We conclude that leptin, in synergy with pro-inflammatory stimuli (IL-1 and the TLR-2 agonist pam2CSK4) selectively enhances MMP-1 and MMP-3 secretion in HGFs and suggest that gingival fibroblast-mediated ECM degradation, may be deleteriously enhanced during conditions of hyperleptinaemia (e.g. obesity, type 2 diabetes mellitus, exogenous leptin therapy). This evidence concerns the gene TLR2 and diabetes mellitus.