Osteoporosis in Rheumatic Diseases

Abstract

The risk of osteoporosis and fragility fracture is increased in patients with autoimmune rheumatic diseases. Although the use of glucocorticoids is the major contributing factor, inflammation mediated by cytokines and growth factors and other medications, including the biologic and targeted disease-modifying antirheumatic drugs, also play important roles in bone remodeling. Pro-inflammatory cytokines such as IL-1, IL-6, IL-17, and TNF[Formula: see text] increase RANK expression and promote osteoclast activity while inhibiting osteoblast-mediated bone formation through the Dickkopf-1 pathway. Certain autoantibodies stimulate differentiation of the osteoclasts, resulting in localized bone resorption. This article covers the prevalence and risk factors for osteoporosis in patients with common rheumatic diseases and the role of inflammatory cytokines and other clinical factors. Controlling disease-related inflammation and optimizing the diagnostic and therapeutic instrumentation is needed to reduce fragility fractures in patients with rheumatic diseases.