Periodontitis is a chronic inflammatory immune disease associated with a dysbiotic state, influenced by keystone bacterial species responsible for disrupting the periodontal tissue homeostasis. Furthermore, the severity of periodontitis is determined by the interaction between the immune cell response in front of periodontitis-associated species, which leads to the destruction of supporting periodontal tissues and tooth loss in a susceptible host. The persistent bacterial challenge induces modifications in the permeability and ulceration of the sulcular epithelium, which facilitates the systemic translocation of periodontitis-associated bacteria into distant tissues and organs. This stimulates the secretion of pro-inflammatory molecules and a chronic activation of immune cells, contributing to a systemic pro-inflammatory status that has been linked with a higher risk of several systemic diseases, such as type 2 diabetes mellitus (T2DM) and gestational diabetes mellitus (GDM). Although periodontitis and GDM share the common feature of systemic inflammation, the molecular mechanistic link of this association has not been completely clarified. This review aims to examine the potential biological mechanisms involved in the association between periodontitis and GDM, highlighting the contribution of both diseases to systemic inflammation and the role of new molecular participants, such as extracellular vesicles and non-coding RNAs, which could act as novel molecular intercellular linkers between periodontal and placental tissues.

Background To explore the diagnostic usefulness of extracellular vesicles (EVs), and their subpopulations (micro‐vesicles and exosomes), and microRNAs (miRNA‐21‐3p, miRNA‐150‐5p, and miRNA‐26a‐5p) in peri‐implant crevicular fluid (PICF) of subjects with healthy, peri‐implant mucositis and peri‐implantitis implants. Methods A total of 54 patients were enrolled into healthy, peri‐implant mucositis, and peri‐implantitis groups. PICF samples were collected, EVs subpopulations (MVs and Exo) were isolated and characterized by nanoparticle tracking analysis and transmission electron microscopy. The expression of miRNA‐21‐3p, miRNA‐150‐5p and miRNA‐26a‐5p was quantified by qRT‐PCR. Logistic regression models and accuracy performance tests were estimated. Results PICF samples show the presence of EVs delimited by a bi‐layered membrane, in accordance with the morphology and size (< 200 nm). The concentration of PICF‐EVs, micro‐vesicles and exosomes was significantly increased in peri‐implantitis implants compared to healthy implants (P = 0.023, P = 0.002, P = 0.036, respectively). miRNA‐21‐3p and miRNA‐150‐5p expression were significantly downregulated in patients with peri‐implantitis in comparison with peri‐implant mucositis sites (P = 0.011, P = 0.020, respectively). The reduced expression of miRNA‐21‐3p and miRNA‐150‐5p was associated with peri‐implantitis diagnosis (OR:0.23, CI 0.08‐0.66, P = 0.007 and OR:0.07, CI 0.01‐0.78, P = 0.031, respectively). The model which included the miRNA‐21‐3p and miRNA‐150‐5p expression had a sensitivity of 93.3%, a specificity of 76.5%, a positive predictive value of 77.8%, and a negative predictive value of 92.9%. The positive and negative likelihood ratios were 3.97 and 0.09, respectively. The area under the receiver operating characteristics curve for the model was 0.84. Conclusions An increase concentration of EVs with a downregulation expression of miRNA‐21‐3p and miRNA‐150‐5p could be related with the peri‐implantitis development.

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Peri-implantitis is one of the leading causes of implant failure and loss, and its early diagnosis is not currently feasible due to the low sensitivity of currents methods. In the current exploratory cross-sectional study, we explored the diagnostic potential of lymphocyte B and Th17chemotactic cytokine levels in peri-implant crevicular fluid (PICF) in 54 patients with healthy, peri-mucositis, or peri-implantitis implants. Periimplant crevicular fluid was collected, and the levels of the molecules under study were quantified by Luminex assay. The concentrations of CCL-20 MIP-3 alpha, BAFF/BLYS, RANKL and OPG concentration in PICF were analyzed in the context of patient and clinical variables (smoking status, history of periodontitis, periodontal diagnosis, implant survival, suppuration, bleeding on probing, periodontal probing depth, clinical attachment level, mean of implant probing depth, and plaque index). Patients with peri-implantitis, appear to have an overregulation of the RANKL/BAFF-BLyS axis. This phenomenon needs to be investigated in depth in further studies with a larger sample size.