Long-Term Use of Glucocorticoid Exacerbates Bone Lesions in Postmenopausal Women With Rheumatoid Arthritis
Abstract Background Glucocorticoid-induced osteoporosis is osteoporosis arising due to long-term use of glucocorticoids. Current despite decades of intense research, the effects of long-term use of glucocorticoids in humans on bone cells and bone structural changes remain unclear. Methods We performed postmortem histomorphometric analysis of bone from two female patients with rheumatoid arthritis aged 64y and 85y. Our two patients had been treated with glucocorticoids for 19 years and 14 years, respectively. Results In case 1, all markers of cancellous bone volume were markedly decreased compared with the age-matched reference range. Connectivity of cancellous bone trabecula was absent. Only a few island bones were noted. There was prominent thinning of the cortical bone, and extension of the bone marrow cavity into the cortical bone with prominent cortical porosis. Cortical nodes between the endocortical surface and the trabecula disappeared due to endocortical resorption. Stoppage of lamellar structure was observed because the bone resorption by osteoclasts surpassed bone formation by osteoblasts. Empty lacunae characterized by disappearance of osteocytes were visible. In case 2, all volume markers of cancellous bone were decreased to the same extent as case 1. However, cortical porosis was more prominent than case 1. Conclusion These two cases suggest that use of glucocorticoid therapy > 10 y can induce severe osteoporosis in elderly RA women with higher disease activity, and that the disappearance of cancellous bone is the common characteristic. The 85 year-old woman was characterized by cortical porosis.