New Way to Slow Osteoporosis

Observation of these animals as they aged revealed that they developed severe osteoporosis, similar to that which appears in humans. These findings were published in the January 9, 2006, online edition of the Proceedings of the [U.S.] National Academy of Sciences.

The underlying mechanism in all cases of osteoporosis is an imbalance between bone resorption and bone formation. Either bone resorption is excessive, or bone formation is diminished. Osteoblast cells manufacture bone matrix, whereas osteoclast cells bring about bone resorption. Trabecular bone is the sponge-like bone in the center of long bones and vertebrae while cortical bone forms the hard outer shell. Since osteoblasts and osteoclasts inhabit the surface of bones, trabecular bone is more active, more subject to bone turnover and to remodeling. The CB2-deficient mice were found to have markedly accelerated age-related trabecular bone loss and cortical expansion, although cortical thickness remained unaltered. These changes were reminiscent of human osteoporosis and may have resulted from differential regulation of trabecular and cortical bone remodeling.

The investigators believe that CB2 offers a molecular target for the diagnosis and treatment of osteoporosis. Towards this end they have developed a new synthetic compound, HU-308, which was shown to activate CB2 and slow the development of osteoporosis in mice. This compound, which has been found to be free of any psychoactive side effects, forms the basis for a cannabinoid-based, anti-osteoporotic type drug.



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