Search

Aim: This study aimed to determine whether periodontitis in early pregnancy and periodontal therapy during gestation affect the incidence of gestational diabetes mellitus (GDM) through a population‐based clinical study. Materials and methods: Subjects without periodontitis at 1–4 weeks of gestation who met our inclusion criteria were enrolled in the non‐periodontitis group. Periodontitis patients who agreed or refused to receive periodontal therapy during pregnancy were separately enrolled in the periodontitis treated or untreated group. At 12–16 weeks of gestation, gingival crevicular fluid (GCF) and venous blood were collected for analyses of bacterial species and serum inflammatory mediators, respectively. At 24–28 weeks of gestation, GDM patients were identified by oral glucose tolerance tests. The association tests were performed using Chi‐squared statistics and regression analyses. Results: The complete data of 3523 pregnant women were recorded during the study period. GDM incidence among the untreated periodontitis participants (84/749, 11.21%) was significantly higher than that among the non‐periodontitis participants (108/2255, 4.79%) (p <.05), and periodontal treatment during gestation reduced the incidence from 11.21% (untreated group) to 7.32% (38/519, treated group) (p <.05). Based on multiple logistic regression analyses, it was found that periodontitis in early pregnancy was associated with GDM, and three‐step regression analyses showed that Porphyromonas gingivalis (P. gingivalis) and the serum TNF‐α and IL‐8 levels played a role in the association between untreated periodontitis and GDM. Furthermore, Pearson's correlation test indicated that the existence of P. gingivalis in GCF was positively correlated with high serum levels of these two inflammatory mediators. Conclusions: This study establishes a connection between periodontitis in early pregnancy and GDM and demonstrates that the presence of P. gingivalis is associated with high levels of inflammatory mediators in serum, and thereby may contribute to the development of GDM. In‐depth mechanistic studies are needed to further support these findings. [ABSTRACT FROM AUTHOR]

Although titanium implants have been applied in dental clinics to replace lost teeth and to restore masticatory function for decades, strategies to design the surface of the transmucosal sites of implants to achieve ideal and predictable biological sealing following implantation remain to be optimized. In this study, we hypothesized that gingival epithelial cell (GEC) adhesion and new tissue attachment to titanium sheets/implants could be promoted by the release of plasmid pLAMA3-CM (encoding a motif of the C-terminal globular domain of LAMA3) from a titanium surface. To test this hypothesis, a chitosan/collagen (Chi/Col) coating was immobilized on the surfaces of titanium substrates with nanotube topography (NT-Ti) through cathodic electrophoretic deposition; it was found that pLAMA3-CM could be released from the coating in a highly sustained manner. After culturing on titanium with nanotube topography coated by Chi/Col with the plasmid pLAMA3-CM (Chi/Col/pLAMA3-CM-Ti), human GECs (hGECs) were found to effectively uptake the incorporated plasmids, which resulted in improved attachment, as evidenced by morphological and immunofluorescence analyses. In addition, Chi/Col/pLAMA3-CM-Ti induced better biological sealing at transmucosal sites following immediate implantation into Sprague-Dawley rats. Our findings indicate that the modification of titanium implants by plasmid-mediated pLAMA3-CM gene transfection points to a practical strategy for optimizing biological sealing around the transmucosal sites of implants. [ABSTRACT FROM AUTHOR]