Osteoporosis in Rheumatic Diseases as a Risk Factor for Pathological Fractures
Osteoporosis (a systemic skeletal disease characterized by reduced bone mass and impaired bone microarchitecture) is one of the most significant comorbid conditions in rheumatic diseases. Systemic inflammation, long-term corticosteroid therapy, and reduced physical activity create conditions for decreased bone mineral density (BMD), substantially increasing the risk of pathological fractures—fractures occurring with minimal or no trauma. This paper aims to examine the mechanisms of osteoporosis development in patients with rheumatic diseases and to assess its impact on pathological fracture risk. A literature review of domestic and international publications from 2010–2023 was conducted, encompassing clinical trials, meta-analyses, and systematic reviews. It was established that patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), and other rheumatic conditions have a 1.5–3-fold higher risk of vertebral and proximal femur fractures compared to the general population. Key pathogenetic mechanisms include RANK/RANKL/OPG axis activation, cytokine-mediated inhibition of osteoblastogenesis, and glucocorticoid-induced adverse effects on bone metabolism. A considerable contributing factor is vitamin D deficiency, frequently detected in patients with chronic inflammatory diseases, which further impairs calcium homeostasis and reduces the efficacy of bone remodeling. Timely dual-energy X-ray absorptiometry (DXA) and anti-osteoporotic therapy (bisphosphonates, denosumab) can reduce fracture risk. The findings confirm the need to incorporate bone health monitoring into the management standards for patients with rheumatic diseases.