Introduction
Periodontitis is the outcome of progressive and persistent inflammation of the supporting
tissues of the teeth leading to clinical attachment loss, alveolar bone loss, and periodontal
pocket formation. As has been clearly documented over the years, periodontitis is a
multifactorial disease involving a microbial challenge, a host immune–inflammatory
response, other local factors, and genetic factors
The interrelationship between diseases in the mouth and body as a whole is not a new
concept as it has been debated for over a hundred years. The theory of “focal infection” was
introduced by William Hunter as a way to connect oral infections or sepsis with infections in
other parts of the body [1]. This led to the removal of many “infected teeth” with the hope
that this would also lead to the cure of distant disease conditions. It was only in the 1980s
and 1990s that there was concerted effort at gathering scientific evidence on the topic,
namely, establishing links between chronic periodontal disease and other systemic diseases
Starting with the debate in the 19th century between non-specific and specific plaque
theories to the later experimental disease and longitudinal models, bacterial plaque and its
byproducts in a susceptible host have been recognized as the primary etiology factor.
The development of epidemiological studies and statistical analysis, the enhanced
understanding of biological plausibility by means of advances in molecular biology,
microbiology, immunology and genetics, the possibility of successfully treating periodontal
diseases, caries and endodontic infections and retaining teeth instead of extracting them, all
these factors have led dental and medical researchers and clinicians to resume the study of
the relationship between oral diseases and systemic conditions with a more scientific
approach.
The Link between Periodontal Diseases and Systemic Conditions
Despite dental plaque biofilm being considered the primary risk factor for periodontitis in
the vast majority of patients that dentists encounter on a daily basis, there are other factors
that can also contribute and/or accelerate the pathologic progressive attachment loss. One
should also recognize that the periodontium may be considered as a reservoir of bacteria,
bacterial products, and inflammatory and immune mediators which can interact with other
organ systems remote from the oral cavity. In the 2012 joint European Federation of
Periodontology (EFP) and the American Academy of Periodontology (AAP) consensus report,
it concluded that periodontitis may induce systemic inflammation via translocated
circulating oral microbiota that impacts upon the development of atherothrombogenesis,
thus suggesting the biological interaction and association between periodontal diseases and
cardiovascular disease
Mechanisms by which chronic periodontal disease may add to systemic disease may be
considered as being via a direct and an indirect route. The direct route is via ulceration in the
lining of periodontal pockets, which can become a passage for bacteria into the systemic
circulation leading to bacteremia that allows periodontal disease bacteria to settle in distant
organs aggravating existing disease conditions. [13]. The indirect route posits that chronic
periodontal disease, being a significant source of inflammation, may play a role in other
disease conditions in which inflammation is a major component. The role of the C-Reactive
protein in this pathogenesis appears to be one that has strong evidence in its favor [14,15].
A recent study, which used ligature-induced periodontal disease in mouse models and
human experimental gingivitis model, demonstrated that periodontal inflammation can
result in increased polymorphonuclear neutrophils (PMNs) and potentially prime the
systemic innate immune response [16]. This PMN-mediated hyperinflammatory innate
immune response could be the plausible biologic crosslink between periodontal disease and
the other chronic inflammatory diseases such as cardiovascular diseases, diabetes and
arthritis.
