Dentin matrix metalloproteinases (MMPs) are involved in collagen degradation of resin-dentin interfaces. This study evaluated if collagen degradation can be prevented by chlorhexidine after different dentin demineralization procedures. Human dentin demineralization was performed with phosphoric acid (PA), EDTA, or acidic monomers (ClearfilSEBond and XENOV). Specimens were stored (24 h, 1 wk or 3 wk) in the presence or absence of chlorhexidine. In half of the groups, active MMP-2 was incorporated into the storing solution. C-terminal telopeptide determination (ICTP) was performed in the supernatants. Collagen degradation was higher in PA and EDTA-demineralized dentin. Chlorhexidine reduced collagen degradation in these groups only for 24 h. When dentin was demineralized with SEBond or Xeno, collagen degradation was reduced up to 30%, but addition of exogenous MMP-2 significantly increased collagen degradation. In self-etchant treated dentin the inhibitory effect of chlorhexidine on MMPs lasted up to 3 wk. Treating dentin with EDTA, PA or self-etching agents produces enough demineralization to permit cleavage of the exposed collagen. Monomers infiltration may exert protection on demineralized collagen, probably through immobilization of MMPs. The partial inhibitory action of CHX on MMP activity produced by self-etching adhesives was prolonged compared to the short-acting in PA or EDTA-treated dentin.

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Regulation of osteoclastic activity is critical for understanding bone loss associated with the postmenopausal period. In vitro and animal studies have revealed the role of OPG as a decoy receptor that neutralizes the effect of RANKL on the differentiation and activation of osteoclasts. However, the role of the OPG-RANKL system in postmenopausal osteoporosis is controversial. Thus, the aim of this study was to investigate the relationship among circulating levels of OPG, RANKL, bone turnover markers (BTM), bone mineral density (BMD) and vertebral fractures in postmenopausal women. We determined anthropometric parameters, circulating OPG and RANKL, BTM, estradiol, BMD by dual X-ray absorptiometry at the lumbar spine (LS) and femoral neck (FN), and pre-existing vertebral fractures in 206 ambulatory postmenopausal women of a mean age of 62 years (SD 7). Circulating OPG was significantly related to age (r =0.158; P =0.023), years since menopause (r =0.167; P =0.016) and BMD (LS Z-score: r =0.240; P =0.001, FN Z-score: r =0.156; P =0.025). Over half of the women had undetectable RANKL (n =113; 54.9%). There were no significant differences in clinical variables, BTM or BMD among women with detectable vs. undetectable RANKL. OPG was found to be independently associated with osteoporosis (OR: 2.9, 1.4-5.9) and prevalent vertebral fractures (OR: 2.5, 1.2-5.4). We conclude that serum OPG levels are independently associated with bone mass and prevalent vertebral fractures in postmenopausal women.

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