Oralmucositis :Supporting cancer
therapy compliancewith oral care

December 2021

Oral mucositis :Supporting cancer therapy compliance with oral care

Content
Executive summary

3

I

Definition

4

II

Epidemiology

5III

Etiology

6IV

Pathogenesis

8

V

Clinical characteristics and diagnosis

11

VI

Prevention and management

13

Bibliography

20

Annex : FDI/Sunstar guidelines on oral cancer

23

Notes

24

This document was developed in collaboration withProfessor Carlo Lajolo
MD, DDS, PhD Associate Professor in the Head and Neck Department
at the “Fondazione Policlinico Universitario A. Gemelli – IRCCS”, Schoolof Dentistry, Catholic University of the Sacred Heart - Rome, Italy.

Professor Giovanni Scambia
Scientific Director. Fondazione Policlinico Universitario A. Gemelli IRCCS, Catholic University of the Sacred Heart - Rome, Italy.

2

Executive
Summary
Patients undergoing cancer treatment,
particularly those receiving a combinationof radiotherapy and chemotherapy for thetreatment of head and neck cancer, areat high risk of developing oral mucositis.
Oral mucositis affects up to 90% of
high-risk patients. Mucositis can be so
debilitating that it prevents patients fromeating and drinking. Some patients may
be hospitalized and fed through a tube
or intravenously. The adverse effects
of mucositis often affect compliance tocancer therapies causing interruptions
or discontinuation of treatment, thus
reducing patient’s chances of survival, andincreasing costs to the healthcare system.
Preventing and managing oral

mucositis is essential in the care ofcancer patients. Oral mucositis requires

an interdisciplinary approach with dentists,
dental hygienists, nutritionists, oncologists
and nurses working together to diagnosepatients early and provide care to alleviate
pain, keep patients nourished and manage
the risk of secondary infections.
3

I

Definition
Oral mucositis is a condition that affects the
mucosa of the mouth. It is one of the mostcommon and debilitating complication of cancer
treatment. It is frequently observed in patients being
treated with chemotherapy and/or radiotherapy inthe oral cavity or in the head and neck area. (1)Mucositis lesions are present in the oral cavity whenassociated with local radiotherapy treatment of
the head-neck area but may extend to the entire
mucous membrane of the gastrointestinal tract
when associated with systemic chemotherapy
treatment. It typically presents itself as an erythemaof the mucous membrane and progresses toulcerations and pseudomembranes (Fig.1).

Fig. 1 – Oral mucositis - Courtesy of Prof. C. Lajolo

The adverse effects of mucositis can interferewith cancer therapies, reduce the effectivenessof radio and/or chemotherapy treatment (3) (5)and lead to hospitalization. Mucositis is associatedwith an increase in patient mortality in the first
100 days from the beginning of therapy. (4)Mucositis symptoms :The symptoms of mucositis include : (2) (3)Intense pain

Dysgeusia

Odynophagia

Difficulty in feeding

Important weight loss

Difficulty in speaking

4

II

EpidemiologyÇakmak and Nural report that oral mucositis
develops in 51.7% of patients undergoing
chemotherapy(7) but the incidence and severityof mucositis vary greatly depending on the typeof treatment, the number of cycles, the modeof administration, the dosages, the possiblecombination of different treatments and on thesusceptibility of the patient.(6) (1) (8)The percentage of patients treated withradiotherapy of the head-neck area who
develops oral mucositis frameworks is very high,sometimes more than 90% of cases. Patients
undergoing a combination of radiotherapy
and chemotherapy face the highest risk, withstudies demonstrating an increased incidenceof severe mucositis among these patients (Grade
3 and 4 on the WHO scale). (9) (10 (11) (12) (Table 1)
Elting et al. conducted a study with patientstreated with radiotherapy in the head-neckarea and reported that when combined withchemotherapy, more than half of patients(66%) developed severe mucositis (Grade 3
and 4) and more than one third (37%) of thisgroup were hospitalized.(10)Patients undergoing chemotherapy and/or
radiotherapy treatments prior to hematopoietic
stem cell transplantation develop oral mucositis
in more than 70% of cases. (13)Table 1: WHO classification (1979) of the grades of oral mucositis :Grade 0

Grade 1

Grade 2

Grade 3

Grade 4

No symptoms of oral
mucositis

Soreness in mouth, noulcer ; patient can eat anormal diet

Sore mouth with ulcers,
patient is still able to eat
a normal diet

Extreme sensitivity whenswallowing solid food,patient needs to be on aliquid diet

Patient is not able toeat, drink or swallow, aparenteral nutrition or
tube feeding is necessary

Incidence :Up to 66% of head & neck cancer
patients undergoing radio-chemo
therapy are likely to develop severe
mucositis, with up to 1/3 requiring
hospitalization

5

IIII

Etiology
Main causes & risk factorsof oral mucositis
Chemotherapy in general and radiotherapy to thehead and neck region for the treatment of headand neck cancers are the main cause of oral
mucositis.
Risk factors play an important role in the etiologyof mucositis as patients suffering from the sameneoplasms and undergoing similar treatments canoften display varying degrees of incidence andseverity.(15) (30) Pico et al. propose two predictive
indices : 1 Treatment related risk factors,
2 Patient associated risk factors (31)1 Treatment-related risk factors
Drugs used in chemotherapy
Treatment-related risk factors :Pharmacological agents most commonly
associated with the onset of oral mucositis

Drug used

include cytarabine, alkylating agents,
methotrexate and 5-fluorouracil used at highdoses.

