory root canal, collateral (medullary canal), andapical pore. Most accessory roots exist in the periapical region (2-3 mm from the root apex); therefore, the deeper
a periodontal pocket, the higher the incidence of periodontal-endodontic lesions. Ascending pulpitis is not caused
by caries in the crown or root, but via the apical pore or accessory root.

❶ Classification of combined periodontic-endodontic lesions
Classifications of periodontal-endodontic lesions include the Simon classification1) and Weine classification2) andconsist of three types of pathogenesis.

（1）Class I (endodontic lesion-derived)
Radiographic findings show bone resorption of advanced periodontitis, but the cause is pulp inflammation andnecrosis. The pulp is devitalized. Endodontic therapy is performed.

（2）Class II (endodontic lesion-derived)

Severe bone resorption due to periodontitis is found and the pulp is infected from the accessory root or apicalpore in periodontal pockets. The pulp is usually vital tooth. In multi- (double-) rooted teeth, only one root is devitalized.

（3）Class III (combined periodontal-endodontic lesion-derived)
Lesions that are due to apical periodontitis-induced periapical bone resorption and periodontitis-induced bone resorption connect with each other and combine. The pulp is devitalized. Endodontic therapy is the first treatment
and is combined with periodontal therapy.

❷ Examination
If periodontal-endodontic lesions are suspected, the following items are examined: [1] pulp viability, [2] probing
depth (position of pocket bottom) and probing of furcation, [3] X-ray image (form and number of the root orroot canal; CBCT definitively shows the range of bone defect and the relationship with the root canal and is considered to be effective), [4] severity of gingival inflammation, [5] pain type, [6] occlusal condition, and [7] root
fracture.

❸ Treatment
Treatment is begun after examination of the above items and diagnosis of the class of periodontal-endodontic lesion. In a case with severe pain, the first therapy is for pain relief. The patient conditions are examined to determine whether treatment of the pulp (pulpectomy) or that of acute symptom of periodontitis (e.g. abscess incision)is necessary. After acute symptoms disappear, endodontic therapy is usually given as a priority, followed by periodontal therapy. For devitalized teeth, attention should be given to root fracture. In a case in which traumatic occlusion is found in the intercuspal position (centric occlusion) or lateral movement, occlusal adjustment is first
performed.

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A Class I lesion is treated with endodontic therapy. Affected cementum and periodontal ligament fibers are likely to recur; therefore, SRP should not be performed early. A Class II lesion with suspected irreversible pulpitis (ascending pulpitis) or partially devitalized roots is treated with pulpectomy (root canal therapy). Single-rooted teeth
sometimes induce asymptomatic pulp necrosis and gangrene. In such a case, both endodontic and periodontal
therapies are necessary. Lesions in molars are treated with root resection, including hemisection. A Class III lesion
is initially treated with endodontical therapy, followed by a combination with periodontal therapy.

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13 Oral rehabilitation:

Choice of splint, bridge, denture and implant
Oral rehabilitation is a collective term for treatment after periodontal surgery to recover oral function lost by periodontal disease, and includes restorative and prosthetic therapy, orthodontic treatment, and implant therapy. Oralrehabilitation for patients with periodontal disease is required for enamel and dentin defect, tooth loss, tooth mobility, decreased occlusal and masticatory function, and esthetics. This treatment is important to recover appropriate occlusal and masticatory function and esthetics, and for long-term stabilization of periodontal tissues for functional maintenance and avoidance of induction of inflammation or occlusal trauma in periodontal tissues. For
moderate or severe advanced periodontitis with decreased support of periodontal tissues, bacterial infection andocclusal trauma are concerns (Figures 12 and 13). Splinted prosthesis and removal of partial denture are often
performed to fix mobile teeth during initial periodontal therapy; consequently, restorative and prosthetic therapy
for patients with advanced periodontal disease is likely to be more difficult than that for patients who are healthy.
Periodontal therapy shows the importance of solving these problems and performing oral rehabilitation, an objective of dental treatment1).

❶ Choice of therapeutic procedures
1）Test items

It is important for oral rehabilitation to avoid induction of inflammation or occlusal trauma in periodontal tissues
and build an oral environment to stabilize these tissues. Therefore, it is important to examine bacterial infection,
inflammation and occlusal trauma, including oral hygiene (O’Leary plaque control record), probing depth and
BOP; and occlusal trauma based on X-ray images (bone resorption, root length, enhanced periodontal ligament
space), tooth mobility and fremitus (slight vibration in occlusal contact), and number, placement and occlusion ofremaining teeth (e.g., bruxism, bite force).

2）Treatment of mobile teeth2,3)
For oral rehabilitation for patients with periodontal disease, it is particularly important to examine and treat thecause of a mobile tooth, after determining whether mobility is due to inflammation or traumatic occlusion, in-• Easy to eliminate bacterial
plaque• Difficult to retain bacterial
plaque• Scaling and root planing areeasy

Consideration ofbacterial infection• Strength of occlusal contact
according to periodontal
tissue supporting force• Avoidance of lateral force• Enforced supporting force of
periodontal tissues by splint

Consideration ofbite force

Figure 12. Bacterial infection and bite force in oral functional restoration in patients with periodontal disease1-4)

Item of note for producing prothesis• Position and compatibilityof margin: Suprabony
tissue attachment(Biological width)• Crown contour• Interdental embrasure• Pontic shape• Position and strength ofcontact point• Appropriate occlusal shape• Polishing conditions ofrestoration and prosthesis

Figure 13. Precautions in production of a prosthesis fororal rehabilitation

68

cluding premature contact and bruxism. Sleep bruxism can exceed the maximum bite force4) and it is important
to treat excessive traumatic force, including sleep bruxism5,6). If tooth mobility is significant, a priority should begiven to plaque control and scaling, although occlusal adjustment and temporary splint are sometimes necessaryduring initial periodontal therapy. For patients with dysfunction due to remaining mobility after these procedures,changes in periodontal tissues including tooth mobility are assessed after occlusal adjustment and temporary
splint, the necessity and range of a permanent splint are determined, and an occlusal splint is used.

3）Temporary splint and splint with provisional restoration
If tooth mobility is found after therapy for bacterial infection, a temporary splint is used and the splint procedures
and range are examined. In using a permanent splint, patients with advanced periodontal tissue destruction havedecreased support from remaining teeth. Consequently, it is often necessary to determine whether the prosthesis isa cause of bacterial infection or occlusal trauma based on chronological data. The process in such a case is to produce devices for periodontal therapy, examine the form of the prosthesis and the splint range, and assess whether aless predictable tooth or a tooth with severe mobility is maintained. Specifically, a splint with devices for periodontal therapy is used for temporal restoration of occlusion and esthetics and also for assessment of cleaning, the formof prosthesis and conservation of remaining teeth.

❷ Choice of procedures for prosthesis and precautions
1）Crown restoration (permanent splint)

Permanent splint is performed when a temporary splint cannot provide sufficient intensity because masticatory
dysfunction or failure in comfortable masticatory function is caused by tooth mobility, or occlusal trauma remains. There are various problems with performance of crown restoration for permanent splint, including abutment tooth preparation, impressive accuracy, model production, compatibility of prosthesis, occlusion, and typeof luting cement. Required root canal therapy may cause additional problems. Interdental embrasure and a contour of the prosthesis should be produced to make it easier to perform plaque control. If these are not appropriate,
the risk for caries increases7). If bite force is strong, a permanent splint should be carefully established using devices
for periodontal therapy (provisional restoration) and a temporary splint is used considering the splint range. An
incorrect splint range may induce occlusal trauma in a splint tooth or other remaining teeth, as well as avulsion
and fracture of prosthesis6). Long-term maintenance of prosthesis requires decreased avulsion and fracture of prosthesis8). For patients with a strong bite force, it is particularly important to consider occlusal trauma (Figure13)5,6).

2）Treatment of partially edentulous arch
For tooth loss, prosthetic therapy is performed with a fixed bridge, denture removal, tooth transplantation, andimplanting. Prosthesis for tooth loss is important to secure a continuous dental arch and occlusion and prevent
occlusal trauma from remaining teeth. Understanding the cause of tooth loss is important to obtain good prognosis. If periodontal disease is the cause of tooth loss, it is necessary to understand whether occlusal trauma is involved in the tooth loss. If this is true, full consideration of the response to occlusion is needed. In a free-end
missing without traumatic dental occlusion, the molar is not used for prosthetic therapy, but the short dental archwith occlusion to the premolar is used for building (Table 13)9).

（1）Bridge

10-17)A prosthetic bridge makes abutment teeth receive a bite force; therefore, it is important to examine the missing
range, distribution of remaining teeth, and conditions of periodontal tissues of abutment teeth, and design prosthetics to avoid overload on abutment teeth. A properly designed bridge has a splinting effect, leading to prevention of occlusal trauma.

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Table 13. Choice of prosthesis
Missing level

Support of periodontal tissue andmasticatory andbite force

Prosthesis
Crown and bridge

Partial denture

Implant

Complete denture

◎

◎

◎

×

○
△
Support of periodontal(Improved support with (Abutment teeth bilattissue < masticatory
erally placed as indirect
splint of remaining
and bite force
retainer)teeth)○(Attention to fractureof antagonist)

×△◎
Support of periodontal (Canine protected artic(Splint of remaining
ulation and molar octissue ≥ masticatory
teeth and bilateral parclusal support are conand bite force
tial denture)firmed)◎×

Support of periodontal
tissue ≥ masticatory
and bite force
Several teeth loss

Numberof occlusal
support:
9-6
Multipleteeth loss
Numberof occlusal
support:6-5

Non-vertical stop
occlusion

Several teeth
remaining×○(Splint of remaining
teeth and bilateral partial denture)○(Attention to fractureof antagonist)

×

Support of periodontal
tissue ≥ masticatory
and bite force×◎(Splint of remaining
teeth and bilateral partial denture)○×

Support of periodontal
tissue < masticatory
and bite force×○(Splint of remaining
teeth and bilateral partial denture)○(Attention to fractureof antagonist)○(Multiple teeth are lost
due to root fracture)

Support of periodontal
tissue ≥ masticatory
and bite force

××◎(Prognosis of remaining
teeth have no problems)◎(Overlay denture)◎(Overlay denture)◎(Overlay denture)

Support of periodontal
tissue < masticatory
and bite force

Support of periodontal
tissue < masticatory
and bite force

××○(Attention to choice ofmaterials for superstructure)

Under any condition

××○(Conditions of residual
ridge and mucosa membrane are appropriate)◎ Recommended, ○ Indicated, △ Indicated by condition, × Inadequate（2）Removal of partial denture
Denture must be designed based on the missing range, number of remaining teeth and position, and number ofantagonists. Denture design may cause load bearing of abutment teeth and induce occlusal trauma; therefore, theload bearing ratio of bite force to remaining teeth and residual ridge mucosa should be carefully determined. The
requirements for stability of partial denture are support (vertical movement), grasp (horizontal movement), andretention (prevention of detachment); however, it is necessary to design denture with consideration of oral cavity
cleansing. Stable denture reduces the load bearing of abutment teeth; however, it is important to design denturewith full consideration of the load bearing capacity of remaining teeth.

