ORAL SUBMUCOUS FIBROSIS RxDentistry

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ORAL SUBMUCOUS FIBROSIS RxDentistry Powered By Docstoc
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                    DEFINITION
(J.J Pindborg and Sirsat 1966)

  It is an insidious chronic disease affecting any part of the

oral cavity and sometimes 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 changes

of the lamina propria with epithelial atrophy leading to

stiffness of the oral mucosa and causing trismus and

inability to eat.


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   The condition of oro -pharyngeal OSMF of oral
    cavity was prevalent even in the days of
    Shushrutha (600 B.C).
   Shushrutha, the greatest practitioner of ancient
    medicine stated in his book "Shushrutha
    Samhita' a condition called 'VIDARI' in his
    classification of diseases of mouth and throat.
   The features of which suit the symptomatology
    of OSMF.


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   First described among five East African women of Indian

    origin under the term Atrophia idiopathica (tropica)

    Mucosae Oris by Schwartz 1952

   Joshi in 1953 is credited to be the first person who

    described it and gave the present term “Oral sub-mucous

    fibrosis”.

   In the year 1954, Su. 1. P. from Taiwan described similar

    condition, which he called "Idiopathic Scleroderma of

    mouth"


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   Paymaster (1956) described the pre-cancerous

    nature of the condition.

    Other names that have been suggested are:

•   Diffuse oral sub-mucous fibrosis (Lal D.1953)

•   Sclerosing stomatitis (Behl 1962)

   Idiopathic palatal fibrosis (Rao 1962)




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   OSMF is a   crippling fibrotic disorder seen commonly in
    India and Indian subcontinent. Sporadic cases are seen in

    Malaysia, Nepal, Thailand and South Vietnam.

   Incidence of OSMF in India is 0.2-0.5% of population.

   Persons between 20 and 40 years of age are most

    commonly affected ,but ages have ranged from 2 to 89

    years of age

   No cast or religious community is especially affected

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   Case reports also include occurrence of

    this condition in a 4 yr old Indian immigrant

    girl in Canada, who had been chewing

    arecanut since the age of 2 yrs.

   Prevalence rate in India ranges from 0.2 to

    1.2%
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  Etiology of OSMF:
   Exact etiology is unknown. The suggested
  factors are,
1. Chronic Irritation
  Chilies
   Lime
   Betel nut
   Tobacco Chewing
2.    Deficiency disease.
3.    Defective iron metabolism
4.    Bacterial Infection
5.    Collagen disorder
6.    Immunological disorders
7.    Genetic disorder.
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    Chronic irritation:

   Pathogenesis of OSMF lies in the continuous

    action of mild irritants.

     Chillies:

   "Capsaicin" a active extract from capsicum.

   The active principle irritant of chillies

    (Capsicum annum and Capsicum frutescence) .


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   The suspicion that chilli is an etiological agent arose on

    the basis of ecological observations and was strengthened

    by the clinical and histological characteristics of this

    condition , i.e.

   Blood eosinophilia,

   Tissue eosinophils in the biopsy specimen and presence

    of sub epithelial vesicles

    suggested an allergic nature of this disease possibly due

    to chilli intake.



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   There are some ecological arguments against

    the chilli hypothesis for example from Mexico

    or other South American countries where chilli

    consumption is widespread, there is no report

    of this condition.

   The overall assessment is that there is no

    evidence substantiating the etiologic role of

    chilli in OSMF
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    Lime:

   Betel nut & lime mixture is used for chewing. This

    also contains arecoline, lime and tannic acid, These

    cause local irritation and damage to the mucosa with

    vesicle and ulceration on susceptible individual.

   Lime in betel quid causes constant aberration of oral

    mucosa, allowing direct access to the carcinogens




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    Tobacco Chewing

   It is a known irritant and a causative factor in oral malignancies

   N’-nitrosonornicotine is produced by bacterial and enzymatic

    nitrosation of nicotine and can be found by reaction of salivary

    nitrates with nornicotine

   N’-nitrosonornicotine levels increased 44% when tobacco was

    mixed with saliva

   N’-nitrosonornicotine extracted from chewing tobacco with

    saliva is approximately 1000 times that found in cigarette

    smoke



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    Betel nut:

   Considered to be one of important etiological

    factor for OSMF

   In India arecanut is chewed by itself or in the

    form of various areca nut preparations such as

    supari, mawa , manipuri , pan masala and in

    betel quid either with or without tobacco

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The factors that contribute to the pathogenesis in

 habitual betel nut chewers.

