Edited by The Japanese Societyof Periodontology

Preface
Periodontal disease is a chronic inflammation induced by chronic bacterial infection andresults in the destruction and loss of periodontal tissue. In severe periodontitis, daily bacteremia from local bacterial infectious lesions occurs and the intensity of total inflammation is aslarge as to influence the whole body. Therefore, chronic infection and inflammation of periodontal tissue affects the establishment or complication of systemic diseases such as diabetes
mellitus, chronic kidney disease, blood vessel disorder, non-alcoholic steatohepatitis, andrheumatoid arthritis. Moreover, tooth loss by severe periodontitis results in oral dysfunctions
such as masticatory dysfunction and induces systemic complication. Adequate periodontal
treatment greatly contributes the promotion of overall health in people. In Japan, there arereports that people without periodontal disease have lower medical costs than others andperiodontal treatment may contribute to reduce total medical cost. Since patient self-care inplaque control is base of periodontal treatment and the period of periodontal treatment isgenerally long, communication with patients is a key to treatment success. It is important for
better results in periodontal treatment that patients understand the significance of periodontal treatment in promotion of not only oral health but also systemic health and that the entire
treatment plan be based on effectual examinations and diagnosis and that patients collaborate
with their periodontists.
This treatment guideline is the English version of“JSP Clinical Practice Guideline for the
Periodontal Treatment, 2015”written in Japanese and published by the Japanese Society of
Periodontology（JSP）in 2016 against the background of a super-aged society. This guideline
covers all clinical procedures of the standard periodontal treatment in Japan. JSP publishes
this English version in order to introduce our concept and treatment flow of periodontal
treatment that JSP has established, and to help the development of and standardization of
periodontal treatment in Asian developing countries. In Asian developing countries, periodontal treatment has not permeated enough to whole country. Periodontal treatment may
reduce the prevalence of systemic diseases and enhance social activity by the health promotion of periodontal treatment in these countries. It will be great pleasure for JSP if this treatment guideline written in English will help the expansion of periodontal treatment in Asiandeveloping countries. Also, JSP expects to develop new relationships with foreign periodontal
specialists through active discussion of the treatment concept or methods.
November 22, 2017

Hidemi Kurihara
President of the Japanese Society of Periodontology（from April, 2017）Foreword to the“JSP Clinical Practice
Guideline for the Periodontal treatment, 2015”
The advent of the super-aging society in Japan in 2007, supported by high levels of education, economy and healthcare, has led to the highest longevity in the world. The increased
number of elderly patients with periodontitis and other diseases is a major problem, and periodontitis is a strong risk factor for systemic health-threatening conditions. Appropriate
guidelines for periodontal therapy including prevention are required because it is extremely
important to manage both oral care and systemic healthcare. The JSP published the“2007
Guidelines for Diagnosis and Treatment of Periodontal Disease”（henceforth referred to as
the 2007 Guidelines）, as an outline of periodontal therapy, and the“2008 Guidelines for
Examination, Diagnosis and Therapeutic Strategies for Periodontal Disease”（the 2008
Guidelines）, which give details of examinations, diagnosis and therapy. However, several
years have passed since these guidelines were published, and thus the JSP has revised theguidelines based on the changes in social conditions described above. Since guidelines proposed by academic societies have major effects on health care, the JSP thoroughly discussed
future periodontal therapy strategies prior to compilation of the current guidelines.
These guidelines were compiled based on the following concepts.
1 ．The guidelines are integrated with the 2007 Guidelines and the 2008 Guidelines.
2 ．The guidelines include examination and diagnosis for periodontal disease, supportive
periodontal therapy, and coping with peri-implant diseases.
3 ．For periodontal therapy in the elderly, sick persons and perioperative patients, the guidelines focus on multiple considerations, including cooperation with medical science.
4 ．The aim of the guidelines is to provide objective criteria for periodontal therapy by dentists, including dental residents.
5 ．The guidelines refer to lectures on periodontology at various educational institutions andquestions in the national dentist examination.
We expect that these guidelines will contribute to maintenance and promotion of oral andsystemic health by providing a correct understanding of periodontal disease and delivery of
appropriate treatment and high-quality periodontal therapy to the public, including elderly
and sick persons. We gratefully acknowledge the chairperson, Dr. Kazuhiro Gomi, and members of the Guidelines Development Subcommittee, Dr. Hidemi Kurihara, chairperson of the
JSP Medicine Committee, the JSP Board members, and Ishiyaku Publishers, Inc.
March 2016

Yuichi Izumi
President of the Japanese Society of Periodontology（April, 2015～March, 2017）

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Edited by the Japanese Society of Periodontology“JSP Clinical Practice Guideline for the periodontal treatment, 2015”
Members of the Guideline Development Subcommittee（＊member of JSP Medicine Committee, ＊＊chairperson of JSP Medicine Committee）（April 2013 to March 2015）
Chairperson＊

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

Hidemi Kurihara（Professor, Hiroshima University, Chief Director of JSP）＊

Hiromasa Yoshie（Professor, Niigata University, Chief Director of JSP）＊

Hiroyuki Kawaguchi（Director of Dentistry, Nihon Koukan Fukuyama Hospital, JSP member）＊

Naoyuki Sugano（Associate Professor, School of Dentistry, Nihon University, JSP member）＊

Toshiaki Yoshino（Director, Yoshino Dental Clinic, Specialist and Instructor of JSP）
Ryuji Sakagami（Professor, Fukuoka Dental College, Chief Director of JSP）
Toshiro Kodama（Professor, Kanagawa Dental University, Chief Director of JSP）
Kenji Wakabayashi（Director, Wakabayashi Dental Clinic, Chief Director of JSP）
Hisao Araki（Professor, School of Dentistry, Meikai University, Chief Director of JSP）
Takeya Uchida（Director, Uchida Dental Clinic, Clinical Professor, Tsurumi University, Specialist and Instructorof JSP）

Acknowledgment
Publication of English version “JSP Clinical Practice Guideline for the periodontal treatment, 2015” was supported by SUNSTAR Group.

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CONTENTS
Contents

1 What is periodontal disease? ・・・・・・・・・・・・・・・・・・・ 9

1．CurrentstatusofperiodontaldiseaseinJapan／9
1 Definition of periodontal disease ／9
2 Morbidity of periodontal disease ／9
3 Visit conditions ／9
2．Typesofperiodontaldisease ／10
1 Gingival lesions（classified into localized andgeneralized types）／10⑴ Plaque‒induced gingivitis ／10⑵ Non plaque‒induced gingival lesions ／10⑶ Gingival overgrowth ／10a）Drug‒induced gingival overgrowth ／10b）Hereditary gingival fibromatosis ／10⑷ HIV infection-related gingival lesions ／10
2 Periodontitis（classified into localized andgeneralized types）／10⑴ Chronic periodontitis ／ 10⑵ Aggressive periodontitis ／ 11
⑶ Periodontitis associated with genetic disorders／11
3 Necrotizing periodontal diseases（classified into
localized and generalized types）／11⑴ Necrotizing ulcerative gingivitis ／12⑵ Necrotizing ulcerative periodontitis ／12
4 Abscesses of periodontium ／12⑴ Gingival abscess ／12⑵ Periodontal abscess ／12
5 Combined periodontal-endodontic lesions ／12
6 Gingival recession ／13
7 Occlusal trauma ／13
3．Characteristicsofgingivallesions ／13⑴ Bacterial plaque is pathogen ／13⑵ Inflammation is localized in the gingiva ／13⑶ Gingival pockets are formed, but without
attachment loss ／13⑷ Gingival lesions are exacerbated by plaqueretention factors ／13⑸ Gingival lesions are improved by plaque control／13⑹ Gingival lesions are considered to be a stageprior to periodontitis ／13
4．Characteristicsofperiodontitis ／13
1 Characteristics of onset of periodontitis ／14⑴ Plaque-induced gingivitis progresses toperiodontitis, resulting in destruction of cementum,
periodontal ligament and alveolar bone ／14⑵ Attachment loss occurs and a periodontal

pocket develops ／14⑶ Periodontopathic bacteria are increased indeep periodontal pockets and inflammation
continues ／14
2 Characteristics of progression of periodontitis ／14⑴ Gingival lesions are exacerbated by plaqueretentions factors ／14⑵ Complicated traumatic occlusion accelerates
periodontitis ／14⑶ Site-specificity in progression rate ／14⑷ Quiescence stage and active stage ／14⑸ Advanced periodontitis produces a vicious
cycle and is likely to advance rapidly ／15
3 Characteristics of periodontal therapy ／15⑴ Cause elimination improves or arrests
periodontitis ／15⑵ Supportive periodontal therapy（SPT）and
maintenance throughout lifetime are requiredin periodontal therapy ／15
5．Characteristicsofocclusaltrauma ／15⑴ Primary occlusal trauma ／15⑵ Secondary occlusal trauma ／15
6．Systemicconditionsandperiodontaldisease ／16

1 Factors affecting periodontal disease ／16⑴ Congenital factors ／16a）Genetic risk factors ／16b）Age and sex ／16c）Racial／ethnic difference ／16⑵ Environmental and acquired risk factors ／16a）Smoking ／16b）Stress stimulation ／17c）Diabetes ／17d）Obesity ／17e）Routine medicines ／17f）HIV infection ／17

2 Diseases influenced by periodontal disease ／17⑴ Angiopathic disorder ／17⑵ Aspiration pneumonia ／17⑶ Preterm and low birth weight infant delivery ／17⑷ Diabetes ／17⑸ Rheumatoid arthritis ／17⑹ Other diseases ／17

2 Process of periodontal therapy ・・・・・・・・・・・・・・ 18

1．Systemicdisease ／18
1 Affected individuals ／19
2 Diabetic patients ／19
3 Elderly patients ／19

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2．Examination‒baseddiagnosis,therapeutic
strategyandinformedconsent ／19
3．Basicperiodontaltherapy ／19
1 Proactive participation of patients in treatment／19
2 Establishment of plaque control ／20
3 Elimination of plaque retention factors ／20
4 Recovery of masticatory function ／20
5 Abstention of palliative treatment ／20
4．Periodontalsurgery ／20
5．Oralrehabilitation ／20
6．Cureanddiseasestabilizationofperiodontal
disease ／20
1 Plaque-induced gingivitis ／21
2 Periodontitis ／21
3 Stable state ／21
4 Treatment after cure ／21

3 Medical interview, patient reference andliaison with medicine ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 22
1．Medicalinterview ／22

2．Referenceofpatientstoperiodontalspecialistsandadvancedcarefacilities ／22
3．Liaisonwithmedicine ／22
1 Disease state and drugs administered ／22
2 Precautions for invasive treatment in the oralcavity ／23

4 Examination, diagnosis and therapeuticstrategy for periodontal disease ・・・・・・・・・・・ 24
1．Periodontalexamination ／24
1）Periodontal examination ／24⑴ Gingival inflammation ／24⑵ Probing depth ／24⑶ Attachment level（AL）／24⑷ Oral hygiene conditions（O’Leary plaquecontrol record）／24⑸ Tooth mobility ／24⑹ Radiograph ／24⑺ Occlusion ／24⑻ Furcation involvement ／24a）Lindhe and Nyman furcation classification ／25b）Glickman furcation classification ／25⑼ Plaque retention factors ／25⑽ Oral photograph ／25⑾ Study model ／252）Microbiological assays ／25⑴ Bacteria test ／25⑵ Serum bactericidal antibody titer test ／25
3）Other examinations ／25⑴ Gingival crevicular fluid（GCF）test（fluid fromperiodontal pockets）／25⑵ Saliva test ／25⑶ Blood test ／25
4 Psychological, social and behavioral assessment／26
2．Diagnosisofperiodontaldisease ／26
1 Diagnostic procedure for plaque-induced gingivitis and periodontitis ／26⑴ Diagnosis by tooth unit ／26a）Periodontitis classification by degree of tissue
disruption ／26b）Periodontitis classification by inflammation
severity ／26c）Diagnosis of periodontitis by tooth unit ／27⑵ Diagnosis at individual levels ／27a）Diagnosis by disease type ／27b）Progression of periodontitis ／27c）Periodontitis severity of the whole oral cavity ／28

2 Diagnostic procedure for occlusal trauma ／28
3．Therapeuticstrategyplanning ／28
1 Basic periodontal therapy（cause elimination）／28

2 Reassessment after basic periodontal therapy ／28

3 Periodontal surgery ／28
4 Reassessment after periodontal surgery ／28
5 Oral rehabilitation ／29
6 Reassessment before SPT ／29
7 Supportive periodontal therapy（SPT）／29
8 Maintenance ／29

5 Home care, perioperative patients andperiodontal therapy ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 30
1．Homecareandperiodontaltherapy ／30
1 Self care ／30
2 Partial support for oral care ／30
3 Full support for oral care ／30

2．Perioperativepatientsandperiodontaltherapy／30
1 Oral function control before surgery（treatment）／31
2 Oral function control during and after surgery（treatment）／31
3 Aspiration and infection in oral hygiene control／31

6 Emergency procedures ・・・・・・・・・・・・・・・・・・・・・・・・・・ 32

1．Identificationofcauseofpain ／32
2．Treatmentofacuteinflammation ／32

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7 Preventive treatment ・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 33
1．Preventionoftransitionfromplaque-induced
gingivitistoperiodontitis ／33
2．Preventivetreatmentforpregnantwomen ／33
8 Basic periodontal therapy ・・・・・・・・・・・・・・・・・・・・・・ 34
1．Conceptsofbasicperiodontaltherapy ／34
2．Therapeuticstrategyforbasicperiodontal
therapy ／34
1 Therapeutic strategy and process of basic periodontal therapy ／34
2 Therapeutic strategy focusing on bacterial infection and inflammation ／34
3．Treatmentofbacterialinfection ／34
1 Plaque control is a high priority in all therapies／34⑴ Motivation ／37⑵ Self-care（supragingival plaque control）／37⑶ Instructions for brushing ／37⑷ Professional care（supragingival andsubgingival plaque control）／37
2 Scaling-root planing ／37⑴ Significance and objective of scaling-root
planing（SRP）／38⑵ Precautions for SRP ／38⑶ Importance of sharpening ／38⑷ Sonic and ultrasonic scalers ／38⑸ Dentin hypersensitivity after SRP ／38
3 Improved plaque retention factors ／38
4 Periodontal pocket curettage ／38
5 Extraction of hopeless tooth ／39
4．Currenttreatmentofbacterialinfection ／39
1 Mechanical supragingival plaque control ／39
2 Mechanical subgingival plaque control ／39
3 Chemical supragingival plaque control ／40
4 Chemical subgingival plaque control ／40⑴ Subgingival pocket irrigation ／40⑵ Administration of antibacterial agents into
periodontal pockets ／41⑶ Oral administration of antibacterial agents ／41
5 Patient’s choice of antibiotic therapy ／41
5．Treatmentofocclusaltrauma ／41
1 Relationship of occlusal trauma with progressionof periodontitis ／41
2 Occlusal adjustment and occlusal reshaping ／42

3 Temporary splint ／42
4 Devices for periodontal therapy（provisional
restoration）／43
5 Treatment of bruxism ／43
6 Orthodontic treatment ／44

9 Risk factors for periodontal disease andrisk control during treatment ・・・・・・・・・・・・・・・・ 45
1 Systemic risk factors ／45
2 Environmental risk factors ／45
1．Periodontaltherapyfortheelderly ／45

2．Periodontaltherapyforpatientswithotherdiseases ／46
1 Metabolic syndrome ／46
2 Obesity ／46
3 Diabetes ／46⑴ Type 1 diabetes ／46⑵ Type 2 diabetes ／46
4 Hypertensive patients ／47
5 Patients with cardiovascular disease（particularly
those taking antithrombotic agents）／47
6 Dialysis ／47
7 Respiratory disease ／47
3．Female-specificperiodontaldisease ／47
1 General precautions ／47
2 Periodontal therapy for pregnant women ／48
3 Patients with osteoporosis（particularly thosetaking BP products and anti-RANKL antibodies）／48
4．Periodontaltherapyforsmokers ／48⓾ Periodontal surgery ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 49