（3）Implant

18,19)

An implant gives strong support and usually reduces the load bearing of remaining teeth. An implant can avoid
splint associated with cutting of neighboring teeth, but may act as a traumatic force on an antagonist. Therefore,
attention should be paid to an implant with a strong bite force. Periodontal therapy for remaining teeth is important because there is a possibility of periodontopathic bacterial infection from natural teeth to peri-implant tissues.

（4）Tooth transplantation

Tooth transplantation is related to complicated factors for outcomes, including the choice of transplanted teeth,
transplant site and transplant technique. Particularly in evulsion of transplanted teeth, as many healthy periodontal ligaments as possible should be kept20).

70❸ Orthodontic treatment
1）Malalignment

Malalignment is classified into that existing before onset of periodontal disease and that induced by periodontal
disease and habit. For cases in which plaque control is difficult, orthodontic treatment is performed to build anenvironment in which it is easier to manage oral hygiene. For cases with causes of occlusal trauma, including occlusal interference, treatment is used to improve malocclusion.

2）Remodeling of the periodontal tissue by orthodontic treatment21,22)
Teeth that have inclination and extrusion, resulting in complication with occlusal trauma, sometimes have an infrabony defect. Osseous defect may be improved by adding orthodontic force (e.g. uprighting, extrusion, intrusion) to this defect after completion of periodontal therapy. Bone leveling is also performed by extruding a toothwith bone resorption. Therefore, orthodontic treatment is significant for improving the environment of periodontal tissues, and not just for moving teeth.

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14 Implant therapy❶ Benefit of implant therapy for oral functional restoration inpatients with periodontal disease

For oral rehabilitation for patients with periodontal disease associated with a defect, it is important to avoid induction of inflammation or occlusal trauma in periodontal tissues after therapy. Application of an implant for defect prosthodontics is useful for protecting remaining teeth with decreased supportive ability and building serialalignment. Implant therapy may avoid removable denture, install rigid prosthetic devices, reduce prosthetic burden against abutment and retaining teeth, secure occlusal stabilization, prevent natural teeth grinding associatedwith restorative and prosthetic therapy, and improve masticatory efficacy and esthetics1,2). However, this is not acriterion for extracting teeth with periodontal disease. Implant therapy can be used, but teeth on the border of extraction approval should be carefully assessed3,4). There are no strict criteria for extracting teeth with periodontal
disease or use of implant therapy, and implant therapy should be determined based on the patient’s preferences, afull examination by the dentist, and informed consent based on test results.

❷ Peri-implant tissue structure
In comparison with periodontal tissues, tissues around implants have markedly different function and structure5).
The important characteristics of periodontal tissues are periodontal ligaments and suprabony connective tissues.
Teeth are supported by alveolar bones and suprabony connective tissues via periodontal ligaments and connective
tissue fiber, whereas implants connecting directly with osseous tissues (osseointegration) have no connective tissue
attachment containing periodontal ligaments because there is no cementum in implants6). Consequently, no physiological movement occurs in implants. In addition, in contrast to natural teeth, hemidesmosomes alone attachedwith epithelia form the adhesion mechanism of gingival tissues, and implant and gingival fibers are not attachedto the surface of implants and run in parallel with the implant surface7).

❸ Implant therapy in patients with periodontal disease

1）Importance of periodontal therapy prior to implant therapy
Implants are exposed to infection of oral bacteria in the oral cavity, with no significant difference between the attachment form of the implant and epithelium and that of natural teeth and epithelia. However, in contrast to natural teeth, subepithelial gingival fibers lie in parallel with an implant and there is no gingival fiber running resistant to probe insertion7). Consequently, external factors are likely to enter tissues8) and implants are less resistant

to infection than natural teeth. Patients with periodontal disease have a lower rate of implant success than patients
without this disease, and also have a significantly high incidence of peri-implantitis9). Pathogenic bacteria in
peri-implantitis are Gram-negative anaerobic bacteria simultaneous with periodontopathic bacteria, and these bacteria spread and infect from the periodontal site of natural teeth to the peri-implant crevice10). Based on these results, periodontal therapy should be performed for remaining teeth to reduce periodontopathic bacteria in the oralcavity as much as possible prior to implantation. To confirm the effect of periodontal therapy, it is preferable toconduct a periodontal tissue examination and a microbiological assay (bacteria test, serum antibody titer test) andevaluate the test results.

2）Precautions for peri-implant mucositis and peri-implantitis
Indications for implants are wide and include patients with maxillofacial deformity, as well as those with edentu-

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lous jaw or partial tooth loss, and implants are also applied as an anchor of orthodontic treatment. Although implants have been applied to various defects in the oral cavity, peri-implant inflammation occurs similarly to that inperiodontal tissues after implant therapy for patients with periodontal disease who have poor plaque control. Implantation also produces new problems, including peri-implant mucositis and peri-implantitis presenting withclinical and histopathological manifestations11,12). The causes of failure in implant therapy are classified as traumatic and infectious. Periodontopathic bacteria in periodontal pockets in the implanted oral cavity are detected in areas surrounding implants developing peri-implantitis that resulted in failure due to bacterial infection13).

3）Precautions for implant trauma

Microflora in implants with disintegrated osseointegration due to trauma are similar to those in a stable implant14).
When bacterial infection and excessive traumatic force simultaneously act on implants, acute and marked disruption of peri-implant tissues occurs. In prosthetic consideration of tissue disruption, reverse of the crown-to-implant (CI) ratio (i.e., implantation of a short implant body and a long upper structure) is caused by widespread
disruption of bone tissues due to periodontal disease, leading to an excessive burden on implants15). To perform
implant therapy for patients with periodontal disease, precautions for both bacterial infection and traumatic force
and therapeutic guidelines are required. Therefore, in implant therapy for these patients, both risk factors for periodontal disease and for implantation should be controlled, in addition to the number of lost teeth and alveolar
ridge conditions.

❹ Implant therapy and maintenance and supportive therapy (ST)after implantation

Implant therapy requires pretreatment including plaque control, removal of the source of infection in basic periodontal therapy, and adjustment of occlusal relationships. Implant therapy is generally performed as a two-stepprocedure: [1] implantation of the implant body into the bone, [2] implant-abutment connection in the transmucosal site in a secondary surgery after an osseointegration period, and [3] production of upper structures. In contrast, in a one-step implant procedure, the transmucosal site is exposed on the oral mucosa simultaneously withimplantation of the implant body. To maintain long-term implant function, it is important to conduct routine assessments, control peri-implant plaques, and maintain appropriate occlusal conditions, similar to management of
natural teeth. The upper structure of implants is likely to be overcontoured, which is a cause of more difficulty in
self-care. The frequency of visits for maintenance or supportive therapy (ST) after completion of implant therapy
depends on a patient’s ability for oral hygiene control and the host response to pathogenic bacteria around implants. Patient recall is generally every 3 months for the first year, followed by every 6 months16).

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15 Treatment of peri-implant disease1）Definition and classification of peri-implant disease
Implants have been established as a therapeutic option for defect prosthodontics, as a replacement for conventional dentures and bridges. However, various complications after implant therapy occur in the clinical course. In particular, the incidence of peri-implantitis is high and increases after implant therapy1,2). Therefore, it is important torecognize peri-implantitis and establish therapeutic procedures in implant therapy.
Peri-implant mucositis and peri-implantitis are defined as peri-implant disease with inflammatory lesions inperi-implant tissues (Table 14). Peri-implant mucositis is a reversible inflammatory process in peri-implant soft
tissues, whereas peri-implantitis is an inflammatory lesion associated with peri-implant bone disruption caused bybacterial infection and an excessive burden on implants3).
Clinical manifestations of peri-implantitis include redness, swelling, pus discharge in peri-implant tissues, BOP,
increased probing depth, bone resorption and recession of surrounding tissues, followed by progression to abscessformation and implant movement. Marked bone resorption in a radiograph is evidence for advancement ofperi-implantitis.
There are many studies of inflammatory lesions caused by bacterial plaque formation in peri-implant tissues, including differences between natural teeth and peri-implant tissues4-6), and the mode of spreading of inflammationin periodontal tissues differs from that in implants. In periodontal tissues, lesions of periodontitis induced by bacterial plaque are localized in connective tissues early, whereas in peri-implant tissues, lesions spread to the alveolarbones6). Bacterial flora in pockets are similar to each other7).
Given this background, if peri-implant tissues are exposed to bacterial plaque for a long period, peri-implantmucositis proceeds to peri-implantitis8). In addition, fracture and crack of the implant body, abutment (screw),
upper structure loosening, and inflammation induced by cement residues after cementing are complications associated with implant therapy and causes of peri-implantitis. To prevent onset of peri-implantitis, early detection of
initial inflammatory lesions in peri-implant soft tissues is required. Therefore, it is important to monitor changes
in clinical findings around implants routinely and continuously using multiple clinical parameters.

