Expression of matrix metalloproteinases in healthy and diseased human gingiva

Background, aims: The aim of our study was to investigate the patterns of s everal metalloproteinases (MMP-1, MMP-2 and MT1-MMP) mRNAs expression using a semi-quantitative reverse transcriptase-polymerase chain reaction (RTPCR ) and to correlate them with clinical parameters and bacteriological diagno sis in healthy versus diseased human gingiva. Methods: To identify the cell origin of MMP production, in situ hybridizati on (ISH) was also performed for the MMPs on the same samples. 17 gingival b iopsies were collected (13 affected by advanced periodontitis and 4 healthy used as controls) and plaque index, gingival index, pocket depth and bleed ing on probing were measured. Subgingival microbial samples were also colle cted to be analysed by a DNA probe technique. The biopsies were processed b oth for RTPCR and ISH. We also investigated a model for bacterial induced M MP expression in human gingival fibroblasts (HGF) infected by Eikenella cor rodens. Results: We found an expression of the mRNA encoding MMP-1 only in diseased gingiva but at low levels relative to beta -actin (mean+/-SD: diseased ver sus healthy: 0.013+/-0.024 versus 0). Although the frequencies and levels o f mRNA encoding for MMP-2 or MT1-MMP are not significantly different betwee n each group (mean+/-SD: 0.329+/-0.344 versus 0.137+/-0.219 for MMP-2; 0.48 5+/-0.374 versus 0.466+/-0.296 for MTI-MMP), using ISH, we observed an expr ession of both mRNAs in fibroblasts of pathological specimens at sites that histologically showed signs of chronic inflammation and connective tissue remodelling. In vitro infection of HGF by Eikenella corrodens stimulated 3- fold the production of the mRNA encoding MMP-2 while other mRNAs remained u nchanged. Conclusion: Our results did not reveal significant differences in the expre ssion of mRNAs encoding for the MMPs between healthy and periodontitis-affe cted patients, reflecting the great heterogeneity in the periodontal status of individuals. However, they indicate that gingival fibroblasts are an ac tive source of MMP-2 production in response to a periopathogen.