Kapila S, Lee C, Tavakkoli Jou M R, Miller A J, Richards D W
Division of Orthodontics, Department of Growth and Development, School of Dentistry, University of California, San Francisco, 94143-0640, USA.
J Dent Res. 1995 Dec;74(12):1870-9. doi: 10.1177/00220345950740121001.
Children with juvenile rheumatoid arthritis or juvenile chronic arthritis often exhibit temporomandibular joint (TMJ) involvement accompanied by pain, dysfunction, and growth abnormalities. Despite the severe functional and developmental consequences of this disease, its pathogenesis remains poorly understood, but important insights may be provided by a suitable animal model of this disease. The purpose of this study was to develop and histologically characterize a juvenile animal model of antigen-induced arthritis of the TMJ. Arthritis was induced with an intra-articular administration of ovalbumin in previously sensitized 10-week-old male New Zealand white rabbits. Sham-treated and untreated rabbits were used as controls. The TMJs were retrieved en bloc at 5, 10, 15, 35, and 55 days post-challenge for histology and matrix histochemistry. Antigen-treated joints demonstrated severe arthritis, including mononuclear cell infiltration, synovial lining and villous hyperplasia, and pannus formation, as early as 5 days after challenge; the arthritis was maintained up to 55 days post-challenge. A decrease in the area of the TMJ disc that stained positively for glycosaminoglycans was observed throughout the experimental period. Loss of collagen staining was primarily localized to sites at the junction of the synovium with bone and fibrocartilage. The histopathologic features of this model of antigen-induced arthritis of the juvenile rabbit TMJ are similar to those observed previously in adult animal models of experimental arthritis and in human rheumatoid arthritis. This animal model will be useful for understanding the pathogenesis of juvenile rheumatoid arthritis of the TMJ, and for exploring the mechanisms for aberrant craniofacial growth.
患有幼年类风湿性关节炎或幼年慢性关节炎的儿童常常表现出颞下颌关节(TMJ)受累,并伴有疼痛、功能障碍和生长异常。尽管这种疾病会导致严重的功能和发育后果,但其发病机制仍知之甚少,但合适的该疾病动物模型可能会提供重要的见解。本研究的目的是建立并从组织学上表征幼年兔颞下颌关节抗原诱导性关节炎的动物模型。通过向先前致敏的10周龄雄性新西兰白兔关节腔内注射卵清蛋白来诱导关节炎。假处理和未处理的兔子用作对照。在激发后第5、10、15、35和55天整块取出颞下颌关节用于组织学和基质组织化学检查。抗原处理的关节在激发后5天就表现出严重的关节炎,包括单核细胞浸润、滑膜衬里和绒毛增生以及血管翳形成;关节炎持续到激发后55天。在整个实验期间,观察到糖胺聚糖染色阳性的颞下颌关节盘面积减小。胶原蛋白染色缺失主要局限于滑膜与骨和纤维软骨交界处。幼年兔颞下颌关节抗原诱导性关节炎模型的组织病理学特征与先前在实验性关节炎成年动物模型和人类类风湿性关节炎中观察到的特征相似。该动物模型将有助于理解颞下颌关节幼年类风湿性关节炎的发病机制,并有助于探索颅面生长异常的机制。