2）Causes of peri-implant mucositis and peri-implantitis
Causes of these diseases include poor oral hygiene conditions9), history of periodontitis10,11), diabetes12), smoking13),
keratinized mucosa deficit14), implant body surface properties15), occlusal contact with the implant, and occlusal
overloading on implants due to occlusal contact and changed occlusal conditions. Overloading is related to the diameter and length of implants, surface structure, number and direction of implants in defects, and bone mass in
implanted sites8). Microflora formed around implants are similar to those around natural teeth and periodontopathic bacteria, with high proportions of Porphyromonas gingivalis, Treponema denticola and Aggregatibacter actinomycetemcomitans16,17). When the remaining teeth are affected by periodontal disease and not treated with plaquecontrol, these teeth are reservoirs of periodontopathic bacteria around implants18); consequently, risks increase in
Table 14. Peri-implant mucositis and peri-implantitis
Peri-implant mucositis

Peri-implantitis

Reversible inflammatory lesion
localized to surrounding mucosa

Irreversible inflammatory lesion
associated with bone resorption

BOP

+

+

Drainage+ or -+

Bone resorption−+ Difficult to detect in early lesions.
Different to progression state

Deflection−+ In a case with progression

Pathology

74

patients with generalized aggressive periodontitis and severe generalized chronic periodontitis (Stage III-IV, GradeC).

3）Clinical examination of peri-implant tissues
Systematic and consecutive modeling of peri-implant tissues based on routine maintenance or SPT is necessaryfor early diagnosis of lesions in peri-implant tissues. The following clinical parameters are proposed to assess conditions from early onset to advanced lesions and for diagnosis of lesions.

（1）Assessment of plaque (biofilm) control

Biofilms form on the surface of implants, similarly to periodontal disease. Oral hygiene is closely related to onsetof peri-implantitis; therefore, removal of biofilms by reliable plaque control is necessary to maintain healthy conditions of peri-implant tissues. Therefore, it is important to perform plaque control, using the modified plaque index (mPI) for objective assessment19).

（2）Probing depth (PD) in peri-implant tissues
Peri-implant probing is an important and reliable method for continuous monitoring of peri-implant tissues. PB
requires appropriate pressure (0.2-0.3 N) based on the conditions of the keratinized mucosa or alveolar mucosa8).
The insertion direction is determined considering the type, mode (platform switching) and depth of the implant
body. The approach using PD should depend on the chronological increase in PD, rather than the absolute valueof PD, because PD changes are correlated with the conditions of peri-implant inflammation1,19). Resistance of tissues in inserting a probe is also helpful to determine whether tissues are healthy.

（3）Bleeding on probing (BOP)The accuracy of BOP diagnosis is higher than that in natural teeth20) and BOP is an important index to monitor
inflammation in peri-implant tissues and disease progression. A BOP(−) status under appropriate probing pressureshows healthy conditions of peri-implant tissues.

（4）Pus discharge

There is a need to examine whether pus discharge from peri-implant pockets is found due to compressed peri-implant mucosa. Drainage is not an appropriate parameter for early peri-implantitis, but suggests that a lesion suspected to be advanced peri-implantitis is associated with bone disruption. Since inflammation of peri-implant tissues is active, it is necessary to treat bacterial infection1,19).

（5）Radiographic assessment (bone resorption)

Radiography is used as a definitive step to examine the bone resorption level of the surrounding bone when clinical indices show a peri-implant lesion. Dental cone-beam computed tomography is used when the three-dimensional bone form or loss needs to be examined for assessment.

（6）Implant deflection

If the upper structure of the implant body is deflected, upper structure loosening and incompatibility or osseointegration loss in the implant body is suspected. Implant body movement after uninstalling upper structures is
considered to be osseointegration loss, which is the criterion for uninstallation of the implant.

（7）Peri-implant keratinized mucosa

Insufficient keratinized mucosa results in poor plaque control and inappropriate probing depth and BOP 1,19).
However, there is no clear evidence showing a requirement for keratinized mucosa.

（8）Occlusal relation

Peri-implant bone disruption progresses acutely due to bruxism and occlusal trauma with advance of peri-implantitis21). Peri-implant bone is lost due to excessive overloading and upper structures are broken and fixation screws
fracture.

（9）Microbiological tests
In general, periodontal bacteria are monitored to determine maintenance intervals for risk diagnosis in maintenance of high risk patients with periodontal disease.

754）Treatment of peri-implant mucositis and peri-implantitis
The priority for treatment of peri-implant mucositis and peri-implantitis is to extinguish inflammatory lesions inaffected areas due to bacterial infection. It is necessary to diagnose and treat affected areas and simultaneously diagnose and treat periodontitis in remaining teeth. The success of conservative therapy or surgical treatment depends on debridement of bacterial biofilms attached to microstructures on the implant surface. The treatment isperformed first according to basic periodontal therapy, followed by reassessment after elimination of inflammationis confirmed. Surgical procedures should be selected based on the test results. Periodontal tissue examination andperiodontal therapy for remaining teeth are essential.

（1）Non-surgical treatment

Therapy for improvement of inflammation includes instructions for oral hygiene (plaque control) debridement of
the implant body, mechanical cleaning, microbicides (antiseptic) therapy, antibiotic therapy, laser coagulation, airablation and photodynamic therapy (PDT), which are consistent with basic periodontal therapy. Bacterial tests arealso important in the treatment process. Remaining teeth including adjacent and opposing teeth are kept to maintain an appropriate relationship between them. Occlusal balance is secured by occlusal adjustment as required after contact with the implant and changed occlusion conditions. In addition, occlusal trauma of remaining teeth
and overloading of occlusion to the implant are prevented22,23). Bruxism is treated considering the patient’s condition, and smoking and systemic disease are also considered. Reassessment is then performed and possible use ofsurgery is determined depending on the patient.

（2）Surgical treatment

Surgery includes resective therapy (gingivectomy and periapical flap procedure) to expose the surface of a contaminated implant body, periodontal plastic surgery for immobile keratinized mucosa deficit surrounding an implant(free gingival graft and connective tissue graft), and regenerative therapy for vertical osseous defect). These respective procedures should be used considering the indications. Particularly in regenerative therapy, debridement ofcontaminated implant surfaces is important, with treatment using curettage with a pure titanium curette, laser, airablation, PDT, and implant plasty; however, no appropriate procedure has been established and further work isneeded1,19). Regenerative therapy includes a combination of membrane and autologous bone or bone grafting materials and application of Emdogain®. The requirements shown in Table 15 should be considered in choosing thesurgical procedure.

（3）Cumulative interceptive supportive therapy (CIST) (Table 14)
For management after implant therapy, it is important to routinely monitor clinical parameters, identify pathological conditions earlier and conduct early treatment. Lang et al.24) recommended a CIST protocol (Figure 14) for
systematically integrated assessments (including bacterial tests) of peri-implant tissue conditions of plaque index(Pl.I), probing depth (PD), BOP and bone resorption in radiography; however, this methodology is not established. This protocol includes four categories (A to D) in accordance with the combination of assessment of clinical parameters.
Table 15. Requirements for surgical therapy• Control of pathogenic bacteria before surgery (including antibiotic therapy)• Confirmation of keratinized mucosa (not movable)• Choice of definite debridement on the implant body surface• Diagnosis of horizontal and vertical osseous defects and choice of surgical procedures• Choice of biomaterials used for regenerative therapy

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PPD ≤3 mm

PPD 4-5 mm

PPD >5 mm

Pl.I <1
BOP (–)
Pl.I ≥1
BOP (+)

Mechanical cleaning
Polishing and scaling
Antibacterial cleaning

Gargling or topical applicationof antiseptics/microbicides

BOP (+)
No crater of alveolar bone

Twice a day, for 3-4 weeks

BOP (+)
Crater of alveolar bone ≤2 mm

Medication with systemic
and topical antibiotics

BOP (+)
Bone resorption >2 mm

Surgical resection
Regenerative therapy

Mobility (+)

Implant removal

Figure 14. Cumulative interceptive supportive therapy (CIST)

A: mechanical plaque removal
B: application of microbicides
C: systemic or localized administration of antibiotics
D: surgical approach (resective or regenerative surgery)
E: implant removal
A flowchart of treatment until surgery is shown in Figure 15: A: initial therapy for peri-implantitis: mechanical plaque removal, B: application of microbicides, including chlorhexidine, and C: systemic or localized administration of antibiotics, for which the priority is thorough removal of pathogenic bacteria. Surgical proceduresshould be chosen, including the need for surgery, after reassessment. After surgery, it is important to design a routine maintenance program based on the patient’s conditions and perform SPT for remaining teeth and implants.
For details, refer to the Therapeutic Strategy and Evidence for Oral Implants in Patients with Periodontal Disease2018 (JSP)25).

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Peri-implantitis histology
Diagnosis/planning of therapeutic strategy

Corresponding
to CIST A

Initial therapy(Plaque control, debridement, polishing and scaling)

Reassessment
Corresponding
to CIST B

Mouth rinse or topical application with disinfectants or microbicides

Reassessment
Corresponding
to CIST C

Medication with systemic or topical antibiotics
Reassessment

Corresponding
to CIST D

Surgical resection or regenerative therapy
Reassessment
Maintenance of supportive therapy

Figure 15. Flowchart of treatment for peri-implantitis

78

16 Follow-up
Bacterial plaque, the main factor for periodontal disease, is always present in the oral cavity. Since traumatic factors are also resident, periodontal pockets of ≥4 mm and furcation involvement remain after completion of appropriate periodontal therapy. Inflammation or BOP is also often found in patients with periodontal pockets of <4mm. The motivation of patients with periodontal disease decreases with time and the environment in the oral cavity, including changes in position and form of the marginal gingiva over time, and systemic factors have effects,
making periodontal disease highly likely to recur1). Therefore, it is important to classify the conditions after periodontal therapy into “healing”, “stable state” and “preventive stage,” which have been incorporated into Social Insurance in Japan, and improve the patient’s motivation to maintain periodontal tissues that are cured or stabilized
by periodontal therapy, with performance of plaque control and SPT based on instructions in daily life, and toprovide continuous management from a dental stand point2,3). As described above, primary care dentists should
consider the patient’s periodontal tissues management status. Such management prevents recurrence, exacerbation,
tooth loss and disruption of periodontal tissues, maintains long term masticatory performance, improves qualityof life (QOL), and increases the healthy lifespan.

