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Osteoporosis has been an understandable concern for children and adult patients with CAH who may receive or have received supraphysiological doses of GCs [49–51]. Chronic GC therapy is known to generate bone loss in many ways: a direct suppression of osteoblastic activity and an inhibition of digestive calcium absorption with secondary hyperparathyroidism and increased bone resorption by osteoclasts [50]. GCs also lead to an inhibition of intestinal calcium absorption and an increase in renal calcium excretion leading to secondary hyperparathyroidism [50]. Some previous reports on BMD in adult CAH patients showed no significant differences in BMD between patients with CAH and controls, but others found a lower BMD in all or certain subpopulations of CAH patients [49–51]. These reports differ with respect to age selections and GC regimens. In reports documenting the BMD reduction, this outcome has been attributed to an accumulated effect of prolonged exposure to excess GCs during infancy and childhood. We conducted a trial to establish the role of the total cumulative GC dose on BMD and showed a negative relationship between total cumulative GC dose and lumbar and femoral BMD [51]. Women might benefit from the preserving effect of estrogens compared to men. In light of this, physicians should bear in mind the potential consequences of GCs on bone by adjusting the treatment and improving clinical and biological surveillance from infancy. CAH patients should thus be considered at risk for osteoporosis and fractures, and physicians have to check systematically BMD in adult CAH patients. Osteoporosis prophylaxis such as physical activities, calcium and vitamin D supplementation should be implemented.