BY Richard H. Nagelberg, DDS
We've come very far in a short period of time in our understanding of the various associations between the mouth and body. During roughly the same time frame, our understanding of the mechanisms involved in the development of periodontal disease also expanded. Not surprisingly, these research findings are linked as well. Unraveling the microbiology of periodontal disease is also well under way.
Research is an evolving activity limited by the methods available at a given period of time. Research methods have also expanded, including DNA analysis and lab on a chip, to name a few examples. Just 30 years ago, these technologies were in their infancy or not available.
Currently, we know there are associations between periodontal disease and insulin resistance, diabetes, atherosclerosis, and cardiovascular disease. While the recent research review by the American Heart Association did not find causality, it did affirm associations. The authors of the study also stated that if there is causality, it likely would have been revealed by now. A more accurate prediction would be that causality would likely be established by now with current research methodologies. Who knows what's coming in the future? We could barely imagine genetic testing and the human genome project in the recent past.
By reflecting on what we've thought in the past, we can shed some light on what we still have to learn. We used to call periodontal disease pyorrhea, and the one salivary enzyme in the oral cavity was called ptyalin. We thought that all the bugs in the mouth contributed to periodontal disease, and that the bacteria were the primary destructive agents of the periodontium. Treatment plans were developed and executed based on the prevailing evidence and theories. We did not know of the existence of biofilms, nor was there such a word to describe this concept. We have come a long way, but we have an even longer way to go. Among the reasons why our knowledge is incomplete at this time are the immunological aspects of periodontal disease. Many inflammatory mediators, processes, and pathways have been identified, but there are more unknown than known. The roles of genetics and epigenetics are also in the early stages of discovery.
We still need to understand the strengths of the various oral-systemic associations, as well as the role of underappreciated agents, such as Plac-2 and others yet to be identified. We need to further understand the level of association and causality of the periodontal pathogens, independent of periodontal disease, to systemic diseases and conditions such as atherosclerosis and cardiovascular disease. Another area that will be quite impactful is the degree of insulin resistance and glycemic control associated with periodontal disease, especially in view of the pandemic nature of diabetes. The role of periodontal pathogens on the development of rheumatoid arthritis (RA) is under investigation. Early evidence implicates the highly pathogenic bacteria Pg in the pathogenesis of RA. In the near future, medical research will classify RA as a cardiovascular risk factor with the same degree of risk as smoking, as research fills in the gaps. Adverse pregnancy events, including the role of periodontal disease and oral bacteria on preterm low-birth-weight infants and preeclampsia, comprise another area of research. The evidence is conflicting at this time, but further studies will shed more light on this association.
Even without data to support causality at this time, the association between oral and systemic diseases is sufficient to proceed with comprehensive periodontal care for the oral and general health of our patients. Educating our patients about these associations in a responsible, accurate manner is completely justified. Making our patients aware that research has demonstrated an association, without proving causality at this point, would fulfill this responsibility.
We need to treat every patient with any level of periodontal disease, every time they present to our care for the health of the oral cavity. Carrying treatment through to the endpoint of therapy, clinically and bacteriologically - such that all sites are healed and the periodontium is free of active disease and the causative bacteria have been reduced or eliminated - is the manner in which we would address the impact of periodontal disease beyond the oral cavity, regardless of demonstrated causality or associations. So the only thing to be avoided at this point is overstating the evidence. It is that simple.
RICHARD NAGELBERG, DDS, has practiced general dentistry in suburban Philadelphia for more than 30 years. He is a speaker, advisory board member, consultant, key opinion leader for several dental companies and organizations, and lecturer on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact him at [email protected].