1. The amount of tannic acid (14-18%)

  contained in the betel nut.

2. The influence of mixed calcium powder.

3. Action of arecoline contained in the betel nut

 affecting the vascular nerve of oral mucosa and

 causing neurotropic disorder

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   Arecanut contain different type of alkaloids-

    arecoline, arecadine, guvacoline, guvacine and

    isoguvacine.

   Nitrosation of arecoline leads to the formation of

    arecanut specific nitrasamine. All arecanut specific

    nitrosamines are found to be powerful carcinogens

    and alkylate DNA.


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   KHANNA AND ANDHARA , have suggested pathogenesis

    of OSMF by dual action of arecanut. They suggested that ,

   Arecoline , stimulate fibroblastic proliferation and collagen

    synthesis.

   The flavonoids catechin and tannins stabilize the collagen

    fibrils rendering them resistant to degradation by

    collagenase.

   The attendent trismus is a result of juxtaepithelial

    hyalinization and secondary muscle involvement (i.e.

    muscular degradation and fibrosis)

   The habit of chewing areca nut leads to muscle fatigue

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   Vitamin B12 and Iron deficiency are

    associated with OSMF. The deficiency

    could be due to the fact that defective

    nutrition due to impaired food intake in

    advanced cases of OSMF, may be the effect

    rather than the cause of the disease


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   Impaired cellular utilization of iron explains the


    presence of hypochromic microcytic anemia.


    There is no definite proof to support the


    hypothesis that defective iron utilization by oral


    mucosa and sub-mucosa is the cause of OSMF

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   Mukherjee and Biswas (1972) suggested
    that there is:
   Rise in mucoprotein and
    mucopolysaccharide level
   Rise in anti-streptolysin - O titre in OSMF
    patients.
     (But these works are not confirmed)

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     Collagen disorder:
   Rao (1962) suggested that OSMF is a
    localized condition of collagen disease.

   He linked it to scleroderma, rheumatoid
    arthritis, duputreyens contracture and
    intestinal fibrosis. Histological features
    were found to be similar in OSMF and
    scleroderma.


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    HARMONAL FACTORS

   There would appear to be predisposition in

    female with a ratio of women to men of 3:1

    (Pillai R et al “pathogenesis of Oral
    submucous fibrosis”, cancer 1992
    ;69:2011-2017)




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    IMMUNOLOGICAL DISORDER:

   Oral Submucous fibrosis is a high risk pre-
    cancerous condition. Raised ESR and globulin
    levels are found, indicative of immune
    inflammatory disorder.

   Serum immunoglobulin levels IgA, IgG and IgM
    levels are raised. These suggest an antigenic
    stimulus in absence of any infection.

   Increased circulating immune complex in OSMF

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   Genetic predisposition to the disease ,

    involving the HLA antigens

    ,A10,DR3,DR7and probably B7 and the

    haplotypic pairs A10/DR3 and A10/B8

    has been demonstrated.




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   The increased evidence of CD4 and HLA-DR-positive cells



    and high ratio of CD4 to CD8 in OSF tissue suggest an



    ongoing cellular immune response leading to imbalance



    of immunoregulation and alteration in local tissue



    architecture.


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    Mast cells

   Mast cells are characterized by numerous cytoplasmic

    granules. Its cytoplasm contains mucopolysaccharides,

    histamine and heparin.

   Many patients with early stage of OSMF give history of

    feeling of itching sensation which could be due to

    release of histamine exact role of mast cells in

    inflammation is not known.


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                              MULTIFACTORIAL PATHOGENESIS


      ARECANUT              TOBACCO                       LIME                 VOLATILE OILS
                                                                              VOLATILE LIQUIDS




                           MECHANICAL          CHEMICAL BURN                  HYPERSENSITIVITY
                             TRAUMA


 TANNIN&
              ARECOLINE
AFLOTOXIN


                                                                                  GENETIC
DEGRADATION        INCREASED SYNTHESIS       ALTERED IMMUNITY                   REDISPOSITION
OF COLLAGEN            OF COLLAGEN




      FIBROBLAST
       FORMATION
                              IRREVERSIBLE FIBROSIS



                             EXPOSURE CONTINOUS                                CACINOMA

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    Brief review : pathogenesis of OSMF

   Section of fibroblasts with a high amount of

    collagen production during long term exposure

    to arecanut ingredients.

