Inflammatory bowel disease (IBD) is a relapsing chronic idiopathic inflammatory condition. The increased risks of fractures in the spine and decreased BMD at all weight-bearing skeletal sites have been reported in IBD patients. The understanding of the mechanisms of IBD-induced bone loss is far from complete. Appropriate animal models are a prerequisite for studying IBD-induced bone loss, which prompted us to undertake quantitative meta-analyses by pooling data from the available IBD models that assessed various bone parameters. Sufficient data for meta-analysis are obtained from chemically- but not genetically induced models. Among the chemically induced models, only the effects of dextran sulfate sodium (DSS) and 2,4,6-trinitrobenzene sulfonic acid (TNBS) on bone parameters have been reported. Meta-analysis showed that both DSS (Hedge’s g = 2.124, p = 0.001) and TNBS (Hedge's g = 6.292, p = 0.000) increased inflammatory disease severity. In pooled analysis, bone volumes in femur (Hedge's g = − 3.42, p = 0.000) and tibia (Hedge's g = − 2.49, p = 0.000) showed significant losses upon DSS administration. Similarly, bone formation rate was significantly reduced upon IBD induction (Hedge’s g = − 3.495, p = 0.006). Besides, cortical thickness was reduced and trabecular microstructure deteriorated by IBD induction. Insufficient data precluded us from determining the effect of IBD on bone strength and calciotropic hormones, as well as the impact of proinflammatory cytokines on bone turnover. This meta-analysis showed that IBD induction in rodents causes significant bone loss. Impaired osteoblast function appears to be the cause of this impact.

炎症性肠病 (IBD) 是一种复发性慢性特发性炎症性疾病。据报道，IBD 患者的脊柱骨折风险增加，所有负重骨骼部位的 BMD 降低。对 IBD 引起的骨质流失机制的了解还远未完成。适当的动物模型是研究 IBD 引起的骨质流失的先决条件，这促使我们通过汇集评估各种骨骼参数的可用 IBD 模型的数据进行定量荟萃分析。荟萃分析的足够数据是从化学诱导模型而非遗传诱导模型中获得的。在化学诱导模型中，仅报道了葡聚糖硫酸钠 (DSS) 和 2,4,6-三硝基苯磺酸 (TNBS) 对骨骼参数的影响。荟萃分析表明，无论是 DSS（Hedge'sg  = 2.124, p  = 0.001) 和 TNBS (Hedge's g  = 6.292, p  = 0.000) 增加炎症性疾病的严重程度。在汇总分析中，股骨（Hedge's g  = - 3.42，p  = 0.000）和胫骨（Hedge's g  = - 2.49，p  = 0.000）的骨量在DSS 给药后显示出显着损失。同样，IBD 诱导后骨形成率显着降低（Hedge's g  = − 3.495, p = 0.006）。此外，IBD 诱导皮质厚度减少，小梁微结构恶化。数据不足使我们无法确定 IBD 对骨强度和促钙激素的影响，以及促炎细胞因子对骨转换的影响。该荟萃分析表明，啮齿类动物的 IBD 诱导会导致显着的骨质流失。成骨细胞功能受损似乎是造成这种影响的原因。