Dosage and therapeutic
protocol

Conditioning protocols used before ahematopoietic stem cell transplant, such as total
body irradiation or the use of doxorubicin ormelphalan, are among those most associatedMethod of administrationand formulation

with the onset of oral mucositis. (8) (35) (36)The association between chemo andradiotherapy, particularly when cisplatin andcetuximab are used, also exposes the patient

Concomitent therapies

to an increased risk of developing
the complication. (34)Time of administrationof therapy

6III
Etiology
Main causes & risk factorsof oral mucositis
Patient-related risk factors :2 Patient-related risk factors
Patient-related risk factors are often conflicting but they dodemonstrate a positive association between smoking and oral
mucositis. (35) Data on age, BMI and gender is less clear a precise definition of patient-related risk based on these factors
is not possible. (39) (35) (40) (36) Some studies report an association
between the incidence of mucositis following chemotherapy
and the female gender (41) (42) (43), while other studies demonstrate
an association between the incidence of mucositis following
chemotherapy for head-neck neoplasms and the male gender. (34)Studies also suggest a possible correlation between genetic
characteristics and the risk of severe events, identifying
the presence of polymorphisms and mutations related to drug
metabolization pathways, DNA repair mechanisms, genes, cellproliferation and immune and inflammatory responses as possible
causes of adverse events. (44) (45) (46) (47) (48) (49) (50) (35)Finally, some studies have highlighted an increased incidence ofsevere mucositis in patients performing radiotherapy sessions in theafternoon and have hypothesized that the circadian rhythm may
also affect the severity of the side effects of radiotherapy. (37) (38)
Although current knowledge on patient-related risk factors is still
limited, the aim of future research will be to sharpen the valueof predictive indices at the individual level so as to enable thedelivery of personalized support therapies before severe mucositis
symptoms arise. (35) (15)Age
Body mass index (bmi)
Sex
Smoke
Genetic factors
Previous infections withherpes simplex (HSV)and papilloma virus (HPV)
Microbiome
Tumor characteristics(localization, size, stage)

Renal and liver function
Oral status
Laboratory parameters
before treatment(neutropenia, lymphopenia,
thrombocytopenia,
ALT (>16U/L), urea, hemoglobin)

Comorbidities
Hyposalivation (32) (33) (34) (35)

Risk factors
Treatment-related risk factors haveshown the strongest predictive
value while patient-related risk
factors need further research. The
future holds opportunities for more
personalized support therapies.

7

IV

NORMALEPITHELIUM

EPITHELIAL LAYER

Pathogenesis

Our understanding of the pathogenesis of mucositis is based almost exclusively on in vitro and animalmodels. The models have helped us understand the multifactorial nature of this condition and thecomplex mechanisms that determine its onset (15) (16).

EPITHELIUMSUBMUCOSA

The model proposed by Sonis (see Fig.2) highlights the importance of endothelial damage (17),PHASE I(15)
pro-inflammatory cytokines (18) (19) (20) (21), extracellular matrix (22), (23), (24) and microbiome
NORMAL .
INITIATION

Fig. 2 : Adaptation of the model of the pathogenesis of oral mucositis by Sonis (14)NORMALEPITHELIUM

PHASE IINITIATION
Radiation and/or
chemotherapy causes
direct cell death andactivates second
messengers

This leads to upregulationin proinflammatory
cytokines, causes injury
to mucosal cells andactivates pathways that
amplify mucosal injury

PHASE IV
ULCERATION(MUCOSITIS)
A significant
inflammatory cell
infiltrate is associatedwith the mucosal
ulcerations

PHASE VHEALINGCHEMOTHERAPYBACTERIASUBMUCOSAEPITHELIAL LAYERRADIATION

PHASES II/III
MESSAGING,
SIGNALING AND
AMPLIFICATIONSUBMUCOSAEPITHELIAL LAYER

Sonis’s model portrays the biological events underlying mucositis in the light of a five-stepRadiation
process:
and/orchemotherapy
initiation, initial damage response, signal amplification, ulceration, and healing. Although
this causes
direct cell death andsecondsubdivision helps understand the complexity of disease progression, it is important to keepactivatesin mindmessengers
that the development of mucositis is a dynamic process that can be triggered either by a single very
RADIATION
intense event (such as chemotherapy treatment for patients waiting for transplantation of hematopoietic
stem cells) or by repeated lower intensity stress (as is the case with fractional therapeutic regimens).
A standard head-neck area radiotherapy treatment for example, involves a dose of 70 Grays divided
into 7 weeks (2 Grays per day) meaning the phases of the model proposed by Sonis overlap, since
the damage is divided into small and numerous daily doses. (14)CHEMOTHERAPYBLOOD VESSELINFLAMMATORY CELLFIBROBLAST

8IV
Pathogenesis

PHASE IINITIATION

Radiation and/or
chemotherapy causes
direct cell death andactivates second
messengers
RADIATION