1．Tissueattachmenttherapy ／50
1 Periodontal pocket curettage ／50
2 Excisional new attachment procedure（ENAP）／50
3 Flap curettage（access flap surgery）／51
4 Modified Widman flap surgery ／51
2．Resectivetherapy ／51
1 Gingivectomy ／51
2 Apically-positioned flap procedure ／52
3．Periodontalregenerativetherapy ／52
1 Bone graft ／53
2 Guided tissue regeneration（GTR）／53
3 Enamel matrix derivative（EMD）-applied surgery ／53
4 Surgical procedure using other biologically
active substances ／53
4．Periodontalplasticsurgery（includinggingival／alveolarmucosaplasty）／54
1 Frenectomy ／54
2 Laterally-positioned flap surgery ／54
3 Coronally-positioned flap surgery ／54
4 Apically-positioned flap surgery ／54
5 Free gingival graft ／54
6 Connective tissue graft ／55
7 Other periodontal plastic surgery ／55

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5．Laserapplicationinperiodontalsurgery ／55⓫ Treatment of furcation involvement ・・・・・ 56

1．Examination ／56
2．Treatment ／56⓬ Treatment of combined periodontic-

endodontic lesions ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 58
1．Classificationofcombinedperiodonticendodonticlesions ／58⑴ Class I（endodontic lesion-derived）／58⑵ Class II（endodontic lesion-derived）／58⑶ Class III（combined periodontic-endodontic
lesion-derived）／58
2．Examination ／58
3．Treatment ／58⓭ Oral rehabilitation―Choice of splint,

bridge, denture and implant ・・・・・・・・・・・・・・・・・・ 60
1．Choiceoftherapeuticprocedures ／60
1 Test items ／60
2 Treatment of moving teeth ／61
3 Temporary splint and splint with provisional
restoration ／61
2．Choiceofproceduresforprosthesisand
precautions ／61
1 Tooth crown restoration（permanent splint）／
61

2 Treatment of dentition with tooth defect ／61⑴ Bridge ／62⑵ Removable partial denture ／62⑶ Implant ／63⑷ Tooth replantation ／63
3．Orthodontictreatment ／63
1 Malalignment ／63
2 Remodeling of the periodontium by orthodontic
treatment ／63⓮ Implant therapy ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 64
1．Benefitofimplanttherapyfororalfunctional
restorationinpatientswithperiodontaldisease／64
2．Implanttherapyinpatientswithperiodontal
disease ／64
1 Importance of periodontal therapy prior to
implant therapy ／64
2 Precautions for peri-implant mucositis andperi-implantitis ／64

3 Precautions for implant with trauma ／64
3．Implanttherapyandmaintenance ／65⓯ Treatment of peri-implantitis ・・・・・・・・・・・・・・・・ 66
1 Broad definition of peri-implantitis ／66
2 Cause of peri-implantitis ／66
3 Examination and diagnosis of peri-implantitis ／67⑴ Plaque（biofilm）control state ／67⑵ Bleeding on probing（BOP）／67⑶ Probing depth（PD）／67⑷ Pus discharge ／67⑸ Radiograph ／67⑹ Implant mobility ／67⑺ Peri-implant keratinized mucosa ／67⑻ Peri-implant crevicular fluid（PICF）／67⑼ Microbiological tests ／67⑽ Occlusal relation ／67
4 Treatment ／68⑴ Treatment process ／68⑵ Cumulative interceptive supportive therapy（CIST）／68⓰ Supportive periodontal therapy（SPT）

and Maintenance ・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・・ 71
1．Termdefinitions ／71
1 Supportive periodontal therapy（SPT）／71
2 Maintenance ／71
3 Stable state ／71
4 Healing ／71
5 Professional tooth cleaning（PTC）／72
6 Professional mechanical tooth cleaning（PMTC）／72
2．Examinationanddiagnosis ／72
1 Decision-making point ／72⑴ Plaque-induced gingivitis ／72⑵ Periodontitis ／73
2 Test items ／73⑴ Periodontal examination ／73⑵ Microbiological assays ／73⑶ Other examinations ／73⑷ Risk assessment in SPT ／73
3．Therapeuticplanning ／74
1 Maintenance ／74
2 Supportive periodontal therapy（SPT）／74
References ／76

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1 What is periodontal disease?
1．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. To maintain dental and oral
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）, andaccounted for 38.3％ in 2011. The mean number of remaining teeth was 13.93）. 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 partially achieved, but the number of elderly people with periodontal pockets ≥4 mm is increasing.
Japan is still among countries with the highest longevity, but Japanese people aged around 80 years have few
remaining teeth. As shown in the＂number of existing teeth＂and＂dental disease survey＂, middle-aged and older
people are likely to lose teeth rapidly1）. Furthermore, the prevalence of periodontal disease in Japan is much higher
than that of other diseases and prevention and treatment of periodontal disease are critical issues.

1）Definition of periodontal disease
Periodontal disease is roughly classified into gingival lesions and periodontitis. Periodontal disease, except for nonplaque-induced gingival disease, is an inflammatory and infectious disorder caused by periodontopathic bacteriathat develops in the periodontium, which consists of the gingiva, cementum, periodontal ligament and alveolarbone. Periodontal disease also includes septic periodontal disease, periodontal abscess, periodontal-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 periodontium4）. Periodontal disease is also considered to be 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 health guidance by dental
professionals. It is necessary for patients to improve their lifestyle by themselves and to be supported by healthcare
professionals（systemic disease）.

2）Morbidity of periodontal disease
The 2011 dental disease survey showed that gingival lesions were found less in youth and more in the elderly. The
prevalence of gingival disease increases with age, reaching a peak at approximately 87％ in the 45-49 age group.
The prevalence in the population of productive workers（35-69 years）accounted for almost 80％. The population
with periodontal pockets ≥4 mm decreased in age groups of 64 years or younger, but increased in those aged 65
years or more. This result suggests increasing tooth number by age3）.

3）Visit conditions
The 2011 dental disease survey3）estimated that approximately 94 million patients had gingival symptoms, but
only about 2.6 million patients visited dental clinics. This number doubled from approximately 1.2 million in
1999, but remains insufficient. The difference suggests that there are many people who are not aware of periodon-

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tal disease and those who are aware of it but are not treated. It is preferable for these patients to visit clinics andhospitals.

2．Types of periodontal disease4）
is shown in Table 1.
The JPS classification system of periodontal disease（2006）

1）Gingival lesions（classified into localized and generalized types）（1）Plaque-induced gingivitis
Plaque-induced gingivitis is gingival inflammation caused by bacteria in the gingival border. Clinical findings are
gingival redness, edema, bleeding, pain and swelling. However, there is no radiographic finding or attachment lossof supporting tissues. Histopathological findings reveal junctional epidermal growth to the periapical or lateralregion, 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 overgrowthGingival overgrowth 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 overgrowth
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 border, interdental papilla and attached gingiva. This disease develops in infants and swelling is found in the
buccolingual side of the maxillary and mandibular bones, but disappears after extraction. Case reports show an
autosomal-dominant and hereditary tendency.
（4）HIV infection-related gingival lesions
The JPS classification system of periodontal disease（2006）does not describe this type of gingivitis; however, HIVinfected 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 gingival borders of multiple teeth. These two characteristic lesions are caused by
reduced immune function（low CD4 lymphocyte counts）; therefore, abnormal gingival findings lead to early
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 border 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 rapidand depends on the defense mechanism in the body. The classification of periodontitis by risk factor is shown in
Table 4.
（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 is generally at 35 years and older. Symptoms include periodontal pocket formation, drainage, bleeding, alveolar bone

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

Classification by virulence factor（risk factor）
1）Gingivitis induced by dental plaque only‡
2）Gingivitis modified by systemic conditions‡
3）Gingivitis modified by malnutrition‡

2．Non-plaque-induced gingival lesions

1）Gingival lesions induced by other infections2）Mucocutaneous disorders‡3）Allergic reactions‡4）Traumatic lesions of gingiva‡

3．Gingival hyperplasia, Gingival overgrowth

1）Drug-induced gingival overgrowth2）Hereditary gingival fibromatosis

Ⅱ．Periodontitis†
1．Chronic periodontitis‡
2．Aggressive periodontitis‡

1）Periodontitis associated with systemic diseases
2）Periodontitis associated with smoking3）Periodontitis associated with other risk factors

3．Periodontitis associated with genetic disorders‡

Note
Table 2

Table 3

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 periodontal-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 New Periodontal Disease Classification System of the American Academy of Periodontology（1999）. Other diseases are defined by JSP.

resorption, and tooth movement. This disease has a chronic course, but results in acute symptoms due to hostdefense 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 age of patients ranges from 10 to the 30s. Some patients have large colonies of Aggregatibacter actinomycetemcomitans（A. actinomycetemcomitans）, and secondary characteristics are 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 Center6）.
（3）Periodontitis associated with genetic disorders
This is rapidly progressive periodontitis that develops as an oral symptom of genetic disorder associated with systemic abnormality. Genetic disorders include familial and cyclic neutropenia, Down syndrome, Papillon-Lefèvre
syndrome, and Chédiak-Higashi syndrome（Table 5）.

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

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 conditions①Puberty-associated gingivitis②Menstrual cycle-associated gingivitis③Pregnancy-associated gingivitis④Diabetes-associated gingivitis⑤Leukemia-associated gingivitis⑥Others3）Gingivitis modified by malnutrition①Ascorbic acid-deficiency gingivitis②Others

1）Gingival lesions induced by other infections①Gingival lesions of specific bacterial origin②Gingival lesions of viral origin③Gingival lesions of fungal origin
2）Mucocutaneous disorders①Lichen planus②Pemphigoid③Pemphigus vulgaris④Lupus erythematosus⑤Others3）Allergic reactions4）Traumatic lesions of gingiva

Table 4．Classification of periodontitis by risk factor

Table 5．Genetic disorders with periodontitis

1）Periodontitis associated with systemic diseases①Leukemia②Diabetes③Osteoporosis／osteopenia④Acquired immunodeficiency syndrome（AIDS）⑤Acquired neutropenia⑥Others2）Periodontitis associated with smoking3）Periodontitis associated with other risk factors

1）Familial and cyclic neutropenia2）Down syndrome3）Leukocyte adhesion deficiency syndrome4）Papillon-Lefèvre syndrome5）Chédiak-Higashi syndrome6）Histiocytosis syndrome7）Infantile genetic agranulocytosis8）Glycogen storage disease9）Cohen syndrome10）Ehlers-Danlos syndrome（TypeⅣ and Ⅷ )11）Hypophosphatasia12）Others（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,
Spirochaeta and Prevotella intermedia（P. intermedia）. The pathogenesis includes poor oral sanitary conditions,stress, smoking, and immunodeficiency. The disorders are also oral findings in HIV-infected patients.

4）Abscesses of 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 periodontal-endodontic lesions
Lesions in periodontal and endodontic regions affect each other. Marginal periodontal and periapical tissues areanatomically close, and lesions are likely to affect each other. Specifically, abnormality in marginal periodontal tissues affects the dental pulp via the root canal lateral shoot and apical pores, whereas lesions in dental pulp haveeffects on periodontal tissues via the root canal lateral shoot, medullary tube and apical pore.

136）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 sensitivity 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 bone impermeability surrounding the tooth root. Disruption of the periodontium is expanded by excessive bite force to tissues with periodontitis（see Page 15,“5. Characteristics of occlusal trauma”）.

3．Characteristics of gingival lesions
Gingival lesions are inflammation only in the gingiva; the cementum, periodontal ligament and alveolar bone are
not disrupted. Of various gingival lesions, plaque-induced gingivitis is clinically important and its characteristics
are given below.
（1）Bacterial plaque is pathogen
Bacteria attached to teeth grow due to poor oral hygiene control and bacterial plaque is formed, resulting in an
inflammatory manifestation. The inflammation grade depends on host resistance, etc.
Bacterial plaque is formed from numerous bacteria attached to teeth, gingiva, and dental repair and prosthesis
products and their metabolites. As a result of bacterial plaque maturation, coaggregation of different bacterial species occurs, and coverage with extracellular polymeric substances（EPS）including glycocalyx, results in bacterial
biofilm formation.
（2）Inflammation is localized in the gingiva
No inflammation expands to the cementum, periodontal ligament or alveolar bone.
（3）Gingival pockets are formed, but without attachment loss
The gingiva swells and proliferates in the crown-side direction due to inflammation, which results in formation ofa gingival pocket（pseudopocket）. Clinically, the bottom of this pocket is positioned at the CEJ. Since the attachment level does not change, there is no attachment loss or alveolar bone resorption.
（4）Gingival lesions are exacerbated by plaque retention factors
If plaque retention factors（factors that make plaque control difficult and accelerate bacterial plaque retention: see
Page 25“（9）Plaque retention factors”and page35“Figure 6-2”
）are present, bacterial plaque is retained orincreased, resulting in aggravated gingivitis.
（5）Gingival lesions are improved by plaque control
Gingival lesions are markedly improved by thorough oral hygiene control, including brushing and elimination or
reduction in bacterial plaque, the major cause. Gingival inflammation is further improved by removal or revisionof plaque retention factors.
（6）Gingival lesions are considered to be a stage prior to 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 generally
advances to periodontitis after it remains untreated for a long time.

4．Characteristics of periodontitis
Periodontitis is a disorder in which inflammation that initially developed in the gingiva expands to deep periodon-

14

tal tissues, including the cementum, periodontal ligament and alveolar bone. Long-term continuous stimulation ofbacterial plaque, the major cause, is required for progression of plaque-induced gingivitis to periodontitis. Suchprogression is strongly associated with lifestyle and plaque retention factors that accelerate bacterial plaque andmake it difficult to remove this plaque.
The progression rate of periodontitis is relatively slow and takes several years. However, traumatic occlusion
accelerates disruption. Furthermore, host defense response has effects on 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 destruction of 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 ligament and alveolar bone.
（2）Attachment loss occurs and a periodontal pocket develops
The attachment function between teeth and periodontal tissues is destroyed, resulting in attachment loss. Specifically, gingival junctional epiderma（attached epidema）and connective tissue attachment transfer from the CEJ
toward the periapical direction and the gingiva detaches from the root. Consequently, a periodontal pocket（truepocket）is formed.
（3）Periodontopathic bacteria are increased in deep periodontal pockets and inflammation continues
The inside of the pocket is under anaerobic conditions, in which periodontopathic bacteria are likely to grow.
Consequently, bacteria and metabolites invade the gingiva through the epiderma 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 retentions factors
Similarly to plaque-induced gingivitis, if plaque retention factors that make plaque control difficult（e.g. calculus,
malalignment, abnormal gingiva and alveolar mucosa, faulty dental restoration, dental morphological defect, food
impaction, mouth breathing, abnormal oral vestibule, caries in the tooth cervix, periodontal pocket）are present,
periodontitis is aggravated. After periodontal pocket formation, the insides of pockets cannot be controlled by thepatient; consequently, bacterial plaque increases and periodontitis progresses.
（2）Complicated traumatic occlusion accelerates periodontitis
Complicated traumatic occlusion including early contact, strong lateral pressure and bruxism, aggravates inflammation in periodontal tissues and tissue disruption rapidly progresses, resulting in angular bone resorption andinfrabony pocket formation. Therefore, traumatic occlusion is a significant local modifier for aggravating periodontitis.
（3）Site-specificity in progression rate
Differences in the quality（type）and mass of infected periodontopathic bacteria and local modifiers induce significant differences in progression of periodontitis between regions in the oral cavity of a patient.
（4）Quiescence stage and active stage
In general, periodontitis is considered to be a chronic disorder; however, disruption of the periodontium does not15always proceed at a constant rate, but rapidly proceeds in active stages. There is no diagnostic procedure for determining resting and active stages in a single test. Rapid progression of attachment loss and alveolar bone resorption
are considered to be the active stage and the region of their occurrence is called active region.
（5）Advanced periodontitis produces a vicious cycle and is likely to advance 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 supporting ability due to alveolar bone
resorption induces secondary occlusal trauma, which is complicated with bacterial infection, and disruption of
periodontal tissues proceeds.

