Way to Recreate Bone Lost to Inflammation?

New research from Swedish is advancing our knowledge of how inflammation-induced bone destruction causes damage. The research makes use of prior work showing that bacteria that cause inflammation to communicate with the body’s cells through Toll-like receptors (TLRs). Since the receptors can also be activated by internal substances in autoimmune diseases, the discovery can also be important in the understanding of how bone loss develops in patients with rheumatoid arthritis.

“We have discovered that Toll-like receptors on the surface of bone cells are activated by bacteria that are suspected to cause of loosening of the teeth or septic arthritis, which leads to the formation of osteoclasts—cells specialised in breaking down bone. If the mechanism controlling new bone formation via these receptors can be revealed it could be used to recreate bone lost due to inflammatory processes, ” Ali Kassem, doctoral student at the Department of Molecular Periodontology at Umeå University.

The dissertation shows how the Toll-like receptors 2 and 5, which can stimulate bone loss, are also a part of the body’s own mechanism for the formation of new bone tissue.

Dr. Kassem told OTW, “We wanted to study the role of TLRs in inflammation-induced bone destruction and the mechanisms by which they cause the destruction. We were surprised to learn that there is a difference between intramembranous and endochondral bone in response to inflammation and diverse stimuli. It was also surprising to see that TLR-induced inflammation activates bone formation independent of (uncoupled to) bone resorption.”

“It is important for orthopedic surgeons to know that flat bones and long bones respond differently to stimuli and inflammation, and that TLRs induce bone destruction independent of inflammatory cytokines.”