PHASES II/III

MESSAGING,
SIGNALING AND
AMPLIFICATIONThis leads to upregulationin proinflammatory
cytokines,
causes injury
CHEMOTHERAPY
to mucosal cells andactivates pathways that
amplify mucosal injury

PHASES II/III

MESSAGING,
SIGNALING AND
AMPLIFICATIONPHASE IV

ULCERATION(MUCOSITIS)

PHASE VHEALINGA significant
inflammatory cellThis leads to upregulation
infiltrate is associatedin proinflammatory
with the mucosal
cytokines, causes injury
ulcerations
to mucosal cells andactivates pathways thatBACTERIA
amplifymucosalPHASE
I : injury
INITIATIONRadiotherapy and chemotherapy can cause very early direct and non-direct DNA and cell
damage regulated by different mechanisms, including the production of reactive oxygen species(ROS). Direct damage to DNA may cause the death of certain cells of the basal layer and those present
in the submucosa, but the extent of this phenomenon is not such as to determine the appearance of
mucositis ; without the contribution of non-direct damage to DNA, the complex processes leading to
PHASE IV
mucousdamage wouldPHASE
not beV triggered. ROS are compounds with high oxidizing capacity potentially
ULCERATIONHEALINGcapableof damaging any macromolecule and determining cell death if not adequately counteracted(MUCOSITIS)
by antioxidant substances. During this phase the mucous membrane does not present any alteration,
A significant
inflammatory cell
but thecascade of events triggered in the submucosa will progressively lead to its destruction. (14)infiltrateis associatedwith the mucosal
BLOOD VESSEL
ulcerations

INFLAMMATORY CELLFIBROBLASTBACTERIA

PHASE II/III : MESSAGING, SIGNALING AND AMPLIFICATION

DNA-induced damage and ROS activation lead to an initial response to damage through threemain routes : the production of ceramide, the increase in the activity of matrix metalloproteinases(MMP) and the activation of transcription factors.
• The complex mechanisms triggered by these three pathways increase tissue damage andstimulate apoptosis. (25) (14) Radiotherapy and chemotherapy can activate certain enzymes dedicatedto the hydrolysis of cell membrane components, sphingomyelinases, which determine the productionof ceramide and the consequent stimulation of cellular apoptosis.
BLOOD VESSEL• Instead, the damage of fibroblasts seems to be mainly due to the activation of activator protein 1(AP1) which
increase in the secretion of MMP, proteins capable of causing the destruction
INFLAMMATORYCELL leads to an FIBROBLAST
of the extracellular matrix and basal membrane ; this phenomenon leads to an increase in apoptosis
both directly and indirectly. (14) (22) (23)• Transcription factors most involved in the initial damage response phase include nuclear factorkB (NF-kB), p53 and erythroid-2 nuclear transcription factor (NRF2) ; the link between these
proteins and DNA is fundamental for the regulation of multiple genes, including those related to the
production of pro-inflammatory cytokines, chemokines, and adhesion molecules. (18) (19) (20) (21)Cells are then stimulated to increase the secretion of pro-inflammatory cytokines, such as tumor
necrosis factor alpha (TNF-α), interleukin 1-beta (IL-1β), interleukin 6 (IL-6) and prostaglandins (PGs),a set of molecules that increase the damage produced in the initiation phase : they reduce theoxygenation of epithelial cells and further feed the mechanisms underlying cell damage induced byradiotherapy and/or chemotherapy. (15) (14) (26)The signals induced by the initial response to the damage are further amplified by establishing acascade of events that stimulates tissue damage again. All these changes involve not only
epithelial cells but all the cells that make up the mucous membrane. (14)Due to the multiple mechanisms that cause direct and indirect damage induced by radiation andchemotherapy drugs, the epithelium loses its normal ability to renew itself and the first signs
and symptoms of mucositis begin to appear. (9) (14)9IVPathogenesis

PHASE IV

ULCERATION(MUCOSITIS)

PHASE VHEALINGA significant
inflammatory cell
infiltrate is associatedwith the mucosal
ulcerations
BACTERIA

PHASE IV : ULCERATION (MUCOSITIS)All the mechanisms described above are part of a dynamic process that continues to damage
the mucous membrane, sometimes until it results in loss of integrity. At this stage, macroscopic
alterations of the oral mucosa become evident, extremely painful ulcers appear, poorly definedand often widespread. The pain associated with the ulcerative phase is so intense because
tissue damage is such as to cause the loss of the myelinic sheath of the nerve endings present
in the mucosa. Mucositis ulcerations are an important problem not only for the symptoms they entail,but also because the loss of integrity of the mucous membrane predisposes patients, especially
if suffering from neutropenia, to infections that can lead to bacteremia and sepsis. (14)PHASE VINFLAMMATORYCELLHEALING

In addition, the products of the cell wall of bacteria manage to penetrate the submucosa by stimulating
FIBROBLAST
the further production of pro-inflammatory cytokines and the consequent activity of other inflammatory
cells ; all this contributes to tissue damage (14) and probably indirectly promotes the expression of proapoptotic genes. (27)

PHASE V : HEALING

In most cases, mucositis is an acute phenomenon that tends to resolve once cancer therapy
is over ; healing times may vary depending on the type of treatment, its duration and the
dosages used. (14)FIBROBLAST

