Aim: To determine the impact of periodontal treatment on systemic markers of inflammation in patients with metabolic syndrome (MetS) and periodontitis. Materials and Methods: In this parallel-arm, double-blind, randomized controlled clinical trial, 63 patients with MetS and severe periodontitis were randomly assigned to receive either intensive periodontal treatment (IPT; scaling and root planing plus azithromycin 500 mg every day for 3 days) or minimal periodontal treatment (MPT; supragingival professional mechanical plaque removal plus a placebo). The primary outcome was the impact of the tested interventions on high-sensitivity C-reactive protein (hs-CRP) serum levels at 6 months. As secondary outcomes, differences in the levels of cytokines, markers of prothrombotic states, carbohydrate and lipid metabolism, as well as blood pressure, were measured at 3 and 6 months after therapy. Results: The intention-to-treat population consisted of 63 subjects randomly assigned to either the MPT (n = 31) or the IPT (n = 32) group. At baseline, mean hs-CRP was 3.9 mg/L (standard deviation [SD] = 2.9) and 3.9 mg/L (SD = 3.4), respectively, and no significant differences in cardiometabolic risk profiles were detected between the groups. Adjusting for baseline hs-CRP, sex, age, smoking status and body mass index, hs-CRP at 6 months was 1.2 mg/L (95% CI 0.4; 2.0; P = .004) lower in the IPT group than in the MPT group. In the secondary outcomes, significant reductions in IL-1β, TNF-α, HbA1c and blood pressure were observed in the IPT group at 3 months compared with the MPT group. Conclusion: Effective periodontal treatment significantly reduced hs-CRP after 6 months in patients with MetS and severe periodontitis. Periodontal therapy might be useful to reduce cardiovascular risk in these patients.

Obesity and periodontitis demonstrated a comorbidity effect on both systemic inflammatory and metabolic dysregulation biomarkers, with increased glucose, dyslipidemia and hepatic damage.

Aim: To analyse, through a pre-clinical in vivo model, the possible mechanisms linking depression and periodontitis at behavioural, microbiological and molecular levels.Materials and methods: Periodontitis (P) was induced in Wistar:Han rats (oral gavages with Porphyromonas gingivalis and Fusobacterium nucleatum) during 12 weeks, followed by a 3-week period of Chronic Mild Stress (CMS) induction. Four groups (n = 12 rats/group) were obtained: periodontitis and CMS (P+CMS+); periodontitis without CMS; CMS without periodontitis; and control. Periodontal clinical variables, alveolar bone levels (ABL), depressive-like behaviour, microbial counts and expression of inflammatory mediators in plasma and brain frontal cortex (FC), were measured.ANOVA tests were applied. Results:The highest values for ABL occurred in the P+CMS+ group, which also presented the highest expression of pro-inflammatory mediators (TNF-α, IL-1β and NF-kB) in frontal cortex, related to the lipoprotein APOA1-mediated transport of bacterial lipopolysaccharide to the brain and the detection of F. nucleatum in the brain parenchyma. A dysregulation of the hypothalamic-pituitary-adrenal stress axis, reflected by the increase in plasma corticosterone and glucocorticoid receptor levels in FC, was also found in this group. Conclusions:Neuroinflammation induced by F. nucleatum (through a leaky mouth) might act as the linking mechanism between periodontal diseases and depression.

Aims:To study the effect of adjunctive systemic administration of melatonin to standard mechanical periodontal therapy in obese rats with experimental periodontitis. Materials and methods:In 42 Wistar rats with an initial body weight of 180 g., half (n = 21) were fed with a high-fat diet to induce obesity. In both obese and normalweight groups, experimental periodontitis was subsequently induced through oral gavages with a combination of Porphyromonas gingivalis and Fusobacterium nucleatum. Both groups were randomly allocated to either no treatment or periodontal treatment consisting on standard mechanical debridement, with either adjunctive chlorhexidine or melatonin. Outcomes were evaluated by the changes in clinical parameters (probing depth modified gingival index, plaque dental index and bleeding on probing [BOP]), in bone resorption and in the levels of biomarkers in plasma and in gingival tissue (inflammatory cytokines, insulin, leptin, osteocalcin, osteopontin, plasminogen activator inhibitor-1, intercellular adhesion molecule 1, E-selectin and lipids). Results:In the obese-periodontitis group, adjunctive melatonin administration resulted in reduced gingival inflammation and BOP, with significant reductions in probing depth and enhanced bone repair demonstrated by micro-CT (15% reduction in alveolar bone destruction) when compared with the same group treated with adjunctive CHX or the normal-weight rats with either melatonin or CHX. In this melatonintreated obese-periodontitis group, a significant impact on biochemical biomarkers was also demonstrated in both gingival and plasma samples, when compared with the other groups, with significant reductions in pro-inflammatory cytokines. Conclusions:Adjunctive melatonin therapy significantly reduced alveolar bone loss and exerted a protective anti-inflammatory effect mainly in those experimental animals affected by the co-morbidity of periodontitis and obesity. K E Y W O R D S chlorhexidine, circadian rhythms, inflammation, melatonin, obesity, periodontitis | 1337 VIRTO eT al.