Periodontitis has been associated with low-grade inflammation as assessed by C-reactive protein (CRP) levels and its treatment can decrease CRP serum levels. The aim of this systematic review was to critically appraise the evidence comparing CRP serum levels (standard and high-sensitivity [hs]) of otherwise healthy patients suffering from periodontitis when compared to controls. The impact of intensive and non-intensive nonsurgical periodontal treatment (NSPT) on hs-CRP was also investigated. Four electronic databases (Pubmed, The Cochrane Central Register of Controlled Trials [CENTRAL], EMBASE and Web of Science) were searched up to February 2021 and the review was completed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines (PROSPERO No. CRD42020167454). Observational and intervention studies that: 1) evaluated CRP and hs-CRP serum levels in patients with and without periodontitis, and; 2) hs- CRP levels after NSPT were included. Following risk of bias appraisal, both qualitative and quantitative analyses were performed. Pooled estimates were rendered through ratio of means (RoM) random-effects meta-analyses. After screening 485 studies, 77 case-control studies and 67 intervention trials were included. Chronic and aggressive periodontitis diagnoses were consistently associated with higher levels of CRP and hs-CRP (p<0.001). Patients with aggressive periodontitis exhibited on average more than 50% higher levels of CRP (RoM [95% confidence interval [CI]]: 1.56 [1.15; 2.12], p=0.0039) than patients with chronic periodontitis. Intensive NSPT induced an immediate increase of hs-CRP followed by a progressive decrease whilst non-intensive NSPT consistently decreased hs-CRP after treatment up to 180 days (p<0.001). These findings provide robust evidence that periodontitis is associated with systemic inflammation as measured by serum CRP levels. Periodontitis treatment induces a short-term acute inflammatory increase when performed in an intensive session, whilst a progressive reduction up to 6 months was demonstrated when performed in multiple visits.

Polycystic ovary syndrome (PCOS) has reproductive and metabolic properties that may be linked to periodontitis (PD). This study aimed to update and render a robust critical assessment on all evidence linking PCOS and PD, and appraising a hypothetical bidirectional association. Five databases (PubMed, Scholar, EMBASE, Web of Science and CENTRAL) were searched up to May 2020. Case-control and cohort studies on the association of PCOS and PD were included. The risk of bias of observational studies was assessed through the Newcastle-Ottawa Scale (NOS). Random effects meta-analyses of standardized mean difference (SMD) and risk ratio (RR) were performed. We followed Strength of Recommendation Taxonomy (SORT) to appraise the strength and quality of the evidence. Twelve case-controls fulfilled the inclusion criteria (876 with PCOS and 48170 healthy controls), all scored as having a low risk of bias. Meta-analysis revealed that PCOS females have 28% more risk towards PD, and PD females have 46% more risk to have PCOS. PCOS females with PD had higher gum bleeding, periodontal pocket depth and clinical attachment loss than non-PCOS females with PD. Populations with undefined periodontal status contribute to underestimated results. On the basis of the available evidence, it is possible to assume a bidirectional link between PCOS and PD. That is, PCOS increases by 28% the risk of having PD and in the same fashion, PD increases by 46% the risk of having PCOS. Furthermore, women with PCOS were associated with worsening clinical characteristics and inflammation of PD. These findings suggest that PCOS and PD may be linked. Hence, further prospective and clinical trial studies with nonsurgical periodontal therapy are necessary to clarify the existence of an increased risk of PCOS in women with PD and vice-versa.

To explore the association between bacterial vaginosis (BV) and periodontitis (PD) and to determine whether PD and BV might be linked with systemic serum alterations. We used the National Health and Nutrition Examination Survey 2001–2004, with women aged 18–49 years old and diagnosed with or without BV according to Nugent’s method. PD was defined according to the 2012 case definition. We compared serum counts according to the presence of PD and the presence of BV. Multivariable regression was used to explore and identify relevant variables towards the presence of BV. 961 women fulfilled the inclusion criteria. In women with BV, PD was associated with higher inflammation, characterized by increased white blood cells (p = 0.006) and lymphocyte (p = 0.009) counts. Predictive models presented a statistically significant association between PD and BV [Odds Ratio (OD) = 1.69, 95% Confidence Interval (CI): 1.09–2.61 for periodontitis; OD = 2.37, 95% CI: 1.30–4.29 for severe PD]. Fully adjusted models for age, smoking, body mass index, diabetes mellitus and number of systemic conditions reinforced this association [OD = 1.71, 95% CI: 1.06–2.76 for PD; OD = 2.21, 95% CI: 1.15–4.25 for severe PD]. An association between BV and PD is conceivable. PD was associated with higher systemic markers of inflammation in women with BV. Our data is novel and could serve as a foundation to guide future studies in the confirmation of this association and the underlying mechanisms.