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Classification System For Oral Submucous Fibrosis

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CLASSIFICATION SYSTEM FOR

ORAL SUBMUCOUS FIBROSIS

CHANDRAMANI BHAGVAN MORE ET.AL

REVIEW ARTICLE By :DR.YASIR SHAFEEQ MOHIYUDDIN


CONTENTS
INTRODUCTION
CLINICAL FEATURES
CLASSIFICATION
CONCLUSION
REFRENCES

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INTRODUCTION

• Oral submucous fibrosis (OSMF) is a potentially malignant disorder


(PMD) and crippling condition of oral mucosa.
• chronic insidious scarring disease of oral cavity, pharynx and upper
digestive tract, characterized by progressive inability to open the
mouth due to loss of elasticity and development of vertical fibrous
bands in labial and buccal tissues.
• predominantly affects people of Southeast Asia and Indian
subcontinent, where chewing of arecanut and its commercial
preparation is high.
• also called as ‘diffuse oral submucous fibrosis’, ‘idiopathic
scleroderma of mouth’, ‘idiopathic palatal fibrosis’, ‘sclerosing
stomatitis’, ‘juxta- epithelial fibrosis’, etc

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• Oral submucous fibrosis is preceded by symptoms like burning
sensation of the oral mucosa, ulceration and pain.
• characteristic features of OSMF are reduced movement and
depapillation of tongue.
• blanching and leathery texture of oral mucosa.
• loss of pigmentation of oral mucosa.
• progressive reduction of mouth opening.
•  advanced cases, nasal twang due to fibrosis of nasopharynx
and hearing impairment due stenosis of eustachian tube is
significantly observed.
• patients with OSMF present with irreversible moderate-to-
severe condition. 
•  changes of OSMF are similar to those of systemic sclerosis
(scleroderma) but are limited to oral tissues

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• OSMF occurs at any age but is most commonly seen in  between
16 and 35 years.
• may be associated with oral leukoplakia.
• potentially malignant disorders or with oral malignancy
• The prevalence rate of OSMF in India is about 0.2 to 0.5%.

• the rapid increase in the prevalence is due to an upsurge in the


popularity of commercially prepared arecanut and tobacco
preparations—gutkha, pan masala, mawa, flavored supari, etc.

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• Etiology of OSMF is multifactorial but arecanut chewing is the main
causative agent.
• OSMF is insidious in origin and is not amenable to reverse at any stage
of the disease process, either spontaneously or with cessation of habit.
• The condition may remain either stationary or become severe, leaving an
individual handicapped, both physically and psychologically.
• Diagnosis and staging thus becomes very important as it affects the
treatment.
• Several classifications based on clinical and histological features, have
been put forth by various researchers, based on different aspects of
OSMF.
• The advantages and disadvantages of these classifications supersede
the other leading to confusion.
• The purpose of the present literature review was to compile and analyze
several classifications of OSMF available at various databases so as to
assist the clinician, researchers and academicians in the categorization
of this potentially malignant disorder according to its biological behavior
and hence its subsequent medical and surgical management

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The details of our search is as under:
 

Classifications based on clinical features of OSMF are as follows:


 

•JV Desa (1957)


 
•Pindborg JJ (1989)
 
•SK Katharia et al (1992)
 
•Lai DR et al (1995)
 
•R Maher et al (1996)
 
•Ranganathan K et al (2001)
 
•Rajendran R (2003)
 
•Nagesh and Bailoor (2005)
 
•Tinky Bose and Anita Balan (2007)
 
•Kiran Kumar et al (2007)
 
•Chandramani More et al (2011)
 

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b.Classifications based on histopathological features:
 
• Pindborg JJ and Sirsat SM (1966)
 
• Utsunomiya H et al (2005)

• Kiran Kumar et al (2007)


C. Classification based on clinical and histopathological features:
 
• Khanna JN et al (1995)

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CLASSIFICATION BASED ON CLINICAL FEATURES
OF OSMF:
• JV Desa (1957) divided OSMF into three stages as follows:
 
– Stage I: Stomatitis and vesiculation
 
– Stage II: Fibrosis
 
– Stage III: As its sequelae

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• Pindborg JJ in 1989 divided OSMF into three stages as follows:
 
– Stage I: Stomatitis includes erythematous mucosa, vesicles, mucosal ulcers,
melanotic mucosal pigmentation and mucosal petechiae.
– Stage II: Fibrosis occurs in healing vesicles and ulcers, which is the hallmark
of this stage.
• Early lesions show blanching of the oral mucosa.
 
