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Oral Submucous Fibrosis

Oral submucous fibrosis is a chronic, precancerous condition of the oral cavity characterized by fibrosis of the submucosa and epithelial atrophy. It predominantly affects people who chew betel nuts and is most common in parts of Asia and India. The condition causes stiffness of the oral cavity and lips and can lead to difficulty opening the mouth. If left untreated, there is a risk of the condition progressing to oral cancer.
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0% found this document useful (0 votes)
441 views18 pages

Oral Submucous Fibrosis

Oral submucous fibrosis is a chronic, precancerous condition of the oral cavity characterized by fibrosis of the submucosa and epithelial atrophy. It predominantly affects people who chew betel nuts and is most common in parts of Asia and India. The condition causes stiffness of the oral cavity and lips and can lead to difficulty opening the mouth. If left untreated, there is a risk of the condition progressing to oral cancer.
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© Attribution Non-Commercial (BY-NC)
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Oral submucous fibrosis

Also known as-asian sideropenic dysphagia


Or Oral mucous disease
Or Oral fibrosis
Or oral soft tissue disease
introduction
In ancient medicine “shushrutha” described a condition “vidari”under
mouth and throat disease.

“Shhwarts” first time reported a case of oral submucous fibrosis and gave
the term”atrophica idiopathica mucosae oris”occurring in indians in east
africa.

Precancerous nature of osf is described by “paymaster” .

“Lal and joshi “first described this condition in india and termed as
o.s.m.f..
It is a chronic and high risk precancerous condition which has highest rate
of malignant transformation among premalignant lesion and condition….
Epidemiology
Indian subcontinent and south east asia
Ocurrs mainly in india
In india-----0.2-1.2% in urban population
 0.4% in rural population
 Geographic distribution------
Primary locations others locations
India china
Pakistan Thailand
Burma Vietnam
Definition
Acc to pindborg n sirsat(1966)
“o.s.m.f is insidious chronic disease affecting any part
of the oral cavity and some times the pharynx.
Although occasionally preceded by and /or associated
with vesicle formation. It is always associated with
juxta epithelial inflammatory reaction followed by a
fibro elastic change of the lamina propria with
epithelial atrophy leading to stiffness of mucosa and
causing trismus and inability to eat..
Etiology
Exact role not clear.
 1.Betal nut-----
 One of the most important etiological factor for the causation of o.s.m.f.
 Areca nut contain different type of alkaloid arecoline,guvacoline,guvacine &isoguvacine.
 Action---they have parasympathomemetic effect, promote salivation, rise B.P,pulse rate.
 Elicit degree of euphoria by virtue of their GABA receptor inhibiting properties which
contributes to dependence and habituation.
 Also has bronchoconstrictor effect &evidence for a role in precipitating &exacerbating
asthma and diabetes..
 Arecoline stimulate fibroblastic proliferation and collagen synthesis
 The flavenoid catachin&flavin stabilize the collagen fibrils rendering them resistance to
degradation by collagenase.
 Trismus is the result of juxtaepithelial hyalinization &sec. muscle involment.
 Increase muscle activity &diminished blood supply ,following C.T changes ,owing to
extensive oralsubmucous fibrosis leads to muscle degeneration & fibrosis.
CHILIES—role in pathogenesis is controversial.
Hypersensitivity reaction to chilies is believe to contribute the occurrence of
O.S.M.F
TOBBACO– known irritant and causative factor of malignancy.
LIME-local irritant, used with betel nut for chewing. damage
to mucosa with vesicle or ulcer formation
NUTRITIONAL DEFICIENCY-malnutrition is more prevalent
in o.s.m.f.several investigators have reported anemia,vit.,iron
and protein deficiency among OSMF patient. iron
metabolism seems to be primary factor,& def. in folic
acid,pyridoxine &vitB-12 is secondary.
Vit-B 12 def. disease characterised by repeated vesiculation&
ulcer in oral cavity.