3）Characteristics of periodontal therapy（1）Cause elimination improves or arrests periodontitis
Basic periodontal therapy mainly using cause elimination improves mild periodontitis and stops its progression.
However, periodontal surgery and oral rehabilitation are frequently used for moderate or severe periodontitis, andmore complicated periodontal therapy is required. In general, it is difficult to regenerate lost periodontal tissues
completely using current periodontal therapy, including periodontal guided tissue regeneration.
（2）Supportive periodontal therapy（SPT）and maintenance throughout lifetime are requiredin periodontal therapy
Periodontitis has a high risk for recurrence because the major causes of bacterial plaque and traumatic factors arealways present inside 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.
SPT and maintenance are necessary as part of periodontal therapy to maintain periodontal tissues that are recovered by basic periodontal therapy, periodontal surgery and oral rehabilitation, or are stable. SPT is performed
mainly using plaque control, scaling, root planing and occlusal adjustment by dental professionals, whereas maintenance consists of self care（home care）by patients and professional care（special care）by specialists. Periodontal disease is likely to recur due to insufficient plaque control; therefore, SPT and maintenance are essential. Teeth
can be preserved by SPT and maintenance for appropriate intervals and this approach can work for a long time.

5．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 films. 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.
Occlusion that causes occlusal trauma is called traumatic occlusion. Causes include malalignment, early contact, biting interference, bruxism, excessive bite force, lateral pressure, oral and labial parafunctional habit, andfood impaction.

16

Genetic factors

Antibody
Polymorphonuclear
leukocyte(PMN)

Microbial
challenge

Antigen
Lipopolysaccharide(LPS)

Hostimmunity
andInﬂammatory
response

Cytokine
andProstaglandin

Matrix
metalloprotease

Connective
tissueandBonemetabolism

Clinical
signofperiodontal
initiation
andprogression

Other
virulencefactors
Environmental and acquired risk factors
Figure 1．Etiology of periodontal disease（ref 7, revised）

6．Systemic conditions and periodontal disease
Patients with periodontal disease who have or are suspected to have systemic disease should receive sufficient consultation before the start of periodontal therapy, and immediate referral to attending physicians about symptoms.
Patients are treated with periodontal therapy together with sufficient control of systemic disease. Some patients
have difficulty 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 abnormal polymorphism and gene expression.
Patients with Down syndrome, Papillon-Lefèvre syndrome and Chédiak-Higashi syndrome are known to havesevere 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/pubertyrelated periodontitis. 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 pockets8）.
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, andunderstanding of dental therapy.
（2）Environmental and acquired risk factorsa）SmokingSmoking is the strongest risk factor among environmental and acquired factors. Smokers are likely to have peri-

17odontal disease 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 stimulation
Stress stimulation is related to aggravation of periodontal disease and stress stimulation-induced mental tension（stress response）has effects on 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 cytokinetargeted 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）at routine medication induce 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 and low birth weight infant delivery
Mothers with moderate periodontitis have higher risks for delivering a low birth weight infant.
（4）Diabetes
TNF-α, a chemical mediator of inflammation caused by periodontitis, increases insulin resistance and aggravate
diabetes.
（5）Rheumatoid arthritis
Patients with rheumatoid arthritis have large attachment loss and dental loss. Periodontal disease has many common causes and pathological conditions to rheumatoid arthritis. Inflammatory cytokines and prostaglandin E2（PGE2）; i.e., enhanced production is involved in tissue disruption.
（6）Other diseases
Periodontal disease has effects on onset and progression of bacteremia, chronic kidney disease and nonalcoholicsteatohepatitis（NASH）.

18

2 Process of periodontal therapy（see Figure 2）

1．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

Medical interview (ﬁrst medical examination)
Periodontal examination
Diagnosis of periodontal disease
Treatment planning
Basic periodontal therapy(Plaque control, scaling and root planing, revision of habit, extraction, occlusal adjustment,
caries treatment, temporal splint, periodontal therapy devices)

Reassessment
Periodontal surgery
Reassessment
Oral rehabilitation(Occlusal therapy, restorative and prosthetic therapy,
orthodontic treatment, implant therapy)

Reassessment

Healing

Stable condition

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

Supportive periodontal
therapy (SPT)19

and progression of periodontal disease, require thorough elimination of local factors for periodontal disease andimprovement of systemic disease by attending physicians1）. Environmental factors including smoking and stressalso induce progression of periodontal disease; therefore, it is important to improve these factors.

1）Affected individuals
Affected individuals are frequently given many agents, and sufficient consultation is required before the start ofperiodontal therapy, with referral to attending physician（s）for symptoms and development of appropriate teamtreatment. In elderly and affected individuals, prevention of complications is needed to determine resting bloodpressure, 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 topoorly-controlled diabetes and those who have endothelial dysfunction due to atherosclerotic disease, combination
with antibiotic therapy is recommended to improve the response of periodontal therapy and reduce adverse effects
on the body and organs2）.

3）Elderly patients
The elderly are likely to have decreased resistance to periodontal disease and develop aspiration pneumonia due toage-related impaired immune functions. There are no particularly specific procedures for periodontal therapy inthe elderly; however, it is important to have sufficient information on past and current medical history and medication, as well as careful observation of patients because of physical dysfunction and various systemic diseases. It isnecessary to refer to physicians with regard to the patient’s systemic conditions, as required.

2．Examination-based diagnosis, therapeutic strategy and informed
consent
For appropriate periodontal therapy, correct examination and diagnosis of the current symptoms of periodontal
disease are required（see Page 24“1. Periodontal disease examination”）. The first step is to conduct a periodontal
tissue examination to confirm gingival inflammation and tissue destruction, 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 start treatment in accordance with the therapeuticstrategy. The standard procedures for periodontal therapy are shown in Table 2. If the test results in each step
indicate no need for therapy, skip and go to the next test.

3．Basic periodontal therapy
The principle of periodontal therapy is to elucidate causes and precipitating factors of periodontal disease andeliminate them.

1）Proactive participation of patients in treatment
Daily plaque control（self care）by patients is important in periodontal therapy3）. This is necessary to prepare
conditions in which patients proactively participate in treatment based on appropriate instructions for oral
hygiene. Therefore, dentists and dental hygienists should fully explain that periodontal disease is caused by bacte-20

rial infection and that systemic diseases are involved in periodontal disease, so that patients recognize the importance of prevention and therapy.

2）Establishment of plaque control
Successful basic 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 essential 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 hygiene4）.

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 mobility due to periodontal destruction after disease are eliminated, it isimportant to splint and install devices for periodontal therapy temporarily for occlusal stabilization and recovery ofmasticatory function5）.

5）Abstention of palliative treatment
It is inappropriate to administer antibiotic and anti-inflammatory agents alone, conduct incisional drainage for theswelling gingiva, and just fix mobile teeth in patients with gingival inflammation and gingival and periodontal
abscess. Such procedures are referred to as palliative treatment, and do not remove bacterial plaque causing periodontal disease. Bacterial plaque temporarily decrease and seem to be relieved by palliative treatment; however,plaque soon increase again, resulting in relapse. Therefore, periodontal therapy should be conducted to eliminate
causes.

4．Periodontal surgery
After completion of basic periodontal therapy, appropriate surgery is conducted to repair and restore lost periodontal tissues in regions requiring this procedure, based on systemic conditions and the general need for surgery,with the goal of improvement of remaining deep periodontal pockets and morphological defects in the oral
mucosa.

5．Oral rehabilitation
After completion of basic 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.

6．Cure and disease stabilization of periodontal disease
Patients who have periodontal pocket（s）＜4 mm without inflammation are considered to be cured by basic periodontal therapy and periodontal surgery or occlusal function restoration; therefore, they are in the maintenancestate. On the other hand, patients who have periodontal pocket（s）≥4 mm and furcation involvement but noinflammation are considered to be clinically stable and in the stable condition. However, they are likely to have

21

relapse of periodontal disease and need to visit a dental clinic at appropriate intervals to undergo SPT. It is important
to continue maintenance and SPT for long-term maintenance of oral health6）. The designation of＂cure＂or＂stablecondition＂depends on the progression of the disease.

1）Plaque-induced gingivitis
Plaque-induced gingivitis is cured by basic periodontal therapy and diagnosed by reassessment after therapy. Periodontal therapy is not discontinued, but maintained at appropriate intervals.

2）Periodontitis
Mild periodontitis is often cured by basic periodontal therapy. Moderate or severe periodontitis depends on
lesions. Periodontal surgery is performed for lesions as required. Furthermore, after completion of this surgery,reassessment（including partial reassessment）is conducted to evaluate the effect of periodontal therapy and thestate of periodontal tissues. Patients who are determined to be stable or cured at the completion of oral rehabilitation transfer to SPT or maintenance.

3）Stable condition

Patients who have healthy periodontal conditions, but periodontal pocket（s）≥4 mm and furcation involvement
without inflammation in the reassessment test are considered to be in the stable condition. 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 bruxism and parafunctional habit,
decreased tooth-supporting volume due to severe alveolar bone resorption resulting in occlusal trauma even withphysiological occlusal force, or have systemic disease（e.g. diabetes）, should also frequently undergo a reassessment
and SPT.

4）Treatment after cure

Patients who have periodontal pocket（s）＜4 mm, but gingival recession and exposed furcation are sometimes
determined to be cured. However, these patients with an exposed root are likely to develop root caries and require
careful maintenance.

22

3 Medicalinterview,patientreferenceandliaisonwith
medicine

1．Medical interview
The major reason（chief complaint）for the patientʼs visit, and particularly their wish for periodontal therapy,
should be asked. This is important to communicate well with patients and conduct treatment without problems.
Patients with a chief complaint of periodontal disease visit a clinic with a strong wish for treatment, and it isimportant to determine anxiety, discomfort and subjective symptoms of periodontal disease. For patients with achief complaint other than periodontal disease, treatment of their chief complaint and 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 health conditions. Furthermore, it is important to obtain information on periodontal disease-related systemic disease, including diabetes, obesity, ischemic heart disease, aspiration pneumonia, preterm
and low birth weight infant delivery, osteoporosis, and immune⊘allergic disease, as well as environmental factors（smoking, stress, etc.）and genetic factors.

2．Reference of patients to periodontal specialists and advanced
care facilities
Patients with severe periodontal disease should be referred to periodontal specialists and advanced facilities withtherapeutic information, including medical history and treatment record.

3．Liaison with medicine
Recently, aging patients with periodontal disease complicated with different systemic diseases have visited 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 immediately 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 prescribed drugs, and should refer patients to appropriate facilities with appropriate timing. With regard
to diseases including diabetes that are deeply involved in onset and progression of periodontal disease（see Page
46＂2. 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
group）, nifedipine（antihypertensive, calcium blocker）and cyclosporine（immunosuppressant, calcineurin
inhibitor）, the patient is informed of this possibility and the effect of the prescribed drugs is communicated to theattending physician. To ask about the possibility of replacing these drugs, close coordination with the attending
physician is important to allow a decision on drug replacement based on mutual understanding.
Bisphosphonate（BP）drugs and 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. There are studies showing that 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

23

procedures3）. Therefore, physicians ask dentists about these agents and an appropriate therapeutic strategy should
be designed in cooperation with each other.

2）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 basic periodontal therapy. The
type and dose of local anesthetics scheduled, use of epinephrine and surgical time are added. Invasive dental procedures including extraction are performed without withdrawal of antiplatelet agents and anticoagulants when possible.

24

4 Examination,diagnosisandtherapeuticstrategyfor
periodontaldisease

1．Periodontal 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
tests systematically for patients, analyze the results, and plan or revise the therapeutic strategy based on theseresults. Tests are also necessary to assess the conditions of periodontal tissues in SPT and maintenance. Test results
are always described in medical records to facilitate planning of the therapeutic strategy and compare with reassessed results.

1）Periodontal examination
A periodontal tissue examination includes the following items.
（1）Gingival inflammation
1）
2,3）
Gingival inflammation is assessed with the gingival index（GI）
and bleeding on probing（BOP）.

（2）Probing depth
The standard method is to measure one tooth at 6 measurement points（6-point method）, with the measurement
points increased or decreased as required.
（3）Attachment level（AL）
The attachment level is the distance from the unchanged baseline such as the enamel cement junction to thepocket base and is measured using a pocket probe as an indicator to examine the status of progression andimprovement in periodontal disease. The standard method is to use the 6-point method, with the measurement
points increased or decreased as required.
（4）Oral hygiene conditions（O’Leary plaque control record）
Bacterial plaque-accumulating conditions are recorded and assessed using plaque charts. A tooth is divided into
four regions, mesial, distal, labiobuccal and lingopalatal sides, and it is determined whether bacterial plaque ispresent in the tooth cervix of each side4）.
（5）Tooth mobility
Tooth mobility is measured using the Millerʼs classification of tooth mobility: Grade 0（physiological mobility≤0.2 mm）, Grade 1（slight: labiolingual 0.2-1 mm）, Grade 2（moderate: labiolingual⊘mesiodistal 1-2 mm）, and
Grade 3（severe: labiolingual⊘mesiodistal ≥2 mm or vertically movement）.
（6）RadiographDigital dental radiography or panoramic radiography is normally used and a combination of these radiographies isalso used, as required. The number of radiographs is variable. Cone-beam computed tomography（CBCT）widelyused in recent years provides a three-dimensional structure of periodontal tissues. CBCT is an excellent procedurefor finding the bone defect type and relationship with periapical lesions.
（7）Occlusion
The occlusal relation in whole tooth alignment（e.g. malocclusion）and traumatic occlusion due to premature
contact and cuspal interference are examined（see Page 28＂2）Diagnostic procedure for occlusal trauma＂）.
（8）Furcation involvement
Furcation involvement in multi（double-）rooted teeth is examined using a furcation probe and a radiographs,
with progression classified into 3 grades（Lindhe and Nyman furcation classification）or 4 grades（Glickman
furcation classification）.

25a）Lindhe and Nyman furcation classification5）
This is a procedure for examining horizontal attachment loss of periodontal support in furcation. ClassⅠ: Horizontal attachment loss of periodontal support not exceeding one-third of the width of the tooth. ClassⅡ: Horizontal attachment loss of periodontal support exceeding one-third of the width of the tooth, but not encompassing the total width of the furcation area. ClassⅢ: Horizontal through-and-through destruction of the attachment
in the furcation and buccolingual or mesiodistal penetration of the periodontal probe.
b）Glickman furcation classification6）
GradeⅠ: Lesion in furcation area, but no clinical or radiographic evidence of bone loss. GradeⅡ: Destruction
and resorption of alveolar bone in partial furcation area, but no penetration of periodontal probe through furcation area. GradeⅢ: Resorption of bone beneath furcation area and buccolingual or mesiodistal penetration of
periodontal probe, but furcation area covered with gingiva. GradeⅣ: Exposed furcation area in oral cavity andcomplete penetration of periodontal probe.
（9）Plaque retention factors
Factors accumulating and increasing plaques to be examined include calculus, faulty dental restoration, caries,
wedge shape detect, malalignment, abnormal gingiva and alveolar mucosa, abnormal frenulum, abnormal oral vestibule, mouth breathing, dental morphological abnormality, food impaction, and periodontal pocket.
（10）Oral photograph
Oral photography provides records of correct oral status that are difficult to record in words or as a figure. Oral
photography is performed at 5 points: frontal, right and left molars, and maxillary and mandibular occlusions, and5 labiobuccal and 6 lingopalatal sides are also photographed.
（11）Study model
Malalignment, attrition and soft tissue morphological abnormalities are examined in a study model.

2）Microbiological assays（1）Bacteria 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 PCR invader are used in bacteria tests. The
procedure for determining enzymes, a chair-side test, does not identify bacterial species, but is used as a convenient method. Bacteria test kits using monoclonal antibody for P. gingivalis are also under development.
（2）Serum bactericidal antibody titer test
An enzyme-linked immuno sorbent assay（ELISA）is used to determine antibodies in serum produced 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）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, etc.
（2）Saliva test
Periodontal disease activity in the whole oral cavity is examined by testing salivary occult blood, free hemoglobin,
lactate dehydrogenase（LDH）, AST, and alkaline phosphatase（ALP）, etc.
（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.

264）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, oralrelated QOL scales are used8,9）.

