EFFECT OF ENDOCRINOPATHIES ON BONE

Progress in bone densitometry, particularly biphotonic absoptiometry, has made it possible to better identify the effects of endocrinopathie s on bone. Both cortical and trabecular bone structures can be evaluat ed quantitatively and topographically revealing important information on the pathophysiology of bone loss. Sex hormones play a major role in the regulation of bone mineralization and hypogonadism, whatever the origin, can lead to deleterious effects, Bone loss is known to be sign ificative in high performance female athletes with amenorrhoea; long-t erm consequences are not yet determined, but stress fractures have bee n reported in up to 50%. Other hypogonadisms leading to bone demineral ization include anorexia nevrosa, chronic intake of gonadotrophin rele asing hormone analogues and anti-oestrogens, and hyperprolactinism. Hy perthyroidism leads to a negative calcium balance and demineralization with remodelling, predominatly in cortical bone. In hypothyroid state s a 10% bone loss is observed in vertebrae. In both cases, bone densit ometry should be performed in order to evaluate the effect of treatmen t. The deleterious effect of spontaneous or iatrogenic hypercortisism is well known, leading to spontaneous wedge fractures of the vertebrae due to predominating trabecular bone loss. The mechanism of action of corticosteroids on bone metabolism is complex, but the major effect i s an inhibition of osteoblast maturation. Recovery may be possible, bu t no large long-term series have yet been reported. Hyperparathyroidis m and acromegaly also affect bone mineralization. The information prov ided by bone densitometry is essential to properly manage patients wit h endocrinopathies affecting bone mineralization.