Olstad K, Ytrehus B, Ekman S, Carlson C S, Dolvik N I
The Norwegian School of Veterinary Science, Department of Companion Animal Clinical Sciences, Section for Equine Medicine and Surgery, Oslo, Norway.
Equine Vet J. 2008 Jan;40(1):30-9. doi: 10.2746/042516407X239836.
Pathological changes in the blood supply to growth cartilage have been implicated in the pathogenesis of osteochondrosis (OC) in horses, but have not been reported using vascular perfusion techniques.
To describe the developmental pattern of cartilage canal vessels in the distal tibial epiphysis and talar growth cartilage of foals.
Nine foals bred from parents with OC were sacrificed between the ages of 0 and 7 weeks to undergo a barium perfusion procedure. The distal end of the tibia and the entire talus were cleared in methyl salicylate and perfused vessels studied in the intact bones. Slabs with a thickness of 4-5 mm from 3 predilection sites for OC were examined in the stereomicroscope and with light microscopy.
Cartilage canals were present for a limited period of growth. Perfused vessels initially entered canals from the perichondrium. Vessels in the proximal portion of canals retained their perichondrial arterial source throughout. With time, the ossification front advanced to incorporate the mid-portion of canals; and anastomoses formed between canal vessels and subchondral vessels. A shift occurred and vessels in the distal terminus of canals came to use subchondral vessels as their arterial source. Twelve histological lesions were found in 7 foals. All contained necrotic vessels surrounded by necrotic growth cartilage and 3 caused macroscopically visible delay in endochondral ossification. Lesions were located where vessels traversed the ossification front to enter the distal terminus of canals.
Cartilage canal vessels are particularly susceptible to failure at the point where they cross the ossification front, with consequences for the viability of those chondrocytes that depend on them.
A better understanding of how lesions of OC arise may improve the ability to identify, monitor, prevent and treat this disorder. Involvement of cartilage canals in the pathogenesis of equine tarsal OC plausibly explains several clinical features of this disease.
生长软骨血液供应的病理变化被认为与马骨软骨病(OC)的发病机制有关,但尚未有使用血管灌注技术的相关报道。
描述幼驹胫骨骺远端和距骨生长软骨中软骨管血管的发育模式。
对9匹父母患有OC的幼驹在0至7周龄时实施安乐死,进行钡剂灌注程序。将胫骨远端和整个距骨在冬青油中清理,并在完整骨骼中研究灌注血管。从OC的3个好发部位切取厚度为4 - 5毫米的薄片,在体视显微镜和光学显微镜下检查。
软骨管在有限的生长时期内存在。灌注血管最初从软骨膜进入软骨管。软骨管近端的血管始终保持其软骨膜动脉来源。随着时间推移,骨化前沿向前推进以包绕软骨管中部;软骨管血管与软骨下血管之间形成吻合。发生了转变,软骨管远端的血管开始以软骨下血管作为其动脉来源。在7匹幼驹中发现了12处组织学病变。所有病变均包含被坏死生长软骨包围的坏死血管,其中3处导致软骨内骨化出现肉眼可见的延迟。病变位于血管穿过骨化前沿进入软骨管远端的部位。
软骨管血管在穿过骨化前沿处特别容易出现功能障碍,这会对依赖它们的软骨细胞的生存能力产生影响。
更好地了解OC病变的发生方式可能会提高识别、监测、预防和治疗这种疾病的能力。软骨管参与马跗骨OC的发病机制,这可能合理地解释了该疾病的一些临床特征。