Periodontal Bone Loss Is Not A Disease

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 remolding 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 results 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 are in fact protective mechanisms developed by the body.
In atherosclerosis, fatty plaques form and if they break free into the vessel, they result in a coronary infarct or stroke. The sclerotic bone that forms in our arteries is a protective mechanism that encloses the plaque and prevents it from breaking free. The calcium deposits in our arteries are not just mineral deposits, but the result of the conversion of smooth muscle cells into mineralizing cells that the body has developed to protect us.
In osteoarthritis, sclerotic bone is formed under the cartilage lining the joint in order to better protect the cartilage and limit the progression of the disease. The sclerotic bone formation in osteoarthritis is another ingenious mechanism developed by our bodies to protect us.

The sclerotic bone that forms around cadaver bone grafts is complex, but is nevertheless the same protective mechanism designed to encapsulate the inflammatory bone graft particles. While the actual cell that forms sclerotic bone around cadaver bone graft particles has not been elucidated, the process of encapsulation is similar to the encapsulation found in atherosclerosis.

The sclerotic bone formation in atherosclerosis, osteoarthritis, and cadaver bone grafts are all similar in that they are all a result of chronic inflammation and are irreversible. As explained in our previous article, Understanding Sclerotic Bone, once sclerotic bone is formed, osteocytes are programmed to produce cytokines that promote bone formation and inhibit bone resorption, thereby the sclerotic bone inherently maintains its protective purpose.

So, what does all of this have to do with periodontal disease?

The previously discussed diseases are the result of chronic inflammation and the body has developed protective mechanisms to limit their progression. Periodontal disease is a chronic inflammatory disease caused by pathogenic bacteria. It destroys the periodontal ligament, but that is the limit of what the disease does to the local tissues. The bone loss associated with the infection is not part of the disease, but a protective mechanism developed by the body to prevent osteomyelitis. In other words, the body sacrifices the tooth to save the host. The alveolar bone in periodontal disease is never infected during periodontal disease progression. The body always resorbs the bone before the bacteria can get to it and infect it.

Without dental treatment, rampant aggressive periodontal disease elicits aggressive bone resorption ahead of the bacteria until all the bone is resorbed and the tooth is exfoliated. If our bodies never developed bone resorption as a protective mechanism, many of us would not be here because our forebearers would likely have died an agonizing death from osteomyelitis of the jaws.

Bone loss in periodontal disease is caused by chronic inflammatory molecules produced in the fight against pathogenic bacteria, stimulating osteoclasts to remove bone. Osteoporosis is the same process. An increase in systemic inflammation caused by the circulation of chronic inflammatory molecules stimulates osteoclasts to remove bone from the skeleton and a primary culprit is found to be the gut bacteria.

Like the oral cavity, the gut contains good and bad bacteria. That bacteria is contained in the gut until the lining begins to fail and this is related to a drop in estrogen that maintains the tight junctions in the gut lining. As estrogen decreases, the junctions open to the inflammatory molecules and bacteria in the gut, resulting in a systemic inflammation that stimulates osteoclasts to remove bone.
At SteinerBio, we consider the bone loss in periodontal disease to be a protective mechanism developed to protect the host. We also believe the same mechanism that was developed as a protective mechanism for the jaws is resulting in the skeletal bone loss that we call osteoporosis. Periodontics and orthopedics are treating the same process.

In the introduction, it was stated that chronic inflammation hijacks the remodeling process, but this is backward. We believe that osteoclasts merely became sensitive to chronic inflammation and responded by removing alveolar bone ahead of the advancing bacteria.

However, the unintended consequences of this adaptation is not a protective mechanism, but the unwanted bone loss found in osteoporosis. Bone loss in periodontal disease and osteoporosis is the same process and collaboration between the two specialties would likely result in improved treatment outcomes. Periodontal therapy has not improved in 25 years, but with a clear understanding of what is and what is not disease, along with collaboration with other scientists and clinicians, we can bring about a much needed improvement in the care we provide our patients.

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