Norrdin R W, Kawcak C E, Capwell B A, McIlwraith C W
Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins 80523, USA.
Bone. 1998 Feb;22(2):133-9. doi: 10.1016/s8756-3282(97)00253-6.
Gross examination of metacarpo-/metatarsophalangeal (fetlock) joints from racehorses revealed defects on the condylar surface that ranged from cartilage fibrillation and erosion to focal cartilage indentations and cavitation in subchondral bone characteristic of traumatic osteochondrosis. Because these lesions represented a spectrum of mechanically induced arthrosis in which microdamage is thought to play a role, a histologic study of sagittal sections was made to study the morphogenesis. Subchondral bone failure developed beneath a flattened section of the condyle where the margin of the sesamoid bone produces compression as well as shear on impact of the foot with the ground. Milder lesions had thickening of subchondral bone and underlying trabeculae. With advancing sclerosis an increased amount of osteocyte necrosis was present. Occasional vascular channels with plugs of matrix debris and cells were present just beneath the cartilage. There was increased prominence of subchondral vessels, and osteoclastic remodeling was seen in and around the sclerotic zone. Apparent fragmentation lines in the subchondral bone suggested increased matrix fragility. Irregular trabecular microfractures developed at a depth of a few millimeters. Increased vascularity with hemorrhage, fibrin, and fibroplasia could be seen in enlarged marrow spaces at this more advanced stage. The overlying articular cartilage was variably indented but remained largely viable with degeneration and erosion limited to the superficial layers. Focally, breaks in the calcified layer appeared to lead to collapse and cartilage infolding. In metacarpal condyles from experimental horses run on a treadmill, there were milder changes at the site. The subchondral bone was increased in volume and there was increased diffuse staining with basic fuchsin, but no increase in the number of microcracks was seen. The findings in the racehorses indicate that the equine fetlock condyle is a consistent site of overload arthrosis in which microfracture and failure in subchondral bone may occur. Controlled exercise in treadmill horses may provide a model in which to study the pathogenesis.
对赛马掌指关节/跖趾关节（球节）进行大体检查发现，髁表面存在缺陷，范围从软骨原纤维形成和糜烂到软骨下骨的局灶性软骨凹陷和空化，具有创伤性骨软骨病的特征。由于这些病变代表了一系列机械性诱导的关节病，其中微损伤被认为起作用，因此对矢状切片进行了组织学研究以探讨形态发生过程。在髁的扁平部分下方发生软骨下骨破坏，籽骨边缘在足部与地面撞击时产生压缩以及剪切力。较轻的病变表现为软骨下骨和下方小梁增厚。随着硬化进展，骨细胞坏死数量增加。在软骨下方偶尔可见带有基质碎片和细胞栓子的血管通道。软骨下血管更加明显，在硬化区及其周围可见破骨细胞重塑。软骨下骨中明显的断裂线表明基质脆性增加。在几毫米深处出现不规则的小梁微骨折。在这个更晚期阶段，在扩大的骨髓腔中可见血管增多伴出血、纤维蛋白和纤维组织增生。上方的关节软骨有不同程度的凹陷，但在很大程度上仍保持存活，退变和糜烂仅限于表层。局部地，钙化层的断裂似乎导致塌陷和软骨折叠。在跑步机上奔跑的实验马的掌骨髁处，该部位的变化较轻。软骨下骨体积增加，碱性品红弥漫性染色增加，但未见微裂纹数量增加。赛马的研究结果表明，马球节髁是过载性关节病的一个一致部位，其中软骨下骨可能发生微骨折和破坏。跑步机上马的控制性运动可能提供一个研究发病机制的模型。
