Dental caries and periodontitis account for a vast burden of morbidity and healthcare spending, yet their genetic basis remains largely uncharacterized. Here, we identify self-reported dental disease proxies which have similar underlying genetic contributions to clinical disease measures and then combine these in a genome-wide association study meta-analysis, identifying 47 novel and conditionally-independent risk loci for dental caries. We show that the heritability of dental caries is enriched for conserved genomic regions and partially overlapping with a range of complex traits including smoking, education, personality traits and metabolic measures. Using cardio-metabolic traits as an example in Mendelian randomization analysis, we estimate causal relationships and provide evidence suggesting that the processes contributing to dental caries may have undesirable downstream effects on health.

Anandamide (AEA) exhibits anti-inflammatory effects. However, its role in the periodontal field remains unknown. Here, we found that gingival crevicular fluid contained a detectable level of AEA. The cannabinoid receptors CB1 and CB2 were expressed by human gingival fibroblasts (HGFs), and markedly upregulated under pathological conditions. AEA significantly reduced the production of pro-inflammatory mediators (IL-6, IL-8 and MCP-1) induced by Porphyromonas gingivalis LPS in HGFs, and this effect was attenuated by AM251 and SR144528, selective antagonists of CB1 and CB2, respectively. Moreover, AEA completely blocked LPS-triggered NF-jB activation, implying that AEA may regulate hyperinflammatory reactions in periodontitis.

We investigated the efficacy, safety, and clinical significance of trafermin, a recombinant human fibroblast growth factor (rhFGF)‐2, for periodontal regeneration in intrabony defects in Phase III trials. Study A, a multicenter, randomized, double‐blind, placebo‐controlled study, was conducted at 24 centers. Patients with periodontitis with 4‐mm and 3‐mm or deeper probing pocket depth and intrabony defects, respectively, were included. A total of 328 patients were randomly assigned (2:1) to receive 0.3% rhFGF‐2 or placebo, and 323 patients received the assigned investigational drug during flap surgery. One of the co‐primary endpoints, the percentage of bone fill at 36 weeks after drug administration, was significantly greater in the rhFGF‐2 group at 37.131% (95% confidence interval [CI], 32.7502 to 41.5123; n = 208) than it was in the placebo group at 21.579% (95% CI, 16.3571 to 26.8011; n = 100; p < 0.001). The other endpoint, the clinical attachment level regained at 36 weeks, was not significantly different between groups. Study B, a multicenter, randomized, blinded (patients and evaluators of radiographs), and active‐controlled study was conducted at 15 centers to clarify the clinical significance of rhFGF‐2. Patients with 6‐mm and 4‐mm or deeper probing pocket depth and intrabony defects, respectively, were included. A total of 274 patients were randomly assigned (5:5:2) to receive rhFGF‐2, enamel matrix derivative (EMD), or flap surgery alone. A total of 267 patients received the assigned treatment during flap surgery. The primary endpoint, the linear alveolar bone growth at 36 weeks, was 1.927 mm (95% CI, 1.6615 to 2.1920; n = 108) in the rhFGF‐2 group and 1.359 mm (95% CI, 1.0683 to 1.6495; n = 109) in the EMD group, showing non‐inferiority (a prespecified margin of 0.3 mm) and superiority of rhFGF‐2 to EMD. Safety problems were not identified in either study. Therefore, trafermin is an effective and safe treatment for periodontal regeneration in intrabony defect, and its efficacy was superior in rhFGF‐2 compared to EMD treatments. © 2015 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research (ASBMR).

Adverse pregnancy outcomes (APOs) have been defined as (a) pre‐term birth, when there is a delivery before 37 completed weeks (<259 days); (b) pre‐eclampsia, which is a multisystem disorder of pregnancy characterized by maternal hypertension and proteinuria after the 20th gestational week; (c) low and very low birthweight, depending on whether the weight of the baby is less of 2500 g or <1500 g and (d) the spontaneous death of the fetus with <20 weeks (miscarriage) or between 20 and 36 weeks (stillbirth). In 2012, during the Consensus Report from the Joint EFP/AAP workshop on periodontitis and systematic diseases the role of periodontal diseases on APOs was reviewed. Some years later, this evidence has grown, and an update on the literature regarding the mechanisms related to this potential association (APOs and periodontal diseases) needs to be presented. The two major pathways (direct and indirect) already accepted in 2012 are still valid nowadays. Most evidence published in the last 5 years deals with a strong and solid evidence coming from the direct pathway while there is as scarce new evidence regarding indirect pathway. In this direct pathway, the haematological dissemination of oral microorganisms and their products, would later induce an inflammatory/Immune response in the foetal‐placental unit. The most plausible route for this direct pathway is the hematogenous transmission through dental bacteremia, although not many new studies dealing with bacteremia has been performed lately.

The TPL women revealed worsened periodontal conditions and elevated serum IL-8 and IL-1beta levels compared to the non-TPL women. The elevated levels of serum IL-8 and IL-1beta could have affected the maintenance of the proper uterine-fetus relationship, resulting in premature uterine contractions.