Importantly, even though we examined

colonization patterns by only a limited number of bacterial species, we found that the variable subgingival bacterial load by several -but clearly not all- species correlated significantly with tissue gene expression. In other words, and to paraphrase both Anton van Leeuwenhoek and George Orwell, our data indicate that all subgingival “”animalcules”" are not “”equal”" in this respect. In a recent publication [10], we presented transcriptomic data from a subset of patients involved in the present report (90 patients and 247 arrays out learn more of the total of 120 patients and 310 arrays included here) and compared

gene expression profiles of clinically healthy and diseased gingival tissues in patients with periodontitis. We documented substantial differential gene expression between states of gingival health and disease that was reflected both by genes that were a priori anticipated to be variably expressed based on current knowledge (e.g., several inflammatory, immune function- and apoptosis-related genes), but also by genes that are not readily associated with gingival inflammation (e.g., the transcription factor POU2AF1, the sperm associated antigen 4 which appears to be associated with apoptosis (own unpublished data), the cell adhesion-mediating Adriamycin solubility dmso protein desmocollin 1, and the signaling lymphocytic

activation molecule family member 7). In the present study, we sought to investigate whether the bacterial content of the selleck chemicals periodontal pocket is also a determinant of gene expression in the adjacent gingival tissues in order to enhance our understanding of the host-bacterial interactions that take place in the interface between the plaque biofilm and the periodontal pocket. We realize that the above question can ideally be addressed in a longitudinal prospective rather than a cross-sectional study. Thus, although our analyses considered bacterial colonization as the independent exposure and tissue gene expression as the outcome, it is impossible to rule out reverse causation, i.e., that the qualitative characteristics of the gingival tissue are the determinants of bacterial colonization. However, given that periodontitis is a bacterially-induced infection, the former approach is reasonable in the discussion of the observed correlations between colonization patterns and tissue gene expression signatures. We also want to draw the reader’s attention to the fact that, despite our inferences on each particular bacterial species’ effect on the gingival tissue transcriptome, we have not studied individual mono-infections.