During this phase, the extracellular matrix plays a fundamental role in stimulating the proliferation,
migration, and differentiation of epithelial cells (24), but it is possible that there are many othermechanisms that can influence tissue healing. Some in vitro studies of oral keratinocytes have shownhow much the presence of bacteria influences this phase. (28) (29) Changes in the oral and gastrointestinal
microbiome induced by cancer therapies most likely play a key role at all stages of mucositis
pathogenesis, but current knowledge, especially on the relationship between oral dysbiosis andmucositis, is still very limited. (26)10V

Clinical characteristics
and diagnosis
Initially, oral mucositis presents itself as an erythema of the oral mucosa that tends to progress withthe formation of very painful and extensive ulcers, characterized by strongly erythematous areas
and areas covered with pseudo membrane consisting of fibrin, cellular debris and bacteria (Fig.3).
Fig.3 : Various clinical appearances of oral mucositis - Courtesy of Prof. C. Lajolo

The grading system proposed by the WHO (see Table 1 p.5) is often used to define the severityof mucositis and incorporates clinical appearance, symptoms and functional status. (11)Patients with a grade 1 or 2 mucositis (Fig.4) usually manage to feed despite the morbidityof such a condition.
Fig.4 : Clinical appearance of oral mucositis Grade 1 and 2 - Courtesy of Prof. C. Lajolo

11

V
Clinical characteristics and diagnosis
If the mucositis progresses towards grade 3 (Fig.5), a liquid diet becomes necessary withhydration also becoming a challenge. At stage 4 oral nutrition and hydration are no longer possible.
Fig.5 : Clinical appearance of oral mucositis Grade 3 and 4 - Courtesy of Prof. C. Lajolo

Mucositis can lead to significant functional impairment, causing malnutrition, dehydration, weight
loss, need for parenteral feeding and hospitalization. In addition, the loss of integrity of the mucous
layer represents a clinically significant risk factor for bacteremia, fungemia and sepsis. (3) (5) (51)
Oral mucositis has an important economic impact – resources need to be allocated to the
management of the patient’s symptoms, the management of secondary infections, the delivery ofadequate nutritional support and in severe cases, hospitalization. (4) (54)Symptoms and complications associated with oral mucositis can also indirectly impair or reduce
the success of antineoplastic treatment, limiting the patient’s ability to tolerate therapy itself. (52)The search for mucositis control therapies is essential because interruptions in radiant or chemotherapy
treatments favor the repopulation of neoplastic cells, resulting in a reduction in tumor control. (53)To ensure compliance with oncological treatment and avoid potentially lethal complications, it is necessary
to support the patient in nutrition and hydration, manage painful symptoms and infections. (11) (35)Despite the strong impact on the quality of life of patients, mucositis tends to resolve spontaneously
between the second and fourth weeks after the end of radiotherapy. In patients undergoing radiochemotherapy treatments, the complication may arise earlier, take a more severe clinical course, andpersist longer. In severe cases, it may be necessary to put patients in intensive care. (55) (56) (9)12VIPrevention andmanagement
Patients who could suffer from oral mucositis must be managed by a multidisciplinary team. Good
communication between all members of the team is essential – dentists, oral-maxillofacial surgeons,dental hygienists, general practitioners, oncologists and nutritionists.
Dentists play an active role in the management of oral mucositis– they help prevent the onset of thedisease, manage disease progression, alleviate symptoms and avoid secondary infections. Their rolehelps support cancer therapy compliance and the maintenance of good oral health. The Multinational
Association of Supportive Care in Cancer and International Society of Oral Oncology (MASCC/ISOO) has
issued clinical practice guidelines for the management of mucositis secondary to cancer therapy. The
new guidelines are based on an extensive systematic review of the literature and provide professionals
an evidence-based tool to help with the management of mucositis. They cover the following interventions
from basic oral care to specific therapies like laser or cryotherapy. (Table 2) (57) (58).

Basic Oral care
The ISOO guidelines suggest different oral care recommendations in function of the treatment pathway before, during or after the chemotherapy or radiotherapy (61).
Overall, basic oral care includes all routine actions performed by the patient or care provider to reduce thebacterial load in the oral cavity, prevent infections, and provide comfort.

Basic oral care includes all routine actions performed by the patient or care provider to reducethe bacterial load in the oral cavity, prevent infections, and provide comfort. Included are :Mechanical cleaning(tooth brushing,interdental cleaning)

Rinsing with mild
mouthwashes, withoutchlorhexidine (CHX), to
reduce bacterial build-up

Application ofmoisturizing agentsfor hydration of the oral
mucosal surfaces. (60)13

VIPrevention and management

1) Mechanical cleaning :• Interdental cleaning : at least once a day if the patient is able.
• Brushing with a soft toothbrush and fluoride toothpaste to avoid tooth decay - if possible,
twice a day after meals and before bed.
• A clean moist gauze or foam swab soaked in mouthrinse can be used to clear the mouth.
• If the patient cannot bear toothpaste, she/he can use a bland mouth rinse.
Even if sore, the mouth will benefit from daily oral care.
2) Rinsing with a mild mouthwash after brushing, flossing and eating or every 1-2 hours while awake, oreven more if the mucus is thick. The ISOO guidelines suggest a recipe for a bland mouthrinse based on
baking soda. The data in the literature on the use of saline-based rinses or baking soda is limited but experts
agree that they can support oral hygiene and give patients a feeling of relief, also reducing xerostomia.

