Abstract
Rheumatoid arthritis (RA), the hallmark of which is the presence of an intense inflammation of the synovium, is a systemic autoimmune inflammatory disease that causes secondarily not only generalized osteoporosis but also paraarticular osteoporosis. Impaired activity of daily livings (ADL), and increased cytokines with osteoclast stimulatory activity within involved joint sites are responsible for the development of generalized osteoporosis but also paraarticular osteoporosis, respectively. The incidence of hip fracture is increased approximately two-fold in RA patients. The risk of vertebral fracture is likely to be increased particularly in those with glucocorticoid administration.
It is increasingly recognized that the increased calcium/phosphate release form the bone resulting from bone resorption might contribute to the development of atherosclerosis. We previous showed in a series of the reports that advanced atherosclerotic changes were observed in RA patients with higher bone resorption. Since evidence has been accumulated to indicate that the administration of anti-bone resorbing agents, such as bisphosphonate, might prevent against the development of atherosclerotic change and the occurrence of acute myocardial infarction.
These data clearly indicate the importance of treatment of abnormal bone metabolism in RA patients not only to prevent fracture but also to attenuate RA-induced aggravation of atherosclerotic changes.
