Biological analyses of articular disk of temporomandibular joint and the adjacent tissues during growth and senescence.

下颌骨关节炎（OA）发病的分子基础尚未阐明。胶原和蛋白多糖在骨骺软骨和软骨下骨的维持以及其他骨的骨关节炎过程中具有重要的结构作用。在蛋白聚糖中，调节胶原原纤维形成的胶原结合小亮氨酸蛋白聚糖（slrp）可能参与了下颌OA的发病和过程。为了验证这一假设，我们使用衰老加速小鼠（SAM）研究了早期OA患者下颌髁突软骨中SLRP的糖胺聚糖（GAGs）的分布以及OA发病前下颌软骨下骨髓中SLRP基因的表达。硫酸软骨素-4 （C4S）和硫酸角蛋白（KS）分布不同；前者分布于软骨各层，而后者仅分布于软骨表面、纤维层和增殖细胞层。然而，一旦软骨出现裂缝，两种GAGs强烈分布在裂缝周围，提示C4S和KS可能在下颌OA软骨退行性变中起作用，它们的结构功能可能补偿退化的胶原网络。在下颌软骨下骨髓中，胶原结合slrp、decorin、biglycan、纤维调节蛋白和lumican的mRNA表达水平在SAMP8伴下颌OA和SAMR1无退行性髁突之间相等。在股骨软骨下骨髓中，biglycan在SAMP8中表达，而在SAMR1中不表达，这可能意味着下颌OA表型的SAMP8与SAMR1相比具有不同的骨质量。总的来说，尽管需要更多的分子生物学和生化分析，胶原结合的slrp可能参与软骨和骨的结构功能以及下颌OA的发生和发展。

Molecular basis of onset of mandibular osteoarthritis (OA) has not been elucidated. It is believed that collagens and proteoglycans have crucial structural roles in maintenance of epiphyseal cartilage and subchondral bone and in process of OA at the other bones. Among proteoglycans, collagen-binding small leucine rich proteoglycans (SLRPs) which regulate formation of collagen fibrils may be involved in the onset and the process of mandibular OA. To test this hypothesis, we investigate distribution of the glycosaminoglycans (GAGs) of SLRPs in mandibular condylar cartilage with an early stage of OA and expression of SLRP genes in mandibular subchondral bone marrow before the onset of OA using senescence-accelerated mice (SAM). Chondroitin-4 sulphate (C4S) and keratin sulphate (KS) had a different distribution ; the former was distributed throughout all layers of the cartilage but the latter was exclusively in the surface of cartilage, fibrous and proliferative cell layers. Once fissures appeared in the cartilage, the two GAGs was, however, strongly located around the fissures, suggesting that C4S and KS may have a role in degenerative cartilage of mandibular OA and that their structural functions possibly compensate those of degenerated collagen networks. In the mandibular subchondral bone marrows, mRNA expression levels of collagen-binding SLRPs, decorin, biglycan, fibromodulin, and lumican, were equivalent between SAMP8 with mandibular OA and SAMR1 with no degenerative mandibular condyles. In the femoral subchondral bone marrows, biglycan was expressed in SAMP8 but not in SAMR1, possibly implying that SAMP8 with mandibular OA phenotype has different bone quality compared with SAMR1. Collectively, although more molecular biological and biochemical analyses are needed, collagen-binding SLRPs may be involved in the structural functions of cartilage and bone and in the onset and the proceeding of mandibular OA.