   Stimulation of fibroblast proliferation and

    collagen synthesis by arecanut alkaloids or by

    fibrogenic cytokines secreted by activated

    macrophages and T lymphocytes in the OSF

    tissue
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   Decreased secretion of collagenase and
    deficiency in collagen phagocytosis by OSF
    fibroblasts
   Production of collagen with a more stable
    structure (collagen type I trimer) by OSF
    fibroblast.
   Stabilization of collagen structure by catechin
    and tannin from arecanut and an increase in
    collagen cross linkage caused by up regulation
    of lysy oxidase by OSF fibroblast
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   Malignant transformation rate is 7.6%
(JIAOM, vol-iv;no.3& 4 July-Dec.1993, p 12-15)




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   The data regarding the sex predilection is
    conflicting. Earlier it was thought to be
    common in females.
   But at present ,study ratio shows 2.3: 1
    =M:F
   Age group common is 2 to 3rd decade of
    life
   But cases have been reported from 4 year
    to 86 yrs

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    Prodromal symptoms :
   Onset is insidious. The most common
    initial symptoms are:
   Burning sensation on eating spicy food
   Blisters on the palate
   Ulceration or recurrent stomatitis
   Excessive salivation
   Defective gustatory sensation
   Dryness of mouth.


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    Later,
   Difficulty in opening mouth
   Inability to whistle, blow
   Difficulty in swallowing
   When fibrosis involves pharynx- referred pain to
    the ear.
   Changes in tone of the voice due to vocal cord
    involvement
   Some times deafness due to occlusion of
    eustachian tubes

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    COMMON SITES INVOLVED

   Buccal mucosa, faucial pillars ,soft palate, lips

    and hard palate.

   The fibrous bands in the buccal mucosa run in a

    vertical direction ,sometimes so marked that the

    cheeks are almost immovable.

   In the soft palate the fibrous bands radiate from

    the pterygomandibular raphe or the faucial pillars

    and have a sear like appearance
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   The uvula is markedly involved , shrinks and
    appears as a small fibrous bud.
   The faucial pillars become thick , short, and
    extremely hard.
   The tonsils may be pressed between the
    fibrosed pillars
   The lips are often affected and upon palpation ,
    a circular band can be felt around the entire
    rima oris
   When gingiva is affected , it is fibrotic, blanched
    and devoid of its normal stippled appearance.

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Clinically signs of OSMF can be grouped as:

   Stage I :         Stage of stomatitis &

                  vesiculation

   Stage ll :        Stage of fibrosis

   Stage III :      Stage of sequelae

                      complication




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    Stage of stomatitis & vesiculation
   It is earliest stage and characterized by recurrent
    stomatitis and vesiculation. Patient complaints
    of burning sensation in the mouth & inability to
    eat spicy food.
   On examination vesicles on palate are seen.
   They rupture and form superficial ulcers.
   Some amount of fibrosis is also present.




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     Stage ll: Stage of fibrosis
   There is inability to open mouth completely and
    stiffness in mastication. As disease advances
    there is difficulty in blowing out cheek &
    protruding tongue. Sometimes pain in ear and
    speech is muffled.On examination there in
    increasing amount of fibrosis in the submucosa.
    This causes blanching of mucosa.
   Lips & checks become stiff & loose their normal
    resistance. Shortening & disappearance of uvula
    in advanced cases.
   Dorsum of tongue shows atrophy of papillae.
   Mucosa of floor of mouth show blanching &
    stiffness


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    Stage of sequelae & Complication
   Patient presents with all the complaints as in
    stage II. Also there may be evidence of
    leukoplakia.

   Changes in mucosa are whitish or brownish
    black-

   Pindborg et al (1967) found the OSMF was found
    in 40%cases of oral cancer than in general
    population 1.2%.


