Moritz Kebschull1, Panos N Papapanou. 1. Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine Columbia University, New York, NY 10032, USA.
Abstract
AIMS: In this review, we summarize data on the association between specific periodontal bacterial profiles and tissue gene/protein expression, generated from cell culture models and in vivo studies. MATERIAL AND METHODS: A PubMed search was conducted to identify publications related to the effects of periodontal microbiota on host cells/tissues. RESULTS AND CONCLUSIONS: The data indicate the presence of specific host tissue responses to particular microbial complexes, evident by differential regulation of gene or protein expression, ultimately resulting in distinct clinical phenotypes. Transcriptomic analyses showed that periodontal pathogens induce a small, "common core" of differentially regulated genes encoding for an inflammatory response, and a larger variable set of genes that may reflect pathogen-specific cellular responses. Limitations of available studies include (i) the unclear role of hundreds of subgingival species not yet investigated, (ii) the fact that in vitro studies utilizing single populations of oral cells challenged with mono-infections of planktonic bacteria may not adequately portray human periodontal diseases and (iii) the cross-sectional nature of most human studies that makes them inherently incapable of allowing temporal or causal inferences. Longitudinal studies in humans hold the potential to be superior to any model, but need to be adequately powered and controlled.
AIMS: In this review, we summarize data on the association between specific periodontal bacterial profiles and tissue gene/protein expression, generated from cell culture models and in vivo studies. MATERIAL AND METHODS: A PubMed search was conducted to identify publications related to the effects of periodontal microbiota on host cells/tissues. RESULTS AND CONCLUSIONS: The data indicate the presence of specific host tissue responses to particular microbial complexes, evident by differential regulation of gene or protein expression, ultimately resulting in distinct clinical phenotypes. Transcriptomic analyses showed that periodontal pathogens induce a small, "common core" of differentially regulated genes encoding for an inflammatory response, and a larger variable set of genes that may reflect pathogen-specific cellular responses. Limitations of available studies include (i) the unclear role of hundreds of subgingival species not yet investigated, (ii) the fact that in vitro studies utilizing single populations of oral cells challenged with mono-infections of planktonic bacteria may not adequately portray humanperiodontal diseases and (iii) the cross-sectional nature of most human studies that makes them inherently incapable of allowing temporal or causal inferences. Longitudinal studies in humans hold the potential to be superior to any model, but need to be adequately powered and controlled.
Authors: Benjamin Krämer; Moritz Kebschull; Michael Nowak; Ryan T Demmer; Manuela Haupt; Christian Körner; Sven Perner; Søren Jepsen; Jacob Nattermann; Panos N Papapanou Journal: Infect Immun Date: 2012-12-17 Impact factor: 3.441
Authors: Jamal M Stein; Helmut K G Machulla; James Deschner; Stefan Fickl; Yvonne Jockel-Schneider; Miriam Tamm; Susanne Schulz; Stefan Reichert Journal: Clin Oral Investig Date: 2015-08-26 Impact factor: 3.573