• Older lesions include vertical and circular palpable fibrous
bands in the buccal mucosa and around the mouth opening or
lips.
 
• This results in a mottled marble like appearance of the mucosa
because of the vertical thick, fibrous bands in association with
a blanched mucosa.
 
Specific findings include reduction of mouth opening, stiff and small tongue,
blanched and leathery floor of the mouth, fibrotic and de-pigmented
gingiva, rubbery soft palate with decreased mobility, blanched and atrophic
tonsils, shrunken bud like uvula and sunken cheeks, not commensurate
with age or nutritional status.

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– Stage III: Sequelae of OSMF are as follows:
• Leukoplakia is found in more than 25% of individuals with OSMF.
• Speech and hearing deficit may occur because of involvement of tongue and the eustachian
tube.
 SK Katharia et al (1992) have given different scores assigned to the patients on the
basis of mouth opening between upper and lower central incisors as follows:– Score
0: Mouth opening is 41mm or more
 
– Score 1: Mouth opening is 37 to 40 mm
 
– Score 2: Mouth opening is 33 to 36 mm
 
– Score 3: Mouth opening is 29 to 32 mm
 
– Score 4: Mouth opening is 25 to 28 mm
 
– Score 5: Mouth opening is 21 to 24 mm
 
– Score 6: Mouth opening is 17 to 20 mm
 
– Score 7: Mouth opening is 13 to 16 mm
 
– Score 8: Mouth opening is 09 to 12 mm
 
– Score 9: Mouth opening is 05 to 08 mm
 

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– Score 10: Mouth opening is 0 to 04 mm.
Lai DR (1995) divided OSMF based on the inter-incisal distance as follows:
 
– Group A: >35 mm
 
– Group B: Between 30 and 35 mm
 
– Group C: Between 20 and 30 mm
 
– Group D: <20 mm
• R Maher et al (1996) had given criteria for evaluation of interincisal distance as
an objective criterion of the severity of OSMF in Karachi, Pakistan. In his
study, he divided intraoral regions into eight anatomical subregions viz palate,
posterior one-third of buccal mucosa, mid one-third of the buccal mucosa,
anterior one-third of buccal mucosa, upper labial mucosa, tongue and floor of
mouth and looked for disease involvement in each to assess the extent of
clinical disease.

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This was further grouped into three categories as follows:

– Involvement of one-third or less of the oral cavity (if three or less of the above sites are
involved).
 
– Involvement of one to two-thirds of the oral cavity (if four to six intraoral sited are involved).
 
– Involvement of more than two-thirds of the oral cavity (if more than six intraoral sites are
involved).

Ranganathan K et al (2001) divided OSMF based on mouth opening as follows:


 
– Group I: Only symptoms, with no demonstrable restriction of mouth opening.
 
– Group II: Limited mouth opening 20 mm and above.
 
– Group III: Mouth opening less than 20 mm.
 
– Group IV: OSMF advanced with limited mouth opening.

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 Rajendran R (2003) reported the clinical features of OSMF as follows:
– Early OSF: Burning sensation in the mouth. Blisters especially on the
palate, ulceration or recurrent generalized inflammation of oral mucosa,
excessive salivation, defective gustatory sensation and dryness of mouth.
 –Advanced OSF: Blanched and slightly opaque mucosa, fibrous bands in
buccal mucosa running in vertical direction. Palate and faucial pillars are
the areas first involved. Gradual impairment of tongue movement and
difficulty in mouth opening.
 Nagesh and Bailoor (1993):
Stage I early OSMF: Mild blanching, no restriction in mouth opening
(normal distance between central incisor tips: Males 35 to 45 mm, females
30 to 42 mm)
• no restriction in tongue protrusion (normal mesioincisal angle of
upper central incisor to the tip of the tongue when maximally extended
with the mouth wide open: Males 5 to 6 cm, females 4.5 to 5.5 cm.
• Cheek flexibility CF = V1-V2 (males = 1.2 cm, females = 1.08 cm)
• Burning sensation on taking spicy food or hot beverages.

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Stage II moderate OSMF:
• Moderate to severe blanching,
• mouth opening reduced by 33%,
• cheek flexibility also demonstrably reduced,
• burning sensation also in absence of stimuli,
• palpable bands felt.
• Lymphadenopathy either unilateral or bilateral and
• Demonstrable anemia on hematological examination.
Stage III severe OSMF:
• Burning sensation is very severe patient unable to do day-to-day
work, more than 66% reduction in the mouth opening, cheek flexibility
and tongue protrusion.
• Tongue may appear fixed.
• Ulcerative lesions may appear on the cheek,
• Thick palpable bands and lymphadenopathy bilaterally evident.