The ISOO recommends as mouthrinse a bland recipe (61) :• 1 level teaspoon (5 mL) of salt
• 1 level teaspoon (5 mL) of baking soda
• 4 cups (1 L) of water
The mix is kept at room temperature in a closed container and renewed every day.

3) Moisturizing :• Nasal passages can be moisturized through the night with a steam vaporizer in the room.
• Oral moisturizing can be achieved with a mouth rinse and water-based lubricants.
• Lip Care can be done with water-soluble, wax-based, or oil-based lubricants4) Patient education
The ISOO guidelines also underline the importance of patient education in supporting compliancewith recommended oral care during cancer therapy. Although the data in the literature on the roleof professional dental hygiene in the prevention of oral mucositis is not sufficient to define a specificguideline, experts agree that the support of a dentist is indicated to prevent the risk of local or systemic
infections caused by oral infections. (57)14

VI
Prevention and management

Topical Soothing agentsThe ISOO guidelines suggest some analgesics and natural agents. (Table 2) (57) (58)
• Analgesics: new evidence supports the suggestion in favor of topical morphine.
• Natural and Miscellaneous Agents: Honey is suggested for the prevention of oral mucositis inpatients with head and neck cancer who receive treatment with either radiotherapy or radiotherapy chemotherapy• Chewing gum is not suggested for the prevention of oral mucositis in pediatric patients with 		
hematological or solid cancer who receive chemotherapy.
Aside from these suggestions from the ISOO, there are also other topical agents that can help sootheand protect the mucosa.
• Protective mucosal agents : drug-free topical agents that deploy their action mainly by forminga protective barrier over the intact mucosa to protect it during radiation therapy and over thebreached mucosa after outburst of oral mucositis. These topical agents have been reported to provide
a safe and gentle approach to reduce oral mucositis and its associated symptoms.

Other interventions• Anti-inflammatory agents : Benzydamine mouthwash is suggested for the prevention of oral 		mucositis in patients with head and neck cancer receiving a moderate dose of radiotherapy or 		radiotherapy – chemotherapy (57).
• Photobiomodulation : Low-laser therapy is used to modulate tissue response, inhibiting mechanisms
such as tissue healing, inflammatory responses, and pain (59). While this is a rapidly growing field,
research indicates that this technology is only able to prevent the onset of oral mucositis in specificpatient populations and only if protocols are followed with extreme precision (57).
• Cryotherapy : Cryotherapy is based on the application of ice cubes or cold water on the oral mucosa,
to obtain a vasoconstriction of the superficial blood vessels, thereby limiting the spread andconcentration of cytotoxic drugs in the cooling area; because cooling and vasoconstriction aretemporary, this treatment option is only useful if the drug is administered in a short period of time or if it
has a short half-life. (57) (60)• Growth Factors and Cytokines : New evidence was identified for the keratinocyte growth factor-1.

15

MASCC/ISOO clinical practice guidelines for the managementof mucositis secondary to cancer therapy
Treatment

Level of
Evidence

Guidelines andrecommendations

III
III

Suggested
Not recommended

II

Recommended

I/II

Recommended

II

Recommended in patients subjected
to conditioning with high dosesof melphalan and/or F-5U

III

Suggested for pain treatment

I

Recommended

GlutamineII

Can be used with caution in patients with T-C
neoplasms undergoing RT-CT treatments (highmortality observed in patients treated with TCSE
undergoing parenteral administration of glutamine)

Honey
Chewing-gum

IIIII

AdvisedNot recommended

Basic Oral Care
Oral hygiene
Chlorhexidine Rinse

Anti-inflammatory agents
Benzidamine

Photobiomodulation
Low Level Laser Therapy

Cryotherapy

Analgesics
Morphine 0.2%

Growth factors and cytokines
KGF-1

Natural agents

Table 2 : Therapeutic and preventive options to counteract oral mucositis – Adapted from Elad et al (57)
F-5U, 5-fluorouracyl; CT, chemotherapy; KGF-1, keratinocyte growth factor-1; RT, radiation therapy; T-C, head-neck;
TCSE, hematopoietic stem cell transplantation; Level of Evidence (I, higher; II, medium; III, lower).

16

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19

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4.

Elting LS, Cooksley C, Chambers M, Cantor SB, Manzullo E, Rubenstein EB. The burdens of cancer therapy.
Clinical and economic outcomes of chemotherapy-induced mucositis. Cancer. 2003 Oct 1;98(7):1531-9.

5.

Saadeh CE. Chemotherapy- and radiotherapy-induced oral mucositis : review of preventive strategies and treatment
Pharmacotherapy. 2005 Apr;25(4):540-54.

6.

Curra M, Soares Junior LAV, Martins MD, Santos PSDS. Chemotherapy protocols and incidence of oral mucositis.
An integrative review. Einstein (Sao Paulo). 2018;16(1):eRW4007.

7.

Çakmak S, Nural N. Incidence of and risk factors for development of oral mucositis in outpatients undergoing cancer
chemotherapy. Int J Nurs Pract. 2019 Feb;25(1):e12710.

