Myofibroblasts could be recruited in a chemokine (C-C motif) ligand 2-dependent manner in pathogenesis of oral submucous fibrosis.

BACKGROUND: Monocyte chemoattractant protein-1 (CCL2) is a major profibrotic mediator with a proven role in fibrosis of different organs of the body. Recently, increased fibrosis in oral submucous fibrosis (OSMF) is linked with betel quid-related chronic irritation and myofibroblast. Hence, this study is designed to investigate expression of CCL2 in OSMF and its correlation with myofibroblasts. MATERIALS AND METHODS: Paraffin-embedded specimens of 30 OSMF and 10 tissues of normal buccal mucosa were subjected to immunohistochemical analysis for CCL2 and alpha-smooth muscle actin (alpha-SMA) expression. RESULTS: CCL2 expression in basal cells (CCL2-B) and connective tissue (CCL2-CT), and alpha-SMA showed significantly increased expression in advanced OSMF as compared with early OSMF and controls. Significant differences were observed in the expression of CCL2-B between control vs. OSMF (P = 0.002), control vs. advanced OSMF (P = 0.005), and early vs. advanced OSMF (P = 0.0377). Similarly, differences in the CCL2-CT expression were statistically significant between control vs. OSMF (P = 0.00086), control vs. early OSMF (P = 0.02914), and control vs. advanced OSMF (P = 0.0006). For alpha-SMA expression, significant differences were observed between control vs. OSMF (P = 0.0003), control vs. early OSMF (P = 0.036), control vs. advanced OSMF (P = 0.00008), and early vs. advanced OSMF (P = 0.0009). In OSMF group, a significant correlation was observed between CCL2-B and CCL2-CT (P < 0.00001), CCL2-B and alpha-SMA (P < 0.00001), and CCL2-CT and alpha-SMA (P < 0.00001). CONCLUSION: CCL2 could be responsible for pathogenesis of OSMF by recruiting myofibroblasts.