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Tinky Bose and Anita Balan (2007) had given clinical classification,
categorized the patients into three groups based on their clinical
presentations:
Group A—mild cases: Only occasional symptoms, pallor, vesicle
formation, presence of one or two solitary palpable bands, loss of elasticity of
mucosa, variable tongue involvement with protrusion beyond vermillion
border. Mouth opening >3 cm.
Group B—moderate cases: Symptoms of soreness of mucosa or
increased sensitivity to chilies, diffuse involvement of the mucosa, blanched
appearance, buccal mucosa tough and inelastic fibrous bands palpable,
considerable restriction of mouth opening (1.5 to 3 cm) and variable tongue
movement.
Group C—severe cases: Symptoms more severe, broad fibrous
bands palpable, blanched opaque mucosa, rigidity of mucosa, very little
opening of mouth (less than 1.5 cm), depapillated tongue and protrusion of
tongue very much restricted.

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• Kiran Kumar et al (2007) categorized three clinical stages of OSMF
on the basis of mouth opening as follows:
 
– Stage I: Mouth opening >45 mm
– Stage II: Restricted mouth opening 20 to 44 mm
– Stage III: Mouth opening <20 mm.
• Chandramani More et al (2011):
– Clinical staging:
• Stage 1 (S1): Stomatitis and/or blanching of oral mucosa.
• Stage 2 (S2): Presence of palpable fibrous bands in buccal mucosa
and/or oropharynx, with /without stomatitis.
• Stage 3 (S3): Presence of palpable fibrous bands in buccal mucosa
and/or oropharynx, and in any other parts of oral cavity, with/ without
stomatitis.
• Stage 4 (S4) as follows:
• Any one of the above stage along with other potentially
malignant disorders, e.g. oral leukoplakia, oral erythroplakia, etc.
• Any one of the above stage along with oral carcinoma.

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– Functional staging:
• M1: Interincisal mouth opening up to or greater than 35 mm.
• M2: Interincisal mouth opening between 25 and 35 mm.
• M3: Interincisal mouth opening between 15 and 25 mm.
M4: Interincisal mouth opening less than 15mm.
Classifications based on histopathological features of OSMF
• Pindborg JJ and Sirsat SM (1966) were the first to
divide OSMF depending only on histopathological features alone are as follows:
– Very early stage: Finely fibrillar collagen dispersed with marked edema.
Plump young fibroblast containing abundant cytoplasm. Blood vessels are
dilated and congested. Inflammatory cells, mainly polymorphonuclear
leukocytes with occasional eosinophils are found.
- Early stage: Juxta-epithelial area shows early hyalinization. Collagen still
in separate thick bundles. Moderate number of plump young fibroblasts is
present. Dilated and congested blood vessels. Inflammatory cells are
primarily lymphocytes, eosinophils and occasional plasma cells.

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-Moderately advanced stage: Collagen is moderately hyalinized. Thickened
collagen bundles are separated by slight residual edema. Fibroblastic
response is less marked. Blood vessels are either normal or compressed.
Inflammatory exudate consists of lymphocytes and plasma cells.
-Advanced stage: Collagen is completely hyalinized. Smooth sheets with no
separate bundles of collagen is seen. Edema is absent. Hyalinized area is
devoid of fibroblasts. Blood vessels are completely obliterated or narrowed.
Inflammatory cells are lymphocytes and plasma cells.
Utsunomiya H, Tilakratne WM, Oshiro K et al (2005) histologically divided
OSMF based on the concept of Pindborg and Sirsat and modified it as
follows:–
Early stage: Large number of lymphocytes in subepithelial, connective tissue, zone
along with myxedematous changes.
– Intermediate stage: Granulation changes close to the muscle layer and
hyalinization appears in subepithelial zone where blood vessels are compressed by
fibrous bundles. Reduced inflammatory cells in subepithelial layer.
– Advanced stage: Inflammatory cell infiltrate hardly seen. Number of blood vessels
dramatically small in subepithelial zone. Marked fibrous areas with hyaline changes
extending from subepithelial to superficial muscle layers. Atrophic, degenerative
changes start in muscle fibers.

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Kiran Kumar et al (2007) proposed histological grading as follows:
– Grade I: Loose, thick and thin fibers.
– Grade II: Loose or thick fibers with partial hyalinization.
– Grade III: Complete hyalinization.