8.

Curra M, Soares Junior LAV, Martins MD, Santos PSDS. Chemotherapy protocols and incidence of oral mucositis.
An integrative review. Einstein (Sao Paulo). 2018;16(1):eRW4007.

9.

Maria OM, Eliopoulos N, Muanza T. Radiation-Induced Oral Mucositis. Front Oncol. 2017 May 22;7:89.

10. Elting LS, Cooksley CD, Chambers MS, Garden AS. Risk, outcomes, and costs of radiation-induced oral mucositis among
patients with head-and-neck malignancies. Int J Radiat Oncol Biol Phys. 2007 Jul 15;68(4):1110-20.
11. Sonis ST, Eilers JP, Epstein JB, LeVeque FG, Liggett WH Jr, Mulagha MT, Peterson DE, Rose AH, Schubert MM, Spijkervet FK,
Wittes JP. Validation of a new scoring system for the assessment of clinical trial research of oral mucositis induced by radiationor chemotherapy. Mucositis Study Group. Cancer. 1999 May 15;85(10):2103-13.
12. Trotti A, Bellm LA, Epstein JB, Frame D, Fuchs HJ, Gwede CK, Komaroff E, Nalysnyk L, Zilberberg MD. Mucositis incidence,
severity and associated outcomes in patients with head and neck cancer receiving radiotherapy with or without chemotherapy :a systematic literature review. Radiother Oncol. 2003 Mar;66(3):253-62.
13. Chaudhry HM, Bruce AJ, Wolf RC, Litzow MR, Hogan WJ, Patnaik MS, Kremers WK, Phillips GL, Hashmi SK. The Incidence
and Severity of Oral Mucositis among Allogeneic Hematopoietic Stem Cell Transplantation Patients : A Systematic Review.
Biol Blood Marrow Transplant. 2016 Apr;22(4):605-616.
14. Sonis ST. The pathobiology of mucositis. Nat Rev Cancer. 2004 Apr;4(4):277-84.
15. Al-Dasooqi N, Sonis ST, Bowen JM, Bateman E, Blijlevens N, Gibson RJ, Logan RM, Nair RG, Stringer AM, Yazbeck R, Elad S,
Lalla RV; Mucositis Study Group of Multinational Association of Supportive Care in Cancer/International Society of Oral Oncology(MASCC/ISOO). Emerging evidence on the pathobiology of mucositis. Support Care Cancer. 2013 Jul;21(7):2075-83.
16. Colley HE, Eves PC, Pinnock A, Thornhill MH, Murdoch C. Tissue-engineered oral mucosa to study radiotherapy-induced oral
mucositis. Int J Radiat Biol. 2013 Nov;89(11):907-14.
17. Paris F, Fuks Z, Kang A, Capodieci P, Juan G, Ehleiter D, Haimovitz-Friedman A, Cordon-Cardo C, Kolesnick R. Endothelial
apoptosis as the primary lesion initiating intestinal radiation damage in mice. Science. 2001 Jul 13;293(5528):293-7.
18. Criswell T, Leskov K, Miyamoto S, Luo G, Boothman DA. Transcription factors activated in mammalian cells after clinically relevant
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a novel target of keratinocyte growth factor action which regulates gene expression and inflammation in the healing skin wound.
Mol Cell Biol. 2002 Aug;22(15):5492-505.
20. Sonis ST, Scherer J, Phelan S, Lucey CA, Barron JE, O’Donnell KE, Brennan RJ, Pan H, Busse P, Haley JD. The gene expression
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21. Ong ZY, Gibson RJ, Bowen JM, Stringer AM, Darby JM, Logan RM, Yeoh AS, Keefe DM. Pro-inflammatory cytokines play a keyrole in the development of radiotherapy-induced gastrointestinal mucositis. Radiat Oncol. 2010 Mar 16;5:22.
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37. Goyal M, Shukla P, Gupta D, Bisht SS, Dhawan A, Gupta S, Pant MC, Verma NS. Oral mucositis in morning vs. evening irradiatedpatients: a randomised prospective study. Int J Radiat Biol. 2009 Jun;85(6):504-9.
38. Bjarnason GA, Mackenzie RG, Nabid A, Hodson ID, El-Sayed S, Grimard L, Brundage M, Wright J, Hay J, Ganguly P, Leong C, Wilson J,
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39. van den Broek GB, Balm AJ, van den Brekel MW, Hauptmann M, Schornagel JH, Rasch CR. Relationship between clinical factors
and the incidence of toxicity after intra-arterial chemoradiation for head and neck cancer. Radiother Oncol. 2006 Nov;81(2):143-50.
40. Robien K, Schubert MM, Bruemmer B, Lloid ME, Potter JD, Ulrich CM. Predictors of oral mucositis in patients receiving
hematopoietic cell transplants for chronic myelogenous leukemia. J Clin Oncol. 2004 Apr 1;22(7):1268-75.
41. Sloan JA, Goldberg RM, Sargent DJ, Vargas-Chanes D, Nair S, Cha SS, Novotny PJ, Poon MA, O’Connell MJ, Loprinzi CL.
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2002 Mar 15;20(6):1491-8.
42. Sloan JA, Loprinzi CL, Novotny PJ, Okuno S, Nair S, Barton DL. Sex differences in fluorouracil-induced stomatitis.
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22

