Osteochondral Interface Stiffening in Mandibular Condylar Osteoarthritis
Osteochondral Interface Stiffening in Mandibular Condylar Osteoarthritis
复制标题
下颌髁突骨关节炎的骨软骨界面硬化
DOI：
10.1177/0022034517748562
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发表时间：
2018-05-01
影响因子：
7.6
通讯作者：
Wang, M.
中科院分区：
文献类型：
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作者：
Zhang, J.;Liao, L.;Wang, M.
颞下颌关节骨关节炎（OA）与牙体生物力学有关。OA进展过程中的一个主要变化是骨软骨界面的骨化。本研究调查了骨软骨界面的形成、放射学可检测性和早期机械性能，其在OA进展中的发病机制意义具有临床意义，但对于TMJ仍然难以理解。单侧前牙反牙合（UAC）进行6周龄大鼠，如我们以前报道。分别于术后4、12、20周取材。使用改良的国际骨关节炎研究协会（OARSI）评分系统评估TMJ OA的进展。通过组织切片的von Kossa染色和通过钙黄绿素注射的体内钙沉积来定量厚度，研究骨软骨界面。通过显微计算机断层扫描（CT）对组织骨化进行成像。使用动态压痕在纳米尺度下测量机械性能。时间依赖性TMJ软骨病变引起的UAC治疗。UAC TMJ的髁状突头几何形状改变和OARSI评分值增加明显。在骨软骨界面处，不仅有增强的深层软骨钙化，而且在骨边界处有钙沉积。骨软骨界面的厚度、密度和刚度均显著增加。骨软骨界面骨化增强是上级区域异常深层软骨钙化和促进下部区域软骨下皮质骨形成的联合结果。因此，从早期阶段的micro-CT检测骨化具有诊断意义。虽然界面的刚度会改变软骨和软骨下骨的环境，但界面的刚度是否会加速OA的进展仍有待证实。有了这些证据，骨软骨界面可能是一个新的诊断和治疗的目标，机械引发的OA在颞下颌关节。
Osteoarthritis (OA) of the temporomandibular joint (TMJ) is associated with dental biomechanics. A major change during OA progression is the ossification of the osteochondral interface. This study investigated the formation, radiological detectability, and mechanical property of the osteochondral interface at an early stage, the pathogenesis significance of which in OA progression is of clinical interest and remains elusive for the TMJ. Unilateral anterior crossbite (UAC) was performed on 6-wk-old rats as we previously reported. TMJs were harvested at 4, 12, and 20 wk. The progression of TMJ OA was evaluated using a modified Osteoarthritis Research Society International (OARSI) score system. Osteochondral interface was investigated by quantifying the thickness via von Kossa staining of histological slices and in vivo calcium deposition by calcein injection. Tissue ossification was imaged by micro–computed tomography (CT). Mechanical properties were measured at nanoscale using dynamic indentation. Time-dependent TMJ cartilage lesions were elicited by UAC treatment. Geometric change of the condyle head and increased value of the OARSI score were evident in UAC TMJs. At the osteochondral interface, there was not only enhanced deep-zone cartilage calcification but also calcium deposition at the osseous boundary. The thickness, density, and stiffness of the osteochondral interface were all significantly increased. The enhanced ossification of the osteochondral interface is a joint outcome of the aberrant deeper cartilage calcification at the superior region and promoted formation of subchondral cortical bone at the inferior region. The micro-CT detectable ossification from an early stage thus is of diagnostic significance. Although the environment of the cartilage and subchondral bone could be changed due to the stiffness of the interface, whether or not the stiffened interface would accelerate OA progress remains to be confirmed. With that evidence, the osteochondral interface could be a new diagnostic and therapeutic target of the mechanically initiated OA in the TMJ.