Chronic arthritides and bone structure: focus on rheumatoid arthritis-an update

Normal bone remodeling depends of a balance between bone forming cells, osteoblasts and bone resorbing cells, the osteoclasts. In chronic arthritides and some inflammatory and autoimmune diseases such as rheumatoid arthritis, there is a great constellation of cytokines produced by pannus that impair bone formation and stimulate bone resorption by inducing osteoclast differentiation and inhibiting osteoblast maturation. Patients with chronic inflammation have multiple causes that lead to low bone mineral density, osteoporosis and a high risk of fracture including circulating cytokines, impaired mobility, chronic administration of glucocorticoids, low vitamin D levels and post-menopausal status in women, among others. Biologic agents and other therapeutic measures to reach prompt remission might ameliorate these deleterious effects. In many cases, bone acting agents need to be added to conventional treatment to reduce the risk of fractures and to preserve articular integrity and independency for daily living activities. A limited number of studies related to fractures in chronic arthritides were published, and future investigation is needed to determine the risk of fractures and the protective effects of different treatments to reduce this risk.

Automated summary

Normal bone remodeling requires a balance between bone forming cells (osteoblasts) and bone resorbing cells (osteoclasts). In certain chronic arthritides and inflammatory diseases like rheumatoid arthritis, cytokines produced by pannus disrupt bone formation, promote bone resorption, and increase the risk of osteoporosis and fractures. Prompt remission and additional bone acting agents are necessary to mitigate these effects and preserve joint integrity and independence in daily activities.