2．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 Page10）
. First, the cause of periodontal disease is roughly identified:［1］bacterial plaque,［2］traumatic occlusion,［3］systemic factors, and［4］lifestyle. Next, each tooth unit is diagnosed with plaque-induced gingivitis or periodontitis. Based on these diagnoses, a patient is identified to have plaque-induced gingivitis or periodontitis. A patientwith periodontitis is diagnosed with 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 mild, 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 destruction and inflammation is also considered in diagnosis.
a）Periodontitis classification by degree of tissue destruction＊Mild periodontitis has bone resorption（bone level: BL）or attachment loss（AL）of ＜30％ of the root
length and no furcation involvement.
＊Moderate periodontitis has BL or AL of 30-50％ and furcation involvement.
＊Severe periodontitis has BL or AL of ≥50％ and ClassⅡ or Ⅲ furcation involvement.
b）Periodontitis classification by inflammation severity＊Mild, moderate and severe periodontitis have probing depths of ＜4 mm, 4 to ＜6, and ≥6 mm. respectively.

Start
Accumulation of bacterial plaque on the tooth surface

No

No

Gingival
inﬂammation

Yes

Yes

Attachment loss
(alveolar bone
resorption)

Gingivitis
classiﬁcation by degree of tissue
destruction

BL or ALoss:
Approx. <30%

Healthy
PD <4 mm

Plaque-induced
gingivitis

Mild
periodontitis

BL or ALoss:
Approx. 30%-50%

Moderate
periodontitis

Periodontitis
classiﬁcation by severity of
inﬂammation

BL or ALoss:
Approx. ≥51%

Severeperiodontitis

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

PD:
<4 mm

Mild
periodontitisPD:≥4 to <6 mmModerate
periodontitis

PD:
≥6mm

Severeperiodontitis

27

Start

Healthy
personPatient with plaqueinduced gingivitis

Conﬁrmation of systemic factors
Periodontal tissue examination

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

Periodontitis:≥1 aﬀected tooth

Diagnostic result
by tooth unit

Patient withperiodontitis

Plaque-induced gingivitis:≥1 aﬀected toothNo

Destruction rate ofperiodontal tissues in comparison
with age

Rapid
Characteristics
・Most patients aged 10s to 30s
・Bacterial plaque and calculus:
relatively small
・Familial clustering: Yes

Characteristics
・Aged 35 years and older
・Bacterial plaque and calculus: many
Patient withchronic periodontitis

Patient withaggressive periodontitis

Attachment loss in theﬁrst molar or incisorsof 2 teeth or more

Patient with periodontitis
associated with genetic disorders

Slow

Bacteria and antibody titertests are recommended.

Aﬀected site

Yes

Genetic disease
related to periodontal
disease

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

Range ofmoderate/severe
periodontitis

Attachment loss inthe ﬁrst molar and 3
teeth or more, otherthan incisors

Diagnostic result
by tooth unit

≤30% ofall sites>30% ofall sites≤30% ofall sites>30% ofall sites

Localized

Generalized

Localized

Generalized

Most advanced toothas reference

Mild

Moderate

SevereFigure 4．Diagnosis of plaque-induced gingivitis and periodontitis at individual levelsc）Diagnosis of periodontitis by tooth unit
The diagnostic classification is based on the degree of tissue destruction 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 estimated by confirming systemic disease, familial onset, smoking andstress.
＊A patient in whom destruction of periodontal tissues is slower than that in the same age group is diagnosed
with chronic periodontitis and those who with a more rapid rate are diagnosed with aggressive periodontitis.
b）Progression of periodontitis＊A patient who has mild, moderate and severe periodontitis is diagnosed with severe periodontitis, which may
be described 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 diagnosed 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 affected teeth is ≤30％ and ＞30％, respectively. On the other hand, the AAP Consensus Report10）indicates that a patient with attachment loss in the first molar or 2 incisors or more（at least
one tooth is the first molar）has localized periodontitis and a patient with attachment loss in at least 3 teeth
other than the first molar and incisors is has generalized periodontitis. It is important to classify patients withconsideration of these definitions.

28c）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 by 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 occlusal force to healthy periodontal tissues and secondary occlusal trauma caused by decreased supporting alveolar bone due to periodontal-induced periodontal
destruction. Occlusal trauma is a diagnostic term used for each tooth unit. A tooth with occlusal trauma of toothmobility Grade 1 or higher and enhanced cavity of the periodontal ligament and bone resorption on intraoral
X-ray is diagnosed with occlusal trauma. Other findings include［1］excessive attrition,［2］pathological toothmigration,［3］tooth fracture,［4］lamina dura defect and hyperplasia, and［5］root resorption on X-ray.

3．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 patientʼs chief complaint and the periodontistʼs technical capability. After planning thisstrategy, it is necessary to give 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 is shown 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 periodontal examination, in principle. Comparison of the results ofthese examinations provides feedback to the patient and an understanding of the correct pathology, and helps tojudge the outcomes and revise the therapeutic strategy. In particularly, it is important to examine gingival inflammation, probing depth, 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 involvements 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 OʼLeary plaquecontrol record, no inflammation including gingival redness, and no smoking are recommended.

3）Periodontal surgery

If active periodontal pocket（s）≥4 mm remain after basic periodontal therapy or periodontal tissues destructed byperiodontal disease are to be regenerated, periodontal surgery is considered. This surgery is roughly classified into
tissue attachment therapy, resective therapy, tissue regenerative therapy, and periodontal plastic surgery. If tissue
regeneration is needed, tissue regenerative therapy is considered, whereas gingival recession and oral vestibule aretreated by periodontal plastic 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 recom-

29

mended. 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, probing depth, attachment leveland furcation involvement. If the therapeutic effect after reassessment is insufficient, the causes are analyzed andrepeated 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 periodontal therapy 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 SPTSPT is performed in the same contents as in the first periodontal examination, in principle. Based on these results,
the need for repeated basic periodontal therapy and periodontal surgery is determined. If this is not necessary, apatient is assessed to be in a stable condition or cured and transferred to SPT 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 andremotivation are added.

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

30

5 Homecare,perioperativepatientsandperiodontal
therapy

1．Home care and periodontal therapy
Most immobile patients at home who cannot visit a dental clinic or hospital have functional impairment and heartdisease and lower hemiparesis, including cerebral infarction sequelae. Long-term immobile status causes joint contracture, muscular atrophy and dementia, resulting in reduced mental and physical performance. Therefore, it isimportant for patients with mastication function to perform oral care to maintain oral health and 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 carepatients have difficulty undergoing radiography, interview and inspection play a role in planning of a therapeuticstrategy. Periodontal tissue examination includes inspection of gingival inflammation and soft tissues, tooth mobility and periodontal pocket depth, if possible. In all cases, dentists are required 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 finger motor activity 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 dentistʼs 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 is maintained, the procedures are almost consistent with those described in 1）. If a clean
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（patientʼs family）
under a dentistʼs instructions. Basic periodontal therapy is also performed, depending on circumstances. Muchattention 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 dentistʼs 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）.

2．Perioperative patients and periodontal therapy
For patients who undergo cancer therapy and major surgery, treatment of periodontal disease and chronic infectious disease reduces postoperative infection and accelerates healing. Therefore, perioperative（preoperative, intraoperative, postoperative）intraoral control is important. In addition to surgical therapy, radiotherapy and pharmacotherapy are used in cancer therapy. Intraoperative and postoperative complications are likely to occur, and dental
care is required. Information sharing and cooperation between physicians and dentists are essential for cancer
therapy.

311）Oral function control before surgery（treatment）
Periodontal disease with inflammatory conditions causes bacteremia, resulting in oral bacteria including periodontopathic bacteria spreading in the body. This is a risk for postoperative infection after major surgery. Before any
major surgery, antibiotics combined with appropriate oral hygiene procedures are necessary for oral bacterial infection. Caries prevention requires fluoride application before radiotherapy, removal of overhang of restoration stimulating soft tissue and scaling. Cancer-related ONJ（osteomyelitis of the jaw after radiotherapy in craniocervicalregions, and ONJ related with osteonecrosis and BMA administration）is a severe adverse event. It is important toperform periodontal therapy before treatment and reduce as many risk factors as possible.

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 craniocervicalregions, the gingiva is highly sensitive to radiation and gingival recession sometimes occurs without indication of
inflammation. In chemotherapy, invasive procedures should be performed with consideration of thrombocytopenia and leukopenia induced by myelosuppression. In cancer radiotherapy and pharmacotherapy, it is important toperform continuous oral hygiene control during and after therapy and prevent oral adverse events.

3）Aspiration and infection in oral hygiene control

Perioperative oral function control（herein oral hygiene control as narrow-sense oral care）reduces risks 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 careand hygiene control with oral care devices induce aspiration pneumonia. To prevent aspiration during oral care, it
is important to assess patients in cooperation with other healthcare professionals and choose appropriate surgicalprocedures. Cross infection via oral care has risks for nosocomial infection. There are studies that show 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 for oral care, and introduction and appropriate use of disposable devices（particularly vacuum hoses and tips）.

32

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

2．Treatment of acute inflammation（see Figure 6［3］）Patients who visit 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 is effective for suppressing inflammation and facilitating periodontitis healing. In an acute symptom of gingival abscessand periodontal abscess, occlusal conditions are confirmed and occlusion is adjusted as required. Furthermore,
periodontal pockets, which are possible causes, are thoroughly irrigated and an abscess with marked fluctuation isincised. A local drug delivery system（LDDS）using depots can be combined with subgingival pocket irrigation1）.
A LDDS is convenient due to its prompt effect and easy-to-use procedures（see Japanese Society of Periodontology：
Guidelines for antibiotic therapy in patients with periodontal disease）. If an abscess moves in a combined periodontal-endodontic lesion, the abscess is incised to make drainage roots. Antibiotics are administered as required
and the priority is early endodontic therapy. Early non-chronic combined periodontal-endodontic lesions are likely
to improve, while prolonged combined periodontal-endodontic lesions with remaining periodontal pockets aretreated by subgingival SRP. Patients with marked tooth movement are treated with a temporary splint.

33

7 Preventive treatment
1．Preventionoftransitionfromplaque-inducedgingivitistoperiodontitis
The 2011 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 transfers to periodontitis in these patients, appropriate preventive procedures for periodontal disease inhibits transfer from gingivitis to periodontitis. Appropriate
preventive procedures for periodontal disease in people aged 15-25 years are expected to decrease patients withperiodontal disease because more than 80％ of people aged 40 years or older have periodontal disease. Periodontal
disease is bacterial infection; therefore, both self and professional care are important. Furthermore, it is life styledisease and community 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 andscaling. Prevention of periodontal disease is closely related to treatment; therefore, routine primary and secondary
prevention is necessary to prevent progression to periodontitis.

2．Preventivetreatmentforpregnantwomen〔seePage48＂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. A study indicated the possibility that chronic inflammatory conditions in the oral cavity
release various chemical mediators in blood, leading to increased preterm delivery and preterm low weight birth.
At present, municipalities conduct dental examinations alone for pregnant women. Early detection and treatment
is important, but preventive treatments are more important. Routine preventive procedures for pregnant women
include periodontal examination, oral hygiene instructions, mechanical tooth cleaning, scaling, scaling-root planing and occlusal adjustment, and health guidance. Active preventive treatments are also recommended for womenplanning pregnancy.

34

8 Basic periodontal therapy
1．Concepts of basic periodontal therapy（Figure 5）
Basic periodontal therapy is treatment to eliminate basic etiological and risk factors for periodontal disease,improve inflammation 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, pathology including sensitivity is considered and a therapeutic strategy is planned. Sensitivity to periodontal disease affects the progression
rate of long-term periodontal therapy, and understanding systemic conditions is important to predict reactivity toperiodontal therapy and the influence of periodontal disease on the whole body.

2．Therapeutic strategy for basic periodontal therapy1）Therapeutic strategy and process of basic 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 basic periodontal therapy
determined. Generally, destruction of periodontal tissues and plaque control conditions are the focus; consequently, brushing instructions and SRP take priority. However, the effect of basic periodontal therapy increases
according to the above-mentioned flow.

2）Therapeutic strategy focusing on bacterial infection and inflammation

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

3．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

Extraction of
etiological and risk
factors for periodontal
diseaseOral problems
Systemic problems
LifestyleConsideration of social background

Pathological diagnosis
including sensitivity

Elimination of
etiological andrisk factors
Figure 5．Concept of basic periodontal therapy

35

Start

Identiﬁcationof presence of bacterial
plaqueOral hygiene Instructions

Poor in maxillary
and mandibular teeth

Locally poor

Motivation and thoroughpatient education

Elimination of plaque retentions
factors and instructions
for appropriate oral hygiene

Progression of tissue destruction
in good oral hygiene conditions

Systemic diseasesuspected

High susceptibility toperiodontal disease

Refer to medical
institution

Antibiotic therapy
as required

Figure 6［1］．Basic therapy according to the level of plaque control

Start

Plaqueretention
factorCalculus anddeposits

Faulty dental
restoration

Caries andwedge shape
defectMalalignment

Mucogingival abnormality
Frenulum abnormality
Narrow oral vestibule

Supragingival Subgingival

Early
scaling
if calculus
anddeposits
inhibitself care.

Scaling androot planing
after
completionofmotivationand self care.

Mouth
breathingExaminationof causes
Reproduction
after conﬁrming
the form using
provisional
restration

Restoration(related to
hyperesthesia)

Orthodontic
treatment

Choice ofcleaning
device andinstructions
for use,
instructions
for cleaningof study
model

Frenectomy,
free gingival
graft,
vestibuloplasty

Inventionofbrushing
methodRefer tootolaryngologist

e.g.,
myofunctional
therapy,oral screen

Figure 6［2］．Basic therapy for plaque retention factors

plaques1）. Elimination of bacterial plaques, the main causes of plaque-induced gingivitis and periodontitis, is thebasis of treatment and prevention of periodontal disease. Insufficient plaque control in periodontal therapy substantially decreases effects of dental therapy, including SRP, temporary splint and periodontal surgery, resulting in
failure of periodontal therapy itself.
Specifically, 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）. Furthermore, self care of oral
hygiene control（not including routine control）does not frequently include cause-related therapy, which is not aneffective periodontal therapy system4,5）.

36

Start

Yes

No

Acute
inﬂammation

Probing
pocket depth[1] Administrationof antibacterial
agents[2] Incision
or SRP[3] Combination
with LDDS

<4 mm

≥4 to
<6 mm

≥6 mm

TBI
SC

SRP

SRP
Combinationof LDDS as
required

Figure 6［3］．Basic periodontal therapy for acute inflammation and probing pocket depth（LDDS: local drug delivery system, TBI: tooth brushing instruction, SC: scaling; SRP: scaling-root planing）

Start

Periodontopathic
bacteria test

Antibody titer test

Periodontopathic
bacteria

High titer(++)(-) or (+)

SRP(+LDDS)

SRP

(+)

(-)

High
activity

Low
activity

SRP(+LDDS)

Normalperiodontal
therapy

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

Periodontal therapy maintains good oral hygiene conditions and inhibits progression of periodontitis6,7）. Therefore, 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 andpatients. Plaque control is roughly classified into self care by patients and professional care by dental specialists.
Bacterial plaque is likely to adhere 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 a periodontal 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 andfaulty dental restoration are found, they should be improved.

37（1）Motivation
Motivation is essential to make patients complete plaque control and perform periodontal therapy successfully.
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 examination, 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. In general, basic procedures are mechanicalplaque control using cleaning devices such as a toothbrush（including interdental brush and dental floss）, and a
combination of mainly mechanical plaque control with chemical control is effective. Chemical plaque control isused for regions in which mechanical control cannot be used immediately after periodontal surgery, and is usefulfor regions in which mechanical procedures cannot be used. Instructions for improving lifestyle are given as
required to decrease 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 is necessary to make patients understand the importance of plaque control by themselves（motivation）
and give them practical cleaning procedures（brushing）. Self care by patients is the basis of periodontal therapy,
and has a great 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, type and shape of defects, and dental restoration）and technical level are chosen andinstructions on effective brushing are given.
Practitioners must fully understand the characteristics of various brushing methods, understand a patient’s conventional brushing method and oral conditions, and give brushing instructions. An appropriate and effective
cleaning instrument（interdental brush, dental floss, electric, sonic and ultrasonic toothbrush）must be recommended. Instructions are given gradually in order and changed according to the patient’s motivation and technicallevel. 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 a interdental brushand 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, practioners eliminate bacterial plaque from the tooth surface and prostheses and simultaneously remotivate and reinstruct for oral hygiene control at the patient’s visit9）. Professionalcare is referred to as professional tooth cleaning（PTC）or professional mechanical tooth cleaning（PMTC）.

