Αρχειοθήκη ιστολογίου

Αλέξανδρος Γ. Σφακιανάκης
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5
Άγιος Νικόλαος Κρήτη 72100
2841026182
6032607174

Τετάρτη 28 Δεκεμβρίου 2016

Myofibroblasts could be recruited in a Chemokine (C-C motif) Ligand 2-dependant manner in pathogenesis of oral submucous fibrosis

Abstract

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 versus OSMF (p = 0.002), control versus advanced OSMF (p = 0.005) and early versus advanced OSMF (p = 0.0377). Similarly, differences in the CCL2-CT expression was statistically significant between control versus OSMF (p = 0.00086), control versus early OSMF (p = 0.02914), and control versus advanced OSMF (p = 0.0006). For α-SMA expression, significant differences were observed between control versus OSMF (p = 0.0003), control versus early OSMF (p = 0.036), control versus advanced OSMF (p = 0.00008) and early versus 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.

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