Classification based on clinical and histopathological features


 •Khanna JN and Andrade NN (1995) developed a group classification system for the surgical
management of OSMF.
Group I:
- Very early cases: Common symptom is burning sensation in the mouth, acute ulceration
and recurrent stomatitis and not associated with mouth opening limitation.
Histology: Fine fibrillar collagen network interspersed with marked edema, blood vessels
dilated and congested, large aggregate of plump young fibroblasts present with abundant
cytoplasm, inflammatory cells mainly consist of polymorphonuclear leukocytes with few
eosinophils. The Epithelium is normal.
.

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– Group II:
-Early cases—Buccal mucosa appears mottled and marble like, widespread sheets
of fibrosis palpable, interincisal distance of 26 to 35 mm.
- Histology: Juxta -epithelial hyalinization present, collagen present as thickened
but separate bundles, blood vessels dilated and congested, young fibroblasts seen
in moderate number, inflammatory cells mainly consist of polymorphonuclear
leukocytes with few eosinophils and occasional plasma cells, flattening or
shortening of epithelial rete-pegs evident with varying degree of keratinization

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Group III: Moderately advanced cases—
• Trismus, interincisal distance of 15 to 25 mm,
• buccal mucosa appears pale firmly attached to underlying tissues, atrophy of
vermilion border,
• vertical fibrous bands palpable at the soft palate,
• pterygomandibular raphe and anterior faucial
• pillars.
- Histology: Juxta -epithelial hyalinization present, thickened collagen bundles,
residual edema, constricted blood vessels, mature fibroblasts with scanty
cytoplasm and spindle-shaped nuclei, inflammatory exudate which consists of
lymphocytes and plasma cells, epithelium markedly atrophic with loss of rete
pegs, muscle fibers seen with thickened and dense collagen fibers.
– Group IVA: Advanced cases—severe trismus,interincisal distance of less than 15
mm,thickened faucial pillars,shruken uvula ,restricted tongue movement, presence
of circular,band around entire lip and mouth.

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– Group IVB: Advanced cases—presence of hyperkeratotic leukoplakia
and/or squamous cell carcinoma.
- Histology: Collagen hyalinized smooth sheet,extensive fibrosis,
obliterated the mucosal blood vessels, eliminated melanocytes, absent
fibroblasts within the hyalinized zones, total loss of epithelial rete pegs,
presence of mild to moderate atypia and extensive degeneration of
muscle fibers.

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CONCLUSION
An attempt is made to provide and update the knowledge of
classification system on OSMF so as to assist the
clinician,researchers and academicians in the categorization
of this potentially malignant disorder in order to help in early
detection and its subsequent management thus reducing the
mortality of oral cancer.

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REFRENCES
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histopathological study in Chennai. Indian Journal of Dental Research 2007;18(3):106-11.
2. Aziz Shahid R. Coming to America: Betel nut and oralsubmucous fibrosis. J Am Dent Assoc 2010;141:423-28.  
3.More C, Asrani M, Patel H, Adalja C. Oral submucous fibrosis-A hospital-based retrospective study. Pearldent 2010;1(4):
4.25-31.Kerr AR, Warnakulasuriya S, Mighell AJ, et al. A systematic eview of medical interventions for oral submucous fibrosis  
and future research opportunities. Oral Diseases 2011;17(1):42-57.
5.Warnakulasuriya S, Johnson Newell W, Waal I van der.Nomenclature and classification of potentially malignantdisorders of
the oral mucosa. J Oral Pathol Med 2007;36:575-80.
 
6.Mohammad Sami Ahmad, SA Ali, AS Ali, KK Chaubey.Epidemiological and etiological study of oral submucous fibrosis
among gutkha chewers of Patna, Bihar, India. Journal of indian society of pedodontics and preventive dentistry 2006;24(2); 84-
89.
7.More Chandramani, Das Sunanda, Patel Hetul, et al. Proposed clinical classification for oral submucous fibrosis. Oral
Oncology; In Press.
8.Moger Ganapathi, Shashikanth MC. Oral submucous fibrosis in a 12-year-old boy-A rare case report. JIDA 2011;5(1);124-25.
9.Dyavanagoudar Sunita N. Oral submucous fibrosis: Review onetiopathogenesis. J Cancer Sci Ther 2009;1(2):72-77.
 
10.Lee Cheng-Kuang, Tsai Meng-Tsan, Lee Hsiang-Chieh, et al. Diagnosis of oral submucous fibrosis with optical coherence
11.tomography. Journal of Biomedical Optics 2009;14(5);1-7.Gnanam A, Kannadasan Kamal, Venkatachalapathy S,David
Jasline. Multimodal treatment options for oral submucous fibrosis, SRM University. Journal of Dental Sciences 2010;1(1):26-29

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