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Microtrauma could lead to the release of thrombin.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Thrombin\u2010induced CCN2 expression and its signaling pathways were assessed by Western blot analyses in human buccal mucosal fibroblasts.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Thrombin stimulated CCN2 synthesis in buccal mucosal fibroblasts via activation of protease\u2010activated receptor\u20101. Pretreatment with antioxidant N\u2010acetyl\u2010L\u2010cysteine, apoptosis signal\u2010regulating kinase 1 inhibitor thioredoxin, and c\u2010Jun NH<jats:sub>2<\/jats:sub>\u2010terminal kinase inhibitor SP600125 significantly reduced thrombin\u2010induced CCN2 synthesis. Epigallocatechin\u20103\u2010gallate completely inhibited thrombin\u2010induced CCN2 synthesis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Thrombin produced by microtrauma may contribute to the pathogenesis of OSF by up\u2010regulating CCN2 expression. This effect could be mediated by protease\u2010activated receptor\u20101, reactive oxygen species, apoptosis signal\u2010regulating kinase 1, and c\u2010Jun NH<jats:sub>2<\/jats:sub>\u2010terminal kinase pathways and prevented by epigallocatechin\u20103\u2010gallate. \u00a9 2011 Wiley Periodicals, Inc. 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