The human microbiome plays important roles in health, but when disrupted, these same indigenous microbes can cause disease. The composition of the microbiome changes during the transition from health to disease; however, these changes are often not conserved among patients. Since microbiome-associated diseases like periodontitis cause similar patient symptoms despite interpatient variability in microbial community composition, we hypothesized that human-associated microbial communities undergo conserved changes in metabolism during disease. Here, we used patient-matched healthy and diseased samples to compare gene expression of 160,000 genes in healthy and diseased periodontal communities. We show that health- and disease-associated communities exhibit defined differences in metabolism that are conserved between patients. In contrast, the metabolic gene expression of individual species was highly variable between patients. These results demonstrate that despite high interpatient variability in microbial composition, disease-associated communities display conserved metabolic profiles that are generally accomplished by a patient-specific cohort of microbes.

Salivary copy-counts of P. gingivalis, T. forsythia and P. intermedia appear to have the potential to identify the presence of periodontitis, whereas the salivary level of the other test infectious agents may possess little or no diagnostic utility. Longitudinal studies are warranted to determine the ability of salivary copy-counts of major periodontopathic bacteria to predict future periodontal breakdown.

Both techniques were effective for maxillary sinus augmentation, and after 6 months of healing, the addition of L-PRF in DBBM did not improve the amount of regenerated bone or the amount of the graft integrated into the newly formed bone under histological and histomorphometric evaluation.

The present findings suggest that OSAS may have an increasing effect on salivary IL-6 and IL-33 concentrations regardless of OSAS severity. Additional investigation is required to elucidate a potential bidirectional relationship between OSAS and periodontal disease.

Within the limits of this study, it may be suggested that elevated salivary and serum TNF-α, APRIL, and BAFF in patients with periodontitis may contribute to the dominance of B cells in periodontitis lesions. Moreover, higher levels in healthy smokers than non-smoking counterparts may play a role in detrimental effects of smoking on periodontal tissues.