❶ Term definitions

1）Maintenance
Maintenance is long-term health management to maintain periodontal tissues cured by initial periodontal therapy,
periodontal surgery and oral rehabilitation. Periodontitis is likely to recur due to insufficient plaque; therefore,routine maintenance is essential. Maintenance consists of self-care (home care) by patients, motivation to makepatients undergo therapy, and professional care by dentists and dental specialists.

2）Preventive periodontal therapy (PPT)Preventive periodontal therapy (PPT) is a follow-up concept that has been newly incorporated in Social Insurancein Japan. Periodontal disease is determined to be in the “preventive stage” when the gingiva is improved withprobing depth <4 mm, but remaining inflammation is confirmed after scaling, SRP or periodontal surgery. Follow-up is performed to prevent progression of periodontal disease. PPT can prevent progression from gingivitis toperiodontitis and worsening of periodontitis. A patient with a worsening disease status during PPT should discontinue PPT and undergo initial periodontal therapy, periodontal surgery, or SPT.

3）Supportive periodontal therapy (SPT)In a case in which most periodontal tissues are cured by initial periodontal therapy, periodontal surgery and oral
rehabilitation, but periodontal pockets remain in a progression-resting stage, the patient is considered to be in a“stable state”. SPT is performed to stabilize the disease stage of periodontal tissues for a long period. SPT is comprehensive therapy consisting of plaque control, PMTC, periodontal pocket cleaning, scaling and root cleaningand occlusal adjustment, with the goal of removing causal factors and giving instructions for oral hygiene and remotivation.

4）Healing
Healing indicates clinically healthy conditions restored in periodontal tissues: no gingival inflammation or BOP,
probing depth <4 mm and tooth movement within physiological ranges. Patients with probing depth <4 mm, but
gingival recession and exposed furcation are also sometimes determined to be “healing”. Dentine reinforcementwith fluoride is used in maintenance.

795）Suppression of progression (a new concept in health insurance)
When reassessment results show that a patient has inflammation in some gingiva, but recovery in all regions withprobing depth <4 mm, the patient is considered to be in a “preventive stage”. In this stage, failure of continuous
maintenance may cause progression of periodontal disease. Therefore, PPT is performed to improve, maintain andstabilize the pathological conditions. It is necessary to assess risks in the patient and continue to conduct reassessment and PPT.

6）Stable lesion
Patients with healthy periodontal conditions, but a periodontal pocket ≥4 mm without BOP, furcation involvement and tooth movement without inflammation in a reassessment test are clinically stable and determined to be
in a “stable state”. These patients undergo SPT. Some of these patients who cannot undergo periodontal surgery
due to systemic disease or other risk factors should frequently undergo a reassessment test and SPT. Patients who
have tooth movement, bruxism and a parafunctional habit, decreased tooth support volume due to severe alveolarbone resorption resulting in occlusal trauma even with physiological bite force, or a systemic disease (e.g. diabetes)should also undergo SPT4).

7）Professional tooth cleaning (PTC)
PTC includes plaque removal, SRP, and polishing of the tooth surface, all of which are periodontal therapy, performed by a dentist or dental hygienist.

8）Professional mechanical tooth cleaning (PMTC)
PMTC is mechanical removal of plaque from teeth by a dentist or dental hygienist using cleaning instruments.
SRP is not included, in principle. In addition, Axelsson defines PMTC as mechanical tooth cleaning by specialists, or procedures for mechanically choosing and removing supragingival and subgingival plaque of 1-3 mm on
all the tooth surface, including the interdental adjacent area using an EVA tip system and paste containing fluoride with a reciprocating Profin band handpiece3).

❷ Examination and diagnosis
Reassessment before transfer to follow-up is performed similarly to the first dental examination, in principle. After
examination results and risk factors are determined, the effect of periodontal therapy and disease state are assessed.
If no repeated basic periodontal therapy or periodontal surgery is necessary, a patient is defined to be in a “preventive stage”, “stable state” or “healing”, and is transferred to PPT, SPT or maintenance. Even during PPT and SPT
as part of periodontal therapy, or maintenance as healthy management, reassessment is conducted in an appropriate period and the disease process is evaluated. If disease has advanced, the causes are found and therapy including
periodontal surgery is performed. Flowcharts for PPT, SPT and the maintenance stage after reassessment and criteria are shown in Figures 16 and 17, respectively.

1）Time of assessment
The time of “healing”, “suppression of progression” or “stable state” depends on the state of progression.

（1）Plaque-induced gingivitis

In a case of plaque-induced gingivitis, “healing” is assessed when a healthy status is recorded by initial periodontal
treatment and PPD <4 mm without inflammation are confirmed by reassessment. Periodontal therapy is not completed at this point, but maintenance is performed at appropriate intervals (e.g. recall, reassessment, oral hygiene
instructions, SRP, and PMTC once every 3 to 6 months). In case of plaque-induced gingivitis, the stage of “suppression of progression” is determined when the gingiva improves with PPD <4 mm, but PPT and reassessment

80

g y

)

Figure 16. Flow of maintenance, SPT, pathological progression and PPTPreventive periodontal therapy (PPT) is a new concept in Japanese health insurance.

Re-evaluation

Probing depth, bleeding on probing (BOP), tooth mobility,
furcation involvement, bacterial test, antibody level test

All PPD <4 mm$WOHDVWRQHVLWHPP

ALL PPD <4 mm

BOP: (–)

BOP: (±)

BOP: (+)

BOP: (+)

Tooth mobility (–)
Furcation involvement (–)
Bacterial count: Low Risk
Antibody level: Low Risk

Tooth mobility (±)
Furcation involvement (±)
Bacterial count: Midium Risk
Antibody level: Midium Risk

Tooth mobility (±)
Furcation involvement (±)
Bacterial count: High Risk
Antibody level: High Risk

Tooth mobility (±)
Furcation involvement (±)

Figure 1�. �etermination of the e�ect of periodontal therap�A comprehensive diagnosis includes reference with PPD, bleeding on probing (BOP), tooth mobility, furcation involvement, and bacterial and serum antibody level test.
For risk assessment of bacterial counts and serum antibody levels, see the “Guidelines for Appropriate use of Antibiotics in Patients with Periodontal Disease 2020”, page 16.
Preventive periodontal therapy (PPT) is a new concept in Japanese health insurance.

should be performed continuously when gingival inflammation remains.

（2）Periodontitis

In a case of slight periodontitis, it is possible to reach a stage where the case can be assessed as “healing” or “suppression of progression” with only initial treatment. Moderate or severe periodontitis may involve areas requiring
periodontal surgery. After periodontal surgery, a reassessment examination should be performed to assess treatment efficacy and periodontal status. Patients who are assessed to be in the “suppression of progression”, “stable lesion” or “healing” stage at completion of oral rehabilitation should transfer to PPT, SPT or maintenance.

81

1XPEHU RI SHULRGRQWDO VLWHV  PP
1XPEHURISHULRGRQWDOVLWHVPP
Percentage of BOP (+) sites/oral cavity
Molar maximum bone resorption %/age
Number missing out of 28 teeth
Systemic disease and genetic predisposition
Smokingg status
1XPEHURI3'PP:

SRLQWVSRLQWVSRLQWV

Bleeding %

:







Bone resorption/age

:





WHHWKWHHWKWHHWK

Number of missing teeth :Systemic disease

:

No

Yes

Yes

Smoking:

0 /dayFLJDUHWWHVGD\

FLJDUHWWHVGD\

Instructions forcontrol of causativeand risk factors:

RIWKHDERYHLWHPVRIWKHDERYHLWHPVRIWKHDERYHLWHPVAs required

Usual

Frequent

Figure 18. Risk assessment in SPT5)2）Items of clinical examination（1）Periodontal tissue examination

The decision to move to SPT or maintenance depends on reassessment of oral hygiene conditions, PPD, BOP,
tooth mobility, radiography, occlusion and furcation involvement.

（2）Bacterial tests

Bacterial tests to monitor periodontopathic bacteria in subgingival plaque, including P. gingivaliss and A. actinomycetemcomitans, and antibody titer (infection marker) tests help to determine therapeutic effects and define thecontents of SPT.

（3）Other examinations
A gingival crevicular fluid (GCF) test also helps to determine therapeutic effects and the details of SPT.

（4）Risk assessment in SPT (revised Lang & Tonetti5), Figure 18)

It is important to classify patients into low- to high-risk levels based on conditions in the oral cavity, to design acare program according to these conditions, and perform patient management.
Lang and Tonetti5) proposed the following risk assessment.
[1] Number of sites with PD ≥5 mm: low risk ≤4 sites, high risk of recurrence ≥8 sites.
[2] Percentage of BOP sites: low risk ≤9%, high risk ≥25%. The cutoff between a stable state and recurrence oradvancement is 25%.
[3] Bone loss and age, measured as radiographic bone loss in percentage of molar root length divided by age ofsubject: low risk ≤0.5%, high risk ≥1.0%.
[4] Number of missing teeth per 28 teeth: low risk ≤4 teeth, high risk of recurrence ≥8 teeth.
[5] Systemic disease/hereditary factors: diabetes or IL-1 genotype-positive is high risk, unknown or IL-1 genotype-negative is no risk.
[6] Environment (lifestyle): non-smoking or smoking cessation ≥5 years is low risk, smoking ≥20 cigarettes/day
is high risk.
Periodontal disease risk is classified into the following three risk groups according to the above six parameters.
*Low periodontal risk: all 6 parameters are low risk or one parameter is moderate risk.
*Moderate periodontal risk: at least 2 parameters are moderate risk, and one at most is high risk.

82*High periodontal risk: at least 2 parameters are high risk.

❸ Therapeutic planning
The contents of therapy after reassessment examination are roughly divided into maintenance6-9) and SPT10), andthe following therapies are chosen.

