β1型整合素在兔颞下颌关节骨关节病组织中的表达变化

目的：探讨颞下颌关节骨关节病发展过程中B1型整合素的作用。方法：通过手术方法制备兔颞下颌关节盘穿孔,在手术后第1、5周取颞下颌关节标本,观察β1型整合素的表达。结果：在颞下颌关节骨关节病的早期,随着髁突软骨细胞和滑膜细胞的增殖,β1型整合素的表达增强,而到了后期随着髁突软骨和滑膜细胞的减少,β1型整合素的表达显著降低。结论：131型整合素在颞下颌关节骨关节病过程中的表达随着疾病的发展程度而变化,在疾病的发展中具有一定的作用。     

无牙颌对兔颞下颌关节影响的组织病理学观察

目的:探讨在无牙颌状态下颞下颌关节的组织学改变。方法:将14只健康成年新西兰白兔等量分为7组,其中1组为对照组,其余6组为实验组。实验组动物在全麻下一次性拔除全口牙齿,使其成为无牙颌状态,分别于术后1、2、4、8、16周和26周将实验动物麻醉过量致死后,将双侧颞下颌关节完整取出,进行组织学观察。结果:实验组动物的髁状突纤维层疏松、玻璃样变性,纤维间的间隙增宽,表面粗糙;增殖层、肥大层和钙化软骨层均变薄或消失;骨髓腔内有灶性出血及显微骨折现象;关节盘纤维间间隙增宽,表面有断裂现象,关节盘软骨细胞灶性增多或聚集;关节盘与髁状突发生粘连。结论:牙列缺失后颞下颌关节发生退行性改变,从而支持无牙颌与颞下颌关节紊乱病有关。     

兔颞下颌关节盘前移位后关节软骨细胞的凋亡及其意义

目的　观察颞下颌关节盘前移位动物模型的关节软骨细胞凋亡动态改变 ,探讨软骨细胞凋亡的意义。方法　日本大白兔 2 6只 ,实验组 2 0只行手术 ,在不打开颞下颌关节囊的情况下制成关节盘前移位动物模型 ,采用原位末端标记法 (TUNEL)观察术后不同病变时期关节区组织学的改变和软骨细胞凋亡的情况。结果　术后 1～ 2周为髁突软骨细胞凋亡的高峰期 ,集中于功能区的肥大层和增殖层。 4～ 6周进入关节改建期。结论　关节盘前移位后可激活软骨细胞的凋亡机制 ,启动关节软骨的适应性改建     

颞下颌关节骨关节病髁突软骨细胞及基质合成代谢特性的研究

目的 探讨颞下颌关节骨关节病(TMJOA)软骨细胞的细胞生物学特性。方法 通过手术切除部分关节盘的方法,制造TMJOA的兔动物模型;从模型动物处于骨关节病病变增殖修复期的髁突软骨组织中获取细胞体外培养,并采用RT-PCR法比较病变软骨细胞与正常对照细胞对软骨基质蛋白、基质胶原酶和内源性生长因子的表达差异。结果 从TMJOA模型的髁突软骨组织中获得细胞经体外培养、鉴定,确认为软骨细胞;骨关节病髁突软骨细胞对软骨基质蛋白的表达不平衡,对内源性基质胶原酶的表达水平和内源性生长因子TGF-β1、IGF-1的表达明显增强。结论 本研究从细胞生物学角度证实了骨关节病早期关节软骨内出现合成代谢活跃的组织学特点,并发现该阶段组织细胞的修复代偿反应可致软骨基质成分合成的不平衡,最终可导致软骨基质环境改变。     

颞下颌关节疾病

正颌外科治疗颞下颌关节强直伴阻塞性睡眠呼吸暂停综合征，颞下颌关节骨关节病髁突软骨细胞及基质合成代谢特性的研究，颞下颌关节滑膜软骨瘤病：病例报告及文献复习，间接性颞下颌关节创伤动物模型的建立，经眶持续牵引颞下颌关节盘前移位动物模型的评价     

