Sharawy M M, Helmy E S, Bays R A, Larke V B
Department of Oral Biology, School of Dentistry, Medical College of Georgia, Augusta 30912.
J Oral Maxillofac Surg. 1994 Mar;52(3):259-70; discussion 270-1. doi: 10.1016/0278-2391(94)90296-8.
Previous studies have demonstrated that experimentally produced perforations in the discs of Macaca fascicularis monkeys lead to osteoarthrosis. Synovial membrane hyperplasia also was demonstrated in monkey and human joints with disc perforations. The hypothesis was advanced that a synovial flap obtained from within the affected joint would be the most appropriate tissue to repair chronic disc perforation. To test this hypothesis, four adult M fascicularis monkeys were anesthetized and 4- to 6-mm perforations were made in the posterolateral aspects of the avascular discs bilaterally. The wounds were sutured leaving the perforations open, and the animals were fed their normal diet. After 4 weeks, one joint in each monkey was reopened and a repair was performed using a double-layered flap from the synovial lining of the superior and inferior recesses. Four weeks after repair, the animals were killed and the temporomandibular joints (TMJs) were removed en bloc and decalcified. The joints were sectioned into lateral, middle, and medial sections and were photographed using a stereomicroscope and then processed for light and electron microscopy. The same processing was done to four intact joints that were used as controls. Eight weeks following perforation, the joint components showed degenerative changes consistent with osteoarthritis. Close to the perforations the disc showed loss of collagen, vacuolation of extracellular matrix, accumulation of dense proteoglycan-like material, and the appearance within the disc of type A or macrophage-like cells of the synovium. The discal tissue away from the perforation showed high cellularity and vascularity. The temporal and condylar surfaces showed denudation, fibrillation, osteophytes, and chondrocytic clustering, all characteristics of osteoarthrosis. The surgically repaired discs were intact and the articular surfaces showed no degenerative changes. Discal collagen was restored and appearance of myofibroblasts and elastogenesis were a consistent feature of the repaired disc. The vascularity of the condylar cartilage of the repaired joints appeared similar to that of embryonic cartilage. The reversibility of the degenerative alterations following discal repair in this experimental model should provide the basis for a rational and useful method for surgical repair of TMJ disc perforation using intraarticular synovial tissue.
先前的研究表明,在食蟹猴的椎间盘上进行实验性穿孔会导致骨关节炎。在有椎间盘穿孔的猴和人类关节中也证实了滑膜增生。有人提出假说,认为取自受影响关节内部的滑膜瓣是修复慢性椎间盘穿孔最合适的组织。为了验证这一假说,对4只成年食蟹猴进行麻醉,在双侧无血管椎间盘的后外侧制造4至6毫米的穿孔。伤口缝合后让穿孔保持开放,动物喂食正常饮食。4周后,每只猴子的一个关节重新打开,使用来自上、下隐窝滑膜衬里的双层瓣进行修复。修复后4周,处死动物,将颞下颌关节(TMJ)整块取出并脱钙。关节被切成外侧、中间和内侧部分,用体视显微镜拍照,然后进行光镜和电镜处理。对4个完整的关节进行同样的处理作为对照。穿孔8周后,关节组件出现了与骨关节炎一致的退行性变化。靠近穿孔处,椎间盘显示胶原蛋白丢失、细胞外基质空泡化、致密蛋白聚糖样物质积聚,以及滑膜A型或巨噬细胞样细胞出现在椎间盘内。远离穿孔的椎间盘组织显示细胞增多和血管增多。颞骨和髁突表面出现剥脱、纤维化、骨赘和软骨细胞聚集,这些都是骨关节炎的特征。手术修复的椎间盘完整,关节表面未显示退行性变化。椎间盘胶原蛋白得以恢复,成肌纤维细胞的出现和弹性生成是修复后椎间盘的一个一致特征。修复关节的髁突软骨的血管分布与胚胎软骨相似。在这个实验模型中,椎间盘修复后退行性改变的可逆性应为使用关节内滑膜组织手术修复颞下颌关节盘穿孔提供一种合理且有用的方法的基础。