Aim: Tenascin, a glycoprotein, is among the major constituents of extracellular matrix, which may function in organizing the stroma in normal and pathological conditions. staining around inflammatory cells, fibroblast and endothelial cells using anti-human tenascin. Result: Most of the OSMF cases showed retention of antigen at ECJ and in deeper CT. Its expression varied in different grades as well as around inflammatory cells, fibroblast and endothelial cells in same tissue section. Highly significant values of 0.001 and 0.003 were obtained for tenascin intensity and pattern, respectively, at ECJ in different OSMF grades. In addition, for the expression of tenascin pattern in deeper CT among different OSMF grades, a significant value of 0.018 was obtained. Conclusion: A differential expression of tenascin was observed with the progression of disease. The expression of tenascin as bright and continuous deposition at ECJ in early and moderate stages of OSMF signifies either proliferative business within the overlying epithelium or an epithelial-mesenchymal conversation. However, a poor immunoreactivity of tenascin at ECJ was observed in advanced stage of OSMF. and but also by epithelial cells.[3] Despite considerable research into numerous aspects of this disease, the actual location of the initiation of fibrosis has eluded researchers and remains inconclusive. It is rather prudent to believe that in some cases of OSMF, the plane of initiation of fibrosis is not in the lamina propria but further down in the submucosa. This seems to be a possible reason for some of the early manifestations of disease such as dryness of the mucosa and functional impairment.[4] While the factors that determine this histological alteration in cases of OSMF remain elusive and in early clinical stages, the histopathological features are not pathognomonic. Further studies on different components of ECM glycoproteins during the progression of OSMF may throw light on early diagnosis of the disease. Therefore, the present study was aimed to study the tenascin expression in early, moderate and advanced cases of OSMF, in individuals exclusively associated with the habit of chewing areca nut, to characterize its role in progression of the disease. MATERIALS AND METHODS A retrospective cross-sectional immunohistochemical (IHC) study was carried out on 35 patients including 30 cases of OSMF and five cases of normal oral mucosa Flumazenil small molecule kinase inhibitor as control group. The samples for the study were collected from 35 formalin-fixed paraffin-embedded tissue blocks, 10 each from histologically confirmed and graded early, moderate and advanced stage of OSMF according to the grading system given by Utsunomiya test was applied for each parameter to minimize the interobserver errors and with this measure of agreement value was nonsignificant. Thus, the observation made by observer 1 was then subjected for further statistical analysis. STATISTICS AND RESULTS All normal oral mucosa sections showed expression of tenascin at the ECJ as faint linear continuous brown staining [Physique 1]. Few cells in the basal cell layer also showed positive staining. In OSMF group, most of the cases showed retention of the antigen. Its expression varied from one case to another and also within the same tissue section. Open in a separate window Physique 1 Normal oral mucosal section showing linear deposition of tenascin along the cellar membrane (IHC stain, 400) Among early OSMF situations, 90% areas exhibited a shiny and constant deposition of tenascin at ECJ, such as a music group [Body 2 and Desk 1]. In these areas, tenascin proteins was transferred diffusely in deeper CT in 80% areas with 20% areas showing patchy regions of tenascin positive areas. Amazingly, tenascin deposition was noticed around endothelial cells, fibroblasts and inflammatory cells in most sections [Desk 2]. Open up in another window Body 2 Early dental submucous fibrosis section displaying shiny immunoreactivity of tenascin on the junction of epithelium and connective tissues with expansion into connective tissues (IHC stain, x200) Desk 1 Evaluation of strength and design of tenascin appearance at epithelium and connective tissues among different levels of dental submucous fibrosis Open up in another window Desk 2 Flumazenil small molecule kinase inhibitor Evaluation of design of tenascin appearance and existence of staining throughout the cells in connective tissues stroma among different levels of dental submucous fibrosis Open up in another screen In moderate Flumazenil small molecule kinase inhibitor OSMF situations, 80% areas exhibited a shiny and 70% areas showed constant deposition of tenascin at ECJ, such as a music group [Body 3 and Desk 1]. In these areas also, tenascin proteins Flumazenil small molecule kinase inhibitor was transferred diffusely in deeper CT in 80% areas with 20% areas showing patchy regions of tenascin positive areas. Nevertheless, the appearance of tenascin, around endothelial cells, fibroblasts and inflammatory cells was seen in less number of instances than in early OSMF areas S1PR4 [Desk 2]. Open up in another window Body 3 Moderate dental submucous fibrosis section displaying shiny immunoreactivity of tenascin on the junction.