Allergy, Immunology & Rheumatology Division, University of Rochester Medical Center, Rochester, NY, 14623, USA.
Calcif Tissue Int. 2018 May;102(5):559-574. doi: 10.1007/s00223-017-0380-2. Epub 2018 Jan 12.
Psoriatic arthritis (PsA) is an inflammatory rheumatic disorder that occurs in patients with psoriasis and predominantly affects musculoskeletal structures, skin, and nails. The etiology of PsA is not well understood but evidence supports an interplay of genetic, immunologic, and environmental factors which promote pathological bone remodeling and joint damage in PsA. Localized and systemic bone loss due to increased activity of osteoclasts is well established in PsA based on animal models and translational studies. In contrast, the mechanisms responsible for pathological bone remodeling in PsA remain enigmatic although new candidate molecules and pathways have been identified. Recent reports have revealed novel findings related to bone erosion and pathologic bone formation in PsA. Many associated risk factors and contributing molecular mechanisms have also been identified. In this review, we discuss new developments in the field, point out unresolved questions regarding the pathogenetic origins of the wide array of bone phenotypes in PsA, and discuss new directions for investigation.
银屑病关节炎（PsA）是一种炎症性风湿性疾病，发生于银屑病患者中，主要影响肌肉骨骼结构、皮肤和指甲。PsA 的病因尚不清楚，但有证据表明遗传、免疫和环境因素相互作用，促进了 PsA 中的病理性骨重塑和关节损伤。基于动物模型和转化研究，已经明确了由于破骨细胞活性增加导致的局部和全身骨质流失。相比之下，尽管已经确定了新的候选分子和途径，但导致 PsA 中病理性骨重塑的机制仍然很神秘。最近的报告揭示了与 PsA 中的骨侵蚀和病理性骨形成相关的新发现。还确定了许多相关的风险因素和促成的分子机制。在这篇综述中，我们讨论了该领域的新进展，指出了关于 PsA 中广泛的骨表型的发病机制起源的未解决问题，并讨论了新的研究方向。
