Etiopathogenesis of Oral Submucous fibrosis

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2 : CONTENTS: Introduction Etiology Pathogenesis Areca alkoloids Tannins & catachine polyphenols Copper in nut & fibrosis Up regulation of cox-2 Fibrogenic cytokines Genetic polymorphism predisposing to osmf Inhibition of collagen phagocytosis Collagen related genes Osmf as an autoimmune disorder Other causes of osmf Precancerous nature & malignant transformation Conclusion References
3 : premalignant condition “It is associated with juxtaepithelial inflammatory reaction followed by fibroelastic change in laminapropria, with epithelial atrophy leading to stiffness of the oral mucosa & causing trismus & inability to eat.” joshi & schwartz(1952) 0.2 – 0.5 % in india , 2,50,000 cases in 1980 2 million cases by 2000 age – 20 – 40 years commonly OSMF
4 : Premalignant lesion: “ a benign , morphologically altered tissue that has a greater than normal risk of malignant transformation.” ex – leukoplakia , erythroplakia Premalignant condition: “a disease or patient habit that does not necessarily alter the clinical appearance of a local tissue but is associated with greater than normal risk of malignant transformation in that tissue.” ex – osmf , lichenplanus, discoid lupus erythematosis , sideropenic dysphagia(plummer vinson syndrome)
5 : OSF is a chronic debilitating disease characterised by a generalised submucosal fibrosis of the oral tissue, resulting in marked rigidity & progressive inability to open mouth. Site – common in buccal mucosa but can occur any part of oral cavity Incidence – 0.2 – 2.3 % in males 1.2 – 4.5 % in females 2.5 million people worldwide , most cases concentrated in indian subcontinent. Age – 14 – 60 years CLINICAL FEATURES
6 : Burning sensation with spicy food Stomatitis , erythematous mucosa, vesicles , mucosal ulcers, pigmentation & mucosal petechia Dryness of mouth PRODROMAL SYMPTOMS (early osf)
7 : Clinically discernible blanching & pallor, Palpable bands , restricted mouth opening, severe burning sensation of mouth , aggrevated by spicy food Dryness of mouth Change of gustatory sensation Hearing loss due to stenosis of eustachian tubes Nasal tonicity to voice Dysphagia to solids( if esophagus is involved) Impaired mouth movements – eating,whistling,blowing,sucking Signs & symptoms ( advanced osf)
8 : Based on history & clinical evaluation Biopsy shows characteristically atropic oral epithelium loss of retepegs epithelial atypia may be observed hyalinization of collagen bundles Diagnosis
10 : Arecanut (betal nut) chewing: areca nut component of betal quid - important role in osf arecoline – alkaloid in betal nut , others – guvacine , guvacholine lime (caoh2) hydrolysis arecoline arecaidine ( active metabolite) fibroblast stimulation collagen production by 150 % collagen breakdown fibrosis pathophysiology
11 : arecholine inhibits metalloproteinase – 2 + Stimulate tissue inhibitors of metalloproteinase overall breakdown of tissue collagen is decreased
12 : arecholine upregulation of keratinocyte growth factor-1 insulin like growth factor interleukin 6 increased tissue fibrogenesis
13 : OSF remains active even after cessation of habit younger people developed OSF in 3.5 years, older people in 6.5 years from start of habit risk is more in below 21 years age group compared to 20-40 years daily use more imp than duration of habit commercial freeze dried products – higher concn. Of arecanut per chew & causes osf more rapidly than self prepared ,ex- panmasala, gutka & mava Recent studies shows
14 : In betalnut increased cross linking & stabilization of collagen reduced collagen degradation by inhibiting collagenases increased collagen production by 1.5 times fibrosis Tanins & catachins polyphenols
15 : copper content in arecanut is high levels of soluble cu in saliva is raised upregulation of lysyl oxidase increased fibroblast cells growth fibrosis
16 : immunohistochemistry study show there was increased expression of the cox2 enzyme in moderate fibrosis and this disappeared in advanced fibrosis 1.4 – 3.4 fold increase in PGE2 production 1.1 – 1.7 fold increase in PGE1 when gingival keratinocyte where exposed to areca nut extracts Upregulation of cyclo-oxygenase
17 : Changes in cytokine secretion in OSF have been investigated & estimated by radioimmunoassay and ELISA shows in OSF – increased pro inflammatory cytokines – IL1, IL6 decreased antifibrotic cytokine – INF-y increased fibrogenic cytokine – TGf-b, PDGF, basic fibroblast growth factor. FIBROGENIC CYTOKINES
18 : the presence of circulating immune complexes, their immunoglobulin contents and the detection of various autoantibodies in patients sera osf patient have high level of HLA – A10 HLA – B7 HLA – DR3 presence of these immunocompetent cells high ratio of complement Cd4 to Cd8 cells in osf pt. raised serum levels of IgG, IgA and IgM all these suggest an ongoing cellular immune response that results in an imbalance of immunoglobulin & alteration in local tissue architecture. Autoimmune cause
19 : Degradation of collagen by fibroblast phagocytosis is an important pathway of physiological remodelling of the extracellular matrix (ECM) in connective tissue Study shows In OSF a gross imbalance in ECM remodeling reduction of phagocytic cells was strongly related to the arecoline levels in fibroblast culture. Inhibition of collagen phagocytosis
20 : Increased and continuous deposition of extracellular matrix may take place as a result of disruption of the equilibrium between matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMP). OSF fibroblasts produced more TIMP-1 protein than normal fibroblasts arecoline reduced the MMP-2 secretion and increased the TIMP-1 levels resulting in increased deposition of collagen in the extracellular matrix Stabilization of extracellular matrix
21 : genetic polymorphism is a predisposing factor for osf. Polymorphisms of the genes coding for TNF-a has been reported as a significant risk factor for OSF. TNF-a is known to stimulate fibroblastic proliferation in vitro. collagen related genes are altered due ingredients of quid. gene – COL1 A1, COL3 A1, COL6 A1 transcriptional activation of procollagen genes by TGF – b increased collagen levels in osmf patient GENETIC
22 : NUTRITIONAL DEFECIENCY: fe def. anemia , vit b complex def.& malnutrition derange the repair of inflamed oral mucosa, atrophic mucosa is more suceptible to effects of betalnut or chillies. INGESTION OF CHILLIES: role of chilles in pathogenesis of osf is controversial capsacin in chillies stimulates fibrosis in some study. but incidence of osf is low in mexico & southamerican than india despite higher dietary intake of chilles.
