Nouveaux marqueurs biologiques du remodelage osseux dans l’ostéoporose

Abstract

Current biological markers of bone turnover have proven useful in improving fracture risk assessment and monitoring treatment efficacy in postmenopausal osteoporosis. Progress in the characterization of important biological pathways regulating bone cell activity and the organic components of bone matrix has led to the development of new biochemical markers. These include the non collagenous protein, bone sialoproteine, the resorption-mediated osteocalcin fragments, the osteoclastic enzymes (isoenzyme 5b of tartrate-resistant acid phosphatase and cathepsin K), the regulators of osteoclastic (osteoprotegerine, RANK-L) and osteoblastic (Wnt signaling molecules) activity and the post-translational modifications of matrix molecules. One of the most interesting developments has been the demonstration that the non-enzymatic modifications of bone collagen, including glycation-mediated crosslinks and the isomerization of aspartic acid, contribute to fracture resistance independent of bone mineral density (BMD). Systemic levels of the glycated crosslink pentosidine and the urinary ratio between native (αCTX) and isomerized (βCTX) type I collagen C-telopeptide are associated with fracture risk in postmenopausal women independent of BMD and may respond differently to the different anti-resorptive therapies and parathyroid hormone. The identification of bone-specific post-translational modifications of bone matrix proteins that influence bone fracture resistance should lead to the development of new biological markers that will be useful in assessing the contribution of changes in bone matrix properties to fracture risk in untreated and treated patients with osteoporosis.