1）Maintenance6-9)
Maintenance is performed to prevent recurrence in patients who are judged to be “healing” in reassessment. The
objectives of maintenance are [1] prevention of recurrence of periodontal disease, [2] early detection of recurrenceof periodontal disease, and [3] long-term maintenance of a good environment of periodontal tissues. Maintenanceprocedures are based on maintaining motivation and confirming appropriate self-care, and PMTC and SRP areadded according to the oral conditions. PTC and PMTC are critical procedures. Dentine reinforcement by application of fluoride and plaque removal by professional care provide an excellent oral hygiene environment. Furthermore, it is necessary to give guidance for improvement of lifestyle corresponding to the patient’s background, including living environment, oral conditions and risk factors. For patients with risk factors such as smoking,dietary habit and drinking and systemic diseases including diabetes, it is necessary to perform management focusing on oral hygiene instructions to maintain reasonable plaque control and give instructions on these environmental factors and systemic risk factors. Recall interval is an important factor and should be decided based on information from various examinations and the condition of periodontal tissue.

2）Suppressive therapy for periodontal disease progression(new follow-up in health Insurance)

Suppressive therapy for periodontal disease progression is treatment to suppress progression from gingivitis toperiodontitis for patients with a probing depth <4 mm, but slight gingival inflammation in reassessment. The objectives of suppressive therapy for periodontal disease progression are [1] prevention of worsening of periodontal
disease, [2] early findings of recurrence of periodontal disease, and [3] long-term maintenance of a good environment of periodontal tissues. Treatment includes maintenance of motivation, enhanced plaque control, SRP and
PMTC. A patient with worsening of disease status or periodontal pockets ≥4 mm should restart initial periodontal
therapy, periodontal surgery, or SPT. Recall every 1 to 3 months is generally recommended.

3）Supportive periodontal therapy (SPT)10,11)
If disease conditions are determined as stable in reassessment, the therapeutic stage moves to SPT. The objectivesof SPT are [1] to provide therapy to maintain or cure lesions in a stable state, [2] to detect new lesions of periodontal disease at an early stage, and [3] to maintain a good environment for periodontal tissues. Therapeuticcontents include enforced plaque control (instructions for oral hygiene), professional mechanical tooth cleaning
and SRP, and periodontal pocket irrigation and occlusal adjustment as required, as well as administration of antibacterial agents into periodontal pockets (Table 16). However, when the disease is advanced (probing depth ≥4mm, BOP (+), many bacteria, high antibody level), periodontal surgery may be performed (Figure 17, Table
16). Recall intervals for SPT depend on periodontal tissue conditions and the plaque control level in each patient,but recall every 1 to 3 months is generally recommended. Recall intervals can increase or decrease as the conditionchanges; e.g. every one month initially, then every 3 months or every 6 months.

83

Table 16. Therapeutic contents of healing, stable state and progression state
Maintenance at appropriate intervals
Oral hygiene instructions (plaque control)
Professional mechanical tooth cleaning (PMTC)
Scaling and root planing

Healing

MaintenancePreventive
stage

Preventive periodontal therapy(PPT)(new follow-up in Japanese healthinsurance)

Preventive periodontal therapy at appropriate intervals
Oral hygiene instructions (plaque control)
Professional mechanical cleaning
Scaling and root planing

Supportive periodontal therapy(SPT)

Based on SPT at appropriate intervals
Oral hygiene instructions (plaque control)
Professional mechanical tooth cleaning (PMTC)
Scaling and root planing
Periodontal pocket cleaning
Administration of antibacterial agents into periodontal pockets
Elimination of traumatic factors (occlusal adjustment, splint)

Stable lesion

Disease evolution

Periodontal surgery, etc.

Periodontal surgery• Flap surgery• Gingivectomy, etc.
Oral rehabilitation

84

References

1 What is periodontal disease?
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3) MHLW Dental Health Div Health Policy Bur: Summary of the Survey of Dental Diseases, 2011.
(http://www.mhlw.go.jp/toukei/list/dl/62-23-01.pdf )4) MHLW Dental Health Div Health Policy Bur: Summary of the Survey of Dental Diseases, 2016.
(https://www.mhlw.go.jp/toukei/list/dl/62-28-02.pdf )5) Japanese Society of Periodontology ed.: Glossary of Periodontal Terms 2019. 3rd edition. Ishiyaku Publishers,
Inc. Tokyo, 20196) MHLW: Community Health and Health Promotion Project Report.
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and regional differences of participation in periodontal screenings. J Dent Hith, 68: 92-100, 2018.
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System for Periodontal Disease by The Japanese Society of Periodontology (2006). J Jpn Assoc Periodontol, 49:
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M, Tonetti MS: A new classification scheme for periodontal and peri-implant diseases and conditions-Introduction and key changes from the 1999 classiffcation. J Periodontol, 89 (Suppl 1): S1-S8, 2018.
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9-11, 1997.
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2 Process of periodontal therapy
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JB Lippincott, Philadelphia, 1991.
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85

and peri odontal disease in adults: results after 30 years of maintenance. J Clin Periodontol, 31: 749-757,
2004.

3 Medical interview, patient referral, and liaison with medicine
1) Ripamonti CI, Maniezzo M, Campa T, Fagnoni E, Brunelli C, Saibene G, Bareggi C, Ascani L, Cislaghi E:
Decreased occurrence of osteonecrosis of the jaw after im plementation of dental preventive measures in solid
tumour patients with bone metastases treated with bisphos phonates: the experience of the National Cancer
Institute of Milan. Ann Oncol, 20: 137-145, 2009.
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Hillner BE, Theriault RL, Zuckerman DS, Von Roenn JH: American Society of Clinical Oncology executive
summary of the clinical practice guideline update on the role of bone-modifying agents in metastatic breast
cancer. J Clin Oncol, 29: 1221-1227, 2011.

4 Examination, diagnosis and therapeutic strategy for periodontal disease
1) Löe H: The Gingival Index, the Plaque Index and the Retention Index Systems. J Periodontol, 38: Suppl: 610616, 1967.
2) Greenstein G: The role of bleeding upon probing in the diagnosis of periodontal disease.A literature review. J
Periodontol, 55: 684-688, 1984.
3) Lang NP, Adler R, Joss A, Nyman S: Absence of bleeding on probing. An indicator of periodontal stability. J
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4) O'Leary TJ, Drake RB, Naylor JE: The plaque control record. J Periodontol, 43: 38, 1972.
5) Nyman S, Lindhe J: Examination of patients with periodontal disease. In: Lindhe J, Karring T, Lang NP. eds,
Textbook of Clinical Periodontology. 2nd ed. Munksgaard, Copenhagen, 1989, 316.
6) Glickman I: Clinical Periodontology. 2nd ed. W.S.Saunders, Philadelphia, 1958, 684-696.
7) Murayama Y, Nagai A, Okamura K, Nomura Y, Kokeguchi S, Kato K: Serum immunoglobulin G antibody toperiodontal bacteria. Adv Dent Res, 2: 339-345, 1988.
8) Williams KB, Gadbury-Amyot CC, Krust-Bray K: Oral health-related quality of life: a model for dental hygiene. J Dent Hyg, 72: 19-26, 1998.
9) Gadbury-Amyot CC, Williams KB, Krust-Bray K, Manne D, Collins P: Validity and reliability of oral healthrelated quality of life instrument for dental hygiene. J Dent Hyg, 73: 126-134, 1999.
10) Saito A, Hosaka Y, Kikuchi M, Akamatsu M, Fukaya C, Matsumoto S, Ueshima F, Hayakawa H, Fujinami K,
Nakagawa T: Effect of initial periodontal therapy on oral health-related quality of life in patients with periodontitis in Japan. J Periodontol, 81: 1001-1009, 2010.
11) Lang N, Bartold PM, Cullinan M, Jeffcoat M, Mombelli A, Murakami S, Page R, Papapanou P, Tonetti M,
Van Dyke T: Consensus Report: Aggressive Periodontitis. Ann Periodontol, 4: 53, 1999.

5 Periodontal therapy and oral biofilm infection in home care, perioperative patients and disabled persons

1) Kato H, Okuyama H: Dental home visits in future. Ishiyaku Publishers, Inc. Tokyo, 109-128, 2000.
2) Yoneyama T, Oiba H, Ota M, Hirota K, Miyake Y, Kajimoto K, Okamoto H: Treatment of Gingivitis in Elderly Patients in a Nursing Home. Japanese Journal of Geriatrics, 34: 120-124, 1997.
3) Tokyo Metropolitan Center for Oral Health of Persons with Disabilities: Special needs dentistry handbook:dental treatment handbook for disabled people, revised edition. Issei Publication, Tokyo, 2015, 170.

864) Osada Y, Mimura K, Imoto T, Nakamura M, Ayuse T: Effect of Combined Treatment of Oral Antimicrobial
Therapy and One-stage Full-mouth Scaling and Root Planing for Severe Periodontitis Patients with Mental
Retardation. J Jpn Soc Disability and Oral Health, 31: 224-231, 2010.
5) Gómez SM, Danser MM, Sipos PM, Rowshani B, van der Velden U, van der Weijden GA: Tongue coating
and salivary bacterial counts in healthy/gingivitis subjects and periodontitis patients. J Clin Periodontol, 28:
970-978, 2001.
6) Minakuchi S, Tsuga K, Ikebe K, Ueda T, Tamura F, Nagao K, Furuya J, Matsuo K, Yamamoto K, Kanazawa M,
Watanabe Y, Hirano H, Kikutani T, Sakurai K: Deterioration of Oral Function in the Elderly. The Position
Paper from Japanese Society of Gerodontology in 2016. Jpn J Gerodont, 31: 81-99, 2016.

6 Emergency procedures
1) Hanes PJ, Purvis JP: Local anti-infective therapy: pharmacological agents: A systematic review. Ann Periodontol, 8: 79-98, 2003.