颞下颌关节软骨损伤治疗的进展

颞下颌关节(temporomandibular joint,TMJ)软骨损伤主要是指髁突和关节结节功能面的软骨损伤。病因复杂,表现为软骨内软骨细胞含量较低且增殖能力差,若治疗不当或治疗不及时,极易形成颞下颌关节病(temporomandibular disorder,TMD),最终出现不可扼制的逐步恶化,导致颞下颌关节骨关节病(temporomandibular joint osteoarthritis,TMJOA)的发生,以及关节功能的丧失。本文就其国内外研究现状及现有的治疗手段和疗效评价进行综述。1颞下颌关节软骨的解剖生理特点TMJ软骨主要分布于髁突和关节结节的表面,是继发性纤维软骨,组织学特点与其他…     

颞下颌关节骨关节病动物模型的建立及组织病理学观察

目的 建立稳定的颞下颌关节骨关节病动物模型。方法 通过外科手术切除部分关节盘的方法，在成年兔上建立较为稳定的颞下颌关节骨关节病动物模型；分别于术后第15天、1个月、2个月、3个月、4个月、5个月和6个月将实验兔处死，取实验侧髁突组织进行组织病理学观察；1％甲苯胺蓝染色，观察病变髁突组织中蛋白多糖的分布范围与水平变化。结果 本研究中的颞下颌关节骨关节病模型从组织病理学上先后观察到了关节盘损伤后早期关节软骨的应激性修复增殖，中期软骨基质渐进性损耗，后期软骨基质损耗丧失、纤维组织修复覆盖及骨赘形成等软骨退行性变过程。甲苯胺蓝染色显示，病变早期肥大增厚的软骨组织中蛋白多糖含量降低，且分布不均匀；病变晚期的髁突较深层软骨组织中仍可见有蛋白多糖的合成与分布。结论 本研究所建立的颞下颌关节骨关节病动物模型能较好地模拟骨关节病的组织病理学变化过程，且具有结果稳定、可重复性好的优点。     

颞下颌关节盘前移位和穿孔的关节内窥镜研究

目的 :探讨颞下颌关节内窥镜下颞下颌关节盘移位和关节盘穿孔的病理改变特征。方法 :76例 84侧临床诊断为颞下颌关节盘前移位以及关节盘穿孔的病例进行颞下颌关节内窥镜检查。结果 :可复性关节盘前移位的病例出现滑膜炎 ,关节腔内有絮状物 ,关节结节表面有纤维形成。不可复性关节结节表面纤维形成 ,关节软骨软化 ,软骨剥脱 ,同时伴有纤维粘连。关节盘穿孔大多数位于双板区与后带。关节盘穿孔出现滑膜增生 ,关节窝及关节结节表面纤维形成 ,软骨剥脱甚至骨质暴露。结论 :关节内窥镜检查可诊断关节盘前移位与关节盘穿孔 ,并能发现病理性改变 ,如滑膜炎 ,滑膜增生 ,纤维变性 ,软骨软化 ,关节内粘连等。在不可复性盘前移位病例中发现关节退行性改变 ,关节盘穿孔为严重的骨关节病。     

兔颞颌下关节盘前移位后关节软骨细胞的凋亡及其意义

目的：观察颞下颌关节盘前位动物模型的关节软骨细胞凋亡动态改变，探讨软骨细胞凋亡的意义。方法：日本大白兔26只，实验组20只行手术，在不打开颞下颌关节囊的情况下制成关节盘前移位动物模型，采用原位末端标记法（TUNEL）观察术后不同时期关节区组织学的改变和软骨细胞凋亡的情况。结果：术后1－2周为髁状软骨细胞凋亡的高峰期，集中于功能区的肥大层和增殖层。4－6周进入关节改建期。结论：关节盘前移位后可激活软骨细胞的凋亡机制，启动关节软骨的适应性改建。     

HGF基因转染软骨细胞治疗兔颞下颌关节骨关节病的研究

目的 建立兔颞下颌骨关节病动物模型,观察携带有GFP-HGF cDNA基因体外转染兔髁突软骨细胞后对兔颞下颌骨关节病的治疗效果。方法 以Ⅱ型胶原酶进行颞下颌关节腔内注射,建立颞下颌骨关节病动物模型。取兔髁状突软骨细胞体外进行培养与增殖,第2代软骨细胞进行GFP-HGFcDNA转染。将收集的转染后的软细胞进行动物模型关节腔内注射,并与对照组(空白质粒组)比较,通过组织切片观察治疗效果。结果 兔颞下颌关节经两次法注射胶原酶可在2周时出现偏侧咀嚼症状;动物模型显示转染细胞可促进关节损伤的修复,促进愈合。结论 转染HGF的软骨细胞可促进颞下颌骨关节病的愈合。     

The immunolocalisation of VEGF in the articular cartilage of sheep mandibular condyles.

