MMP-13 and TIMP-1 determinations in progressive chronic periodontitis

Abstract

Matrix metalloproteinase (MMP)-13 is a collagenase involved in extracellular matrix degradation either by its direct degradative effects or by processing bioactive substrates. The aim of this study was to determine the levels of MMP-13 and tissue inhibitor of metalloproteinase (TIMP)-1 in gingival crevicular fluid (GCF) and gingival biopsies obtained from active and inactive sites during chronic periodontitis progression. MATERIALS AND METHODS: This was a longitudinal study in which chronic periodontitis patients with moderate to severe disease were included and followed until they developed progression determined by the tolerance method. GCF samples were obtained from periodontitis, active, inactive and healthy sites and additional gingival biopsies were taken from active and inactive sites. MMP-13 and TIMP-1 determinations were carried out by immunodot blots and immunowestern blots. RESULTS: In progressive periodontitis, MMP-13 and TIMP-1 remained unchanged between active and inactive sites, but as the TIMP-1 relative levels increased together with MMP-13 elevation in inactive samples, an inverse correlation was observed in active sites. Besides, MMP-13 was undetectable in healthy controls. CONCLUSION: Chronic periodontitis is characterized by increased MMP-13 expression. During disease progression, active sites tended to decrease TIMP-1 levels in association with MMP-13 elevation.

Matrix metalloproteinase (MMP)-13 is a collagenase involved in extracellular matrix degradation either by its direct degradative effects or by processing bioactive substrates. The aim of this study was to determine the levels of MMP-13 and tissue inhibitor of metalloproteinase (TIMP)-1 in gingival crevicular fluid (GCF) and gingival biopsies obtained from active and inactive sites during chronic periodontitis progression. MATERIALS AND METHODS: This was a longitudinal study in which chronic periodontitis patients with moderate to severe disease were included and followed until they developed progression determined by the tolerance method. GCF samples were obtained from periodontitis, active, inactive and healthy sites and additional gingival biopsies were taken from active and inactive sites. MMP-13 and TIMP-1 determinations were carried out by immunodot blots and immunowestern blots. RESULTS: In progressive periodontitis, MMP-13 and TIMP-1 remained unchanged between active and inactive sites, but as the TIMP-1 relative levels increased together with MMP-13 elevation in inactive samples, an inverse correlation was observed in active sites. Besides, MMP-13 was undetectable in healthy controls. CONCLUSION: Chronic periodontitis is characterized by increased MMP-13 expression. During disease progression, active sites tended to decrease TIMP-1 levels in association with MMP-13 elevation.