Ferrari S
Service des maladies osseuses, Département de réhabilitation et gériatrie, Faculté de médecine et HUG, Genève.
Rev Med Suisse. 2009 Jun 10;5(207):1325-8.
High bone remodeling leads to bone loss and microarchitectural deteriorations characteristic of osteoporosis. Bisphosphonates and selective estrogen receptor modulators decrease bone remodeling by preventing osteoclast-mediated bone resorption, whereas parathyroid hormone/teriparatide increase bone remodeling in favor of new bone formation. Better understanding of the molecular processes of bone remodeling has led to the development of agents to inhibit bone resorption, such as the human monoclonal antibody Denosumab targeting osteoclast-activating factor RANK Ligand, and odanacatib targeting the collagen-degrading enzyme cathepsin K. Agents capable to stimulate bone formation independently of bone resorption, such as antagonists of the osteoblast-inhibitory factor sclerostin, may provide new therapeutic approaches to osteoporosis.
高骨重塑会导致骨质流失以及骨质疏松所特有的微结构恶化。双膦酸盐和选择性雌激素受体调节剂通过阻止破骨细胞介导的骨吸收来减少骨重塑，而甲状旁腺激素/特立帕肽则增加骨重塑以促进新骨形成。对骨重塑分子过程的更好理解促使了抑制骨吸收药物的开发，例如靶向破骨细胞激活因子RANK配体的人单克隆抗体地诺单抗，以及靶向胶原蛋白降解酶组织蛋白酶K的odanacatib。能够独立于骨吸收刺激骨形成的药物，例如成骨细胞抑制因子硬化蛋白的拮抗剂，可能为骨质疏松症提供新的治疗方法。
