期刊
REUMATOLOGIA
卷 61, 期 4, 页码 305-317出版社
TERMEDIA PUBLISHING HOUSE LTD
DOI: 10.5114/reum/170312
关键词
obesity; diabetes; thyroid dysfunction; musculoskeletal disorders
类别
Many medical conditions, such as thyroid dysfunction, obesity, and diabetes, have an impact on the skeletal system, increasing the risk of fractures. Thyroid hormones are crucial for proper bone development and strength, and untreated hyperthyroidism can lead to decreased bone mineral density, osteoporosis, and pathological fractures. Hypothyroidism alters the quality of bone structure and increases the frequency of fractures. Excessive body weight, as seen in obesity, negatively affects fracture risk and accelerates the development of rheumatoid arthritis and osteoporosis. Both type 1 and type 2 diabetes are associated with an increased risk of bone fractures, influenced by factors such as disease duration, inflammation, incorporation of advanced glycation end products (AGEs) in the bone matrix, and microvascular disorders.
Many medical conditions affect the skeletal system and constitute independent risk factors for fractures. The action of thyroid hormones is necessary to maintain adequate development, mineralization, and bone strength. Untreated hyperthyroidism can lead to a decrease in bone mineral density (BMD), os-teoporosis, and pathological fractures. In hypothyroidism, the changes in the quality of bone structure lead to an increase in the frequency of fractures. Excessive body weight negatively impacts fracture risk, increases the risk of osteoarthritis and accelerates the development of rheumatoid arthritis and osteoporosis. Type 1 and type 2 diabetes are associated with an increased risk of bone fractures despite different etiopathogenesis due to the duration of the disease and the pro-inflammatory state, the incor-poration of advanced glycation end products (AGEs) into the bone matrix, and microvascular disorders. This study summarizes the current literature on the influence of thyroid dysfunction, obesity, and diabetes on the skeletal system.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据