A Mechanism Linking Inflammation and Bone Loss

Your bones are not as static as you might think, and are constantly being remodeled on the small scale by the activities of distinct populations of cells. It is known that a growing imbalance between the activities of osteoblasts, cells responsible for creating bone, and osteoclasts, cells responsible for breaking down bone, is involved in age-related loss of bone mass and strength. Researchers are making some progress towards understanding why inflammation causes more rapid bone loss, and one of the mechanisms turns out to be very similar:

Gum disease affects millions of North Americans each year. In fact, as much as $125B is spent each year in the US in an attempt to tackle periodontitis - considered an "osteoimmune" condition similar to osteoarthritis and osteoporosis - and its attendant complication: bone loss. Osteoinflammation produces larger osteoclasts. These "superosteoclasts" cause damage as they form on the bone surface, and, once attached, spit out enzymes that chew away at the bone - and loosen the teeth in the process. The larger the osteoclasts, the more efficient they are at resorbing bone. The question has always been, though: why does inflammation create larger osteoclasts?

To find the answer, the group looked carefully at the role of cytokines, chemicals released by cells in the body as part of an immune response. The team discovered that the cytokines spurred the production of adseverin, and from there, were able to trace a clear role for the protein through study models. "Adseverin appears to be critical for the generation or formation of super large osteoclasts responsible for the rapid bone loss associated with periodontal disease - and potentially other bone-related diseases such as osteoarthritis and osteoporosis. Adseverin has a very limited distribution in the body and very few cells express this protein at significant levels, which make it easier to target from a pharmacotherapeutic standpoint. It's an exciting drug target."

Link: http://www.eurekalert.org/pub_releases/2015-04/uot--pai042215.php

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