Inflammation Pathway May Inform New Therapeutic Options for Better Outcomes
Findings from a recent study shed new light on the mechanism behind inflammation and bone loss that frequently occurs following joint replacement surgery. The research, conducted by a team from the Center for Immunity and Inflammation at Rutgers New Jersey Medical School, investigated the action of microparticles called “wear debris” that are shed from prosthetic devices, causing pain and inflammation and leading to the loss of bone tissue and subsequent loosening and failure of the implant. Lead author William Gause, PhD, commented “Bone degradation can occur within 10-15 years and often requires complex revision surgery to replace the implant and treat bone loss. However, many people start experiencing pain from this inflammation shortly after surgery. They are prescribed medications for the pain, but the loosening continues.”
The mechanism by which the wear debris lead to inflammation has been poorly understood. The Rutgers team discovered that white blood cells, or macrophages, deploy against the microparticles as foreign invaders. When these cells die, they release a molecule that in turn triggers a second immune response including inflammation. Dr. Gause continued “Although we typically think of infectious agents or toxins as causing disease, apparently the response of the body to these particles, which have essentially no intrinsic activities, can result in considerable tissue damage and pathology.” He expressed hope that the findings may prompt the development of new responses to this inflammation and bone loss that do not compromise other aspects of the body’s immune response defenses. The findings were reported earlier this week in the journal Nature Materials
Learn more about joint replacement surgery.
Read about the study.
The journal article may be read here.
Did you enjoy this article?
Subscribe to the PAINWeek Newsletter
and get our latest articles and more direct to your inbox