Abu-Amer Yousef
Department of Orthopedic Research, Washington University School of Medicine, St Louis, MO 63110, USA.
Curr Drug Targets Immune Endocr Metabol Disord. 2005 Sep;5(3):347-55. doi: 10.2174/1568008054863808.
Osteoclasts are the sole bone resorbing cells. These cells are essential for skeletal development and remodeling throughout the life of animal and man. Deficiency of osteoclasts leads to osteopetrosis, a diseases manifested by increased non-remodeled bone mass, which ultimately leads to bone deformities and functional failure of other body systems. On the other hand, increased number and activity of osteoclasts under certain pathologic conditions causes accelerated bone resorption and may lead to osteoporosis and osteolytic diseases. To better understand the mechanisms underlying osteoclast-based diseases and design relevant therapies, one should unveil the molecular basis of osteoclast differentiation and function and regulatory mechanisms of osteoclast signaling. This review will outline up-to-date information regarding osteoclast differentiation and activation. Molecular mechanisms underlying osteoclast signaling pathways in inflammatory osteolysis and arthritis will be discussed. In addition, stimulators and inhibitors of osteoclasts, as well as current therapies for osteoclast activity will be addressed.
破骨细胞是唯一的骨吸收细胞。这些细胞对于动物和人类一生中的骨骼发育和重塑至关重要。破骨细胞缺乏会导致骨质石化症，这种疾病表现为未重塑的骨量增加，最终导致骨骼畸形和其他身体系统的功能衰竭。另一方面，在某些病理条件下，破骨细胞数量增加和活性增强会导致骨吸收加速，并可能导致骨质疏松症和溶骨性疾病。为了更好地理解破骨细胞相关疾病的潜在机制并设计相关治疗方法，人们应该揭示破骨细胞分化和功能的分子基础以及破骨细胞信号传导的调节机制。本综述将概述有关破骨细胞分化和激活的最新信息。还将讨论炎症性骨溶解和关节炎中破骨细胞信号通路的分子机制。此外，还将探讨破骨细胞的刺激剂和抑制剂，以及目前针对破骨细胞活性的治疗方法。