2）Scaling-root planing
Scaling-root planing are extremely important procedures, in addition to plaque control, for periodontal therapy,
and are performed during basic periodontal therapy and periodontal surgery and SPT. Scaling mechanically eliminates supragingival and subgingival bacterial plaque adhered to teeth, calculus and other prostheses using various
scalers. Calculus is calcified bacterial plaque. It has a crude surface on which many bacterial plaques accumulate.

38

Therefore, calculus is the most important local plaque retention factor. The objectives of scaling are to eliminate
factors attached to bacterial plaques and build an environment in which bacterial plaque is easily eliminated bypractitioners 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-root planing is performed in series
as SRP.
（1）Significance and objective of scaling-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 affect 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 considering systemic pain and past history because SRP involves invasive
procedures. Patients with systemic disease are given antibiotics and antiinflammatory agents, as required by bacteremia. After SRP, debridement＊ including calculus and residual contaminants are cleaned out. There are studies
concluding 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 operator fatigue, resulting in poor efficiency. Therefore, sharpening（grinding）of thehand scaler is important for successful SRP.
（4）Sonic and ultrasonic scalers
Bacterial plaque, calculus and other deposits can be mechanically eliminated using sonic and ultrasonic scalers.
These scalers are effective for elimination of supragingival calculus, and recently improved scaler tips are also available for subgingival scaling, with high elimination effects for certain regions13）. Studies have shown clinical effects
similar to those of hand scalers14,15）.
（5）Dentin hypersensitivity after SRP
Elimination of calculus, deposits and infected tooth substances sometimes cause transient hypersensitivity after
SRP. This should be explained to patients in advance. Patients with hyperesthesia should be appropriately treated.

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

4）Periodontal pocket curettage
If SRP provides no improvement, periodontal tissues can be improved and periodontal pockets shortened byeliminating bacterial plaque and calculus on roots facing periodontal pockets and cementum on the surface ofcontaminated roots, together with periodontal curettage of epithelia and inflammatory connective tissues in periodontal pockets containing junctional epithelia in the inner walls of periodontal pockets, using a curette typescaler.

＊Debridement: procedure for elimination of foreign stimuli and denatured tissues. In periodontal therapy, eliminationof bacterial plaque, calculus, contaminated roots, and inflammatory granulation tissue.

395）Extraction of hopeless tooth
Teeth that cannot be saved are extracted in basic periodontal therapy. However, such a tooth that maintains occlusal relation or plays an important role in oral function may be extracted after teeth in other regions are treated tomaintain occlusal relation and oral function. If a tooth cannot be evaluated in the initial examination, it is notextracted in basic periodontal therapy and is reassessed after completion of this therapy. In particular, teeth withacute inflammation are likely to have increased mobility as periodontal pockets become deeper. Therefore, theseteeth are evaluated after elimination of acute inflammation to diagnose the condition correctly. When extraction is
performed or scheduled, but teeth in other regions are treated before extraction in basic periodontal therapy, or
extraction is indicated in reassessment, it is important to explain to patients and obtain informed consent, because
most patients who undergo periodontal therapy desire to keep as many teeth as possible. Even for teeth that clearlyrequire extraction dentally and medically, informed consent is required for extraction.

4．Current treatment of bacterial infection（Table 6）
1）Mechanical supragingival plaque control
The major oral hygiene control is brushing by patients using a toothbrush. Use of a cleaning instruments including an interdental brush, dental floss, and electric⊘sonic⊘ultrasonic toothbrushes is necessary considering the periodontal severity, treatment period, and patientʼs technique and lifestyle. Scaling and mechanical tooth cleaning by
medical staff are likely to help plaque control and enhance and maintain a patientʼs motivation1）. Adjustment andremoval of faulty dental restoration disturbing supragingival plaque control and occlusal reshaping are performed
as required. Subgingival plaque control is combined for periodontal pockets ≥4 mm. 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）. Decreases of periodontal pockets with depth of 5-7 mm were 1-2 mm and attachment gain was 0.5-1

Table 6．Basic periodontal therapy chosen by diagnostic classification
Mechanical plaque control

Diagnostic
classification

Systemic
control＊Supragingival Subgingival（liaison with （brushing, （scaling-root
physicians）
scaling）
planing）

Chemical plaque control
Supragingival

Subgingival

Application of antimicrobial
and antiseptic agents
Mouthwash

subgingival
pocketirrigation

Antibiotic therapy
Administration
to periodontal
pocketsOraladministration

Plaque-induced
gingivitis

▲

●

▲

▲

▲

Chronic
periodontitis（mild）

▲

●

●

▲

▲

▲

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

40

Table 7．Major drugs used for chemical plaque control
Concentrations of
Product
antibiotics used in Europe
type
and the United States

Antibiotics

Inhibitory
effect of the
drug at thisconcentration onplaqueInhibitory Upper limit of theReference
effect of the concentration in
Presentation type⊘drug at thisthe Japan
analysis method⊘concentrapharmaceutical
Reference
selected RCTs
tion inaffairs guidelines
periodontitis （as a quasi drug） （study period）

Chlorhexidine
gluconate

Mouthwash

0.12～0.20％－0.67
in QHI

－0.32
in GI

0.05％

systematic review J Clin Periodontol,
3 9 : 1 0 4 2 -10 5 5 ,Meta-analysis
30 RCTs（≥4W） 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
J Periodontol, 78:
Meta-analysis
1218-1228, 2007.
7 RCTs（≥6W）

Triclosan⊘
copolymer

Dentifrice

0.3％／2％－0.48
in QHI

－0.26
in GI

0.1％／NL

systematic review J Clin Periodontol,
3 1 : 1 0 2 9 -10 3 3 ,Meta-analysis
15 RCTs（≥6W） 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 Periodontol 2000,
6 RCTs（≥6W） 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 Periodontol 2000,
5 RCTs（≥6W） 48: 23-30, 2008.

Cetylpyridinium
chloride

Mouthwash⊘
Dentifrice

0.05～0.1％－0.42
in QHI

－0.15
in GI

0.01％

systematic review
Int J Dent Hyg, 6:
Meta-analysis
290-303, 2008.
4 RCTs（≥6W）

Tin fluoride

Dentifrice

0.45％

－3～
－33％

＋1～
－40％

NL

systematic review Int J Dent Hyg, 3:
10 RCTs（≥6W） 162-78, 2005.

Amine fluoride⊘
Tin fluoride

Dentifrice

1,400 PPMF-／
250 PPMF-－3.5～－11.8％

－4.3～
29.9％

1,000 PPMF-

systematic review Int J Dent Hyg, 3:
4 RCTs（≥6W） 162-78, 2005.

Sanguinarine

Mouthwash

0.01％

＋4～
－33.9％＋5～－33.8％

NL

systematic review Int J Dent Hyg, 3:
6 RCTs（≥6W） 162-78, 2005.

Delmopinol

Mouthwash

0.1～0.2％

－9.3～
－35％

＋1～
－18％

NL

systematic review Int J Dent Hyg, 3:
3 RCTs（≥6W） 162-78, 2005.

RCT: randomized controlled trial; QHI: Quigley & Hein Plaque Index, GI: Gingival Index; NL: not listed in the quasi drug additives list PFSB⊘ELD
0327004, March 27, 2008. Cited from reference 5］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 inhibits bacterial plaque formation and deposition on the tooth surface. Phenols, povidone-iodine, cetylpyridinium chloride, and essential oils are also used4）. In
basic periodontal therapy, continuous use for 2-4 weeks after scaling prevents regrowth of periodontopathic bacte5）
ria（Table 7）.

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］understand that chemical plaque control is not needed in mostcases of chronic periodontitis and in regions with a good response to SRP.
（1）Subgingival pocket irrigation
The inside of a periodontal 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.

41（2）Administration of antibacterial agents into periodontal pockets
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 after basic
periodontal therapy. However, irresponsible administration may induce microbial substitution and drug resistance,
and there is no validation of repeated administration of antibiotics in SPT.
（3）Oral administration of periodontal antimicrobial therapy
Oral administration of antibiotics are considered for patients with periodontitis that is not improved by basic
therapy, patients who cannot undergo invasive treatment, immunocompromised patients with periodontitis,
patients with generalized aggressive periodontitis, and severe generalized chronic periodontitis. Antibacterial therapy must be performed after［1］thorough planning,［2］clarified 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 drug-resistant⊘refractory periodontitis that was not clinically improved by mechanical plaquecontrol［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. bacterial
endocarditis, aortic valve disease, cyanotic congenital disease, prosthetic valve shunt）.
The details of antibacterial therapy for patients with periodontal disease are described in the JSP 2010＂Guidelines for antibiotic therapy in patients with periodontal disease＂.

5．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 15＂5. Characteristics of occlusal trauma＂）. Occlusal trauma is associatedwith degenerative necrosis in the pressed region of periodontal ligament and alveolar bone resorption（see Table8）. Before treatment, occlusal trauma should be accurately diagnosed（see Page 28＂2）Diagnostic procedure forocclusal 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 8:＂tooth mobility＂and＂enhanced periodontal ligament space＂are important2）.

1）Relationship of occlusal trauma with progression of periodontitis
Traumatic occlusion is not an initial factor for periodontitis, but 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 formarked symptoms and manifestations of occlusal trauma found after completion of procedures for bacterial infection. The specific procedures are below.
［1］Basic periodontal therapy for bacterial infection. If functional impairment is found, occlusal adjustment may

42

Table 8．Clinical and radiographic findings of occlusal trauma（revised 1999 AAP New Periodontal Disease Classification）
One or more clinical findings are included.
1）Increased tooth mobility2）Premature contact3）Marked attrition4）Deep periodontal pocket formation
5）Pathological tooth migration
6）Abfraction（wedge shape detect）
7）Tooth fracture
One or more radiographic findings are included.
1）Widened PDL space
2）Changed alveolar bone（loss, hyperplasia）
3）Bone loss（furcation, vertical, circumferential）
4）Root resorption5）Cementum hyperplasia

be a priority.
［2］Occlusal adjustment or splint when basic periodontal therapy for bacterial infection causes inflammation todisappear and reduces tooth mobility in partial regions; however, mobility remains or increases in someteeth.
［3］Occlusal adjustment and splint for teeth without improved mobility.
［4］Occlusal adjustment and splint for teeth with increasing mobility.
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 occlusal force on periodontal tissues during dental occlusion and calm inflammation in periodontal tissues by correcting traumatic occlusion. Selective grinding makes
occlusal 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 mobility. The objectives of occlusal adjustment
are to improve occlusal trauma in periodontal tissues as a priority, and improve temporomandibular joint disorderand bruxism, stabilize occlusion after tooth crown restoration and orthodontic treatment, improve food impaction, and eliminate premature contact interfering with orthodontic treatment. Occlusal reshaping5）is performed
to revise the ridge and buccolingual diameter of crown or reshape crown morphology, including the cuspal angle
and cusp, to eliminate and distribute traumatic occlusion caused by a poor crown shape. Occlusal reshaping is performed regardless of premature contact; however, occlusal force is reduced by reserving the contact site of theintercuspal 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 athorough 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 returnto the 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, severe
tooth mobility is detected, or periodontal tissues are destructed, resulting in secondary occlusal trauma6）. Temporary splint is performed to distribute and stabilize occlusal pressure to periodontal tissues, improve occlusal

43

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 mobility issevere 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 mobility is temporally increased by invasion after periodontal surgery and may affect healing, temporary splint is performed before surgery and the splint
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 and range ofdestruction of 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］Check plaque control conditions, premature contact and damage of the splint device because routine observation and 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 occlusal force on the splint site.

4）Devices for periodontal therapy（provisional restoration）
For patients with a tooth defect who require extraction or elimination of a faulty dental restoration, 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 occlusal force toremaining teeth, and are referred to as devices for periodontal therapy and denture base and crown type devices7）.
If faulty dental restoration is deeply involved in the onset of periodontal disease, periodontal tissues are stabilized
by eliminating the restoration and installing devices for periodontal therapy during basic 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 basic
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 periodontal tissue conditions during installation of devices for periodontal therapy, confirm regionswith possible recurrence, consider appropriate forms, and incorporate these results into the final prosthesis
design.
［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 occlusal 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

44

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（occlusal base for bruxism）is installed, followed by observation. It is not recommended to adjust wide occlusion
and make 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 noestablished 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 destruction. Occlusal adjustment after orthodontic treatment is essential and it is important to obtain finally balanced occlusal conditions and continue to follow up. An improved dental arch by orthodontic treatment makes oral hygiene control easier and stabilizes periodontal tissues.

45

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 plaque retention factors as local factor, see“Page 25. Characteristics and procedures for the elderly, illpersons, women and smokers”.

1）Systemicriskfactors（seePage16“6.Systemicconditionsandperiodontal
disease”）
Systemic risk factors include age, sex, ethnic differences, genetics, systemic disease, and individual susceptibility of
periodontal disease. For patients with systemic risk factors, including systemic disease such as 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 alchol. In particular, smoking is an important risk factor for progression of periodontal
disease2）, and the necessity of smoking cessation for periodontal therapy should be explained to smokers and theyshould 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.

1．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 dental therapy. 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 isextremely important for elderly people, both physically and mentally. In periodontal therapy for the elderly, it isnecessary to consider the general characteristics of the elderly, mental and physical conditions, the level of finger
function, 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, nonsurgical treatment should be
repeated: mainly debridement in periodontal pockets including plaque control, SRP, periodontal pocket curettage
as required, and supplemental combined chemical plaque control. Elderly people also often develop new systemic
disease during maintenance and SPT; consequently, medication is changed or increased. Therefore, it is required to
ask about new disease or medication at every visit. Cognitive decline may also occur. If a patient’s fingers or brush-46

ing actions during maintenance and SPT pose a problem for the first time, it is necessary to contact their family
and provide the assistance according to cognitive function and brushing actions. More attention is given to physical, mental and environmental changes in periodontal therapy for elderly people, compared to therapy for those inlate middle age.

2．Periodontaltherapyforpatientswithotherdiseases
Patients with periodontal disease often also have diseases such as hypertension, cardiovascular disease, diabetes andosteoporosis.5,6）. 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 medical 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 be difficult 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 onrisk 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 berelated 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.

3）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”（Japanese Society of Periodontology）.
（1）Type1diabetes
Avoidance of development of hypoglycemia is a concern if eating is limited by long-term treatment, including
extraction and periodontal surgery.
（2）Type2diabetes
It is generally preferable not to perform SRP until patients achieve plaque control by themselves; however, peri-

47

odontopathic 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, thepatientʼs 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 to
an attending physician and understanding these conditions. Invasive dental procedures, including extraction, arecommonly 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 administration of antibiotics, see the＂Guidelines for antibiotic therapy in patients with periodontal disease＂（Japanese Society of Periodontology）

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.

3．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.

482）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 mechanicalplaque control, 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 be performed after delivery. Periodontal disease is a risk factor for preterm and low weight birth; 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 33“2. Preventive treatment for pregnant
women”）.

3）Patients with osteoporosis（particularly those taking BP products and antiRANKL 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 22“3. Liaison with medicine”）. Patients taking BP products and antiRANKL 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.

4．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 a heavy smoker, 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.

