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Myofibroblasts could be recruited in a chemokine (C‐C motif) ligand 2‐dependent manner in pathogenesis of oral submucous fibrosis
Author(s) -
Sarode Gargi,
Sarode Sachin C.,
Deshmukh Revati,
Raktade Prashant,
Patil Shankargouda
Publication year - 2017
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12543
Subject(s) - oral submucous fibrosis , ccl2 , fibrosis , myofibroblast , chemokine , immunohistochemistry , pathology , medicine , pathogenesis , sma* , inflammation , mathematics , combinatorics
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 (α‐SMA) expression. Results CCL2 expression in basal cells (CCL2‐B) and connective tissue (CCL2‐CT), and α‐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 α‐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 α‐SMA ( P < 0.00001), and CCL2‐CT and α‐SMA ( P < 0.00001). Conclusion CCL2 could be responsible for pathogenesis of OSMF by recruiting myofibroblasts.