Innovative i-PRF semisurgical method for gingival augmentation and root coverage in thin periodontal phenotypes: a preliminary study.

OBJECTIVES: The aim of the study was to evaluate the effect of injectable platelet-rich fibrin (i-PRF) on gingival thickness and gingival recession in individuals with thin periodontal phenotypes. METHOD AND MATERIALS: In this prospective study, i-PRF was applied via a semisurgical method to augment 53 tooth regions with thin periodontal phenotypes. In order to ensure that sufficient blood clot formed on the side of the gingiva facing the bone and that i-PRF reached the area, a minimal incision was made with the help of a scalpel in the apical region of the relevant region, and the periosteum was elevated with a microsurgical instrument. To ensure sustained exposure to angiogenetic growth factors and enhance the histoconductive properties, i-PRF injection was applied to the relevant areas in four sessions at 10-day intervals. RESULTS: An increase in gingival thickness was achieved in 92.5% of the areas treated with i-PRF, and the desired gingival thickness (0.8 mm) was achieved in 44.9% of these areas. In addition, significant reductions in the amount of recession were observed in 83.3% of the 12 gingival recession areas (P = .005). Moreover, complete coverage was achieved in 60% of these regions. CONCLUSION: With the new i-PRF semisurgical method, it was shown that gingival thickness can be increased in tooth regions with thin gingiva, and that areas of gingival recession can be covered. Further comprehensive studies are needed to fully understand the role of i-PRF in enhancing angiogenesis and the histoconductive properties of this fully autogenous blood concentrate.

Localization and expression profiles of gingival monocyte chemoattractant protein-1-induced protein-1 (MCPIP-1) and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1).

OBJECTIVES: The purposes of this study were to localize monocyte chemoattractant protein-1-induced protein-1 (MCPIP-1) and its suppressor mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1) in gingival tissues and to profile their protein expression levels in relation to the clinical inflammation, Porphyromonas gingivalis colonization, and interleukin (IL)-8 levels. MATERIALS AND METHODS: Study samples were collected from two independent study populations: (1) Gingival tissues were collected from eight periodontally healthy individuals and eight periodontitis patients to localize MCPIP-1 and MALT-1 immunohistochemically, and (2) forty-one gingival tissue samples with marginal, mild, or moderate to severe inflammation were collected from 20 periodontitis patients to determine MCPIP-1 and MALT-1 levels using immunoblots, P. gingivalis levels with qPCR, P. gingivalis gingipain activities with fluorogenic substrates, and IL-8 levels with multiplex technique. RESULTS: MCPIP-1 was detectable in the epithelium and in connective tissue, being especially prominent around the blood vessel walls in healthy periodontal tissues. MALT-1 was observed at all layers of gingival epithelium and especially around the accumulated inflammatory cells in connective tissue. No difference in gingival tissue MCPIP-1 and MALT-1 levels was observed in relation to the severity of gingival inflammation. MALT-1 levels were elevated (p = 0.023) with the increase in tissue P. gingivalis levels, and there was an association between MALT-1 and IL-8 levels (ß = 0.054, p = 0.001). CONCLUSIONS: Interactions of MALT-1 levels with gingival tissue P. gingivalis counts and IL-8 levels suggest that activation of MALT-1 can take part in P. gingivalis-regulated host immune responses. CLINICAL RELEVANCE: Pharmacological targeting the crosstalk between immune response and MCPIP-1/MALT-1 may have benefits in periodontal treatment.

Regulation of gingival keratinocyte monocyte chemoattractant protein-1-induced protein (MCPIP)-1 and mucosa-associated lymphoid tissue lymphoma translocation protein (MALT)-1 expressions by periodontal bacteria, lipopolysaccharide, and interleukin-1ß.

BACKGROUND: The aim of this study was to evaluate oral bacteria- and interleukin (IL)-1ß-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-1ß. 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-1ß. 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-1ß, 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-induced modifications in MCPIP-1 and MALT-1 responses can be a part of periodontal disease pathogenesis.

Tissue Levels of CD80, CD163 and CD206 and Their Ratios in Periodontal and Peri-Implant Health and Disease.

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.

Ultrasonographic evaluation of the titanium-prepared platelet-rich fibrin effect in free gingival graft procedures.

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.

Analyses of Gingival Adhesion Molecules in Periodontitis: Theoretical In Silico, Comparative In Vivo, and Explanatory In Vitro Models.

BACKGROUND: A deeper understanding of periodontitis pathophysiology is central to future development of novel biomarkers and therapeutics. The following is reported here: 1) an in silico network model of interactions among cell adhesion molecules and a network-focused microarray analysis of the corresponding genes in periodontitis; 2) analysis of secretions of adhesion molecules in gingival tissue samples from patients with periodontitis and healthy controls; and 3) effect of the human neutrophilic peptide-1 (HNP-1) on epithelial adhesion molecules. METHODS: The network model identified 85 nodes in relation to the interactions of adhesion molecules. Subsequently, the relative gene expression was overlaid on the network model. Differential gene expression was analyzed, and false discovery rate control was performed for statistical assessment of the microarray data. Both tissue and cell culture samples were immunostained for desmocollin (DSC)2, occludin (OCLN), desmoglein (DSG)1, tight junction protein 2, and gap junction protein α. RESULTS: The differential gene expression analysis revealed that the epithelial adhesion molecules were significantly lower in abundance in individuals with periodontitis than controls. In contrast, the genes for leukocyte adhesion molecules showed a significant upregulation. Immunostainings revealed elevated secretions of both DSG1 and OCLN in periodontitis. An in vitro model suggested reduced DSC2 and OCLN secretions in the presence of HNP-1. CONCLUSIONS: 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.