49

 Periodontal surgery
The indications for periodontal surgery are［1］remaining a deep periodontal pocket after basic periodontal
therapy,［2］poor plaque control and relapse of periodontitis due to soft tissue morphological abnormality, and［3］esthetic dysfunction and anatomical morphological abnormality preventing installation of appropriate dental restoration1）. A patient should also meet the following conditions before periodontal surgery:［1］provision of
informed consent after a full explanation,［2］good systemic conditions,［3］good oral hygiene, and［4］current
non-smoker. Periodontal surgery is classified into four types: tissue attachment therapy, resective therapy, periodontal regenerative therapy, and periodontal plastic surgery. The type of surgery is determined based on the bone
defect type, oral hygiene, periodontal pocket depth, BOP, and radiographic findings（Table 9 and Figure 7）.
The indications for periodontal surgery are periodontal pocket depth ≥4 mm in reassessment and BOP; however,
surgery is conducted to improve poor gingival forms in cases with a lower periodontal pocket depth and no BOP.
Bone defect conditions are important criteria in the choice of the surgical procedure（Figure 8）.
Definition of flap surgery
Flap surgery is periodontal surgery to detach the gingiva from a mucoperiosteal flap containing the periosteum or amucosal flap with the periosteum remaining on the bone surface, curette plaque, calculus and inflammatory granTable 9．Bone defect type and periodontal surgical procedures
Tissue attachment therapy
Vertical osseous
defectHorizontal
osseous defect・Flap curettage（access flap surgery）
・Modified Widman flap surgery

Resective therapy

・Apically-positioned flap procedure＋ostectomy and osteoplasty

Periodontal regenerative
therapy

・Bone transplantation
・Guided tissue regeneration（GTR）
・Enamel matrix derivative（EMD）applied surgical procedure・Surgical procedure using other biologically active substances

Tissue attachment therapy

・Periodontal pocket curettage
・Excisional new attachment procedure（ENAP）
・Flap curettage（access flap surgery）
・Modified Widman flap surgery

Resection

・Apically-positioned flap procedure（＋osteoplasty）
・Gingivectomy

Criteria to start
Periodontal pocket depth: ≥4mm
Bleeding on probing (+)
・Systemic conditions are good?
・Oral hygiene conditions are good?
・Non-smoker?
・Informed consent obtained after an
explanation was given?

<Objectives>

To modify the form
and reduce gingival/
periodontal pocket

Resection

To clean up a root
and attach soft
tissues to the root.

Tissue attachment
therapy

To regenerate
tissues andachieve new
attachment.

Periodontal
regenerative therapy

Figure 7．Selection criteria of periodontal surgery by purpose

To modify
the formand obtain
esthetics
and function.
Periodontal
plastic surgery

50

Start
osseousdefectHorizontal osseous defect only

Vertical (wedge shape) osseous defectOsseousdefect depth<4 mm

Osseousdefect width

≥2 mm

≥4 mm

≥2 mm

Osseousdefect width<2 mmTissue attachment
therapy orresective therapy

Numberof bone
walls

<2 mm
1 or 4 walls

Tissueattachment
therapy

2 or 3 walls
Periodontal regenerative therapy(tissue attachment therapy)

Figure 8．Selection criteria for periodontal surgery by bone defect type＊The depth and width of the bone defect are radiographic findings.

ulation tissues with clear visibility, and eliminate or decrease periodontal pockets.

1．Tissue attachment therapy
Tissue attachment therapy is a surgical procedure to eliminate bacteria and bacteria-derived contaminants on roots
and inside periodontal pockets, and facilitate attachment of gingival soft tissues on roots3）. Tissue attachment
therapy does not include positive ostectomy, osteoplasty or apically positioned flap surgery, but includes periodontal pocket curettage, excisional new attachment procedure（ENAP）, flap curettage（access flap surgery）, andmodified Widman flap surgery. The major inclusion criteria for tissue attachment therapy, surgical characteristics
and indications are shown in Figure 9. In patients with fully controlled oral hygiene, tissue attachment therapy
results in better attachment than resective therapy3）.

1）Periodontal pocket curettage
Periodontal pocket curettage treats roots（e.g., elimination of bacterial biofilm, calculus and pathological cementum）with simultaneous curettage of inflammatory lesions（periodontal pocket epithelium, inflammatory gingival
tissue）on the inner walls of periodontal pockets. This is a procedure for promoting attachment of the gingiva androot surfaces and decreasing periodontal pockets. This procedure is performed to relieve inflammation in the tissues surrounding periodontal pockets and stabilize the pathology even for deep periodontal pockets difficult toeliminate.
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 periodontal pocket curettage using a surgical scalpel. Inner walls of periodontal pockets are eliminatedby internal bevel incision from the gingival margin to the bottom of a periodontal pocket, the root surface istreated with SRP, and the gingiva is pressed and attached to the root, followed by suturing.
Characteristics: Similarly to periodontal pocket curettage, ENAP is less invasive and results in less gingival

51

Start
access to the root
surface in a bright ﬁeld
Deep periodontal pocket
or complicated root shape

Shallow periodontal pocket
or simple root shape

Esthetic
requirement level(gingival recession)
High

Periodontal pocket
curettage or new
attachment procedure

Flap curettage

Low

Modiﬁed Widman
ﬂap surgery

Figure 9．Selection criteria for tissue attachment therapy

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

3）Flap curettage（access flap surgery）
Flap curettage has objectives and procedures that are close to modified Widman flap surgery（see below）. The differences from modified Widman flap surgery are addition of intracrevicular incision and removal of gingival flaps
from the mucoperiosteal flap to allow access to the root surface and further remove the gingival flap to expose thebone tip slightly.
Characteristics: Root cleaning with clear visibility, less surgical invasion, and low gingival recession.

4）Modified Widman flap surgery
This is a surgical procedure for eliminating periodontal pocket epithelium and removing the mucoperiosteal flap
accessible to the root surface to eliminate contaminants on roots and give clear visibility. The original procedure
introduced by Ramfjörd4）specifies steps of incision from outside 1-2 mm from the gingival margin and removal ofthe mucoperiosteal flap by 2-3 mm from the alveolar crest, but no ostectomy or osteoplasty. However, the procedure used for ostectomy and periodontal pocket elimination associated with modified Widman flap surgery is notstrictly classified as tissue attachment therapy.
Characteristics: Periodontal pocket depth decreased by gingival attachment and resection during healing, andusually it will be attachment between the gingiva and root surface is long epithelial attachment4）.

2．Resective therapy
Resective therapy includes gingivectomy, 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 hypersensitivity are needed.

1）Gingivectomy
Gingivectomy is a procedure for gingivectomizing with external bevel incision to decrease or eliminate gingival（false）pockets or shallow suprabony periodontal（true）pockets.
Characteristics: This is a simple procedure for definite elimination of gingival and periodontal pockets, and

52

Start

Attachment
loss

Yes
Bone
resorption
type

No
Gingival
hyperplasia
Yes

Horizontal osseous
defect only

Attached
gingiva width

Vertical (wedge shape)
osseous defectAttached
gingiva width

InsuﬃcientSuﬃcient

Insuﬃcient

Attached
gingiva widthSuﬃcient

GingivectomyORSuﬃcient＊

Flap surgery+ osteoplasty

Gingivectomy

Flap surgery(+osteoplasty)
Apically-positioned
ﬂap procedure

Apically-positioned ﬂap procedure+ ostectomy and osteoplasty

Figure 10．Selection criteria for resective therapy＊
Incise further outside of the gingival margin.

outcomes after surgery are easily predictable. However, gingivectomy sometimes causes 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 fromthe indication.

2）Apically-positioned flap procedure
This procedure is periodontal plastic surgery that eliminates periodontal pockets and is included in resective therapy. The gingival flap over the mucogingival junction is removed, and the soft tissue flap is transferred to the apicalside before suture. Simultaneously with elimination of periodontal pockets, the attached gingiva width is allowed
to increase. However, the gingival flap of the maxillary palate cannot be transferred to the apical root and the gingival thickness and height are adjusted by scallop-shaped incision. The gingival flap can be removed on the mucoperiosteal and mucosal flaps, respectively. For removal on the mucoperiosteal flap, the gingival flap is tightly incontact with the alveolar bone 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 apicalroot and sutured. In apically positioned flap surgery, ostectomy and osteoplasty are usually combined to eliminate
vertical osseous defects and bone torus because periodontal pockets remain or the postoperative gingival form
worsens if the bone margin is not smooth when transferring the gingival flap to the apical root.
Characteristics: Reduction of periodontal pockets, but the root exposed area increases; therefore, it is necessary to give instructions on careful oral hygiene control. This procedure is also used as a clinical crown lengthening
procedure.

3．Periodontal regenerative therapy（see“2012 Guidelines for regenerative therapy
in patients with periodontal disease”（Japanese Society of Periodontology5））
Several periodontal regenerative therapies are based on recent studies of periodontal generation. There is a long53

history of bone transplantation and guided tissue regeneration（GTR）as regenerative therapy. Recent clinicalapplications include use of biologically active substances. The main procedure is enamel matrix derivative（EMD）
applied surgery, which was approved as“highly advanced medical technology for periodontal surgery”in 2007 by
the Ministry of Health, Labour and Welfare in Japan and is currently used in clinical practice in several university
hospitals. This therapy is aimed at regenerating periodontal tissues, and it is important to assess the amount ofregenerated bone and the attachment level gain accurately for a certain period after surgery using standardized
radiography measurements. Several other materials for regeneration have not been approved in Japan. These
guidelines describe these materials to allow an understanding of the current conditions of periodontal regenerative
therapy, but do not recommend surgical procedures using the materials. Many regenerative materials are approvedin Japan and are currently used off-label; therefore, particular attention including medical ethics is required in useof this therapy.

1）Bone graft
Bone graft is performed to stabilize periodontal tissues with regeneration of bone defects and maintain dental
function and esthetics by supporting or enhancing teeth. Bone graft also includes heterogenous bone grafts andxenografts, but mainly uses autogenous grafts and artificial bone grafts（e.g. hydroxyapatite, tricalcium phosphate）
as bone graft materials for safety.
Characteristics: Indications are various bone defects and furcation. Good outcomes of bone regeneration is
expected when many bone walls support graft materials. Bone graft is clinically applied in combination with GTR
and EMD; however, there is no clear evidence of an additional effect. Therefore, careful consideration should begiven 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 an absorbable or nonabsorbable GTR membrane.
Characteristics: Indications are vertical bone loss in 2 or 3 walls and class Ⅱ furcation involvement. In suchcases, GTR provides significant attachment gain and improved horizontal bone loss in comparison with flap surgery. For class Ⅲ furcation involvement, there is no definite evidence for regeneration.

3）Enamel matrix derivative（EMD）-applied surgery
This is a surgical procedure for introducing cementum and facilitating regeneration of periodontal tissues byapplying EMD extracted and purified from tooth germs of juvenile pigs to roots with attachment loss.
Characteristics: The indications are vertical bone loss in 2 or 3 walls. EMD is considered to have outcomessimilar to those of GTR（nonabsorbable membrane）for periodontal pocket depth and attachment gain one year
after surgery. For furcation involvement, there are studies showing that EMD provides significantly improved
attachment gain and improved horizontal bone loss in comparison with flap surgery; however, furcation involvement is not currently included in indications of EMD in Japan and its use requires careful consideration.

4）Surgical procedure using other biologically active substances
Regenerative materials combined with tricalcium phosphate, as bone graft materials, and platelet-derived growth
factor（PDGF）are produced in the United States are used for periodontal regenerative therapy. A surgical procedure using basic fibroblast growth factor has completed clinical trials in Japan and is scheduled to be used for periodontal regenerative therapy. Platelet-rich plasma（PRP）therapy for regenerating periodontal tissues using biological substances such as PDGF is also applied clinically. The Law on Safety of Regenerative Medicine, wasenforced on December 25, 2014 and PRP is classified as a Regenerative Medicine Class Ⅲ.

54

4．Periodontal plastic surgery（including gingival／alveolar mucosaplasty）
Periodontal plastic surgery is a collective term for surgical procedures for improving anatomical problems, including lack and loss of attached gingiva, shallow oral vestibule and frenulum, and muscle attachment, which inhibit
the marginal gingiva, to treat and prevent periodontal disease, confirm the oral environment facilitating plaquecontrol, and improve esthetics6）.

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.
Characteristics: This is a standard procedure that has been used for many years to cover a solitary exposedroot of mild（≤4 mm）gingival recession or a severe case with a narrow width. A marked osseous defect in theregion to be covered, a large area of the exposed root, and a shallow oral vestibule are excluded from indications.
The disadvantages are the complicated operation because a pedicle flap is produced by combination of mucoperiosteal and mucosal flaps, and a high possibility that new gingival recession will develop in teeth adjacent to thetransplanted marginal gingiva.

3）Coronally positioned 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. The procedure is also used to cover a bone graft and GTR membrane in periodontal regenerative therapy. However, forcepressing on a gingival flap sometimes causes recurrence and necrosis. Semilunar coronally positioned flap surgery
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 inpatients with a narrow attached gingiva width or a periodontal pocket bottom beyond the mucogingival junction.
For details, see the resective therapy described above.

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

55

Characteristics: A graft meeting the size of the recipient site can be collected, but the graft requires two surgical sites. Laterally positioned and coronally positioned flap surgery are sometimes combined with grafting. A disadvantage is that grafted gingiva forms a keloid. Miller classified gingival recession into Class Ⅰ and Ⅱ and proposed therapeutic guidelines: Class Ⅰ root coverage can be achieved with a free gingival graft, whereas Class Ⅱroot coverage requires GTR.

6）Connective tissue graft
Connective tissue graft is a procedure for transplanting subepithelial connective tissues collected from the palate.
The objectives include expanded oral vestibules and alveolar ridge augmentation in a region requiring coverage andesthetics of exposed roots, and protection of GTR membranes and newly formed tissues on the GTR membrane.
The indications are gingival recession in wide ranges and exposed roots of many teeth.
Characteristics: A graft in the recipient site is supplied with blood from the periosteal and epithelial sides;
consequently, the graft is likely to engraft in comparison with a free gingival graft. This grafting is superior to freegingival graft in esthetics and is currently the best method.

7）Other periodontal plastic surgery
Besides the periodontal plastic surgery mentioned above, double papilla laterally positioned flap surgery and vestibular extension procedures are included in periodontal plastic surgery.

5．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 with highwater-absorbability has particularly been used in debridement of pathologic roots, including calculus elimination.
The Er: YAG laser output is absorbed by water in calculus and the internal pressure increases as vaporization is
produced, with contaminants including calculus are transpired by＂micro-explosion＂. The laser is likely to havebactericidal action on the irradiated area and effects on endotoxin degradation and removal. However, a laser islight therapy with a noncontact action and is completely different from 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 for treatment 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 Dentistry7）.

56

 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 depend onroot form and divergence, root trunk length and local anatomical factors, including enamel projection in the toothcervix. 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 is important to make an appropriate diagnosis in accordance with the Lindhe and Nyman furcation classification or Glickman furcation classification1）.

1．Examination
In the examination of furcation involvement, the cause and lesion range should be identified; therefore, precise
probing using a furcation probe and examination by dental x-ray film 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）.

2．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.
［1］Class Ⅰ or mild Class Ⅱ lesion: treated with basic periodontal therapy, selective grinding and removal ofClass 1

Scaling and root planing
Periodontal pocket curettage
Furcation plasty

Upper jaw
Root resection

Start

Furcation
involvement

Class 2orPeriodontal regenerative therapy(GTR: combination with bone graft material is allowed)orTissue attachment
therapy

TrisectionorLower jaw
Root separation

Class 3
* Decision-making
based on root
conditions andremaining alveolar boneorUpper jaw

Root resection

Lower jaw

Tunnel preparation or

Figure 11．Selection criteria for therapy for furcation involvement

Trisection

Root separation

orHemisection

57

enamel 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.

58 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 combined periodontic-endodontic lesions. Ascending pulpitis is
not caused by caries in the crown or root, but via the apical pore or accessory root.

1．Classification of combined periodontic-endodontic lesions
Classifications of combined periodontic-endodontic lesions include the Simon classification1）and Weine classification2）and consist 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 and necrosis. The pulp is devitalized. Endodontic therapy is performed.
（2）Class Ⅱ（endodontic lesion-derived）: Severe bone resorption due to periodontitis is found and thepulp is infected from the accessory root or apical pore in periodontal pockets. The pulp is usually vital tooth. In
multi（double-）rooted teeth, only one root is devitalized.
（3）Class Ⅲ（combined periodontic-endodontic lesion-derived）: Lesions that are due to apical periodontitis-induced periapical bone resorption and periodontitis-induced bone resorption connect with each otherand combine. The pulp is devitalized. Endodontic therapy is the first treatment and is combined with periodontal
therapy.

