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논문 기본 정보

자료유형
학술저널
저자정보
김윤경 (Division of Rheumatology Department of Internal Medicine Kosin University Gospel Hospital Kosin University College of Medicine Busan Korea) 김근태 (Division of Rheumatology Department of Internal Medicine Kosin University Gospel Hospital Kosin University College of Medicine Busan Korea)
저널정보
대한류마티스학회 대한류마티스학회지 대한류마티스학회지 제30권 제1호
발행연도
2023.1
수록면
3 - 17 (15page)
DOI
10.4078/jrd.22.0046

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Osteoporosis is a systemic skeletal disorder that causes vulnerability of bones to fracture owing to reduction in bone density and deterioration of the bone tissue microstructure. The prevalence of osteoporosis is higher in patients with autoimmune inflammatory rheumatic diseases, including rheumatoid arthritis (RA), than in those of the general population. In this autoimmune inflammatory rheumatic disease, in addition to known risk factors for osteoporosis, various factors such as chronic inflammation, autoantibodies, metabolic disorders, drugs, and decreased physical activity contribute to additional risk. In RA, disease-related inflammation plays an important role in local or systemic bone loss, and active treatment for inflammation can help prevent osteoporosis. In addition to conventional synthetic disease-modifying anti-rheumatic drugs that have been traditionally used for treatment of RA, biologic DMARDs and targeted synthetic DMARDs have been widely used. These agents can be employed more selectively and precisely based on disease pathogenesis. It has been reported that these drugs can inhibit bone loss by not only reducing inflammation in RA, but also by inhibiting bone resorption and promoting bone formation. In this review, the pathogenesis and research results of the increase in osteoporosis in RA are reviewed, and the effects of biological agents on osteoporosis are discussed.

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