actinomycetemcomitans, P. gingivalis and C. rectus, and tissue-infiltrating neutrophils are a conceivable source for these transcripts. In general, the magnitude of the

differential expression of host tissue genes according to levels of A. actinomycetemcomitams (with a total of 68 genes exceeding an absolute fold change of 2 when comparing tissue samples in the upper and lowest quintiles of subgingival colonization; Additional File 1) was more limited than that of bacteria in the ‘red complex’ (488 genes for P. gingivalis, 521 genes for T. forsythia, 429 genes for T. denticola; Additional Files 2, 3, 4) or C. rectus (450 genes; Additional File 8). The null hypothesis underlying the present study, i.e., that variable subgingival bacterial load by specific bacteria results

in no differential gene expression in the selleck chemical adjacent pocket tissues, was rejected by our data. Indeed levels of only 2 of the 11 species investigated appeared to correlate poorly with differential gene expression in the tissues: A. naeslundii, whose levels were statistically associated with differential expression of only 8 probe sets out of the approximately 55,000 analyzed, and E. corrodens with <1% of the probe sets being differentially regulated between pockets with the highest versus the selleck chemicals llc Y-27632 2HCl lowest levels of colonization. In contrast, 15-17% of the examined probes sets were differentially expressed according to subgingival levels of the “”red complex”" species and C.

rectus, whose levels were the most strongly correlated with gingival tissue gene expression signatures among all investigated species. Importantly, the above associations between bacterial colonization and gingival tissue gene expression signatures were confirmed in analyses adjusting for clinical periodontal status, although they were expectedly attenuated. In other words, the difference in the tissue transcriptomes between periodontal pockets with high versus low levels of colonization by the particular species identified as strong regulators of gene expression cannot solely be ascribed to differences in the clinical status of the sampled tissues [10] which is known to correlate well with bacterial colonization patterns [31]. Instead, our analyses based on either statistical adjustment or restriction to ‘diseased’ tissue samples consistently demonstrate that, even among periodontal pockets with similar clinical characteristics, the subgingival colonization patterns still influence the transcriptome of the adjacent gingival tissues.