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    GRADE-I            GRADE-II          GRADE-III               GRADE-IV
    Incipient            Mild             Moderate                severe
(very early stage)   (early stage)   Moderately advanced         advanced
                                            stage                  stage



    1.Burning        1.Burning       1.Burning sensation,        1.Burning
    sensation,       sensation,        dryness of mouth          sensation,
dryness of mouth,    dryness of                                  dryness of
   vesicles or         mouth                                       mouth
    ulceration
 2.Irritation with    2.Irritation     2.Irritation with         2.Irritation
     spicy food           with             spicy food                with
                       spicy food                                 spicy food


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3.No change in 3. Oral mucosa 3.Blanched        3.Blanched
mucosal colour is blanched and ,opaque, leather ,opaque, leather
               loses        its like mucosa     like mucosa
               elasticity


4.  No     fibrous 4. No clear cut 4.       Vertical 4. Thick fibrous
bands              fibrotic bands  fibrotic  bands bands occurring
                                   on        buccal on both buccal
                                   mucosa making mucosa,           in
                                   it stiff          retromolar area
                                                     and           at
                                                     ptrygomandibul
                                                     ar raphe

5. Mouth opening 5.          Slight 5.Considerable   5. Very little
normal           restriction     of restriction   of mouth opening
                 mouth opening mouth opening



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6.Tongue      6.Tongue      6.        Tongue 6.Restricted
protrussion   protrussion   protrussion not tongue
normal        normal        much affected    protrussion

                            7.Difficulty            in 7. Speech and
                            eating                and eating     very
                            speaking                   much impaired

                            8.Oral        hygiene 8.Oral hygiene
                            poor                  very poor




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    DIAGNOSIS IS BASED ON :

   Clinically discernible blanching and pallor

   Palpable bands and restriction-of mouth

    opening.

   Severe burning sensation of mouth, aggravated

    by use of even moderate spicy food.

   Biopsy report characteristically showing

    histopathologically


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   Atrophic Oral epithelium.

   Loss of rete pegs .

   Epithelial atypia may be observed.

   Hyalinization of collagen bundles.

   Fibroblasts decreased and blood
    vessels obliterated.

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     Stage 1: Early OSMF
   Mild blanching.
   No restriction in mouth opening .Central
    incisor tip Males... 35-45mm to tip of
    same side. Females 30-42mm.
   No restriction in tongue protrusion .Mesio
    incisal angle of upper central incisor to
    the tip of the tongue when maximally
    extended with mouth wide open-Males 5-
    6 cms and Females 4.5-5.5 cms.




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    Stage 2 : Moderate OSMF…

   Moderate to severe blanching .

   Mouth opening reduced by 33%.Flexibility also
    demonstrably decreased.

   Burning sensation even in absence of stimuli.

   Palpable bands felt.

   Lymphadenopathy either unilateral or bilateral.

   Demonstrable anemia on hematological
    examination.




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    Stage 3: Severe OSMF
   Burning sensation very severe. patient
    unable to do day to day work.
    More than 66% reduction in the mouth
    opening cheek flexibility and tongue
    protrusion, the tongue may appear fixed.
   Ulcerative lesions may appear on the
    cheek.
   Thick palpable bands.
   Lymphadenopathy bilaterally evident..


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   Lab findings reflect the nature of tissue
    changes in this condition rather than any
    diagnostic importance.
   Increased ESR
   Anemia
   High eosinophil count
   Hyper gammaglobulinaemia
   Lower serum vitamin A levels


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    MANAGEMENT
   Various modalities of treatment have been
    tried.
1.Restriction of habits/ Behavioral therapy
2.     Medicinal therapy
3.     Surgical therapy.
4.     Oral Physiotherapy




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      Restriction of habits/behavioral therapy
   The consumption of pan, betel nut, chillies, spices, &
    commercially available, pan masalas, guthkas with or
    without tobacco is increasing in India. So people
    should be encouraged to stop these habits

   Affected patients should be explained about the
    disease and possible malignant potential of OSMF.

   Possible irritants should be removed

   Nutritional supplements.


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    MEDICINAL THERAPY

   Antioxidants

   Intralesional injections of hyaluronidase.

   Use of Placentrix 2ml solution at interval

    of 3 days in five divided region

   Topical application of 4% Acetic acid

    (variable) 3 times daily.

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    Topical application of   immunomodulators:


   5 Fluorouracil


    Systemic administration of immunomodulators


   Levamisole 150mg for 3 weeks


   Dapsone 75 mg O.D for 90 days


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    SURGICAL TREATMENT


   Fibrotomy


   Cryosurgery


   Laser treatment




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