Kawaguchi Hiroshi
Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo.
Clin Calcium. 2009 Nov;19(11):1608-14.
Little is known about molecular mechanism underlying osteoarthrits. Recent mouse genetic approaches by others and us found that the proteinases produced during the endochondral ossification process cause cartilage degradation at the center of the joint and osteophyte formation at the periphery. The difference of the two sites may depend on the vascularity. At the periphery, vascularity is accessible from the synovium or tendon, which completes endochondral ossification and forms osteophytes, just as it does at the embryonic and growth plate cartilage. However, in the center, the vascularity is not accessible from the edge, so that it may end up with cartilage degradation without being replaced by bone. Molecules related to the endochondral ossification will be a therapeutic target of osteoarthritis.
关于骨关节炎的分子机制，人们了解甚少。最近，我们和其他人通过小鼠遗传学方法发现，软骨内骨化过程中产生的蛋白酶会导致关节中心的软骨降解和周边的骨赘形成。这两个部位的差异可能取决于血管分布。在周边，血管可从滑膜或肌腱进入，这完成了软骨内骨化并形成骨赘，就像在胚胎和生长板软骨中一样。然而，在中心部位，血管无法从边缘进入，因此可能最终导致软骨降解而无法被骨替代。与软骨内骨化相关的分子将成为骨关节炎的治疗靶点。