7 Preventive treatment
1) MHLW Dental Health Div Health Policy Bur: Summary of the 2011 dental disease survey results.

8 Initial periodontal therapy❸ Treatment of bacterial infection
1) Löe H, Theilade E, Jensen SB: Experimental gingivitis in man. J Periodontol, 36: 177-187, 1965.
2) Sanz M, Herrera D: Role of oral hygiene during the healing phase of Periodontal therapy. In: Lang NP, Attstrom R, Loe H, eds, the European Workshop on Mechanical Plaque Control.Quintessence, London, 1998,
248-267.
3) Cortellini P, Tonetti MS, Pini-Prato G: Periodontal regeneration of human intrabony defects: Ⅳ .determinantsof healing response. J Periodontol, 64: 934-940, 1993.
4) Loos B, Claffey N, Crigger M: Effects of oral hygiene measures on clinical and microbiological parameters of
Periodontal disease. J Clin Periodontol, 15: 211-216, 1988.
5) Lindhe J, Okamoto H, Yoneyama T, Haffajee A, Socransky SS: Longitudinal changes in periodontal disease in
untreated subjects. J Clin Periodontol, 16: 662-670, 1989.
6) Axelsson P, Lindhe J, Nystrom B: On the prevention of caries and periodontal disease: results of a 15-year longitudinal study in adults. J Clin Periodontol, 18: 182-189, 1991.
7) Kaldahl WB, Kalkwarf KL, Patil KD: A review of longitudinal studies that compared Periodontal therapies. J
Periodontol, 64: 243-253, 1993.
8) Hugoson A, Koch G: Oral health in 1000 individuals aged 3-70 years in the community of Jonkoping, Sweden: a review. Swed Dent J, 3: 69-87, 1979.
9) Axelsson P: Mechanical Plaque control. In: Lang NP, Karring T, eds, the 1st European Workshop on Periodontology. Quintessence Publishing, London, 1993, 215-243.
10) Nyman S, Sarhed G, Ericsson I, Gottlow J, Karring T: Role of “diseased” root cementum in healing following
treatment of periodontal disease: an experimental study in the dog. J Periodontal Res, 21: 496-503, 1986.
11) Nyman S, Westfelt E, Sarhed G, Karring T: Role of “diseased” root cementum in healing following treatmentof Periodontal diseasea clinical study. J Clin Periodontol, 15: 464-468, 1988.
12) Oberholzer R, Rateitschak KH: Root cleaning or root smoothing: an in vivo study. J Clin Periodontol, 23:326-330, 1996.
13) Oda S, Ishikawa I: In vitro effectiveness of a newly-designed ultrasonic scaler tip for furcation areas. J Periodontol, 60: 634-639, 1989.
14) Badersten A, Nilveus R, Egelberg J: Effect of nonsurgical Periodontal therapy: I. Moderately advanced peri-

87

odontitis. J Clin Periodontol, 8: 57-72, 1981.
15) Oda S, Nitta H, Setoguchi T, Izumi Y, Ishikawa I: Current concepts and advances in manual and power-driven instrumentation. Periodontol 2000, 36: 45-58, 2004.

❹ Current treatment of bacterial infection

1) Lindhe J (trans. Okamoto H: Lindhe Clinical periodontology and implant. 4Th ed. Clinical version. Quintessence Publishing Co., Ltd. Tokyo, 2005.
2) Minabe M: Scientific evidence for the effect of sub-gingival biofilm control. Journal of the Japan Health Care
Dental Association, 5: 42-61, 2003.
3) Heitz-Mayfield LJ: How effective is surgical therapy compared with nonsurgical debridement?. Periodontol
2000, 37; 72-87, 2005.
4) Klaus H. Rateitschak: Color Atlas of Periodontology. Nagasue Shoten Inc., 2008.
5) Furuichi Y: Chemical Plaque Control. Journal of the Japanese Association of Periodontology, 55: 3-8, 2013.
6) Murayama Y, Nomura Y, Yamaoka A, Ueda M, Hori T, Minabe M, Umemoto T, Ishikawa I, Uraguchi R,
Ueno K, Watanabe K, Ogawa N: Local Administration of Minocycline for Periodontitis Double Blind Comparative Study of LS-007. J Jpn Soc Periodontol, 30: 206-222, 1988.
7) Preus HR, Lassen J, Aass AM, Ciancio SG: Bacterial resistance following subgingival and systemic administration of minocycline. J Clin Periodontol, 22: 380-384, 1995.
8) Walker CB, Godowski KC, Borden L, Lennon J, Nango S, Stone C, Garret S: The effects of sustained release
doxycycline on the anaerobic flora and antibiotic-resistant patterns in subgingival plaque and saliva. J Periodontol, 71: 768-774, 2000.
9) Herrera D, Sanz M, Jepsen S, Needleman I, Roldan S: A systematic review on the effect of systemic anti-microbials as an adjunct to scaling and root planing in periodontitis patients. J Clin Periodontol, 29 (Suppl 3):
136-159, 2002.
10) Haffajee A, Socransky SS, Gunsolley JC: Systemic anti-infective periodontal therapy. A systematic review. Ann
Periodontol, 8: 115-181, 2003.

❺ Treatment of occlusal trauma
1) The American Academy of Periodontology: Glossary of Periodontal Terms. The American Academy of Periodontology, Chicago, 1992, 34.
2) Ramfjörd SP, Ash MM Jr: Significance of occlusion in the etiology and treatment of early, moderate and advanced periodontitis. J Periodontol, 52: 511-517, 1981.
3) Svanberg G, Lindhe J: Vascular reactions in the Periodontal ligament incident to trauma from occlusion. J
Clin Periodontol, 1: 58-69, 1974.
4) Lauritzen AG: Atlas of occlusal analysis. HAH publication, Colorado Springs, 1974.
5) Krogh-Poulsen WG, Olsson A: Management of the occlusion of the teeth. In: Schwartz LS, Chayes CM, eds,
Facial pain and mandibular dysfunction. WB Saunders, Philadelphia, 1968.
6) Howard LW: Manual of clinical periodontics. CV Mosby, Saint Louis, 1973, 147-159.
7) Amsterdams M, Abrams L: Periodontal prosthesis. In: Goldman HM, Cohen DW eds, Periodontal therapy.
Mosby, Philadelphia, 1980, 1121-1154.
8) Lindhe J: The text book of periodontology. Munksgard, Copenhagen, 1986, 451-479.
9) Pierce CJ, Gale EN: A comparison of different treatment for nocturnal bruxism. J Dent Res, 67: 597-601,
1988.
10) Carranza FA: Glickman's clinical periodontology. 7th ed. WB Saunders, Philadelphia, 1990, 264-285, 750758.

❻ Support for smoking cessation
1) Inagaki K, Naito T, Ishihara , Kaneko T, Nakayama Y, Yamamoto T, Yoshinari N, Morita M, Kurihara H:
Smoking cessation manual for periodontal practice. J Jpn Assoc Periodontol, 60:201-219, 2018.

882) WHO: WHO Monograph on Tobacco cessation and oral health integration. (https://www.who.int/publications/i/item/who-monograph-on-tobacco-cessation-and-oral-health-integration, Accessed for Aug 8, 2021)
3) Leite FRM, Nascimento GG, Baake S, Pedersen LD, Scheutz F, López R: Impact of smoking cessation on
periodontitis: A systematic review and meta-analysis of prospective longitudinal observational and interventional studies. Nicotine Tob Res, doi: 10.1093/ntr/nty147. Jul 13, 2018.
4) Hanioka T, Morita M, Yamamoto T, Inagaki K, Wang PL, Ito H, Morozumi T, Takeshita T, Suzuki N, Shigeishi H, Sugiyama M, Ohta K, Nagao T, Hanada N, Ojima M, Ogawa H: Smoking and periodontal microorganisms. Jpn Dent Sci Rev, 55: 88-94, 2019.
5) Nakayama Y, Mizutani K, Tsumanuma Y, Yoshino H, Aoyama N, Inagaki K, Morita M, Izumi Y, Murakami S,
Yoshimura H, Matsuura T, Murakami T, Yamamoto M, Yoshinari N, Mezawa M, Ogata Y, Yoshimura A,
Kono K, Maruyama K, Sato S, Sakagami R, Ito H, Numabe Y, Nikaido M, Hanioka T, Seto K, Fukuda J,
Warnakulasuriya S, Nagao T: A multicenter, prospective cohort study on the effect of smoking cessation on
periodontal therapies in Japan. J Oral Sci, 63: 114-118, 2020.

9 Risk factors for periodontal disease and risk control during treatment
1) Kinane DF, Chestnutt IG: Relationship of diabetes to periodontitis. Curr Opin Periodontol, 4: 29-34, 1997.
2) Kinane DF, Chestnutt IG: Smoking and periodontal disease. Crit Rev Oral Biol Med, 11: 356-365, 2000.
3) Holm-Pedersen P, Löe H: Watanabe M (ed.) Elderly odontolgy. Nagasue Shoten Inc., Kyoto, 111-117, 2000.
4) Uematsu H: Navigation for the elderly in dental practice corresponding to internal medicine emergency by
disease Ishiyaku Publishers, Inc., Tokyo, 16, 2003.
5) Nakamura T, Hasegawa H, Yoshimoto T, Yuda A, Sakota K, Goto H, Nakajima Y, Morimoto Y, Kadomatsu H,
Okina M, Takeuchi H, Miyamoto M, Iwatani Y, Setoguchi H, Izumi Y: Relationship between Systemic Diseases and Periodontal Conditions: A Clinico-statistical Study. Journal of the Japanese Association of Periodontology, 47: 250-257, 2005.
6) Georgiou TO, Marshall RI, Bartold PM: Prevalance of systemic diseases in Brisbane general and periodontal
practice patients. Australian Dent J, 49: 177-184, 2004.
7) Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S: Periodontal disease and cardiovascular disease. J Periodontol, 67 (10 Suppl): 1123-1137, 1996.
8) Nakagawa S, Fujii H, Machida Y, Okuda K: A longitudinal study from prepuberty to puberty of gingivitis:correlation between the occurrence of Prevotella intermedia and sex hormones. J Clin Periodontol, 216: 5865, 1994.
9) Jeffcoat MK, Hauth JC, Geurs NC, Reddy MS, Cliver SP, Hodgkins PM, Goldenberg RL: Periodontal disease
and preterm birth: results of a pilot intervention study. J Periodontol, 74: 1214-1218, 2003.
10) Committee for Bisphosphonate-Related Osteonecrosis of the Jaw: position paper of bisphosphonate-related
osteonecrosis of the jaw. The Japanese Society for Bone and Mineral Research, Japan Osteoporosis Society,Japanese Society for Oral and Maxillofacial Radiology, Japanese Society of Periodontology, Japanese Society ofOral and Maxillofacial Surgeons, 2016.
11) Akhtar NH, Afzal MZ, Ahmed AA: Osteonecrosis of jaw with the use of denosumab. J Cancer Res Ther, 7:499-500. 2011.
12) Hellstein JW, Adler RA, Edwards B, Jacobsen PL, Kalmar JR, Koka S, Migliorati CA, Ristic H: Managing thecare of patients receiving antiresorptive therapy for prevention and treatment of osteoporosis: executive summary of recommendations from the American Dental Association Council on Scientifc Affairs. J Am Dent Assoc, 142: 1243-1251, 2011.
13) Bergstrome J, Peter H: The influence of cigarette smoking on the development of experimental gingivitis. J
Periodontal Res, 21: 668-676, 1986.
14) Kaldahl WB, Johnson GK, Kashinath DP, Kalkwarf KL: Levels of cigarette consumption and response to

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periodontal therapy. J Periodontol, 67: 675-681, 1996.