2．Examination
If combined periodontic-endodontic lesions are suspected, the following items are examined:［1］pulp viability,［2］periodontal pocket depth（position of pocket bottom）and probing of furcation,［3］X-ray（form andnumber of the root or root canal; CBCT definitively shows the range of bone defect and the relation 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.

3．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. A Class Ⅰ lesion is treated with endodontic therapy. Affected cementum and periodontal ligament

59

fibers are likely to recur, therefore, SRP should not be performed early. A Class Ⅱ lesion with suspected irreversible 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.

60 O ral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 occlusal treatment, restorative and prosthetic therapy, orthodontic treatment, andimplant therapy. Oral rehabilitation for patients with periodontal disease is required for dentin defect, tooth
defect, tooth movement, decreased occlusal and masticatory function, and esthetics. This treatment is important torecover 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 and occlusal trauma are concerns（Figures 12 and 13）. Joint splint with extensive prosthesis to fix
mobile teeth during basic periodontal therapy and removal partial denture are often performed; consequently,
restorative and prosthetic therapy for patients with advanced periodontal disease is likely to be more difficult thanthat for patients who are healthy. Periodontal therapy is completed by solving these problems and performing oral
rehabilitation, an objective of dental treatment1）. In this chapter, the concepts and choices of procedures for oral
rehabilitation are described.

1．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
and inflammation, including oral hygiene（O’Leary plaque control record）, periodontal pocket depth and BOP;
and occlusal trauma based on roentgenograms（bone resorption, root length, enhanced periodontal ligament
space）, tooth mobility and fremitus（slight vibration in occlusal contact）, and number, placement of remaining
teeth and occlusion（e.g., bruxism, bite force）. For patients with lateral differences in jaw movement or clicks onmouth opening and closing, it is necessary to examine the temporomandibular joint. Jaw dysfunction may bediagnosed in patients with periodontitis complicated with occlusal trauma due to load bearing of the force originally on the jaw joint on teeth and periodontal tissues due to articular disc dislocation.

・Easy to eliminate
bacterial plaque・Diﬃcult to eliminate
bacterial plaque・Scaling and root planingare easy

・Strength of occlusal
contact consistent withsupporting force
・Avoidance of lateralforce
・Enhanced supporting
force by splint

Consideration ofbacterial infection

Consideration of
Occlusal force

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

Item requiring attention in
producing prosthetic device

・Position and compatibility of margin ・Pontic shape(Biological width)

・Position and strength of contact point

・Crown contour

・Appropriate occlusal shape・Interdental embrasure

・Polishing conditions of prosthetic device

Figure 13．Precautions in production of a prosthetic devicefor oral rehabilitation

612）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,
including early contact and bruxism. Sleep bruxism can exceed the maximum bite force4）and it is important totreat excessive traumatic force, including sleep bruxism5,6）. If tooth mobility is significant, priority should be given
to therapy for infected bacteria, although occlusal adjustment and temporary splint are sometimes necessary during basic periodontal therapy. For patients with dysfunction due to remaining mobility after treatment of infectedbacteria, 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 movement 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 disruption
have decreased support from remaining teeth and are likely to have recurrent inflammation. Consequently, it isoften necessary to determine whether dental restoration is a cause of bacterial infection or occlusal trauma basedon chronological data. The process in such a case is to produce provisional restration for periodontal therapy,
examine the form of dental restoration and the split range, and assess whether a less predictable tooth or a toothwith wide movement is also maintained. Specifically, a splint with devices for periodontal therapy is used for temporal restoration of occlusion and esthetics and also for assessment of occlusion, cleaning and occlusal trauma.

2．Choice of procedures for prosthesis and precautions
1）Tooth 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 movement, or occlusal trauma
remains. There are various problems with performance of tooth crown restoration for permanent splint, including
abutment tooth preparation, impressive accuracy, model production, restoration compatibility, and type of cementum for attachment. ne produced to make it easy 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 forperiodontal therapy（provisional restoration）and a temporary splint is used considering the splint range. Incorrect
splint range may induce new or advanced periodontal disease in a splint tooth or other remaining teeth. Furthermore, insufficient consideration about traumatic occlusion causes restoration avulsion and fracture6）. For longterm maintenance of restoration, it is necessary to decrease restoration avulsion and fracture8）, and particularly forpatients with a strong bite force, it is important to consider occlusive trauma for long-term maintenance of resto5,6）
ration（Figure 13）.

2）Treatment of dentition with tooth defectFor a tooth defect, prosthetic therapy is performed with a fixed bridge, removable denture, tooth transplantation,and implanting. Prosthesis for defects is important to secure a continuous dental arch and occlusion and prevent
remaining teeth from occlusal trauma. Understanding the cause of a defect is important to obtain good outcomes.
It is necessary to understand whether the cause of tooth loss is caries or periodontal disease, if periodontal diseaseis the cause of a defect, and whether occlusal trauma is involved in the defect. When traumatic occlusion is
involved in a defect, the outcomes are poor if the type of traumatic occlusion, assessment of traumatic force, andprospect of therapy are not definitively determined, regardless of whether the procedure is used at any site. In a
distal extension defect of a molar less influenced by occlusal trauma, the molar is not used for prosthetic therapy,
9）
but the short dental arch with occlusion to the premolar is used for building（Table 10）.

62

Table 10．Choice of prosthetic devices
Support and masticatory and bite force of
periodontal tissue

Defect level

Prosthetic device
Crown and bridge

Partial denture

Implant

Completedenture

◎

◎

◎

×

Support of periodontal
tissue≥masticatory andbite force
Several teeth loss

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

Non-vertical stop
occlusion

Several teeth
remaining◎Recommended○△
Support of periodontal○（Improved support with （Clasp-anchored teeth
tissue＜masticatory and（Attention to fracture ofconnective splint ofbilaterally placed asbite force
pair teeth）
remaining teeth）
joint-stabilizing devices）

×△◎（Canine tooth instruc- （Connective splint oftion and molar occlusal
remaining teeth andsupport are confirmed） bilateral partial denture）

×

Support of periodontal
tissue≥masticatory andbite force◎

Support of periodontal
tissue＜masticatory andbite force

×○○（Connective splint of（Attention to fracture of
remaining teeth andpair teeth）
bilateral partial denture）

×

Support of periodontal
tissue≥masticatory andbite force

×◎（Connective splint ofremaining teeth andbilateral partial denture）

×

Support of periodontal
tissue＜masticatory andbite force

×

○
○
○
（Connective splint of（Multiple teeth（Attention to fracture of
remaining teeth andare lost due topair teeth）
bilateral partial denture）
root fracture）

Support of periodontal
tissue≥masticatory andbite force

×

×

◎
◎
（Outcomes of remaining（Cross bite,
teeth have no problems） overlay denture）

Support of periodontal
tissue＜masticatory andbite force

××○（Attention to choice ofmaterials for upper
structures）◎（Cross bite,overlay denture）

×○（Conditions of alveolar
ridge and mucosa areappropriate）◎（Overlaydenture）

Under any condition○Indicated×△Indicated by condition○

×Inadequate（1）Bridge10-17）
A prosthetic bridge makes abutment teeth receive a bite force; therefore, it is important to examine the defectrange, 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 fixing effect, leading to preventionof occlusive trauma, whereas an inappropriate design induces new or advanced periodontal disease in abutment
teeth.
（2）Removable partial denture
Denture must be designed based on the defect range, number of remaining teeth and position, and number ofpaired teeth. An inappropriate denture design may cause load bearing of clasp-anchored teeth and induce occlusal
trauma; therefore, the load bearing ratio of bite force to remaining teeth and denture mucosa should be carefully
determined. Stable retention of partial denture are support（vertical movement）, grasp（horizontal movement）,
and maintenance（prevention of withdrawal）. Stable denture reduces the load bearing of clasp-anchored teeth;
however, it is important to design denture with full consideration of load bearing capacity of remaining teeth. In acase with many defective teeth, it is important to determine the cause, analyze the patientʼs background on daily
life, and take measures.

63（3）Implant18,19）
An implant gives strong support and usually reduces the load bearing of remaining teeth. An implant can avoid
the fixing prosthesis with cutting of neighboring teeth, but may act as a traumatic force on a teeth pair. 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 bacteria infection from natural teeth to peri-implant tissues.
（4）Tooth replantation
Tooth replantation is related to complicated factors for outcomes, including the choice of replanted teeth, replanting site and technology, and occlusal trauma. However, if problems with these respective factors are solved, goodlong-term outcomes are likely. In evulsion of replanted teeth, as many healthy periodontal ligaments as possible
should be kept. The outcomes depend on the surgeonʼs plan and technique, and further establishment of conditions and approaches is required20）.

3．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 occlusal abnormality.

2）Remodeling of the periodontium 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.

64 Implant therapy
1．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 serial alignment. Implant therapy may avoid removable denture, occlusal stabilization,
prevent natural teeth cutting associated with restorative and prosthetic therapy, increase masticatory efficacy andimprove esthetics. However, this is not a criterion for extracting teeth with periodontal disease. Implant therapy
can be used, but teeth on the border of extraction approval should be carefully assessed1,2）. There are no strict criteria for extracting teeth with periodontal disease or use of implant therapy, and implant therapy should be determined based on a full examination by dental staff and informed consent based on test results.

2．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 theattachment form of the implant and epithelium and that of natural teeth and epithelia. However, the attachment
mechanism of epithelia and implants is built only at the deep site of epithelial attachment, and not near the
implant pocket base. Consequently, external factors are likely to enter tissues3）and implants are less resistant toinfection 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-implantitis4）. Pathogenic bacteria in periimplantitis 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 crevice5）. Based on these results,
periodontal therapy is performed for remaining teeth before implantation. To confirm the effect of periodontal
therapy, it is preferable to conduct a periodontal tissue examination and a microbiological assay（bacteria test,
serum bactericidal antibody titer test）.

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 edentulous jaw or partial tooth loss, and implants are also applied as an anchor of orthodontic treatment. Althoughimplants have been applied to various defects in the oral cavity, peri-implant inflammation occurs similarly to thatin periodontal tissues after implant therapy for patients with periodontal disease who have poor plaque control.
Implant treatment also produces new problems, including peri-implant mucositis and peri-implantitis presenting
with clinical and histopathological manifestations6,7）. The causes of implant failure are classified as traumatic andinfectious, and periodontopathic bacteria in periodontal pockets in the implanted oral cavity are detected in areas
surrounding implants and result in failure due to bacterial infection.

3）Precautions for implant with trauma
Microflora in implants with disintegrated osseointegration due to trauma are similar to those in a stable implant.
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-toimplant ratio（i.e., implantation of a short implant body and a long upper structure）is caused by widespread

65

disruption of bone tissues due to periodontal disease, leading to excessive burden to implants8）. To perform
implant therapy for patients with periodontal disease, precautions for both bacterial infection and traumatic force
and therapeutic guidelines are required. Therefore, for implant therapy for patients with periodontal disease, bothrisk factors for periodontal disease and for peri-implantitis should be controlled, in addition to the number of lost
teeth and alveolar ridge conditions.

3．Implant therapy and maintenanceIn comparison with periodontal tissues, tissues around osseointegration-type implants have markedly different
function and structure9）. Important characteristics of periodontal tissues that differ from peri-implant 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 have no connective tissue attachment because there is no cementum in implants10）. Consequently, no physiological movement occurs in
implants. Collagen fibers are not attached to the surface of implants, but form circular fibers running parallel with
the implant surface. Implant therapy requires pretreatment including removal of the source of infection in basic
periodontal therapy and adjustment of occlusal relations. 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 osseointegration periods, 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 managementof natural teeth. The upper structure of implants is likely to be markedly overcontoured, which is a cause of difficulty in self care. The frequency of visits for maintenance after completion of implant therapy depends on apatientʼs 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 months. For details, see the＂2008 Guidelines for implant treatment in patients with periodontal disease＂（Japanese Society of Periodontology）.

66 Treatment of peri-implantitis
1）Broad definition of peri-implantitis
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 with time after implant therapy1,2）. Therefore, it isimportant to elucidate the mechanism of peri-implantitis and establish therapeutic procedures in implant therapy.
Peri-implantitis is inflammatory lesions associated with bone disruption in peri-implant tissues that develops
due to bacterial infection and the burden on implants under osseointegration. Clinical manifestations include redness, swelling, pus discharge in peri-implant tissues, BOP, increased probing depth and recession, followed by progression to abscess formation and implant movement. 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 inclinical findings around implants routinely and continuously using multiple clinical parameters.
Peri-implant mucositis and peri-implantitis are defined as inflammatory lesions in peri-implant tissues（Table
11）. Peri-implant mucositis is a reversible inflammatory process in peri-implant soft tissues, whereas peri-implantitis is an inflammatory process causing supporting bone loss3）. Marked bone resorption in a radiograph is evidence for advancement of peri-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 inflammation in implants differs from that in periodontal tissues. In periodontal tissues, periodontal lesions induced by bacterial plaque are localized in connective tissues, whereas in peri-implanttissues, lesions spread to alveolar bones6）. Bacterial flora in pockets are similar to each other7）. Considering thisbackground, if peri-implant tissues are exposed to bacterial plaque for a long period, peri-implant mucositis proceeds to peri-implantitis8）. However, fracture and crack of the implant body, abutment（screw）, upper structureloosening, and inflammation induced by cementum residues after cementation are similar clinical findings thatneed to be differentiated from clinical findings of peri-implant mucositis and peri-implantitis.

2）Cause of peri-implantitis
Microflora around implants are similar to those around natural teeth and periodontopathic bacteria, with highproportions of A. actinomycetemcomitans, P. gingivalis, P. intermedia, and T. denticola are present in high proportion9-11）. When the remaining teeth are affected with periodontal disease and not treated with plaque control,
these teeth are reservoirs of periodontopathic bacteria around implants12）, consequently, risks increase in patientswith generalized aggressive periodontitis and severe generalized chronic periodontitis.
Other risk factors include systemic disease-related periodontitis（particularly complication with diabetes andrheumatoid arthritis）, smoking-related periodontitis, occlusal trauma in remaining teeth due to changed occlusal
conditions, and occlusal overloading on implants. 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）.
Table 11．Peri-implant mucositis and peri-implantitis

Pathology

Peri-implant mucositis

Peri-implantitis

Reversible inflammatory lesion localized to surrounding mucosa

Irreversible inflammatory lesion associated with bone
resorption

BOP
Drainage＋＋orBone resorption－

Deflection

－

＋
－

＋
＋

Difficult to detect in early lesions. Different toprogression state＋

In case with progression

673）Examination and diagnosis of peri-implantitis
Systematic and consecutive monitoring 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 to diagnose lesions.
（1）Plaque（biofilm）control state
Plaque control is closely related with onset of peri-implantitis and peri-implant bone resorption. Biofilms form on
the surface of implants, similarly to periodontal disease. Therefore, it is important to perform plaque control, using
the modified plaque index（PI）for objective assessment13）.
（2）Bleeding on probing（BOP）
The accuracy of BOP diagnosis is higher than that in natural teeth14）and BOP is an important index to monitorchanges in peri-implant tissues. The modified gingival index（GI）is generally used for assessment of inflammation
13）
in peri-implant tissues. In addition, a BOP（－）status under appropriate probing pressure（0.15-0.25 N）
shows

healthy conditions of peri-implant tissues.
（3）Probing depth（PD）
Probing of a peri-implant crevice requires appropriate pressure based on conditions of keratinized mucosa or alveolar mucosa. The insertion direction is determined considering the type, mode（platform switching）and depth of
the implant body. The approach using PD depends on the chronological increase in PD, rather than the absolutevalue of PD. PD changes are correlated with the conditions of peri-implant inflammation1,13）. Resistance of tissues
in inserting a probe is also helpful to determine whether tissues are healthy.
（4）Pus discharge
Pus discharge is not an appropriate parameter for early peri-implantitis, but suggests that a lesion suspected to beadvanced peri-implantitis is associated with bone disruption. Since inflammation of peri-implant tissues is active,
it is necessary to treat bacterial infection1,13）.
（5）RadiographRadiography is less sensitive for diagnosis of early peri-implantitis and does not show changes in the alveolar boneon the buccolingual（palatal）side. The criterion for implant success is mean resorption in the marginal bone after
loading implant function ＜0.2 mm per year; however, this criterion requires reassessment8,14）.
（6）Implant mobility
Diagnosis to peri-implantitis is less sensitive and clinical evidence for the diagnostic accuracy of devices for quantitative evaluation of mobility（Periotest（Siemens, Germany）and Osstell（Integration Diagnostics, Sweden））isinsufficient13）. If movement is detected, osseointegration is considered to be lost,, which is a definitive result foruninstallation of the implant.
（7）Peri-implant keratinized mucosa
There is no clear evidence showing that keratinized mucosa is necessary. However, insufficient keratinized mucosa
results in poor plaque control and inappropriate probing depth and BOP1,13）.
（8）Peri-implant crevicular fluid（PICF）
The amount of PICF is correlated with the inflammatory severity and bone resorption in peri-implant tissues;
however, the diagnostic accuracy is not always high13）.
（9）Microbiological tests
When antibiotic therapy for peri-implantitis is given in accordance with cumulative interceptive supportive therapy（CIST）, bacterial tests combined with BOP improves diagnostic accuracy12,15）.
（10）Occlusal relation
Peri-implant bone disruption is progresses acutely due to bruxism and occlusal trauma as peri-implantitis advances
16）（perio-implant-load-titis）. Peri-implant bone is lost due to excessive overloading and upper structures are bro-

ken and fixation screws fracture.