INTRODUCTION: Vascular endothelial growth factor (VEGF) has recently been found to be essential for hypertrophic chondrocyte apoptosis and angiogenesis at the growth plate of long bones, indicating a central role in endochondral ossification. VEGF has more recently, also been shown to be expressed in articular cartilage chondrocytes in human osteoarthritic and rheumatoarthritic joints but not healthy adult joints. To investigate the role of VEGF in the fibrocartilage of the temporomandibular joint, this study aimed to document the presence and distribution of VEGF in the condylar articular cartilage of sheep temporomandibular joints. METHODS: Mandibular condyles of the temporomandibular joints of five 18-month old Wether sheep were fixed, decalcified, paraffin embedded and sectioned. The sections were analyzed using immunohistochemistry for VEGF. RESULTS: VEGF was found to be localised predominantly to the proliferative and maturing layers of chondrocytes in the condylar fibrocartilage of the temporomandibular joints. Articular cartilage is an avascular and alymphatic tissue. As such, the localisation of VEGF to the articular cartilage of normal temporomandibular joint condyles suggests a role for VEGF other than angiogenesis. CONCLUSION: VEGF is shown here for the first time to be present in mandibular condylar cartilage, leading us to propose a possible role in non-angiogenic extracellular matrix remodeling.     

Ultrastructure of the articular cartilage of the mandibular condyle: aging and degeneration

To obtain more insight into the pathogenesis of osteoarthrosis of the temporomandibular joint, we examined the ultrastructure of articular cartilage of six healthy and sixteen osteoarthrotic human mandibular condyles. Ultrastructural changes due to aging and osteoarthrosis are described and compared with the findings of other ultrastructural studies of articular cartilage of synovial joints. Aging was accompanied by some slight degenerative signs. Osteoarthrotic hyaline cartilage and fibrocartilage showed a striking similarity. The only ultrastructural difference was the presence of elastic fibers in the latter. Therefore, both seem to have the same pathogenesis. Several current statements on the pathogenesis of osteoarthrosis are discussed.     

Expression of matrix metalloproteinase-2 in osteoarthritic fibrocartilage from human mandibular condyle

Matrix metalloproteinase (MMP)-2 is expressed in osteoarthritic cartilage and synovial fluid and is thought to be involved in the degradation of cartilage extracellular matrix. However, MMP-2 expression and osteoarthritic changes in internal derangement of the temporomandibular joint are unknown. In the present study, we have examined the histological relationship between osteoarthritic changes on articular cartilage with or without articular disc perforation, and MMP-2 expression, in 85 mandibular condyles from cadavers. The expression and tissue immunolocalization of MMP-2 in fibrocartilages from these condyles was examined histochemically. The Mankin grade of histological criteria for specimens with disc perforation was significantly higher than that of specimens without perforation. MMP-2 immunostaining was positive in the cytoplasm of chondrocytes and in their surrounding matrix. There was a linear correlation between MMP-2-positive cell rates and Mankin grade. Our data suggest that MMP-2 plays an important role in fibrocartilage degradation in internal derangement of the temporomandibular joint.     

Dissertations 25 years after date 28. Degenerative diseases of the temporomandibular joint

In 1985, the dissertation 'Temporomandibular joint. Articular cartilage structure and function' was published. Much was known at the time concerning the (clinical) pathogenesis of osteoarthrosis of the temporomandibuIar joint, the associated radiographical characteristics and the results of non-surgical treatment. Little was known, however, concerning the processes that lead to the loss of bone tissue and other degenerative changes. The current idea that osteoarthrosis was histopathologically characterized by defects in the joint surfaces did not seem to apply to temporomandibular joints. In temporomandibular joints, the phenomenon was recognized of degenerative changes in the deeper layers of the articular cartilage and the subchondral bone, while the articular surface could be microscopically intact. A dislocated articular disc was seen as part of the disease osteoarthrosis. Clear insight into the origins of osteoarthrosis was not achieved.     