⓾ Periodontal surgery
1) Takei HH, Carranza FA (translated by Shin M et al.): Principle of Periodontal surgery Carranza's Clinical
Periodontology 9th ed. Quintessence Publishing Co., Ltd., Tokyo, 731-736, 2005.
2) Hall WB: Critical Decisions in Periodontology. 4th ed., BC Decker, Hamilton, 2003.
3) Cortellini P, Tonneti MS: A Minimally Invasive Surgical Technique with an Enamel Matrix Derivative in the
Regenerative Treatment of Intrabony Defects: A Novel Approach to Limit Morbidity. J Clin Periodontol, 34:
87-93, 2007.
4) Cortellini P, Tonneti MS: Improved Wound Stability with a Modified Minimally Invasive Surgical Techniquein the Regenerative Treatment of Isolated Interdental Intrabony Defects. J Clin Periodontol, 36: 157-163,
2009.
5) Cortellini P, Pini-Prato G, Tonneti MS: The Modified Papilla Preservation Technique. A New Surgical Approach for Interproximal Regenerative Procedures. J Periodontol, 66: 261-266, 1995.
6) Cortellini P, Pini-Prato G, Tonneti MS: The Simplified Papilla Preservation Flap. A Novel Surgical Approachfor the Management of Soft Tissues in Regenerative Procedures. Int J Periodont, 19: 589-599, 1999.
7) Rosling B, Nyman S, Lindhe J, Jern B: The healing potential of the periodontal tissue following different
techniques of periodontal surgery in plaque-free dentitions. A 2 year clinical study. J Clin Periodontol, 3: 233250, 1976.
8) Ramfjörd SP, Nissle RR: The modified Widman flap. J Periodontol, 45: 601-607, 1974.
9) Japanese Society of Periodontology. Guidelines for regenerative therapy in patients with periodontal disease.
2012 Ishiyaku Publishers, Inc., Tokyo, 2014.
10) Miller PD Jr, Allen EP: The development of periodontal plastic surgery. Periodontol 2000, 11: 7-17, 1996.
11) Aoki A, Mizutani K, Watanabe H, Izumi Y, Ishikawa I, Fujitani M, Senda A, Yoshida K, Kurihara H, Yoshie H,
Ito K: Position paper Dental calculus removal with lasers. J Jpn Assoc Periodontol, 52:180-190, 2010.

⓫ Treatment of furcation involvement
1) Ammons WF, Harrington GW translated by Shin M et al.): Furcation area: its problems and management
Carranza's Clinical Periodontology 9th edition. Quintessence Publishing Co., Ltd., Tokyo, 841-855, 2005.

⓬ Treatment of combined periodontic-endodontic lesions
1) Simon JH, Glick DH, Frank AL: The relationship of endodontic-periodontic lesions. J Periodontol, 43: 202208, 1972.
2) Weine FS: Endodontic therapy. 5th ed. CV Mosby, St. Louis, 1996, 640-673.

⓭ Oral rehabilitation: Choice of splint, bridge, denture and implant
1) Kato H: A Textbook of Periodonology. Ishiyaku Publishers, Inc., Tokyo, 1994.
2) Harrel SK, Nunn ME: The effect of occlusal discrepancies on periodontics. II. Relationship of occlusal treatment to the progression of periodontal disease. J Periodontol, 72: 495-505, 2001.
3) Nunn ME, Harrel SK: The effect of occlusal discrepancies on periodontitis. I. Relationship of initial occlusal
discrepancies to initial clinical parameters. J Periodontol, 72: 485-494, 2001.
4) Nishikawa K, Bando E, Nakano M: Study of Bite Force during Sleep Associated Bruxism. Ann Jpn Prosthodont Soc, 42: 740-746, 1998.
5) Ikeda M: How Occlusion and mastication impact periodontal disease? Lion Foundation for Dental Health.
Overview of periodontal disease and systemic health. Ishiyaku Publishers, Inc., Tokyo, 144-153, 2004.
6) Tomonaga A, Ikeda M, Kato H, Ohata N: Influence of Sleep Bruxism on Dislodgement of Dental Resto-

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rations. Ann Jpn Prosthodont Soc, 49: 21-230, 2005.
7) Fujimoto J: Contemporary Fixed Prosthodontics 3rd Edition. Ishiyaku Publishers, Inc., Tokyo, 2002.
8) Morita M, Ishimura H, Ishikawa A, Koizumi K, Watanabe T: Causes of Failure of Various Types of Dental
Restorations and Their Longevity. J Dent Hith, 45: 788-793, 1995.
9) Kayser AF: Limited treatment goals-shortened dental arches. Periodontol 2000, 4: 7-14, 1994.
10) Nyman S, Lindhe J, Lundgren D: The role of occlusion for stability of fixed bridges in patients with reduced
periodontol tissue support. J Clin Periodontol, 2: 53-66, 1975.
11) Nyman S, Ericsson I: The capacity of reduced periodontal tissues to support fixed bridgework. J Clin Periodontol, 9: 409-414, 1982.
12) Nyman SR, Lang NP: Tooth mobility and the biological rationale for splinting teeth. Periodontol 2000, 4: 1522, 1994.
13) Nevins M: Periodontal prosthesis reconsidered. Int J Prosthodont, 6: 209-217, 1993.
14) Nevins M, Langer B: The successful use of osseointegrated implants for the treatment of the recalcitrant periodontal patient. J Periodontol, 66: 150-157, 1995.
15) Priest GF: Failure rates of restorations for single-tooth replacement. Int J Prosthodont, 9: 38-45, 1996.
16) Lindquist E, Karlsson S: Success rate and failures for fixed partial dentures after 20 years of service: Part I. Int
J Prosthodont, 11: 133-138, 1998.
17) Scurria MS, Bader JD, Shugars DA: Meta-analysis of fixed partial denture survival: Prostheses and abutments.
J Prosthet Dent, 79: 459-464, 1998.
18) Karoussis IK, Salvi GE, Heitz-Mayfield LJ, Bragger U, Hammerle CH, Lang NP: Long-term implant prognosis in patients with and without a history of chronic periodontitis: a 10-year prospective cohort study of the
ITI Dental Implant System. Clin Oral Implants Res, 14: 329-339, 2003.
19) Sumida S, Ishihara K, Kishi M, Okuda K: Transmission of periodontal disease-associated bacteria from teeth
to osseointegrated implant regions. Int J Oral Maxillofac Implants, 17: 696-702. 2002.
20) Hamano H, Hayashi H, Muramatsu K, Marumori H, SImotsuke M: Series for clinical feeling verification.
Extrusion as transplantation conditioning - healing process of transplanted teeth and the role of periodontal
ligaments. Dental outlook, 108: 469-496, 2006.
21) Polson A, Caton J, Polson AP, Nyman S, Novak J, Reed B: Periodontal response after tooth movement into
intrabony defects. J Periodontol, 55: 197-202, 1984.
22) Nevins M, Wise RJ: The use of orthodontic therapy to alter infrabony pockets Part II. Int J Periodontics Restorative Dent, 10: 199-207, 1990.

⓮ Implant therapy
1) Japanese Society of Periodontology ed.: Therapeutic strategy and evidence of oral implant for patients withperiodontal disease. 2018. Ishiyaku Publishers, Inc. Tokyo, 2019.
2) Japanese Society of Oral Implantology ed.: Treatment Guidelines for Oral Implants. Ishiyaku Publishers, Inc.
Tokyo, 2020.
3) Jovanovic SA (translated by Shin M et al.): Clinical aspect of dental implantation. Carranza's Clinical Periodontology 9th ed. Quintessence Publishing Co., Ltd., Tokyo, 904-912, 2005
4) Akagawa Y (trans): New consensus of the criteria for implant assessment-details of Toronto Conference.
Quintessence Publishing Co., Ltd., Tokyo, 2001.
5) Abrahamsson I, Berglundh T, Wennström J, Lindhe J: The peri-implant hard and soft tissues at different implant systems: a comparative study in the dog. Clin Oral Implants Res, 7: 212-219, 1996.
6) Berglundh T, Lindhe J: Dimension of the periimplant mucosa: biological width revisited. J Clin Periodontol,
23: 971-973, 1996.

