Secondary osteoporosis and the microanatomy of trabecular bone

Osteoporosis is a generic term implying a decrease in bone mass which increases the risk of fracture. It is now becoming appreciated that decreases in bone mass alone are not the sole factor in increasing the risk of osteoporotic fracture, and that other skeletal and extraskeletal factors also contribute significantly to this risk. Extraskeletal factors include the propensity to falls and responses to falls, whereas additional skeletal factors include bone turnover, the ability to repair fatigue damage and the tertiary structure of bone, particularly trabecular tissue. There are a large number of causes of secondary osteoporosis each with their own specific pathophysiological mechanisms. It is therefore not surprising that they have heterogeneous effects on the skeleton. A good example is provided in corticosteroid osteoporosis which is characterised by thinning of trabecular elements, whereas postmenopausal osteoporosis is characterised less by thinning and more by destruction of trabecular elements which derange trabecular continuity. A variety of techniques are now being developed to address the heterogeneity of trabecular osteoporosis. These include direct histomorphometric techniques to assess trabecular continuity, and indirect techniques such as the attenuation of ultrasound. These different pathophysiological mechanisms in osteoporosis have important therapeutic implications, particularly with agents that affect bone remodelling. Since bone remodelling is a surface-based phenomenon, if trabecular surfaces are destroyed, the augmentation of bone mass may thicken remnant structures without restoring trabecular continuity. Since most treatments for osteoporosis affect bone remodelling they are likely to have a greater effect in restoring structural integrity of the skeleton in corticosteroid than in postmenopausal osteoporosis.