Our complete skeleton grows and changes throughout life with no physiologic interaction with inflammation. Normal bone formation and remodeling does not share metabolic pathways with inflammation. Acute inflammation is involved in fracture healing, but that response is primarily for the purpose of removing damaged tissue making way for bone regeneration. Chronic inflammation hijacks the bone remodeling process by stimulating osteoclasts that remove bone and inhibiting osteoblasts that form bone with the net result of significant bone loss.
Two of our most prevalent and destructive diseases are involved with chronic inflammation that result in bone resorption: periodontal disease and osteoporosis.
In both of these diseases, it appears that the ability of our bones to remodel has been hijacked by chronic inflammation, resulting in bone resorption that leads to tooth loss and skeletal failure. Understanding how chronic inflammation has developed into the driving force for these two diseases may help guide us to better therapeutic options for both.
In our previous article, we discussed inflammation-induced sclerotic bone (Understanding Sclerotic Bone). More specifically, we discussed how inflammation-induced sclerotic bone formation in atherosclerosis, osteoarthritis, and cadaver bone grafts is not part of the disease, but is in fact a protective mechanism developed by the body.