Annex :FDI/Sunstar guidelines
on oral cancer
In 2018, Sunstar and FDI World Dental Federation launched Oral Cancer : Prevention and patientmanagement, a toolkit for oral health professionals that aims to mitigate the effects of oral cancer bypromoting comprehensive oral cancer screenings as an integral part of routine dental check-ups.
It highlights the most common risk factors for oral cancer and underlines the importance of early
diagnosis and treatment by providing practical solutions for the care pathway.
The chairside guide provides information about oral cancer prevention, risk factors and management,
and also helps them navigate the clinical examination and diagnosis through a decision tree. It focuseson the most common sites of oral cancer : the tongue, the insides of the cheeks, and the floor of the mouth.

Get your copy of the toolkit
and chairside guideor go to sunstar.com

DOWNLOAD

er
Oral Cancmanagement

Chairside
guide ford patientvention an

Oral Cancer
Prevention and patient management

Up to 70% of oral cancers are preceded by premalignant oral lesions, such as persistent red or white patches in the mouth.
This chairside guide focuses on the most common sites of oral cancer: the tongue, the insides of the cheeks, and the floor of the mouth.

Pre

TOBACCO FACTS
Tobacco use

Types of tobacco use

800 million
men smoke.
ORAL CANCER
FACTS

Effects of tobacco on oral health

MAIN RISK FACTORS
Smoking

Smokeless

200 million women smoke.

snuff, dry

OTHER RISK FACTORS

Increases risk of:• oral cancer

Facts aboutoralindividuals
cancer die each year from cigarettes
Risk factors and moist
Profile of those at highest risk
• smoker’s palate
600,000
TOBACCO FACTS secondhand smoke: 156,000 men, 50% bidisCigarette smoking is the most • periodontal disease
A typical high-risk profile for oral cancer
281,0005-year
women survival
and 166,000 children.
The average
TOBACCOTobacco useFACTS
Types of tobacco useof tobacco
health toothis alossman, over age 40, who uses tobacco
common form Effects
of tobaccouse,on •oralpremature
At least 300 million people use
Tobacco use rate of patients with oralTypes
use kreteks
EffectsofAll
tobaccooral health
threeof alcohol
and/or is a heavy user of alcohol.
but all forms ofchewing
tobaccoare
Smokeless
Increasesrisk
of: on forms
90%ofoftobacco
these aresmokelesstobacco and Smoking
800 millionmen• gingivitis
tobaccocancerissmoke.
about 50%. Smoking
linked with increased
riskof:ofspirits, and wine)
in Southeast Asia.
Smokeless
Increases(beer,risk

Tobacco800200
millionmen womensmoke. smoke.
millioncigarettes

2011, manufacturers spent about
200
millionIn
women
600,000
individuals
die eachsmoke.
year from
US$9.5 billion on advertising
cigarettes
secondhand
smoke:
156,000
600,000
individuals
die eachmen,
year
95%
cigarettes
and fromsmokelesstobacco.
bidis
281,000 women
and
166,000
children.
About
95% of all
secondhand
smoke:
156,000
men,
bidis
Governments
spend less
than
TOBACCO FACTS 281,000
women
and 166,000
At least 300
millionpeoplechildren.
usecancers occur
US$1oralbillionon tobacco
controlkreteks
Tobacco use
ofuse
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smokelessandTypes
90%
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least 300tobacco
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eachyear.
in Southeast
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tobaccoSmoking
years of age. Smokeless
800 million mensmokelesssmoke.
pipes

Oralcancer is
10
among themonmost com cancancers, but ented
prevlargely be cingby reduto risk
exposure
factors

Alcoholsmokeless
All three forms of alcohol

inInSoutheast
Asia.
2011, manufacturers
spent about
From The Challenge of Oral Disease – A call for global•action
FDI World Dental
Federation.
•• staining
oralbycancerhalitosis (bad breath)snus(beer, spirits andwine)•• halitosis(badandbreath)• smoker’s
palateassociatedloss ofwith
taste
smell
snus
have beencigarssecondhand smoke: 156,000
men,cigarettes
and smokelessGovernments
spend lesstobacco.
thandissolvables• loss of taste and smell•
periodontal
diseasediagnosis
bidis at the time of waterpipes
oral cancer,
although
281,000 women and 166,000
US$1 children.
billionon less
tobaccocontrol
Governments
spendthanisdissolvables
60
about 60. waterpipes
spirits and• premature
toothbeerloss have a
each
year.
At least 300 millionUS$1
peopleusebillionon tobacco control
chewingkreteks
higher associated risk.
smokeless tobacco andeach
90%of these areyear.
• gingivitis
tobaccoin Southeast Asia.
From The Challenge of Oral Disease – A call for global action by FDI World Dental Federation.
• staining
pipes
Maps and graphics © Myriad
Editions 2015
From
The Challengeof Oral– A callglobalaction by
World
Federation.
In 2011, manufacturers
spent
aboutFrom
TheDisease
Challenge
offor
Oral
Disease– FDI
A callforDental
globalaction by FDI World Dental Federation.
and graphics © Myriad Editions 2015
• halitosis (bad breath)
US$9.5 billion onMaps
advertisingsnus
Maps and graphics © Myriad Editions 2015
cigarscigarettes and smokeless tobacco.
• loss of taste and smell
Governments spend less thandissolvables
waterpipes
US$1 billion on tobacco control

