CIA is a well-studied animal model of autoimmune arthritis. It resembles rheumatoid arthritis as far as histopathological changes and molecular pathogenesis are concerned. CIA is induced by immunization with collagen type II in susceptible strains. The purpose of this review is to assess the use of CIA animal model on bone metabolism and the potential therapeutic agents that could reverse this effect. A database search from their inception to 2019 was conducted to identify experimental animal studies pertinent to CIA model and bone examination. Studies including ovariectomy or without a direct comparison between control and CIA groups were excluded. Forty-eight articles were considered suitable for inclusion. Imaging techniques, biomechanical analysis, histopathological studies, and molecular biology techniques were employed. A decrease in bone mineral density in CII arthritic animals was established. Bone loss was either periarticular, generalized or both. Although trabecular bone loss was clear, the effect on cortical bone is yet to be determined. The proposed mechanism is an imbalance between bone formation and resorption as a result of osteoclast activation. The signal pathways implicated appear to be the RANKL/RANK/OPG and the Wnt pathway. Many therapeutic targets were investigated with promising results.

CIA是一种经过充分研究的自身免疫性关节炎动物模型。就组织病理学变化和分子发病机理而言，它类似于类风湿关节炎。通过在易感菌株中用II型胶原免疫来诱导CIA。这篇综述的目的是评估CIA动物模型在骨代谢上的应用以及可能逆转这种作用的潜在治疗剂。从开始到2019年进行了数据库搜索，以鉴定与CIA模型和骨骼检查有关的实验动物研究。排除包括卵巢切除术或未与对照组和CIA组直接比较的研究。四十八篇文章被认为适合列入。使用了成像技术，生物力学分析，组织病理学研究和分子生物学技术。已确定CII关节炎动物的骨矿物质密度降低。骨丢失是关节周围的，全身性的或两者兼有。尽管小梁骨丢失很明显，但对皮质骨的影响尚待确定。拟议的机制是破骨细胞活化导致骨形成与吸收之间的不平衡。暗示的信号途径似乎是RANKL / RANK / OPG和Wnt途径。对许多治疗靶标进行了研究，结果令人满意。暗示的信号途径似乎是RANKL / RANK / OPG和Wnt途径。对许多治疗靶标进行了研究，结果令人满意。暗示的信号途径似乎是RANKL / RANK / OPG和Wnt途径。对许多治疗靶标进行了研究，结果令人满意。