Expression of cyclooxygenase 2 in oral submucous fibrosis: An immunohistochemical pilot study

Abstract

Introduction: Oral submucous fibrosis (OSF) is associated with inflammatory changes in at least some stages of the disease. Prostaglandin is one of the main inflammatory mediators and its production is controlled by various enzymes such as cyclooxygenase (COX). The genetic and pharmacological data strongly indicate that COX-2 should be investigated as a potential target for the prevention and treatment of OSF. Methodology: The study group comprised histologically confirmed specimens ( n = 10 each) of early OSF, moderate OSF, advanced OSF and normal oral mucosa for comparison. Immunohistochemistry was performed with avidin–biotin technique and evaluated with scoring methods. Results: The difference in percentage of expression in normal tissue and OSF was statistically highly significant ( P < 0.001). Positive COX-2 exhibited cytoplasmic staining. One-way analysis of variances test was performed to evaluate COX-2 expression in different grades of OSF. Cytoplasmic staining assessed in terms of intensity, percentage of expression and Q Score did not show any statistical difference (percentage of expression F = 0.029, P = 0.971; Q Score F = 0.154, P = 0.858). Conclusions: Our study indicates that COX-2 may be an important marker of disease progression and might be a reliable prognostic indicator.

Clinicopathological Correlation of Cyclooxygenase 2 Expression in Oral Submucous Fibrosis

“…The immunoexpression of COX 2 in the present study was significantly increased in the OSMF group, when compared with controls, with none of the normal patients showing positivity to COX 2, the results of which were in correlation with a similar study. [ 17 ] Similar correlation with the present study was observed in a study done by Tsai et al ,[ 35 ] in which COX 2 expression was upregulated in OSMF specimens compared with normal buccal mucosa, with strong immunostaining for COX-2 being detected in epithelial cells, fibroblasts, and inflammatory cells. Statistically significant expression of COX 2 was observed on comparison with normal, OSMF, and OSCC, with increased expression of advanced stage of OSMF in a study done by Singh et al .…”

“…In an attempt to find the association of dysplasia connected with OSMF with COX 2 expression, it was found to be statistically insignificant, probably attributed to the lower sample size. [ 17 ] However, in the present study on comparison with normal, atrophic, mild, and moderately dysplastic epithelium, statistically significant difference was noted with the expression of COX 2. Evaluation of clinical and histopathological parameters, using univariate and multivariate analyses, showed that COX 2 expression along with nature of the epithelium and vascularity together as a model would help in identification of disease progression in OSMF.…”

“…The association of COX 2 with histopathological parameters such as degree of fibrosis and vascularity showed statistically significant difference. The study done by Rangaswamy et al [ 17 ] showed no significant correlation with histopathological grading of OSMF. Though, in the current study, correlation of COX 2 with histopathological grading was not done, it was observed that the COX 2 expression significantly increased with the increase in severity of fibrosis.…”

“…[ 5 ] The array of diagnostic markers studied using IHC in OSMF includes cell proliferation markers such as Ki 67 and cyclin D1,[ 5 6 ] tumor suppressor genes p53, p63, and p16,[ 6 7 ] transcription markers c-Jun, β-catenin, growth factor receptors c-Met and insulin-like growth factor II mRNA-binding protein 3 (IMP3),[ 5 ] epithelial to mesenchymal transition markers,[ 8 ] oncoproteins such as Bcl2,[ 9 ] apoptotic markers such as caspase 8, caspase 3,[ 10 11 ] cancer stem cell markers such as CD (cluster differentiation) 44,[ 12 ] pan endothelial markers associated with tumor angiogenesis CD34, CD105, growth factor markers such as basic fibroblast growth factor,[ 13 14 ] transforming growth factor-β1,TGF-β2,[ 15 ] cytokeratin markers such as CK 19,[ 16 ] and inflammatory markers such as cyclooxygenase (COX) 2. [ 17 ]…”

Immunohistochemical biomarkers in oral submucous fibrosis: A scoping review

“…α‐SMA, 23 podoplanin, 41 cyclooxygenase‐2 (COX2), 42 α‐enolase, 43 p53, 24 p63, 44‐46 ΔNp63, 44 p16, 24 Ki67, 23,27 cytokeratin (CK‐5/6), 44 VEGF, 47 CD105, 23,45,47 vimentin, 48 PCNA, 49 caspase‐3, 50 SOX2, Bmi1, 27 and cytoplasmic expression of E‐cadherin and β‐catenin 49 were upregulated in OSF with dysplasia compared with OSF without dysplasia and normal subjects. Loss of membranous E‐cadherin and β‐catenin was evident in OSF with moderate and severe dysplasia 45–47 …”