Periodontitis has been independently associated with the chronic noncommunicable diseases that most frequently lead to death worldwide. The aim of the present systematic review was to study whether people with periodontitis/edentulism are at increased risk of all-cause and cause-specific mortality as compared with those without periodontitis/edentulism. Cohort studies were included that 1) evaluated periodontitis or edentulism as exposures in relation to all-cause or cause-specific mortality as an outcome and 2) reported effect estimates as hazard ratios, risk ratios, or odds ratios with 95% CIs or crude numbers. Two review authors independently searched for eligible studies, screened the titles and abstracts, did full-text analysis, extracted the data from the published reports, and performed the risk-of-bias assessment. In case of disagreement, a third review author was consulted. Study results were summarized through random effects meta-analyses. A total of 57 studies were included, involving 48 cohorts and 5.71 million participants. Periodontitis was associated with increased risk of all-cause mortality (risk ratio, 1.46 [95% CI, 1.15 to 1.85]) and mortality due to cardiovascular diseases (1.47 [1.14 to 1.90]), cancer (1.38 [1.24 to 1.53]), coronary heart disease (2.58 [2.20 to 3.03]), cerebrovascular diseases (3.11 [2.42 to 3.98]), but not pneumonia (0.98 [0.69 to 1.38]). Edentulism (all types) was associated with increased risk of all-cause mortality (1.66 [1.46 to 1.88]) and mortality due to cardiovascular diseases (2.03 [1.50 to 2.74]), cancer (1.55 [1.24 to 1.94]), pneumonia (1.72 [1.07 to 2.78]), coronary heart disease (2.98 [2.43 to 3.65]), and cerebrovascular diseases (3.18 [2.24 to 4.51]). Periodontitis and its ultimate sequela (edentulism) are associated with an increased risk of all-cause and cause-specific mortality (PROSPERO CRD42018100095).

As the whole world is epidemically aging, the burden of periodontitis and tooth loss is becoming a major health concern. Growing meta-epidemiological data implicate chronic systemic inflammation/infection due to periodontitis as an independent risk factor for aging-related diseases and mortality. However, because people age differently, chronological age is not a reliable marker of an individual’s functional status. Recent advances in geroscience have shown that various biomarker signatures of biological aging are longitudinally associated with declined physical function, morbidity, and mortality due to major age-related diseases, including periodontitis. Here, we emphasize novel research developments bidirectionally linking periodontitis to accelerated biological aging. Using a composite biomarker age estimator, a striking increase in periodontitis and tooth loss was observed in subjects whose biological age at baseline was higher than their chronological age. Moreover, significantly shortened telomeres were encountered in populations affected by severe periodontitis. Second, we elucidate the cellular and molecular pillars of the aging process at the periodontal level. Accumulating evidence suggests that cellular senescence, stem cell exhaustion, and immunoaging are hallmarks of biological aging implicated in the impairment of periodontal homeostasis and the pathophysiology of periodontitis. Indeed, persistent bacteria-derived lipopolysaccharide stimulation influences cellular senescence in osteocytes, driving alveolar bone resorption. Moreover, inflammaging status induced by chronic hyperglycemia elevates the burden of senescent cells in gingival tissues, impairing their barrier function. Lastly, we reviewed a recent breakthrough in senotherapy to directly target the mechanisms of aging at the periodontal level. Physical exercise and intermittent fasting, together with natural compounds, senolytic drugs, and cell therapy, are increasingly being evaluated to rejuvenate the oral cavity. Following these innovations in geroscience, further advancements could provide oral clinicians the chance to intercept biological aging when still “subclinical” and set interventions for halting or delaying the trajectory toward aging-related diseases while patients are still chronologically young.

Objective: To answer the following PICO question: “In patients requiring surgical treatment of peri‐implantitis (P), is any implant surface decontamination protocol (I) superior to others (C) in terms of clinical and radiographic parameters (O)?”Methods: Randomized clinical trials (RCTs) comparing two or more decontamination protocols as part of the surgical treatment of peri‐implantitis were included. Two authors independently searched for eligible studies, screened titles and abstracts, did full‐text analysis, extracted data, and performed the risk‐of‐bias assessment. Whenever possible, results were summarized through random effects meta‐analyses.Results: Twenty‐two manuscripts reporting on 16 RCTs were included, testing mechanical, chemical and physical decontamination protocols. All of them resulted in an improvement in clinical parameters; however, the superiority of specific protocols over others is mainly based on single RCTs. The use of titanium brushes and implantoplasty showed favorable results as single decontamination methods. Meta‐analyses indicated a lack of added effect of Er:Yag laser on probing pocket depth (PPD) reduction (n = 2, WMD = −0.24 mm, 95% confidence interval [CI] [−1.10; 0.63], p = .59); while systemic antimicrobials (amoxicillin or azithromycin) showed an added effect on treatment success ([PPD ≤5 mm, no bleeding or suppuration, no progressive bone loss]; n = 2, RR = 1.84, 95% CI [1.17;2.91], p = .008), but not in terms of PPD reduction (n = 2, WMD = 0.93 mm, 95% CI [−0.69; 2.55], p = .26), even if with substantial heterogeneity.Conclusions: No single decontamination method demonstrated clear evidence of superiority compared to the others. Systemic antibiotics, but not Er:Yag laser, may provide short‐term clinical benefits in terms of treatment success (CRD42020182303).

Mounting evidence indicates that periodontitis-related oral bacteria may contribute to gut microbial dysbiosis. This clinical study aimed to explore the oral–gut microbial signatures associated with periodontitis and to longitudinally evaluate the effect of periodontal treatment on the oral and gut microbial composition. Stool and saliva samples from generalized stage III/IV periodontitis patients ( n = 47) were collected and analyzed by 16S ribosomal RNA gene amplicon sequencing, before and 3 mo after steps I to II of periodontal therapy. Periodontally healthy matched subjects ( n = 47) were used as controls. Principal component analysis was carried out to identify oral–gut microbial profiles between periodontitis patients at baseline and healthy subjects; periodontitis samples were longitudinally compared before and after treatment. β-Diversity of gut microbial profiles of periodontitis patients before treatment significantly differed from healthy controls ( P < 0.001). Periodontal therapy was associated with a significant change in gut microbiota ( P < 0.001), with post-treatment microbial profiles similar to healthy volunteers. A higher abundance of Bacteroides, Faecalibacterium, Fusobacterium, and Lachnospiraceae was noted in fecal samples of periodontitis patients at baseline compared to healthy controls. In contrast, Lactobacillus was the only genus more abundant in the latter. Additionally, periodontal therapy led to a parallel reduction in the salivary carriage of periodontal pathobionts, as well as gut Bacteroides, Lachnoclostridium, Lachnospiraceae, Oscillospiraceae, and Ruminococcaceae, to levels similar to healthy controls. Collectively, discriminating oral–gut microbial signatures of periodontitis were found. Periodontal treatment both mitigated oral dysbiosis and altered gut microbial composition, signifying potential broader implications for gastrointestinal health and disease.