Systemic inflammation induced by periodontitis is suggested to be the link between periodontitis and cardiovascular disease. The aim of this work was to explore the oral microbiome in periodontitis in relation to disease severity and systemic inflammation. The saliva and subgingival microbiome from periodontal pocket samples of patients with severe (n = 12) and mild periodontitis (n = 13) were analyzed using metagenomic shotgun sequencing. The taxa and pathways abundances were quantified. The diversity was assessed and the abundances to phenotype associations were performed using ANCOM and linear regression. A panel of inflammatory markers was measured in blood and was associated with taxa abundance. The microbial diversity and species richness did not differ between severe and mild periodontitis in either saliva or periodontal pockets. However, there were significant differences in the microbial composition between severe and mild periodontitis in the subgingival microbiome (i.e., pocket samples) and, in a lower grade, in saliva, and this is positively associated with systemic inflammatory markers. The “red complex” and “cluster B” abundances in periodontal pockets were strongly associated with inflammatory markers interleukin-6 and the white blood cell count. Our data suggest that systemic inflammation in severe periodontitis may be driven by the oral microbiome and may support the indirect (inflammatory) mechanism for the association between periodontitis and cardiovascular disease.

The aim of this comprehensive review is to summarize recent literature on associations between periodontitis and neurodegenerative diseases, explore the bidirectionality and provide insights into the plausible pathogenesis. For this purpose, systematic reviews and meta-analyses from PubMed, Medline and EMBASE were considered. Out of 33 retrieved papers, 6 articles complying with the inclusion criteria were selected and discussed. Additional relevant papers for bidirectionality and pathogenesis were included. Results show an association between periodontitis and Alzheimer’s disease, with odds ratios of 3 to 5. A bidirectional relationship is suspected. For Parkinson’s disease (PD), current evidence for an association appears to be weak, although poor oral health and PD seem to be correlated. A huge knowledge gap was identified. The plausible mechanistic link for the association between periodontitis and neurodegenerative diseases is the interplay between periodontal inflammation and neuroinflammation. Three pathways are hypothesized in the literature, i.e., humoral, neuronal and cellular, with a clear role of periodontal pathogens, such as Porphyromonas gingivalis. Age, gender, race, smoking, alcohol intake, nutrition, physical activity, socioeconomic status, stress, medical comorbidities and genetics were identified as common risk factors for periodontitis and neurodegenerative diseases. Future research with main emphasis on the collaboration between neurologists and dentists is encouraged.

Scaling and root planning is a key element in the mechanical therapy used for the eradication of biofilm, which is the major etiological factor for periodontitis and peri‐implantitis. However, periodontitis is also a host mediated disease, therefore, removal of the biofilm without adjunctive therapy may not achieve the desired clinical outcome due to persistent activation of the innate and adaptive immune cells. Most recently, even the resident cells of the periodontium, including periodontal ligament fibroblasts, have been shown to produce several inflammatory factors in response to bacterial challenge. With increased understanding of the pathophysiology of periodontitis, more research is focusing on opposing excessive inflammation with specialized pro‐resolving mediators (SPMs). This review article covers the major limitations of current standards of care for periodontitis and peri‐implantitis, and it highlights recent advances and prospects of SPMs in the context of tissue reconstruction and regeneration. Here, we focus primarily on the role of SPMs in restoring tissue homeostasis after periodontal infection.

Aim: Chemoattractants, such as stromal cell‐derived factor‐1α (SDF‐1α), can offer an advantage for periodontal regeneration by recruiting the patient’s own stem cells to stimulate self‐repair. We here developed a chemoattractive construct for periodontal regeneration using SDF‐1α and evaluated its efficacy in vivo.Materials and Methods: SDF‐1α was loaded on gelatin sponge and tested in vitro for SDF‐1α release. Subsequently, SDF‐1α constructs were implanted into rat periodontal defects for 1 and 6 weeks, with unloaded materials and empty defects as controls. The regenerative efficacy was evaluated by micro‐CT, histological and histomorphometrical analyses.Results: In vitro results showed limited SDF‐1α release up to 35 days. In contrast, SDF‐1α constructs significantly improved periodontal defect regeneration in terms of alveolar bone height, new bone area and functional ligament length. Additionally, SDF‐1α constructs decreased the inflammatory response at Week 6.Conclusion: Chemoattractive constructs significantly improved periodontal regeneration in terms of alveolar bone height, new bone area and functional ligament length.

Background: Perioperative oral care has been proposed as an effective intervention to reduce postoperative complications in patients undergoing major cancer surgery, however, its effectiveness across different cancer types and surgical procedures remains unclear. Objective: To evaluate the effectiveness of perioperative oral care in reducing postoperative complications among patients undergoing major cancer surgery. Materials and methods: A systematic literature search was conducted across five databases to identify studies evaluating the effect of perioperative oral care on postoperative outcomes following oncological surgery. Twenty-six studies were included, comprising retrospective and prospective cohort and case–control studies. The primary outcomes were postoperative pneumonia, surgical-site infection (SSI), and mortality. Meta-analyses were performed for postoperative pneumonia and SSI, whereas mortality was analyzed descriptively because of clinical and methodological heterogeneity. Results: Perioperative oral care was significantly associated with reduced odds of postoperative pneumonia (OR = 0.47; 95% CI: 0.40–0.54; P < 0.00001) and SSI (OR = 0.45; 95% CI: 0.36–0.56; P < 0.00001). Subgroup analyses demonstrated variation in effect sizes across cancer types, with the greatest benefits observed in lung, esophageal, colorectal, and pancreatic cancer surgery. Mortality outcomes showed a trend toward lower mortality in patients receiving perioperative oral care. However, these data could not be quantitatively synthesized because of differences in outcome definitions, follow-up periods, and study populations. Variation in oral care protocols, study design, and potential residual confounding contributed to the observed clinical and methodological heterogeneity. Conclusion: The current evidence suggests that perioperative oral care is associated with lower rates of postoperative pneumonia and SSI in patients undergoing major cancer surgery. However, because the available evidence is derived predominantly from observational studies conducted in Japan, well-designed multicenter randomized controlled trials in different countries and healthcare systems are needed to confirm these findings, improve generalizability, and establish standardized perioperative oral care protocols.