Mechanisms for exposing the host to bacterial material in periodontitis

Posted 12.10.2017

This blog is based on the concept that periodontitis is a chronic, low-grade bacterial infection that, contrary to acute infections, is multispecies and mostly asymptomatic. For a century, researchers tried to find ‘The periodontitis pathogen’, but despite several bacterial candidates were proposed this approach did not succeed in defining a single pathogen that would explain this complex disease. However, starting from the 1990s, bacterial biofilm science has brought a completely new insight into chronic infections. It generated a groundbreaking progress in the comprehension of the nature of disease in chronic infections, among them periodontitis. Along with rapidly advancing molecular biological technology new, detailed information started to flood of biofilms living as organized bacterial communities with regulated life style. Concomitantly with the advancing biofilm research a link was found between chronic infections and cardiovascular disease. The finding that atherosclerosis is an inflammatory disease and the primary cause of cardiovascular disease rapidly lead to further progress. Of fundamental importance was the research that produced the concept that systemic inflammation induces pathogenic events in arterial walls leading to development of atheroma plaques and their complications such as thromboembolia. What then triggers the systemic inflammation was the next question, to which one answer was - infection.


Good so far, but how can a chronic local infection such as periodontitis, where subgingival bacterial biofilms grow outside the epithelial lining of the body, contribute to systemic inflammation? For decades, it has been known that typical periodontal bacteria can be found in circulating blood and that they occasionally cause infections in various body parts. The most important source for these bacteria is the bacterial biofilm in subgingival tooth surfaces. From periodontal pockets bacteria disseminate through microulcerations in pocket epithelium into the sterile body compartment and participate in causing systemic inflammation. Since bacteria that detach from biofilm upregulate virulence properties for an acute infection, it would be worthwhile studying if these bacteria differ in chronic and active phases of periodontitis or in chronic and aggressively progressing periodontitis etc. For this purpose, gingival crevicular fluid could serve as practical bacterial sampling material.


Another interesting aspect in search for mechanisms how periodontitis contributes to systemic inflammation is the release of free molecules and outer membrane vesicles from bacteria living as sessile members of subgingival biofilm. This phenomenon provides continuous spread of bacterial material into blood circulation while bacteria remain living in biofilm ‘outside’ the body. An advantage over whole bacterial cells is that these bacterial parts are not restricted to certain species and that their small size enables them to readily pass biological membranes. Experimental studies have demonstrated that bacterial components spontaneously detach from biofilms and induce proinflammatory response in human blood, supporting the idea that it also occurs in vivo. In addition, proteomic analyses have revealed hundreds of proteins, among them tens of virulence-related proteins, in extracellular secretome of periodontal bacteria during their biofilm growth. If there are temporal or species-related differences in extracellular secretion or release activity among subgingival biofilm bacteria awaits new studies.


To sum up, besides infective bacterial cells also the release of free-soluble virulence-related molecules and outer membrane vesicles from subgingival biofilm provides a mechanism that exposes periodontitis patients to constant systemic spread of proinflammatory bacterial material. Even if periodontitis had a limited role in the development of cardiovascular disease, it would have a vital impact on human health. Early diagnostics and efficient treatment of initial periodontitis would easily abolish this threat to systemic health.

Prof. Sirkka Asikainen

Professor Emerita, Umeå University, Sweden & Adjunct Professor, University of Helsinki, Finland