Gene expression of gingival adhesion molecules in periodontitis is regulated by leukocyte transmigration, whereas the neutrophilic antimicrobial peptide HNP-1 is noted as a putative regulator of epithelial adhesion molecules. These observations contribute to the key mechanisms by which future biomarkers might be developed for periodontitis.

Background:The aim of this study was to evaluate oral bacteria-and interleukin (IL)-1β-induced protein and mRNA expression profiles of monocyte chemoattractant protein-1-induced protein (MCPIP)-1 and mucosa-associated lymphoid tissue lymphoma translocation protein (MALT)-1 in human gingival keratinocyte monolayers and organotypic oral mucosal models. Methods: Human gingival keratinocyte (HMK) monolayers were incubated with Porphyromonas gingivalis, Fusobacterium nucleatum, P. gingivalis lipopolysaccharide (LPS) and IL-1β. The protein levels of MCPIP-1 and MALT-1 were examined by immunoblots and mRNA levels by qPCR. MCPIP-1 and MALT-1 protein expression levels were also analyzed immunohistochemically using an organotypic oral mucosal model. One-way analysis of variance followed by Tukey correction was used in statistical analyses. Results: In keratinocyte monolayers, MCPIP-1 protein expression was suppressed by F. nucleatum and MALT-1 protein expression was suppressed by F. nucleatum, P. gingivalis LPS and IL-1β. P. gingivalis seemed to degrade MCPIP-1 and MALT-1 at all tested time points and degradation was inhibited when P. gingivalis was heat-killed. MCPIP-1 mRNA levels were increased by P. gingivalis, F. nucleatum, and IL-1β, however, no changes were observed in MALT-1 mRNA levels. Conclusion: Gingival keratinocyte MCPIP-1 and MALT-1 mRNA and protein expression responses are regulated by infection and inflammatory mediators. These findings suggest that periodontitis-associated bacteria-inducedThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Background Complications after free gingival graft (FGG) operations are generally related to the donor site. The titanium‐prepared, platelet‐rich fibrin (T‐PRF) placement in the donor site accelerate the wound healing and prevent postoperative complications such as pain and hemorrhage. We aim to evaluate the effect of T‐PRF regarding vascularization and tissue thickness and to report the advantages of the ultrasonography (US) in FGG. Methods Ten individuals were divided into two groups as T‐PRF and control. While the T‐PRF membrane was placed at the donor site in the T‐PRF group, a gelatin sponge was placed in the control group. All patients underwent US examination in terms of vascularization and tissue thickness of left and right donor sites. The correlation between the right and left donor sites was analyzed with the Pearson correlation test. Tissue thicknesses and pulsatility index (PI) were analyzed with independent samples t‐test. The results were evaluated statistically at the P <0.05 significance level. Results The T‐PRF group showed increased vascularity which can be interpreted to improve healing in soft tissue. However, not a difference, but a positively very high correlation was observed between the right and left tissue thicknesses (P = 0,00; r = +0902). Conclusions Evaluation of tissue thickness and vascularization density of donor sites with US not only increases clinical success rate but also reduces the risk of complications during surgery and postoperative pain in FGG. Studies evaluating T‐PRF membrane as palatal dressing after FGG are only clinical, however, the efficiency of T‐PRF was evaluated radiologically in this study for the first time.

This study aimed to compare tissue levels of CD80 (pro-inflammatory macrophage-related surface marker), CD163, and CD206 (anti-inflammatory macrophage-related surface markers), and their ratios in periodontal and peri-implant health and disease. Altogether, 36 tissue samples were obtained from 36 participants with clinically healthy gingiva (n = 10), healthy peri-implant mucosa (n = 8), periodontitis lesions (n = 9), and peri-implantitis lesions (n = 9). CD80, CD163, and CD206 levels were assessed with immunoblotting. CD163 levels were found to be decreased (p = 0.004), and the CD80/CD163 ratio was found to be elevated (p = 0.002) in periodontitis lesions compared to healthy gingiva. Peri-implantitis lesions showed a tendency towards a higher CD80/CD163 ratio than in healthy peri-implant mucosa with a borderline difference (p = 0.054). No statistically significant difference was detected in CD80, CD163, and CD206 levels of periodontitis lesions when compared to peri-implantitis, and in healthy gingiva when compared to healthy peri-implant mucosa. A disruption in CD80/CD163 balance seems to be related to the pathogenesis of periodontitis and peri-implantitis, being less prominent in the latter. The reason behind this phenomenon may be either suppressed CD163 expression or reduced CD163+ anti-inflammatory macrophage abundance.