Osteoblast role in the pathogenesis of rheumatoid arthritis

被引:49
作者
Berardi, S. [1 ]
Corrado, A. [1 ]
Maruotti, N. [1 ]
Cici, D. [1 ]
Cantatore, F. P. [1 ]
机构
[1] Univ Foggia, Policlin Riuniti Foggia, Dept Med & Surg Sci, Rheumatol Clin, Viale Pinto 1, I-71121 Foggia, Italy
关键词
Osteoblasts; Rheumatoid arthritis; RANKL; RANK; Bone loss; Cytokines;
D O I
10.1007/s11033-021-06288-y
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In the pathogenesis of several rheumatic diseases, such as rheumatoid arthritis, spondyloarthritis, osteoarthritis, osteoporosis, alterations in osteoblast growth, differentiation and activity play a role. In particular, in rheumatoid arthritis bone homeostasis is perturbed: in addition to stimulating the pathologic bone resorption process performed by osteoclasts in course of rheumatoid arthritis, proinflammatory cytokines (such as Tumor Necrosis factor-alpha, Interleukin-1) can also inhibit osteoblast differentiation and function, resulting in net bone loss. Mouse models of rheumatoid arthritis showed that complete resolution of inflammation (with maximal reduction in the expression of pro-inflammatory factors) is crucial for bone healing, performed by osteoblasts activity. In fact, abnormal activity of factors and systems involved in osteoblast function in these patients has been described. A better understanding of the pathogenic mechanisms involved in osteoblast dysregulation could contribute to explain the generalized and focal articular bone loss found in rheumatoid arthritis. Nevertheless, these aspects have not been frequently and directly evaluated in studies. This review article is focused on analysis of the current knowledge about the role of osteoblast dysregulation occurring in rheumatoid arthritis: a better knowledge of these mechanisms could contribute to the realization of new therapeutic strategies.
引用
收藏
页码:2843 / 2852
页数:10
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