Dr. Gerald Crabtree and pre-doctoral fellow Monte Winslow report slightly increasing the activity of a protein called NFATc1 causes massive bone accumulation, suggesting NFATc1 or other proteins that regulate its activity will make good targets for drugs to treat osteoporosis.

In vertebrates, bone is constantly being formed and broken down throughout life. Cells called osteoclasts continuously degrade bone, while cells called osteoblasts replenish it.

Ideally, they are perfectly balanced, said Crabtree, the senior author of the study. Over the course of a lifetime, if everything goes well, we’ll maintain almost exactly identical bone mass.

But if the balance is upset, and more bone is destroyed than formed, osteoporosis results, increasing the risk of fractures.

If you could find a small molecule that would flip 10 percent of the existing NFATc into the active form, you could favor the formation of osteoblasts and make stronger bones, said Crabtree.

The research is reported in the journal Developmental Cell.