Generalized bone loss (osteoporosis) and fragility fractures can occur in rheumatic and musculoskeletal diseases including rheumatoid arthritis and spondyloarthritis (SpA; including ankylosing spondylitis and psoriatic arthritis). In addition, rheumatoid arthritis can involve localized, periarticular bone erosion and, in SpA, local (pathological) bone formation can occur. The RANK–RANKL–osteoprotegerin axis and the Wnt–β-catenin signalling pathway (along with its inhibitors sclerostin and Dickkopf 1) have been implicated in inflammatory bone loss and formation, respectively. Targeted therapies including biologic DMARDs and Janus kinase (JAK) inhibitors can stabilize bone turnover and inhibit radiographic joint damage, and potentially also prevent generalized bone loss. Targeted therapies interfere at various points in the mechanisms of local and generalized bone changes in systemic rheumatic diseases, and they effect biomarkers of bone resorption and formation, bone mass and risk of fragility fractures. Studies on the effects of targeted therapies on rates of fragility fracture are scarce. The efficacy of biologic DMARDs for arresting bone formation in axial SpA is debated. Improved understanding of the most relevant therapeutic targets and identification of important targeted therapies could lead to the preservation of bone in inflammatory rheumatic and musculoskeletal diseases.

全身性骨质流失（骨质疏松症）和脆性骨折可发生在风湿性和肌肉骨骼疾病中，包括类风湿性关节炎和脊柱关节炎（SpA；包括强直性脊柱炎和银屑病关节炎）。此外，类风湿性关节炎可涉及局部的关节周围骨侵蚀，并且在 SpA 中，可发生局部（病理性）骨形成。RANK-RANKL-骨保护素轴和 Wnt-β-连环蛋白信号通路（及其抑制剂硬化蛋白和 Dickkopf 1）分别与炎症性骨丢失和形成有关。包括生物 DMARD 和 Janus 激酶 (JAK) 抑制剂在内的靶向治疗可以稳定骨转换并抑制放射学关节损伤，并且还可能预防全身性骨质流失。靶向治疗在全身性风湿病的局部和全身骨变化机制的不同点上进行干预，并且它们影响骨吸收和形成、骨量和脆性骨折风险的生物标志物。关于靶向治疗对脆性骨折发生率影响的研究很少。生物 DMARDs 阻止中轴 SpA 骨形成的功效存在争议。更好地了解最相关的治疗靶点和识别重要的靶向治疗可能会导致在炎症性风湿病和肌肉骨骼疾病中保存骨骼。关于靶向治疗对脆性骨折发生率影响的研究很少。生物 DMARDs 阻止中轴 SpA 骨形成的功效存在争议。更好地了解最相关的治疗靶点和识别重要的靶向治疗可能会导致在炎症性风湿病和肌肉骨骼疾病中保存骨骼。关于靶向治疗对脆性骨折发生率影响的研究很少。生物 DMARDs 阻止中轴 SpA 骨形成的功效存在争议。更好地了解最相关的治疗靶点和识别重要的靶向治疗可能会导致在炎症性风湿病和肌肉骨骼疾病中保存骨骼。