Osteoporosis: an Independent Determinant of Bone Erosions in Rheumatoid Arthritis?

Rossini, Maurizio; Adami, Giovanni; Viapiana, Ombretta; Idolazzi, Luca; Orsolini, Giovanni; Fassio, Angelo; Giollo, Alessandro; Gatti, Davide

doi:10.1002/jbmr.3209

Cited by 13 publications

(10 citation statements)

References 20 publications

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“…Dkk-1 production is enhanced mainly by inflammatory cytokines, such as TNF [18], but emerging evidence has shown that PTH can mediate part of the secretion of Dkk-1 [21,22,23], especially in RA [19]. The PTH-driven increase of Dkk-1 might explain, at least in part, the unfavorable outcome of RA patients with low-vitamin D status [24,25,26]. Other independent factors associated with bone destruction in RA are autoantibodies against citrullinated proteins (ACPA) [27,28].…”

Section: Rheumatoid Arthritismentioning

confidence: 99%

Osteoporosis in Rheumatic Diseases

Adami

Fassio

Rossini

et al. 2019

IJMS

114

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Osteoporosis is a chronic disease characterized by an increased risk of fragility fracture. Patients affected by rheumatic diseases are at greater risk of developing osteoporosis. The purpose of the present review is to discuss the pathogenesis, epidemiology, and treatment of osteoporosis in patients affected by rheumatic diseases with special focus for rheumatoid arthritis, psoriatic arthritis, spondyloarthritis, systemic lupus erythematosus, systemic sclerosis, vasculitides, Sjogren syndrome, and crystal-induced arthritis.

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Section: Rheumatoid Arthritismentioning

confidence: 99%

Osteoporosis in Rheumatic Diseases

Adami

Fassio

Rossini

et al. 2019

IJMS

114

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“…Moreover, a possible association between low systemic BMD and atlantoaxial subluxation occurrence was suggested in subjects affected by RA ( 27 ). This evidence suggests that OP could increase susceptibility to bone erosions in RA patients ( 28 , 29 ).…”

Section: Rheumatoid Arthritismentioning

confidence: 87%

Osteoporosis in Inflammatory Arthritides: New Perspective on Pathogenesis and Treatment

et al. 2020

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Osteoporosis is a skeletal disorder characterized by impaired bone strength and increased risk of fragility fracture and is among the most relevant comorbidities of rheumatic diseases. The purpose of the present review is to discuss the pathogenesis of local and systemic bone involvement in inflammatory arthritides, especially Rheumatoid Arthritis, Psoriatic Arthritis, and Spondyloarthritides, as well as the effect of anti-rheumatic treatments and anti-osteoporotic medication on bone health and fracture incidence, including recent data on novel therapeutic perspective.

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“…Patients with RA are also prone to periarticular and systemic bone loss, which further contributes to morbidity due to osteoporosis and fragility fractures [5][6][7]. Furthermore, as osteoporosis can facilitate the development of erosions, there is a close interrelationship between systemic and local bone loss [8,9].…”

Section: Introductionmentioning

confidence: 99%

Osteoimmunology in rheumatoid and psoriatic arthritis: potential effects of tofacitinib on bone involvement

2020

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Chronic inflammation, such as that present in rheumatoid arthritis (RA) and psoriatic arthritis (PsA), leads to aberrations in bone remodeling, which is mediated by several signaling pathways, including the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. In this light, pro-inflammatory cytokines are now clearly implicated in these processes as they can perturb normal bone remodeling through their action on osteoclasts and osteoblasts at both intra-and extra-articular skeletal sites. As a selective inhibitor of JAK1 and JAK3, tofacitinib has the potential to play a role in the management of rheumatic diseases such as RA and PsA. Preclinical studies have demonstrated that tofacitinib can inhibit disturbed osteoclastogenesis in RA, which suggests that targeting the JAK-STAT pathway may help limit bone erosion. Evidence from clinical trials with tofacitinib in RA and PsA is encouraging, as tofacitinib treatment has been shown to decrease articular bone erosion. In this review, the authors summarize current knowledge on the relationship between the immune system and the skeleton before examining the involvement of JAK-STAT signaling in bone homeostasis as well as the available preclinical and clinical evidence on the benefits of tofacitinib on prevention of bone involvement in RA and PsA. Key Points • Chronic inflammation in rheumatoid arthritis (RA) and psoriatic arthritis (PsA) leads to disturbances in bone remodeling • Bone remodeling is mediated by several signaling pathways, including the JAK-STAT pathway • Tofacitinib, a selective inhibitor of JAK1 and JAK3, is active in RA and PsA and may help limit systemic bone loss through inhibiting disturbed osteoclastogenesis • Clinical trials show that tofacitinib reduces articular bone erosion

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Osteoporosis: an Independent Determinant of Bone Erosions in Rheumatoid Arthritis?

Cited by 13 publications

References 20 publications

Osteoporosis in Rheumatic Diseases

Osteoporosis in Rheumatic Diseases

Osteoporosis in Inflammatory Arthritides: New Perspective on Pathogenesis and Treatment

Osteoimmunology in rheumatoid and psoriatic arthritis: potential effects of tofacitinib on bone involvement

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