Osteoarthritis of the temporomandibular joint: a light microscopic and scanning electron microscopic study of the articular cartilage of the mandibular condyle

The aim of this study was to investigate the organization of collagen fibrils and the histopathologic alterations as well as the morphologic aspects of osteoarthritic articular cartilage of the human mandibular condyle. Nine osteoarthritic condyles, three obtained at necropsy and the other six during surgery, were examined by light microscopy and scanning electron microscopy. Light microscopic observations revealed features of progressive and regressive remodeling and the presence of clefts. Scanning electron microscopic observations showed the presence of thick, coiled fibrils at the joint surface and numerous osmiophilic lipid globules scattered between the collagen fibrils. The collagen fibrils were disordered. It was concluded that collagen fiber network disintegration and fatty degeneration comprise the osteoarthritic changes of the articular cartilage of the human mandibular condyle.     

Temporomandibular joint: surgically created disk displacement causes arthrosis in the rabbit.

To document a causal relationship between temporomandibular joint disk displacement and arthrosis, the disk was surgically displaced in one temporomandibular joint in each of three rabbits. The rabbits were sacrificed after 4 weeks and the mandibular condyles were studied radiographically and histologically. All three joints that underwent disk displacement had radiographic and histologic evidence of arthrosis, which included erosion of the bone, irregularity and fissure formation of the articular soft tissue cover, disruption of the subchondral layer of cartilage cells, and chondrocyte proliferation. No radiographic or histologic changes occurred in the joints that were untouched. The results suggest that surgically created disk displacement can cause arthrosis in the temporomandibular joint of the rabbit.     

Microscopic changes in the condyle and disc in response to distraction osteogenesis of the minipig mandible.

PURPOSE: Unilateral mandibular distraction osteogenesis (DO) has been shown to cause gross changes in the mandibular condyle and articular disc. The purpose of this study was to correlate histologic findings with these gross changes in a minipig distraction model. MATERIALS AND METHODS: Semiburied distractors were placed via submandibular incisions in 15 minipigs. Two unoperated animals served as controls. The protocol consisted of 0-day latency and rates of 1, 2, or 4 mm/day for a 12-mm gap. After the minipigs were killed (at 0, 24, or 90 days), ipsilateral and contralateral condyles and discs were harvested, decalcified, prepared for standard paraffin embedding, and evaluated to determine changes in 1) morphology and thickness of the articular cartilage and subchondral bone and 2) morphology of the disc. RESULTS: In control animals, there were no degenerative changes in the articular cartilage and underlying condylar bone; there were no significant differences in the mean articular cartilage thickness. The temporomandibular joint discs were normal. In experimental animals, distracted condyles showed increasing degenerative changes and mean articular cartilage thickness as the DO rate increased. The discs were thinner. These changes were present, but to a lesser degree, in the contralateral condyles. After 90 days, degenerative changes in the condyles and discs were reduced, after remodeling, except in the 4 mm/day DO group. CONCLUSIONS: Histologic changes in the condyles and temporomandibular joint discs in response to mandibular DO correlated with previously reported gross changes. These changes were greater at higher distraction rates and remodeling back to normal occurred in mandibular condyles distracted at 1 mm/day.     

An experimental model of osteoarthrosis of the temporomandibular joint in monkeys

The purpose of this study was to develop a model of osteoarthrosis of the temporomandibular joint in monkeys, which is remarkably similar in structure and function to that of humans. Nine juvenile monkeys, two as controls and seven as an experimental group, were used in this study. In the experimental group, the articular eminence on both sides was surgically made steeper. Two animals were killed at 1 week, four at 6 months, and one at 1 year postoperatively and the temporomandibular joints were examined macroscopically and microscopically. Typical changes of osteoarthrosis were observed in the 6-month and 1-year specimens. These comprised clustering of chondrocytes which resulted in vertical and horizontal splitting in the articular cartilage, and fibrillation of the articular surface resulting in fibrous union in the joint cavity. These degenerative changes advanced progressively over time. Slight anterior displacement and degenerative changes in the articular disc were also seen.