Effect of Calcium Supplementation in Glucocorticoid-Induced Osteoporosis

Abstract

The commonest secondary cause of osteoporosis is glucocorticoid-induced osteoporosis (GIO) which is also the commonest cause of iatrogenic osteoporosis. Chronic glucocorticoids (GCs) treatment may cause fractures in 30-50% of patients. Fracture risk is increased specially among those using oral glucocorticoids. On longterm glucocorticoids therapy, deterioration of cortical bone progressively detected and long bones became increasingly fragile. Any patient with chronic glucocorticoid therapy should be suspected to suffer from GIO. Patients on glucocorticoids should receive supplementation with calcium. These deleterious influences are the result of suppression of bone formation that occurs with an early but temporal rise in the process of bone resorption. Numbers of osteoclast rapidly rise, and accompanied by inactivation of osteoblast with the decline of bone formation, these changes cause the fastest bone loss during the initial phase of the disease. Glucocorticoids cause inhibition of osteoblasts replication and function and accelerate their apoptosis. Calcium is fundamental for bone, and assuring sufficient calcium intake is important. It is said that when children and adolescents ingest large amount of calcium could result in a decrease in the danger of developing osteoporosis when they got old, however, some researches propose that solitary use of calcium supplementation might not be enough for lowering the danger for fractures. Conflicting results were reported about the effects of the use of supplemental calcium on the bone mineral content in those taking glucocorticoids therapy. Whereas, calcium supplementations were used in most bone protective treatment trials and therefore should be used as an adjunct to GIO therapy.