7) Lang NP and Lindhe J: Clinical periodontology and implant dentistry. sixth ed. Willey Blackwell, Chichester,

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2015.
8) Ikeda H, Shirakawa M, Yamaza T, Yoshinari M, Kido MA, Ayukawa Y, Inoue T, Koyano K, Tanaka T: Difference in penetration of horseradish peroxidase tracer as a foreign substance into the peri-implant or junctional
epithelium of ret gingivae. Clin Oral Implants Res, 13: 243-251, 2002.
9) Karousis IK, Salvi GE, Heitz-Mayfield LJ, Brägger U, Hämmerle CHF, Lang NP: Long-term implant prognosis in patients with and without a history of chronic periodontitis: a 10-year prospective cohort study of the
ITI Dental Implant System. Clin Oral Implants Res, 14: 329-339, 2003.
10) Sumida S, Ishihara K, Kishi M, Okuda K: Transmission of periodontal disease-associated bacteria from teeth
to osseointegrated implant regions. lnt J Oral Maxillofacial lmplant, 17: 696-702, 2002.
11) American Academy of Periodontology (translation supervisor: Okada H): Implant therapy I. AAP, Consensus
of periodontal therapy. 1996. Quintessence Publishing, Tokyo, 78-81, 1999.
12) Newman MG, Flemmig TF: Periodontal considerations of implants and implant associated microbiota. J
Dent Educ, 52: 737-744, 1988.
13) Leonhardt A, Berglundh T, Ericsson I, Dahlén G: Putative periodontal pathogens on titanium implants andteeth in experimental gingivitis and periodontitis in beagle dogs. Clin Oral Implants Res, 3: 112-119, 1992.
14) Andrea M, Niklaus PL: Microbial aspects of implant dentistry. Periodontol 2000, 4: 74-80, 199415) Miyata T, Kobayashi Y, Araki H, Ohto T, Shin K: The influence of controlled occlusal overload on periimplant tissue. Part 3: a histologic study in monkeys. Int J Oral Maxillofac Implants, 15: 425-431, 2000.
16) Japanese Society of Oral Implantology ed.: Academic opinion on implant maintenance by the Japanese Society of Oral Implantology and Japanese Society of Periodontology. 2018.

⓯ Treatment of peri-implant disease1) Izumi U, Kodama To, Matsui T: New approach for implantitis. Nagasue Shoten Inc., Kyoto, 2010.
2) Tatsumi J, Shin M, Kodama T, Kusakabe Y, Ota M, Sato S, Ishihara Y, Kubota T, Sato T, Hasegawa Y, Hirose T,
Ogata Y, Ito K, Yoshie H: Report of a questionnaire survey regarding dental implant therapy among membersof the Japanese Society of Periodontology. Journal of the Japanese Association of Periodontology, 54: 265-276,
2012.
3) Allbrektsson T, Isidor F, Consensus report: Implant therapy. In: Lang NP, Karring T, Eds., Proceedings of the
1st European Workshop on Periodontology. Quintessence, Berlin, 1994, 365-369.
4) Berglundh T, Lindhe J, Ericsson I, Marinello CP, Liljenberg B, Thomsen P: The soft tissue barrier at implants
and teeth. Clin Oral Implants Res, 2: 81-90, 1991.
5) Ericsson I, Berglundh T, Marinello CP, Liljenberg B, Lindhe J: Long-standing plaque and gingivitis at implants and teeth in dog. Clin Oral Implants Res, 3: 99-103, 1992.
6) Lindhe J, Berglundh T, Ericsson I, Liljenberg B, Marinello CP: Experimental breakdown of periimplant andperiodontal tissues.A study in the beagle dog. Clin Oral Implants Res, 3: 9-16, 1992.
7) Leonhardt A, Berglundh T, Ericsson I, Dahlen G: Putatize periodontal pathogens on titanium implants andteeth in experimental gingivitis and periodontitis in beagle dogs. Clin Oral Implants Res, 3: 112-119, 1992.
8) Lang NP and Lindhe J: Clinical periodontology and implant dentistry. sixth ed. Willey Blackwell, Chichester,
2015.
9) Ferreira SD, Silva GL, Cortelli JR, Costa JE, Costa FO: Prevalence and risk variables for peri-implant disease
in Brazilian subjects. J Clin Periodontol, 33: 929-935, 2006.
10) Roccuzzo M, Bonino F, Aglietta M, Dalmasso P: Ten-year results of a three arms prospective cohort study on
implants in periodontally compromised patients. Part 2: clinical results. Clin Oral Implants Res, 23: 389-395,
2011.
11) Pjetursson BE, Helbling C, Weber HP, Matuliene G, Salvi GE, Brägger U, Schmidlin K, Zwahlen M, Lang
NP: Peri-implantitis susceptibility as it relates to periodontal therapy and supportive care. Clin Oral Implants

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Res, 23: 888-894, 2012.
12) Zupnik J, Kim SW, Ravens D, Karimbux N, Guze K: Factors associated with dental implant survival: a 4-year
retrospective analysis. J Periodontol, 82: 1390-1395, 2011.
13) Strietzel FP, Reichart PA, Kale A, Kulkarni M, Wegner B, Küchler I: Smoking interferes with the prognosis ofdental implant treatment: a systematic review and meta-analysis. J Clin Periodontol, 34: 523-544, 2007.
14) Lin GH, Chan HL, Wang HL: The significance of keratinized mucosa on implant health: a systematic review.
J Periodontol, 84: 1755-1767, 2013.
15) Teughels W, Van Assche N, Sliepen I, Quirynen M: Effect of material characteristics and/or surface topography on biofilm development. Clin Oral Implants Res, 17 (Suppl 2): 68-81, 2006.
16) Renvert S, Lindahl C, Renvert H, Persson GR: Clinical and microbiological analysis of subjects treated withBrånemark or AstraTech implants: a 7-year follow-up study. Clin Oral Implants Res, 19: 342-347, 2008.
17) Shibli JA, Melo L, Ferrari DS, Figueiredo LC, Faveri M, Feres M: Composition of supra- and subgingival biofilm of subjects with healthy and diseased implants. Clin Oral Implants Res, 19: 975-982, 2008.
18) Salvi GE, Furst MM, Lang NP, Persson GR: One-year bacterial colonization patterns of Staphylococcus aureus and other bacteria at implants and adjacent teeth. Clin Oral Implants Res, 19: 242-248, 2008.
19) Katsuyama H (trans): Minutes of the 3rd ITI Consensus Conference. Quintessence Dental Implantology Annex. Quintessence Publishing Co., Ltd., 2005.
20) Schwartz-Arad D, Herzberg R, Levin L: Evaluation of long-term implant success. J Periodontol, 76: 16231628, 2005.
21) Schou S, Holmstrup P, Worthington HV, Esposito M: Outcome of implant therapy in patients with previous
tooth loss due to periodontitis. Clin Oral Implants Res, 17: 104-123, 2006.
22) Renouard F, Rangert B (translated by Maeda Y and Yonehata Y): Risk factors in implant dentistry. Quintessence Publishing Co., Ltd., Tokyo, 2000.
23) Tasumi S, Naito T, Yokota M: Measurement of Implant Displacement with Vertical Loading on Periimplantitis. Journal of the Japanese Association of Periodontology, 44: 21-31, 2002.
24) Lang NP, Berglundh T, Heitz-Mayfield LJ: Consensus statements and recommended clinical procedures regarding implant survival and complications. Int J Oral Maxillofac Implants, 19 (Suppl): 150-154, 2004.
25) Japanese Society of Periodontology ed.: Therapeutic Strategy and Evidence of Oral Implant for Patients with
Periodontal Disease. 2018. Ishiyaku Publishers, Inc. Tokyo, 2019.

⓰ Follow-up
1) Becker W, Becker BE, Berg LE: Periodontal treatment without maintenance.A retrospective study in 44 patients. J Periodontol, 55: 505-509, 1984.
2) Rosling B, Nyman S, Lindhe J, Jern B: The healing potential of the periodontal tissues following different
techniques of periodontal surgery in plaque free dentitions. A 2-year clinical study. J Clin Periodontol, 3: 233250, 1976.
3) Axelsson R, Lindhe J: The significance of maintenance care in the treatment of periodontal disease. J Clin
Periodontol, 8: 281-294, 1981.
4) The American Academy of Periodontology.Supportive treatment.In: Proceedings of the World Workshop in
Clinical Periodontics. Chicago: American Academy of Periodontology: IX-24, 1989.
5) Lang NP, Tonetti MS: Periodontal risk assessment (PRA) for patients in supportive periodontal therapy (SPT).
Oral Health and Preventive Dentistry, 1: 7-16, 2003.
6) Kitamura M, Terakura M, Kobayashi S, Yamashita G, Okuda K, Hayashi H, Yamada H, Ozato H, Takayama S,
Saho T, Nozaki T, Hirano H, Shimabukuro Y, Murakami S, Okada H: The Longitudinal Effects of Supportive
Periodontal Therapy on Maintenance of Periodontal Patients. Japanese journal of conservative dentistry, 46:
613-618, 2003.

937) Omori M, Sakai Y, Morozumi Y, Hasegawa A: Evaluation of the Effectiveness of Long-term MaintenanceCare of Periodontal Patients. Journal of the Japanese Association of Periodontology, 46: 185-192, 2004.
8) Hitomi S, Ishihata H, Inomata H, Shimauti H: Study of Long-Term Periodontal Maintenance in Private
Practice --Evaluation of Supportive Periodontal Therapy Managed by a Dental Hygienist--. Journal of the Japanese Association of Periodontology, 48: 123-134, 2006.
9) Position Paper, Periodontal Maintenance. J Periodontol, 74: 1395-1401, 2003.
10) Wada H, Fujise O, Hamaji T, Miura M, Matsumoto A, Inoue K, Noda D, Kaida H, Hirai T, Maeda K: Microbiological status necessitating preventive scaling and root planning in the early period of supportive periodontal therapy. Journal of the Japanese Association of Periodontology, 49: 20-26, 2007.
11) Renvert S, Persson GR: Supportive periodontal therapy. Periodontol 2000, 36: 179-195, 2004.

JSP Clinical Practice Guidelines for the Periodontal Treatment 2022
First edition published (Japanese version) on March 25, 2022
First edition published (English version) on September 5, 2023
Edited by

The Japanese Society of Periodontology

Issuer: Yorimasa Ogata (Japanese version)
Issuer: Yukihiro Numabe (English version)
Production support:

Ishiyaku Publishers, Inc.

A book with defective or missing pieces will be replaced with a complete one.
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