Clinical application of bone metabolism markers to disuse bone atrophy

Abstract

Mechanical stress on bone is one of the determinants of bone morphology, bone mineral density and bone strength. Therefore, disuse accelerates bone resorption, especially of cancellous bone, and consequently bone becomes atrophic and fragile. Osteocytes embedded in the bone matrix respond to mechanical load and changes of bone metabolism. The gapjunction of the long processes of osteocytes plays an important role in transmitting mechanical load through intracellular signal transmitters (cAMP, cGMP) and extracellular signal transmitters (PGE(2), IGF- I , IGF- II , TGF-beta) , to induce bone formation by osteoblasts and bone resorption by osteoclasts, or a combination of the two. Bone metabolism markers reflect activities of osteoblasts and osteoclasts, so they provide information on bone turnover and bone metabolism. Bone resorption markers characteristically increase and remain high during bed rest and disuse, whereas ambulation and exercise, as in kinesiotherapy, decrease bone resorption markers. As for treatments of disuse bone atrophy, from the bone metabolic and pharmacological viewpoint, anti-resorption agents are recommended to inhibit bone loss. Bisphosphonates which are strong anti-resorption agents, are expected to inhibit bone resorption. Calcitonin and vitamin K(2) which are also anti-resorption agents effectively, reduce bone loss due to disuse and bed rest.