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下颌骨髁突骨关节炎中的软骨-骨界面僵硬。

Osteochondral Interface Stiffening in Mandibular Condylar Osteoarthritis.

机构信息

1 State Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Diseases & Shaanxi International Joint Research Center for Oral Diseases, Department of Oral Anatomy and Physiology and TMD, School of Stomatology, the Fourth Military Medical University, Xi'an, China.

2 Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, Department of Implant Dentistry, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.

出版信息

J Dent Res. 2018 May;97(5):563-570. doi: 10.1177/0022034517748562. Epub 2018 Jan 3.

DOI:10.1177/0022034517748562
PMID:29298566
Abstract

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.

摘要

颞下颌关节(TMJ)的骨关节炎(OA)与牙齿生物力学有关。OA 进展过程中的主要变化是骨软骨界面的骨化。本研究调查了早期骨软骨界面的形成、放射学可检测性和力学特性,其在 OA 进展中的发病机制意义对 TMJ 具有临床意义,但仍不清楚。如前所述,我们对 6 周龄大鼠进行单侧前牙反颌(UAC)。4、12 和 20 周时收获 TMJ。使用改良的骨关节炎研究协会国际(OARSI)评分系统评估 TMJ OA 的进展。通过 von Kossa 染色组织切片和 calcein 注射测量体内钙沉积来量化厚度,从而研究骨软骨界面。通过微计算机断层扫描(CT)对组织骨化进行成像。使用动态压痕在纳米尺度测量力学性能。UAC 治疗可诱发 TMJ 软骨病变的时间依赖性。UAC TMJ 中明显出现髁突头的几何变化和 OARSI 评分的增加。在骨软骨界面,不仅深层软骨钙化增强,而且骨边界也有钙沉积。骨软骨界面的厚度、密度和刚度均显著增加。骨软骨界面的增强骨化是上区异常深层软骨钙化和下区促发软骨下皮质骨形成的关节结果。因此,早期微 CT 可检测到的骨化具有诊断意义。尽管由于界面的刚度,软骨和软骨下骨的环境可能会发生变化,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,骨软骨界面可能成为 TMJ 机械性引发 OA 的新的诊断和治疗靶点。

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