23 : Physical staging by – pindborg 1989, murti 1992, cox 1996, aziz 1999 Stage1: early osmf mild blanching mouth opening normal males – 35-45mm, females – 30-42mm no restriction in tongue protrusion burning sensation only on taking spicy/hot food. Stage 2: moderate osmf moderate to severe blanching mouth opening reduced by 33%, flexibility also reduced burning sensation even in absence of stimuli palpable bands felt lymphadenopathy – unilaterally/bilaterally Staging of osmf
24 : Stage3: severe osmf burning sensation very severe more than 66% reduction in mouth opening, cheek flexibility, tongue protrusion, tongue appears fixed. ulerative lesions may appear on cheek thick palpable bands bilaterally evident lymphadenopathy
25 : A GROUP CLASSIFICATION SYSTEM FOR THE SURGICAL MANAGEMENT OF TRISMUS BY KHANNA AND ANDRADE, 1995 Group1: earliest stage , no trismus , interincisal distance greater than 35mm Group2: interincisal distance – 26 -35mm Group3: moderately advanced cases, interincisal distance – 15-26mm Group4A: trismus severe, interincisal distance – less than 15mm & extensive fibrosis of all oral mucosa Group4B: disease is most advanced , with premalignant & malignant changes throughout the mucosa.
26 : Clinical staging : 1 – faucial bands only 2 – faucial & buccal bands 3 – faucial , buccal & labial bands Functional staging: A – mouth opening more than 20mm B - mouth opening 11- 19 mm C – mouth opening less than 10mm BY HAIDER SM ETAL IN 2000
27 : MORTALITY / MORBIDITY OF OSMF high rate MALIGNANT POTENTIAL OF OSMF: osmf to squamous cell carcinoma – 7.6% chance in 10 year period (aziz 1999). epithelial atrophy , increased rate of cell division decreased cell cycle time DNA strands break
28 : The precancerous nature of OSF was first described by Paymaster in 1956 Pindborg in 1972 put forward five criteria to prove that the disease is precancerous high occurrence of OSF in oral cancer patients, higher incidence of SCC in patients with OSF, histological diagnosis of cancer without any clinical suspicion in OSF, high frequency of epithelial dysplasia higher prevalence of leukoplakia among OSF cases
29 : dense fibrosis and less vascularity of the corium, in the presence of an altered cytokine activity creates a unique environment for carcinogens from both Oral submucous fibrosis , tobacco and areca nut to act on the epithelium. carcinogens from areca nut accumulate over a long period of time either on or immediately below the epithelium Less vascularity may deny the quick absorption of carcinogens into the systemic circulation.
31 : REFERENCES Shafer, Hine & Levy:Benign & malignant tumours of oral cavity – A textbook of oral pathology. 4th edition. 1993: 92 – 110 Oral & maxillofacial pathology , neville,damm Vernon J. Brightman: Red & white lesions of the oral mucosa – Burket’s oral medicine, diagnosis and treatment. 9th edition. 1994: 51 – 111. J. N. Khanna & N. N. Andrade: Oral submucous fibrosis, a new concept in surgical management. Report of 100 cases. International Journal of Oral & Maxillofacial Surgery. 1995: 24: 433 – 439 SM HAIDER etal :CLINICAL & functional staging of osmf , BJOMS,2000,38
32 : OSMF REVIEW OF ETIOLOGY & PATHOGENESIS:oral oncology,(2006) 42, 561- 568. Oral Submucous Fibrosis A Distressing Disease with Malignant Potential, N. Afroz1, S.A. Hasan2, S. Naseem1, Indian Journal of Community Medicine Vol. 31, No. 4, October-December, 2006
33 : Thank you


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