Ketoprofen lysine salt inhibits disuse-induced osteopenia in a new non-traumatic immobilization model in the rat.

Immobilization and the consequent unloading can cause osteopenia both in humans and in animals due to an increased bone resorption and a parallel reduction in bone formation. Non-steroidal anti-inflammatory drugs (NSAIDs), and in particular the aryl propionic acids, are described to prevent bone loss by inhibiting the cyclo-oxygenase activity. In this study we evaluated the role of a classical aryl propionic acid, ketoprofen lysine salt (KLS), in a new model of disuse-induced osteoporosis in the rat. Tail immobilization evoked a time-dependent bone loss in the caudal vertebral bodies, measured densitometrically as a reduction of bone mineral density (BMD) and content (BMC). KLS was administered once daily for 10 days by subcutaneous route at 0.5 mg kg-1, a dose lower than that effective to elicit an anti-inflammatory response. In these conditions, KLS completely abolished BMD and BMC decrease observed in the caudal vertebrae after 10-day immobilization, without affecting bone mass in normal (non-immobilized) rats. These results suggest that KLS can exert, besides to its anti-inflammatory effect, an anti-resorptive activity on bone that could be useful in the prevention of disuse-induced osteopenia.