.
DEFECTIVE IRON METABOLISM-microcytic hypochromic
anaemic with high serum irom have reported in osmf.
BACTERIAL INFECTION-steptocaccal toxicity is also a factor in
etiology of osmf..
COLLEGEN DISORDER—scleroderma,rhematoid
arthritis,intestinal fibrosis.
IMMUNOLOGICAL DISORDER—serum immunoglobulin leven
of ig A,ig B,ig M are raised significantly o.s.f circulating auto
antibodies are also seen..
GENETIC SUSCEPTIBLIY-familial occurrence also been reported.
HLA DR 10,HLA DR 3,&DR 7 are found in OSMF in inceased
freqency.
PATHOGENESIS
Increase collagen production.

Stabilization of collagen.

Decrease collagen breakdown


ROLE OF ARECANUT IN O.S.M.F
ARECA NUT

Alkaloids trauma during tannins & copper


catechins
chewing
CLINICAL FEATURES
AFFECT BOTH SEX(F>M) SITE- BUCCAL MUCOSA,RETROMOLAR
AREA,TONGUE,LABIAL MUCOSA,PALATAL
AGE-12 TO 62(MEAN 40) FAUCES,UVULA,&SOME TIME FLOOR OF MOUTH
 SYMPTOMS  SIGN
 Burning sensation &pallor or  Stiff and small
blanching of oral mucosa. tongue,blanched and leathery
 Increase salivation,change in floor of mouth,
gustatory sensation,hering  Fibrotic and depigmented
loss due to stenosisof gingiva.
eustachian tube,impaired  Rubbery soft palate with
mouth movement. decrease mobility. blanched
and atrophic tonsils.
 Mouth opening progresively
reduced.
STAGING OF OSMF
STAGE- 1( EARLY OSMF)
Mild blanchingnded
No restriction in mouth opening
No ristriction in tongue protussion upto mesioincisal
angle of upper central incisor when maximmaly
extended with mouth wide opening.
Burning sensation only on taking spicy food or hot
liquid.
STAGE-2(MODERATE OSMF)
Moderate to severe blanching
Mouth opening reduced by 33%,tongue protrusion
reduced by 33% &reduced flexibility.
Burning sensation even in the absence of stimuli.
Presence of palpable band
Lymphadinopathy either unilateral or bilateral.
Demonstrable anemia on hematological examination.
STAGE-3(SEVERE OSMF)—
o Burning sensation very severe
o Moore than 66% reduction in the mouth opening
,cheek,flexiblity&tongue protrusion.
o Ulcer over buccal mucosa
o Thick palpable band
o Bilateral lymphadenopathy definite
o Angular chelitis&iron def. group.
CLINICAL STAGING FUNCTIONAL
STAGE 1-faucial band only STAGING
STAGE 2-faucial &buccal STAGE A-mouth
band opening 13-20 mm
STAGE 3-faucial &labial STAGE B-mouth
bands opening 10-12 mm
STAGE C-mouth
opening less than 10mm
HISTOPATHOLOGY
EPITHELIAL CHANGE CONNECTIVE TISSUE
CHANGES
Epithelial hyperplasia or
Its shows vesicle which are
atrophy which is caused by sub epithelial
associated with increase accumulation of fluid.
tendency for keratinizing C.T changes include
metaplasia hyalinization with moderate no.
of chronic inflammatory cells.
Liquefaction
Most striking feature of c.t is
degeneration of the basal the presence of dense collagen
cell layer of cells. bundles randomly oriented &
Rate pegs completely lost. extending into the underlying
striated muscle
TREATMENT
CORTICOSTEROIDS
PLACENTAL EXTRACTS
HYALURONIDASE
INTERFERON GAMMA
LUCOPENE
PENTOXIFYLLINE
SUGICAL CARE—

SIMPLE EXCISION OF THE FIBROUS BAND---


excision can result in contracture of the tissue
exacerbating the condition.
SPLIT THICKNESS SKIN GRAFTING FOLLOWING
BILATERAL TEOMPORALIS MYOTOMY OR
CORONOIDECTOMY--
COMPLICATION

Oral dysplasia & sq.cell carcinoma


In patient with osf,the risk of developing carcinoma is
7-14% over a 10 year period
PROGNOSIS----
No treatment is effective in patient with osmf &the
condition is irreversible.
Recent report claims improvement of the condition. If
the habit is discontinue following diagnosis at early
stage

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