A research group led by Professor Masaki Noda of Tokyo Medical and Dental University has found that one of the causes of osteoporosis is a decrease in the motility of osteoblasts that produce bone.It will contribute to the development of new treatments and the full picture of osteoporosis in the future.

 Once the bone is made, it is not intact, and the old parts are destroyed by osteoclasts.Bone is repaired by the osteoblasts moving (migrating) inside the bone.If the balance of these actions is maintained, the original amount of bone will be maintained.Conversely, if the speed of repair becomes slower than the speed at which it is destroyed, bone mass will decrease steadily.The group focused on the migration of osteoblasts to the part where the bone was broken and chipped.Although the genes associated with migration were known, their direct association with osteoporosis was unclear.

 To clarify this, the gene N that controls cell shape and migrationckWas destroyed and transplanted to the bone defect.Then, we found that migration was suppressed and the range of cell spread became narrower than that of normal cells.Further NckWhen we investigated how the bone condition changed in animals that suppressed the disease, we were able to confirm that they also showed symptoms of osteoporosis.

 Thus, it became clear that osteoblast migration is important for bone maintenance, and that impaired function leads to osteoporosis.In other words, experiments have shown that even if bone is destroyed by osteoclasts, the osteoblasts to be repaired will remain if they cannot move to that extent.If the lost migratory function can be regained, the treatment of osteoporosis will make great strides.In addition, if it is known in advance from genetic analysis that migration is likely to be lost, it should be useful for prevention.


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