Understanding and Managing Corticosteroid-Induced Osteoporosis

Abstract

Glucocorticoids are effective immunosuppressants used in a wide variety of diseases. Their use results in secondary osteoporosis in about 30–50% of chronic glucocorticoid users. Glucocorticoids cause a rapid decline in bone strength within the first 3–6 months mostly due to increased bone resorption by osteoclasts. This is followed by a more gradual loss of bone partly due to decreased osteoblastogenesis and osteoblast and osteocyte apoptosis. The loss of bone strength induced by glucocorticoids is not fully captured by bone mineral density measurements. Other tools such as the trabecular bone score and advanced imaging techniques give insight into bone quality; however, these are not used widely in clinical practice. Glucocorticoid-induced osteoporosis should be seen as a widely preventable disease. Currently, only about 15% of chronic glucocorticoid users are receiving optimal care. Glucocorticoids should be prescribed at the lowest dose and shortest duration. All patients should be counselled on lifestyle measures to maintain bone strength including nutrition and weight-bearing exercise. Pharmacological therapy should be considered for all patients at moderate to high risk of fracture as there is evidence for the prevention of bone loss and fractures with a favourable safety profile. Oral bisphosphonates are the current mainstay of therapy, whereas osteoanabolic agents may be considered for those at highest risk of fracture.

Multidisciplinary Care of a Vertebral Fracture in a Patient with Hematopoietic Stem Cell Transplant: Safety Appropriateness in Interventional Pain Management and Rehabilitation Considerations

“…All patients with a high risk of corticosteroid induced bone loss should be counseled on lifestyle measures to maintain bone strength including nutrition and weight-bearing exercise. Pharmacological therapy should be considered for all patients at moderate to high risk of fracture because a favorable safety profile using oral bisphosphonates as the current mainstay of therapy showed evidence for preventing steroid-induced bone loss and reducing fracture risk [ 24 ].…”

Distinct Glucocorticoid Receptor Actions in Bone Homeostasis and Bone Diseases

“…It is well known that patients undergoing long-term GC medication are at a significantly increased risk for bone fractures ( 23 , 70 ). Even though steroid use has not been found to be a major risk factor for non-union fracture healing in clinical studies ( 71 ), preclinical studies indicate that GCs also influence the complex fracture healing process ( 6 , 72 ).…”

Status of Glucocorticoid-Induced Osteoporosis Preventive Care in Korea: A Retrospective Cohort Study on the Korean National Health Insurance Service Database

“…Approximately 1% of the adult population worldwide are treated with long-term systemic glucocorticoids (GC), which are widely used for the management of a variety of disorders due to their anti-inflammatory and immunosuppressive properties; these disorders include systemic autoimmune diseases, inflammatory bowel diseases, chronic pulmonary diseases, allergic diseases, hematologic malignancy, and following organ transplants [1,2]. However, long-term use of GC can cause a myriad of adverse effects, among which the most serious one is the reduction of bone density and derangement of bone quality, leading to glucocorticoid-induced osteoporosis (GIOP), the most common form of secondary osteoporosis.…”

“…However, long-term use of GC can cause a myriad of adverse effects, among which the most serious one is the reduction of bone density and derangement of bone quality, leading to glucocorticoid-induced osteoporosis (GIOP), the most common form of secondary osteoporosis. GIOP develops in approximately 30-50% of patients receiving long-term GC therapy, and the risk of fracture increases by more than 50% in these patients [1], which imposes a significant clinical burden due to increased morbidity and mortality [3,4]. Although GC can affect both trabecular and cortical bones, fragility fractures occur more commonly in the trabecular bone, such as the lumbar vertebrae [5].…”

“…Bone loss occurs rapidly within the first 3 to 6 months of GC initiation and persists at a slower rate thereafter; thus, the risk of fracture peaks at 12 months [4,5]. Fractures can occur even with low daily dose exposure of long-term GC and are independent of bone mineral density (BMD) and age [1]. Thus, GC should be administered at the lowest dose for the shortest period of time, and if long-term glucocorticoid treatment is inevitable, special attention is required to prevent fractures.…”