What will it take to prove the oral-systemic links?

A mountain of evidence has accumulated indicating associations between the mouth and the body. However, the lack of proof is the reason why our patients are not benefitting from those mouth-body connections at this point. Dr. Richard Nagelberg looks at the reasons why and discusses what is involved in establishing causality from the research gathered.

Jan 17th, 2018
Content Dam De En Articles Print Volume 108 Issue 1 Science Tech Gp Perio The Oral Systematic Connection Leftcolumn Article Thumbnailimage File

Richard H. Nagelberg, DDS

A mountain of evidence has accumulated indicating associations between the mouth and the body; however, they have not yet been proven. The lack of proof is the reason for the reluctance of many companies, organizations, and individual health-care professionals to accept and, more importantly, act on those mouth-body connections for the benefit of our patients.

What do we know for certain at this point? There is an overwhelming body of evidence indicating that the untreated or inadequately treated periodontal lesion results in ulceration of the gingival epithelium due to the destruction of the subjacent connective tissue. The ulcerations are a gateway to the bloodstream and points distant, for live bacteria, bacterial toxins, and inflammatory mediators. No one disputes this. It is also known that periodontitis is a bacterially induced, localized, chronic inflammatory disease. And it is this inflammatory component of periodontitis that causes clinically significant connective tissue and bone destruction. No one disputes this.

One way to prove causality of different systemic events and conditions from periodontal disease and/or periodontal pathogens would be to conduct an interventional study concluding that successful treatment of periodontitis and/or reduction of periodontal pathogens results in lower incidence of atherosclerosis, cardiovascular events, adverse pregnancy events, etc. This type of study would take decades to conduct and require enormous resources due to the length of time it takes for the systemic events to occur and manifest. The logistics of such a study would also be a nightmare: patients relocate throughout their lives, others drop out of the study for various reasons ... not to mention mortality unrelated to the systemic conditions being studied.

Another way to prove oral-systemic links would be to objectively quantify the degree of periodontitis-induced inflammation that is produced in the oral cavity and measure how much of that oral inflammation seeps into the systemic circulation. This is a metric that is not yet obtainable. We are stuck with the binary measurement of bleeding on probing—BOP or NoBOP—after jamming a notched stick between the teeth and gums. BOP does indicate the presence of infection, but it tells us nothing about how much of the epithelial lining is ulcerated, how much inflammation is present, or how much of the inflammation gets into the rest of the body.

How should we proceed with the current absence of proof? Our philosophy and approach to periodontal disease need to change, because we now know that periodontal disease is a complex entity with many moving parts. Merely scaling and root planing is too simplistic to achieve disease resolution for many individuals, hence the large number of refractory cases. Focusing on what we know will guide us on how to proceed.

We know that inflammation is the root cause of many of the chronic diseases of aging. We also know that the mouth can add significantly to the total inflammatory burden and that maximal control of biofilm short-circuits the host inflammatory response, preventing periodontal tissue destruction. Maximal periodontal therapy involves identifying and managing risk factors, host modulation to tamp down the inflammatory response, and maximum disruption of the biofilm. We must add to that providing patients with all the tools they need to keep a lid on the bacterial population on a daily basis.

Biofilm is microscopic. If allowed to grow and mature, it then becomes clinically visible. Calculus is also initially microscopic, and, similarly, if undisturbed grows to the point where it, too, is visible. All forms of biofilm and calculus need to be removed as much as possible. But how do you treat what you cannot see? This is where adjunctive antimicrobials become invaluable, because they increase the likelihood that the maximum amount of microscopic biofilm will be knocked out. Removal of visible plaque and calculus is apparently insufficient to maximize periodontal disease resolution for many patients.

Wait for proof or act on what we now know? All clinicians decide how far they are willing to go for their patients.

Author’s note: Thanks to Dr. Tim Donley, a periodontist in Bowling Green, Kentucky, for sharing his thoughts and approach to patient care as discussed in this column.

Richard H. Nagelberg, DDS, has practiced general dentistry in suburban Philadelphia for more than 30 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact Dr. Nagelberg at gr82th@aol.com.

More in Science & Tech