“Inflammation and dysbiosis in periodontitis: Mechanisms and therapeutic intervention”
George Hajishengallis, DDS, PhD, Thomas W. Evans Centennial Professor, University of Pennsylvania, Penn Dental Medicine – Microbiology, Philadelphia, PA
Wednesday, March 8, 2017; 12:00 noon
Dixon Lecture Hall, UNMC, College of Dentistry
40th & Holdrege (UNL East Campus)
Presentation will be livestreamed to CON 2017 on the UNMC campus in Omaha
Hosted by: Dr. Tom Petro
Recent human microbiome analyses and animal model-based mechanistic studies collectively suggest that the pathogenesis of periodontitis is not mediated by a select few bacteria (traditionally known as ‘periopathogens’) but rather involves polymicrobial synergy and dysbiosis. The dysbiosis of the periodontal microbiota represents an alteration in the relative abundance or influence of individual members of the polymicrobial community (relative to their abundance or influence in health) leading to dysregulated host-microbial interactions that mediate destructive inflammation and bone loss. Functional specialization of community participants has given rise to several newly appreciated designations within the commensal-to-pathogen spectrum (e.g., accessory pathogens, keystone pathogens, and pathobionts). Although necessary, the bacteria are not sufficient to cause periodontitis, as it is the host inflammatory response to this polymicrobial challenge that predominantly inflicts damage to the periodontium. It is now well appreciated that the control of periodontal inflammation can indirectly exert antimicrobial effects. This is because periodontitis-associated bacteria thrive in an inflammatory environment. Indeed, the release into the gingival crevicular fluid of inflammatory breakdown products of connective tissue favors the outgrowth of certain species (e.g., proteolytic and asaccharolytic) that can benefit from these microenvironmental alterations. Briefly stated, an initial inflammatory response (e.g., due to incipient dysbsiosis associated with poor oral hygiene) may select for those bacteria that can give rise to full-blown dysbiosis, thereby exacerbating inflammation and ultimately causing clinically evident periodontitis in susceptible individuals. Therefore, the control of inflammation should not only inhibit tissue damage but also suppress a nutritionally favorable environment that fuels dysbiosis.
All interested faculty, staff and students are invited to attend this presentation. The seminar will be recorded and available for those who cannot attend.