The prevailing understanding of periodontal disease in the dental profession includes the localized nature of the disease, which then extends to the rest of the body through ulcerations in the gingival epithelium. The ulcerated pocket lining is an open door to the capillary beds in the subjacent connective tissue. The bacteria walk right through that open door into the blood vessels, the heart pumps a few times, and live bacteria and their endotoxins are spread all around the body. But is this scenario really the case?
Local or systemic?
Is periodontal disease, perhaps, a systemic disease with localized oral manifestations even though it originates in the mouth? Is diabetes localized to the pancreas due to the inadequacy or lack of insulin production, or is it a systemic disease? The systemic effects of diabetes are well-known, but there are also localized effects from the two- to threefold increased risk of pancreatitis in diabetic individuals. The same can be said for other diseases and conditions, including rheumatoid arthritis.
Does it really matter?
Indeed, it does matter for both periodontal disease and diabetes. If the medical profession concentrated merely on the pancreas instead of the total-body manifestations of uncontrolled diabetes, many people would suffer diminished quality of life and diminished life span. Unfortunately, that is exactly what we do in the dental profession. We concentrate only on the oral cavity without consideration of the systemic effects of periodontal disease.
The oral contribution to the total inflammatory burden is not minimal; on the contrary, it is very significant. If one ingrown toenail can elevate blood sugar levels, think of the surface area of the gingiva involved in moderate to severe periodontitis. Estimates indicate it is about the size of the palm. The total inflammatory burden contributes to an elevated likelihood of cardiovascular diseases, among others. Every inflammatory condition from an ingrown toenail to periodontal disease and everything in between contributes to the total inflammatory burden.
Exactly what are we trying to accomplish in our efforts to manage periodontal disease?
It varies depending on how we think about it. If we consider periodontal disease as limited to the oral cavity, then our endpoint is reduction in pocket depths, bleeding, swelling, etc., without regard to the rest of the body. If we consider periodontal disease to be a systemic disease with local lesions, the endpoint is lifelong reduction of inflammation to minimize the oral contribution to the total inflammatory burden.
Will both approaches accomplish the same thing?
They might, depending on the thoroughness of the clinician. This includes debriding every lesion meticulously and using adjunctive antimicrobials, because mechanical instrumentation, while necessary, has limitations. Bacteria are hiding around the microscopic nooks and crannies around the cementoenamel junction inside dentinal tubules and gingival epithelial cells. The instruments that can access these areas have not been invented yet. Clinical thoroughness would also entail understanding why bacteria accumulate where they do for each patient, recommending home-care instruments for each of these sites, and scheduling different maintenance intervals for each patient depending on how their disease responds to treatment and home care.
Considering pocket depth reduction, the endpoint of therapy is inadequate as is, accepting bleeding around the same sites, visit after visit, month after month, year after year. If we shift our thinking to lifelong reduction of inflammation, we are going to figure out how to get those bleeding sites under control—whatever it takes.
Just something to think about.
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