68

Table 12．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 therapy4）Treatment
The priority for treatment of peri-implantitis is to extinguish inflammatory lesions in affected areas due to bacterial infection. It is necessary to diagnose and treat the affected area and simultaneously diagnose and treat periodontitis in remaining teeth. For conservative therapy or surgical treatment, success depends on debridement ofbacterial biofilms attached to microstructures on the implant surface. Reassessment should be performed after
elimination of inflammation is confirmed, as in periodontal therapy, and surgical procedures should be selected as
required.
（1）Treatment process
Therapy for improvement of inflammation includes reinstruction for plaque control, debridement, mechanicalcleaning, disinfectant therapy and antibiotic therapy, which are consistent with basic periodontal therapy and arechosen depending on the patient. Bacterial tests are also important parameter in the treatment process. Occlusal
adjustment for overloading and bruxism are performed depending on patients. Periodontal tissue examination andperiodontal therapy for remaining teeth are essential, and smoking and systemic disease are considered. Reassessment is then performed and use of surgery is determined depending on the patient. Possible surgery includes
resective therapy to expose the surface of the contaminated implant body, apically-positioned flap surgery（applied
to horizontal bone resorption and not applied to esthetic regions）, periodontal plastic surgery for immobile keratinized mucosa deficit（free gingival graft, connective tissue graft）, and regenerative therapy（e.g. vertical bone
defect）. Particularly in regenerative therapy, the success of re-osseointegration depends on the procedure fordebridement of contaminated implant surfaces, including curettage with pure titanium curette, laser, air ablation,
photodynamic therapy（PDT）, and implant plasty1,13）. The outcomes of these therapies should improve with time.
In regenerative therapy, a combination of autologous bone and membrane is the standard. The requirements
shown in Table 12 should be considered in choosing the surgical procedure.
（2）Cumulative interceptive supportive therapy（CIST）（Figure 14）
For patient management after implant therapy, it is important to monitor various clinical parameters continuously
and evaluate the results. Lang et al. recommended a CIST protocol（Figure 14）for systematically integrated
assessments of peri-implant tissue conditions of plaque index（Pl.I）, probing depth（PD）, BOP, bone resorption
in radiography, and bacterial test17,18）. This protocol includes four categories（A to D）in accordance with the
combination of assessment results of clinical parameters. A: mechanical plaque removal, B: application of disinfectants, C: systemic or localized administration of antibiotics, and D: regenerative or resective surgery. With regard
to disinfectants［B］, chemical plaque control requires gargling with 0.1-0.2％ chlorhexidine or use of 0.2％
chlorhexidine gel for topical application. However, these agents are currently unavailable in Japan. In applicationof antibiotics［C］, the recommended agents are ornidazole（1,000 mg×1）or metronidazole（250 mg×3）for10 days, or a combination of amoxicillin（375 mg×3）and metronidazole（250 mg×3）for 10 days, as required.
These agents are available, but should be used carefully based on the results of bacterial tests and under the responsibility of a clinician. In surgical treatment［D］, even for resective or regenerative surgery, judgment should bemade considering wound closure and membrane exposure if no keratinized mucosa is present around implants.
The flowchart of treatment until surgery is shown in Figure 15: A, basic therapy for peri-implantitis: mechanical plaque removal, B: application of disinfectants, and C: systemic or localized administration of antibiotics, for69PD≤3mmPD 4 to 5mm

PD >5mm

Absence of plaque
BOP negative
Mechanical debridement
PolishingA

Antibacterial cleaning
0.1% chlorhexidine gel
Twice a day, for 3-4 weeks

B

BOP(+)
Bone loss ≤2 mm

Systemic or local
antibiotic therapy

C

BOP(+)
Bone loss >2 mm

Resective orregenerative surgery

D

Mobility(+)

Implant removal

E

Presence of plaque
BOP(+)

BOP(+)
No bone loss

Figure 14．Cumulative interceptive supportive therapy（CIST）

which the priority is thorough removal of pathogenic bacteria. Surgical procedures should be chosen, including theavailability of 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. Particularly for the high risk
group, including generalized aggressive periodontitis, severe generalized chronic periodontitis, systemic diseaserelated periodontitis（complication with rheumatoid arthritis and diabetes）, and smoking-related periodontitis,
bacterial tests are required, in addition to conventional clinical parameters1,12）. In addition, it is necessary to maintain an appropriate occlusal relationship of remaining teeth, including neighboring and pairing teeth, secure occlusal balance against contact with implants and changed occlusal conditions using occlusal adjustment as required,and prevent occlusive trauma in remaining teeth and overloading of occlusion to implants19,20）.

70

Peri-implantitis histology
Diagnosis/planning of therapeutic strategy
Corresponding
to CIST A

Basic therapy(Plaque control, mechanical 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 or supportive implant therapy
Figure 15．Flowchart of treatment for peri-implantitis

71 Supportiveperiodontaltherapy（SPT）andMaintenanceBacterial plaque, the main factor for periodontal disease, always exists in the oral cavity. Since traumatic factors arealso resident, periodontal pockets of ≥4 mm and furcation involvement sometimes remain after completion of
appropriate periodontal therapy. The motivation of patients with periodontal disease decreases with time and theenvironment in the oral cavity, including changes in position and form of the marginal gingiva over time, and systemic factors have effects and periodontal disease is highly likely to recur1）. Therefore, it is important to improve
patient motivation to maintain periodontal tissues that are cured or stabilized by periodontal therapy, with performance of plaque control in SPT or maintenance based on instructions in daily life, and view point of odontology2,3）. As described above, family dentists should consider a patient self care permanently for patients gettingback the healthy periodontal tissues. Such management prevents recurrence, tooth loss and disruption of periodontal tissues, maintains long term masticatory performance, improve quality of life（QOL）, and increases thehealthy lifespan.

1．Term definitions
1）Supportive periodontal therapy（SPT）
After basic periodontal therapy, periodontal surgery and oral rehabilitation, most periodontal tissues are cured, but
periodontal pockets remain in a progression-resting stage, 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 cleaning and occlusal adjustment, with the goal of removing causal factors andgiving oral hygiene instructions and remotivation.

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

3）Stable state

Patients who have healthy periodontal conditions, but periodontal pocket（s）≥4 mm without BOP, furcation
involvement and tooth movement without inflammation in the 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 have a reassessment test and SPT. Patients
who have tooth movement, bruxism and parafunctional habit, decrease tooth-supporting volume due to severe
alveolar bone resorption resulting in occlusal trauma even with physiological bite force, or systemic disease（e.g.
diabetes）should also have SPT4）.

4）Healing
Healing is a clinically healthy condition recovered in periodontal tissues. The conditions are no gingival inflammation or BOP, periodontal pocket depth ＜4 mm and tooth movement within physiological ranges. Patients withperiodontal pocket（s）of depth ＜4 mm, but gingival recession and exposed furcation, might be determined to be
cured. Dentine reinforcement with fluorine is necessary in maintenance.

725）Professional tooth cleaning（PTC）
Plaque removal, SRP, and polishing of the tooth surface by a dentist or dental hygienist.

6）Professional mechanical tooth cleaning（PMTC）
PMTC is mechanical removal of plaque from teeth by a dentist or dental hygienists using cleaning instruments.
SRP is not included, in principle. PMTC is defined as mechanical tooth cleaning by specialists, or procedures formechanically choosing and removing supragingival and subgingival（from 1 to 3 mm）plaque on all the tooth
surface, including the interdental adjacent area3）.

2．Examination and diagnosis
Reassessment before SPT is performed similarly to the first dental examination, in principle. After review of examination results and risk factors, the effect of periodontal therapy is assessed and the disease is diagnosed. If norepeated basic periodontal therapy or periodontal surgery is necessary, a patient is defined to be in a stable state or
cured, and is transferred to SPT or maintenance. Even during SPT as part of periodontal therapy or maintenanceas health management, reassessment is conducted at 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 in
SPT and the maintenance stage after reassessment and criteria are shown in Figures 16 and 17, respectively.

1）Decision-making point
The determination of cure or stable state depends on the progression state.
（1）Plaque-induced gingivitis
Plaque-induced gingivitis is cured by basic periodontal therapy and diagnosed by reassessment after therapy. 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）.

Start(During SPT or
maintenance)

Reassessment

Healing

Pathologic
progression

Stablecondition

Maintenance

Periodontal
surgery, etc.

Supportive
periodontal therapy(SPT)

Reassessment
Figure 16．Flowchart in SPT and maintenance stage

73

Start during SPT or maintenance
Reassessment
Periodontal pocket depth
Bleeding on probing
Furcation involvement
Bacteria test
Antibody titer test

Periodontal pockets in allteeth: <4 mm
BOP: Bacterial count: below thedetection limit or small
Antibody titer: low

Tooth with periodontal
pockets ≥4mm
BOP: Bacterial count: moderate
Antibody titer: moderate

Tooth with periodontal
pockets ≥4mm
BOP: +
Bacterial count: large
Antibody titer: highHealing

Stable conditiondiseaseprogression

Maintenance

SPT

Periodontal
surgery, etc.

Figure 17．Diagnoses by tooth unit and individual levels
Comprehensive diagnosis is made based on reassessment, periodontal pocket depth, bleeding on probing, bacteria test, and antibody titer test（2）Periodontitis
Slight periodontitis is often diagnosed with cure in basic periodontal therapy. Moderate or severe periodontitis
depends on lesions. Surgical periodontal therapy is performed in lesions as required. Furthermore, after completion of surgical periodontal therapy, reassessment（including partial reassessment）is conducted to evaluate theeffect of periodontal therapy and the state of periodontal tissues. Patients who are determined to be in a stablestate or cured at completion of oral rehabilitation transfer to SPT or maintenance.

2）Test items（1）Periodontal examination
The requirements for stepping to SPT or maintenance are reassessment of oral hygiene conditions, periodontal
pocket depth, BOP, tooth mobility, radiograph, occlusion and furcation involvement.
（2）Microbiological assays
Bacterial tests to monitor periodontopathic bacteria in subgingival plaque, including P. gingivalis and A. actinomycetemcomitans, and antibody titer（infection marker）tests are useful to assess therapeutic effects and define thecontents of SPT.
（3）Other examinations
A gingival crevicular fluid（GCF）test is also useful to assess therapeutic effects and determine the details of SPT.
（4）Risk assessment in SPT（revised Lang & Tonetti6）, 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］PD ≥5 mm: low risk ≤4 sites, high risk of recurrence ≥8 sites.
［2］BOP ratio: low risk ≤9％, high risk ≥25％. The cutoff between a stable state and recurrence or advancement is 25％.
［3］Bone loss depending on age, using ％ maximum loss of molar alveolar bone divided by age: low risk ≤0.5％,high risk ≥1.0％.
［4］Number of lost teeth per 28 teeth: low risk ≤4 teeth, high risk of recurrence ≥8 teeth.
［5］Systemic disease⊘genetic factor: diabetes and IL-1 genotype-positive are high risk, unknown and IL-1 genotype-negative are no risk.

74

Prevalence of residual pockets ≥5 mm
Percentage of sites with BOP
Posterior bone loss in relation to the patient’s age
Loss of teeth from a total of 28 teeth
Systemic and genetic aspects
Cigarette smoking

Prevalence of PD ≥5 mm
BOP %Bone loss/age
Loss of Teeth
Syst./Gen.
Smoking≤4 points≤9%≤0.5≤4 teethNo
0/day

5-7 points
10-24%
0.6-0.9
5-7 teeth
Yes
1-19 cigarettes/day≥8 points≥25%≥1.0≥8 teethYes≥20 cigarettes/day

Consistent with ≥5 of the 6 items

Consistent with ≥2 of the 6 items

Consistent with ≥2 of the 6 items

Low risk

Moderate risk

High risk

As required

Usual

Stronger

Instructions forcontrol of causal
and risk factors

Figure 18．Risk assessment in SPT5）［6］Environment（lifestyle）: non-smoking and smoking cessation ≥5 years are low risk, smoking ≥20 cigarettes⊘day is high risk.
The risk for periodontal disease is assessed using the above 6 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.

＊

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

3．Therapeutic planning
The contents of therapy after reassessment examination are roughly divided into maintenance7-9）and SPT10）andthe following therapies are chosen.

1）Maintenance6-9）
Maintenance is used to prevent recurrence in patients who are cured in reassessment. The objectives of maintenance are［1］prevention of recurrence of periodontal disease,［2］early detection of new sites of periodontal onset,
and［3］long-term maintenance of a good environment of periodontal tissues. After confirming whether motivation is maintained or appropriate self care is being performed, PMTC and SRP are performed to eliminate causal
factors. PTC and PMTC are important procedures and dentine reinforcement by application of fluoride andplaque removal by professional care provide a good oral hygiene environment. Furthermore, it is necessary tounderstand the patientʼs living environment, oral conditions and risk factors, and give instructions for improving
lifestyle. For patients who have lifestyle 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 goodplaque control and give instructions on these environmental factors and systemic risk factors. It is important for
maintenance to schedule the next visit. Recall intervals are determined based on information from various tests
and therapy.
10,11）
2）Supportive periodontal therapy（SPT）

If disease conditions are determined as stable in reassessment, the therapeutic stage moves to SPT. The objectives

75

Table 13．Therapeutic contents of healing, stable state and progression state
Healing

MaintenanceStable state

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

Pathologic Periodontal surgery, etc.
progression

Based on recall at appropriate intervals
Oral hygiene instructions（plaque control）
Professional mechanical tooth cleaning（PMTC）
Scaling and root planing

Periodontal surgery
Flap surgery
Gingivectomy, etc.
Oral rehabilitationof 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 pocket irrigation and occlusal adjustment as required, as well as administration of antibacterial
agents into periodontal pockets（Table 13）. However, when the disease is advanced（periodontal pocket depth ≥4 mm, BOP（＋）, many bacteria, high antibody titer）, periodontal surgery may be performed. Recall intervals of
SPT depend on periodontal tissue conditions and plaque control level in each patient, and recall every 1 to 3
months is generally recommended. Recall intervals can increase or decrease based on condition changes, e.g. every
one month initially, then every 3 months or every 6 months

76

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JSP Clnical Practice Guideline for the Periodontal lreatment, 2015
The first edition first published（Japanese version）on March 25, 2016
The first edition first published（English version）on December 15, 2017

Edited by

The Japanese Society of Periodontology

IssuerIssuerYuichi Izumi （Japanese version）
Hidemi Kurihara（English version）

Production support

Ishiyaku Publishers, Inc.

A book with defective or missing pieces will be replaced with a complete one.
Printed and bound by Sanposha Printing Co., Ltd.

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