200 millionInUS$9.5
women smoke.
pipesbillion onMaps
advertisingsnuff,
dry2015
and aboutgraphics © Myriad
Editions
2011, manufacturers
spentcigarettes
cigarscigarettes
andfromsmokelesstobacco.
andmoist
600,000 individualsUS$9.5
dieeach year
billionon advertising
The average age

UV sun exposure
UV radiation

UVB rays

UVA rays

2015

1950

Environmental, infectious,and other factors• Poor oral hygiene• Chronic candidiasis• Herpes virus infections• Immunosuppressive
conditions (HIV…)

PATIENT MANAGEMENT

each year.

From The Challenge of Oral Disease – A call for global action by FDI World Dental Federation.
Maps and graphics © Myriad Editions 2015

HPV

• oral cancer• staining
snuff, drypipesoral cancer: regularuse of been associatedhave•• oralcancerand moistsmoker’spalate • halitosis (bad breath)snuff,
dry
However, the male–female ratio has
snuspipes,
cigars, waterpipes,
aswithoral cancer, although
and
moist
•• smoker’s
palatecigarsperiodontal
disease• loss of taste andwell as all formsofsmokelessspirits
and beer havedropped
asmell from 6 to 1 in 1950•• periodontal
diseasepremature toothloss
to about 2 to 1 at present.
tobacco (snus,dissolvables
chewing
waterpipes
haigher associated risk.
chewing•• premature
Effectsof tobacco
on oralhealth tooth loss
gingivitis
tobacco,etc.).
tobaccochewing•• gingivitis
Increases risk of:staining
tobacco

BEFORE CANCER TREATMENT

DURING CANCER TREATMENT

AFTER CANCER TREATMENT

Prepare patients
before cancer treatment

Minimize the side effects ofradiotherapy

Monitor the healing process andpossible recurrence of oral cancer

STEP 1Eliminate oral
infectious focus

STEP 2 Conduct non-invasive

treatment
STEP 3 Apply fluoride dental tray
STEP 4 Recommend maxillofacial
prosthesis if indicated•

Use local antiseptic, anaesthetic gel andnon-alcoholic alkaline rinses in case ofpost radiotherapy mucositis.

•

Prevent caries by recommending brushing
twice daily with a soft toothbrush andfluoride toothpaste between 2800ppm
and 5000ppm and/or apply fluoride
dental tray.

•

Recommend sugar-free chewing gum andsalivary substitutes in case of xerostomia.

•

Follow-up and recall at least twicea year.

•Use antibiotic therapy in caseof traumatic dental procedures
after radiotherapy.

•

Conduct non-traumatic prosthetics
for rehabilitation within 6 to
12 months.

Oral screening

STEP 1

STEP 2

STEP 3

STEP 4

Oral health professionals are well-placed toscreen high-risk patients for early signs oforal cancer. Survival rates can be improved
with early detection and timely referral tomulti-disciplinary treatment centres.

Examine theinner cheekExamine thelateral border of
the tongue

Examine the floorof the mouth

Examine thepalateSTEP 5

Diagnosis
UNIQUE ULCERATION

WHITE LESIONS

It is
recommended
to use two mirrors
and to palpate oral
mucosa in all oral
screening steps

SCREENING BY PALPATION
Ask patient if he/she is a smoker
REMOVABLE

SWAB TESTNON-REMOVABLE

Lichen planous,
pemphigus

TobaccoLeukoplakia

Homogenous
If candidiosis,
anti-fungal
treatment
is needed

If no candidiosis,
consultationneeded regarding
oral hygiene(plaque bacteria)(smooth andtranslucent)

Stop tobacco

NG
LEADI

THE

WORLD

TO

A
OPTIM

L

ORAL

H E A LTand regular follow-up

H

Oral Can cer:

Prev entio

nt mann and patieagem ent

1

FDI World Dental Federation
Avenue Louis-Casaï 51 • 1216 Genève • Switzerland
T +41 22 560 81 50 • info@fdiworlddental.org ©2018 FDI World Dental Federation

Idiopathic
Leukoplakia

SCREENING BY PALPATIONTRAUMATIC

INFECTION LESIONS(tuberculosis, HIV, syphilis, etc.)

Eliminate all traumatic factors
and conduct two week follow-up

Biopsy and timelyreferral

APHTOSIS

Local or systemictreatment

Non-homogenous(thick, white with red
spots, rugous)

Biopsy to confirm if
oral cell carcinoma andtimely referral

Stop tobacco
Biopsy: OIN, Dysplasia, SCC(Squamous Cell Carcinoma)

DISCLAIMER Please note that in this document ‘oral cancer’ refers to squamous cell carcinoma.
NOTE Please consult national guidelines and recommendations on oral cancer management and prevention.

www.fdiworlddental.org/oral-cancer

This chairside guide wasmade possible through anunrestricted grant from23

Route de Pallatex 111163 Etoy, Switzerland
www.sunstar.com

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