Glucocorticoid-Induced Osteoporosis: From Basic Mechanisms to Clinical Aspects

Abstract

Glucocorticoid (GC)-induced osteoporosis (GCOP) is the most common cause of osteoporosis in adults aged 20–45 years as well as the most common cause of iatrogenic osteoporosis. GC excess, either endogenous or exogenous, induces bone loss in 30–50% of cases. Indeed, bone loss leading to fractures is perhaps the most incapacitating, sometimes partially irreversible, complication of GC therapy. Nevertheless, GCOP is often underdiagnosed and left untreated. The following article provides an update on the cellular and molecular mechanisms implicated in the pathophysiology of GC-induced bone loss, as well as some guidelines on diagnostic, preventive and therapeutic strategies for this medical condition, in an effort to promote a better knowledge and greater awareness of GCOP by both the patient and the physician.

The prevalence and risk factors for osteoporosis in patients with inflammatory bowel disease

“…The duration of disease may have a measurable impact on bone metabolism in IBD for several reasons including chronic systemic infl ammation and drug therapy. Corticosteroids are more often given to patients with frequent relapse of the disease but an increased level of infl ammatory cytokines seems to be an important independent risk factor for accelerated bone loss (49,50).…”

Bone health in ambulatory individuals with multiple sclerosis: Impact of physical activity, glucocorticoid use, and body composition

“…Other factors, a major one of which is glucocorticoid medication use, may predispose MS patients to osteoporosis. Glucocorticoid use has been established as a common cause of osteoporosis [11][12][13]. The effect of glucocorticoid exposure in the MS population, however, is not clear.…”

“…Importantly, the use of glucocorticoids is a risk factor for osteoporosis [11][12][13]. The severity of bone loss depends on dose and duration of treatment [12].…”

“…Lean mass appears to be a stronger predictor in young women, whereas fat mass has a stronger association with BMD in postmenopausal women [21][22][23]. Glucocorticoid medication can lead to loss of lean mass [24], which together with the demyelination process of MS, can result in muscle weakness [11]. To our knowledge, only one study has assessed the effect of glucocorticoid therapy on lean mass and the association between lean mass and WB bone mineral content (BMC) in those with MS [7].…”

Assessment and management of low bone density in inflammatory bowel disease and performance of professional society guidelines1

“…[1][2][3] Hence, low BMD has been established as an extraintestinal manifestation of IBD 4 and is believed to result from a combination of direct effects of systemic inflammation on bone, vitamin D malabsorption, and glucocorticoid use. [5][6][7] The overall prevalence of osteoporosis is estimated between 10%-14% of a relatively young IBD population (mean age 33-41 years). [8][9][10][11] Most studies have shown that the prevalence of low BMD is similar for patients with ulcerative colitis (UC) and Crohn's disease (CD) 3,12,13 ; however, other studies suggest a higher prevalence among CD patients.…”