Burr D B
Department of Anatomy, Indiana University School of Medicine, Indianapolis 46202, USA.
Curr Opin Rheumatol. 1998 May;10(3):256-62. doi: 10.1097/00002281-199805000-00017.
This article reviews evidence that subchondral bone plays a role in the degeneration of cartilage in osteoarthrosis. Whether the bony changes precede the cartilage degeneration remains unproven but may best be considered necessary for progression of the disease. Epidemiologic studies clearly show increasing subchondral sclerosis with disease progression. Recent evidence demonstrates specific architectural changes in the subchondral trabecular bone in osteoarthrosis that are consistent with an acceleration of bone turnover, which appears to be a part of the pathophysiologic process in progression of the disease. The now well-documented acceleration of bone turnover in osteoarthrosis decreases the stiffness of the bone as a material, but because of structural modifications in both trabecular bone (i.e., increased trabecular number and reduced separation) and subchondral bone (i.e., increased plate thickness), the stiffness (rigidity) of the structure as a whole undoubtedly increases. There is no evidence that growth factors, cytokines, or enzymes play any role in the bony changes associated with the disease, other than as the naturally occurring sequelae of normal bone remodeling processes.
本文综述了有关软骨下骨在骨关节炎软骨退变中起作用的证据。骨改变是否先于软骨退变尚未得到证实,但可能最好被视为疾病进展所必需的。流行病学研究清楚地表明,随着疾病进展,软骨下骨硬化加剧。最近的证据显示,骨关节炎中软骨下小梁骨存在特定的结构变化,这与骨转换加速一致,而骨转换加速似乎是疾病进展病理生理过程的一部分。目前已充分证明,骨关节炎中骨转换加速会降低骨作为一种材料的硬度,但由于小梁骨(即小梁数量增加和间距减小)和软骨下骨(即板层厚度增加)的结构改变,整个结构的硬度(刚性)无疑会增加。没有证据表明生长因子、细胞因子或酶在与该疾病相关的骨改变中起任何作用,除非是作为正常骨重塑过程的自然后续结果。