Periodontitis is characterized by subgingival biofilm dysbiosis, inflammation and tissue destruction. Current treatment involves mechanical biofilm disruption known as non-surgical periodontal therapy (NSPT). This study sought to characterise the impact of treatment on microbial diversity and overall community, and the parallel impact on host inflammation in the oral cavity. Fourty-two periodontitis patients were included in this study, with periodontal clinical parameters, subgingival plaque and saliva samples collected at baseline and 90 days after treatment. Salivary cytokines were quantified, and subgingival plaque was analysed using 16S rRNA sequencing. After treatment, there were marked health-associated alterations in microbial composition and diversity, including differential abundance of 42 genera and 61 species. These changes were accompanied by substantial clinical improvement (pockets ≥ 5 mm, 27.50% to 9.00%,p < 0.001) and a decrease in salivary IL-1β (p < 0.001)—a putative marker of periodontal inflammation. Despite significant reductions in disease associated anaerobes, several genera (Fusobacterium, Prevotella, Tanenerella, Treponema) remained present and formed a distinct subnetwork associated with residual disease. Collectively, this study shows that current periodontal treatment results in partial restoration of a healthy microbial ecosystem, but features of biofilm dysbiosis and host inflammation remain in some patients, which were surprisingly independent of clinical response.

Periodontitis (PD) shows an association with rheumatoid arthritis (RA) and systemic inflammation. Periodontal pathogens, namely Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, are proposed to be capable of inducing citrullination of peptides in the gingiva, inducing the formation of anti-citrullinated protein antibodies (ACPAs) within susceptible hosts. Here, we sought to investigate whether periodontal treatment influenced systemic inflammation and antibody titres to P. gingivalis, A. actinomycetemcomitans, Prevotella intermedia and ACPA in 42 systemically health patients with periodontal disease. Subgingival plaque and serum samples were collected from study participants before (baseline) and 90 days after treatment to analyse the abundance of specific bacteria and evaluate anti-bacterial antibodies, C-reactive protein (CRP), tumour necrosis factor α (TNF-α), interleukin 6 (IL-6) and ACPA in serum. Following treatment, all patients showed reduced periodontal inflammation. Despite observing a weak positive correlation between CRP and IL-6 with periodontal inflammation at baseline, we observed no significant reductions in any indicators of systemic inflammation 90 days after treatment. In contrast, anti-P. gingivalis IgG significantly reduced post-treatment (p < 0.001, Wilcoxon signed rank test), although no changes were observed for other antibody titres. Patients who had detectable P. gingivalis in subgingival plaques had significantly higher anti-P. gingivalis IgG and ACPA titres, suggesting a potential association between P. gingivalis colonisation and systemic antibody titres.

Objective: This study sought to investigate whether the immediate systemic inflammatory response following full‐mouth debridement differs following use of hand compared with ultrasonic instruments.Methods: Thirty‐nine periodontitis patients were randomized to treatment with full‐mouth debridement using either hand or ultrasonic instrumentation completed within 24 hr. Serum and periodontal clinical parameters were collected at baseline, day 1, day 7 and day 90 post‐treatment. Differences in systemic inflammatory markers were assessed using general linear models at each timepoint, corrected for age, gender, smoking status, body mass index and baseline levels of each marker.Results: Across all patients, serum C‐reactive protein increased at day 1, with no differences between hand and ultrasonic groups (p(adjusted) = .22). There was no difference between groups in interleukin‐6 (p(adjusted) = .29) or tumour necrosis factor α (p(adjusted) = .53) at day 1. Inflammatory markers returned to baseline levels by day 7. Treatment resulted in equal and marked improvements in clinical parameters in both groups; however, total treatment time was on average shorter for ultrasonic instruments (p(adjusted) = .002).Conclusions: Ultrasonic instrumentation resulted in shorter treatment time with comparable clinical outcomes. Levels of serum C‐reactive protein at day 1 were similar following debridement with hand or ultrasonic instruments.

Background: The reduction of nitrate to nitrite by the oral microbiota has been proposed to be important for oral health and results in nitric oxide formation that can improve cardiometabolic conditions, such as hypertension and diabetes. Studies of bacterial composition in subgingival plaque suggest that nitrate-reducing bacteria are associated with healthy conditions, but the impact of periodontitis on nitrate-reducing capacity and therefore nitric oxide availability has not been evaluated. The aim of the current study is to see assess how periodontitis and periodontal treatment affect the nitrate reduction capacity of the oral microbiota. Methods: First, 16S rRNA sequencing data of five studies from different countries were analysed with the Dada2 pipeline to compare nitrate-reducing bacteria in health and periodontitis. Additionally, subgingival plaque, saliva and plasma samples from 42 periodontitis patients were collected before and after non-surgical periodontal therapy (NSPT). The subgingival plaque bacterial composition was determined using Illumina sequencing of the 16S rRNA gene and the quantity of the nitrate-reducing biomarker genus Rothia was determined by qPCR. Measurements of nitrate and nitrite in saliva and plasma were performed and the salivary nitrate reduction capacity (NRC) was determined after three hours of incubation in vitro and compared with the NRC of 15 healthy individuals. Results: Nitrate-reducing bacteria were significantly lower in subgingival plaque of periodontitis patients compared with healthy individuals (p < 0.05 in all five datasets). After NSPT, nitrate-reducing bacteria increased in subgingival plaque (p < 0.05) and correlated negatively with periodontitis-associated bacteria (p < 0.001). A post-treatment increase in the genus Rothia was confirmed by qPCR (p < 0.05), as well as an increase in the salivary NRC (p < 0.05). No significant effect was found of NSPT on the plasma nitrate and nitrite levels in this population. Conclusion: The levels of nitrate-reducing bacteria of the subgingival microbiota decrease in periodontitis and both their levels and the salivary NRC increase after NSPT. We hypothesize that an impaired NRC can affect nitric oxide availability and can therefore be an instrumental link between periodontitis and systemic conditions.