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Delayed gingival wound healing is widely observed in periodontal patients with diabetes. However, the molecular mechanisms of the impaired function of gingival fibroblasts in diabetes remain unclear. The purpose of this study was to investigate changes in the properties of human gingival fibroblasts (HGFs) under high-glucose conditions. Primary HGFs were isolated from healthy gingiva and cultured with 5.5, 25, 50, and 75 mM glucose for 72 h. In vitro wound healing, 5-ethynyl-2'-deoxyuridine (EdU), and water-soluble tetrazolium salt (WST-8) assays were performed to examine cell migration and proliferation. Lactase dehydrogenase (LDH) levels were measured to determine cytotoxicity. The mRNA expression levels of oxidative stress markers were quantified by real-time PCR. Intracellular reactive oxygen species (ROS) were also measured in live cells. The antioxidant N-acetyl-l-cysteine (NAC, 1 mM) was added to evaluate the involvement of ROS in the glucose effect on HGFs. As a result, the in vitro wound healing assay showed that high glucose levels significantly reduced fibroblast migration and proliferation at 6, 12, 24, 36, and 48 h. The numbers of cells positive for EdU staining were decreased, as was cell viability, at 50 and 75 mM glucose. A significant increase in LDH was proportional to the glucose concentration. The mRNA levels of heme oxygenase-1 and superoxide dismutase-1 and ROS levels were significantly increased in HGFs after 72 h of exposure to 50 mM glucose concentration. The addition of NAC diminished the inhibitory effect of high glucose in the in vitro wound healing assay. The results of the present study show that high glucose impairs the proliferation and migration of HGFs. Fibroblast dysfunction may therefore be caused by high glucose-induced oxidative stress and may explain the delayed gingival wound healing in diabetic patients.

Background: This study aimed at comparing gingival depigmentation by locally injected vitamin C with surgical depigmentation, in terms of effectiveness and patient acceptability. Methods: Forty‐two patients presenting with ethnicity‐related hyperpigmentation were randomly divided into two groups, Group I ( n  = 21) was treated with locally injected vitamin C and Group II ( n  = 21) was treated by surgical depigmentation. The outcome was assessed using Gingival Pigmentation Index (GPI) and Skin Hyperpigmentation Index (SHI). Results: Both the techniques were successful in treating gingival hyperpigmentation, but the patients who underwent vitamin C–based depigmentation showed significantly higher satisfaction with the treatment result, based on patient reported Visual Analog Scale (VAS) scoring. Conclusion: Based on the findings of this study, it was concluded that locally injected vitamin C and surgical depigmentation are comparable in their effectiveness for treating gingival hyperpigmentation. Trial Registration: ClinicalTrials.gov identifier: CTRI/2023/02/050127 .

In order to treat MAGRD in the maxillary anterior region, the VISTA approach was evaluated and compared with and without A-PRF. A split mouth RCT was designed with 216 MAGRD that were assigned to VISTA alone and VISTA with A-PRF. The complete root coverage (CRC) and gingival thickness (GT) were measured using CBCT at baseline and 12 months post-operatively, while the clinical parameters of probing depth (PD), clinical attachment level (CAL), width of keratinized gingival (WKG), gingival recession depth (GRD), and gingival recession width (GRW) were recorded at baseline, 6 months, and 12 months. From baseline to 12 months, there was a significant decrease in the mean values of GRD and GRW with an increase in WKG. CBCT scans showed a significant increase in GT mean values. According to these results, the Test group's CRC was higher (95.92%) than the Control groups (85.02%). In contrast to the Control group, the Test group demonstrated superior MAGRD resolution in achieving a decrease in GRD and GRW as well as a higher increase in WKG and GT. These findings resulted into a substantially more CRC for the Test group. Registration no. CTRI/2022/09/045845. Registered on: 26/09/2022.

Porphyromonas gingivalis is a major pathogen of periodontal disease that affects a majority of adults worldwide. Increasing evidence shows that periodontal disease is linked to various systemic diseases like diabetes and cardiovascular disease, by contributing to increased systemic levels of inflammation. Lipopolysaccharides (LPS), as a key virulent attribute of P. gingivalis, possesses significant amount of lipid A heterogeneity containing tetra- (LPS1435/1449) and penta-acylated (LPS1690) structures. Hitherto, the exact molecular mechanism of P. gingivalis LPS involved in periodontal pathogenesis remains unclear, due to limited understanding of the specific receptors and signaling pathways involved in LPS-host cell interactions. This study systematically investigated the effects of P. gingivalis LPS1435/1449 and LPS1690 on the expression of TLR2 and TLR4 signal transduction and the activation of pro-inflammatory cytokines IL-6 and IL-8 in human gingival fibroblasts (HGFs). We found that LPS1435/1449 and LPS1690 differentially modulated TLR2 and TLR4 expression. NF-κB pathway was significantly activated by LPS1690 but not by LPS1435/1449. In addition, LPS1690 induced significant expression of NF-κB and p38 MPAK pathways-related genes, such as NFKBIA, NFKB1, IKBKB, MAP2K4 and MAPK8. Notably, the pro-inflammatory genes including GM-CSF, CXCL10, G-CSF, IL-6, IL-8 and CCL2 were significantly upregulated by LPS1690 while down-regulated by LPS1435/1449. Blocking assays confirmed that TLR4-mediated NF-κB signaling was vital in LPS1690-induced expression of IL-6 and IL-8 in HGFs. The present study suggests that the tetra- and penta-acylated lipid A structures of P. gingivalis LPS differentially activate TLR4-mediated NF-κB signaling pathway, and significantly modulate the expression of IL-6 and IL-8 in HGFs. The ability to alter the lipid A structure of LPS could be one of the strategies carried-out by P. gingivalis to evade innate host defense in gingival tissues, thereby contributing to periodontal pathogenesis.

Rationale Electronic cigarettes (ECs) are becoming popular alternatives for smokers, but there has been limited study of their abuse liability. Objectives The objective of this study was to evaluate the abuse liability of three Vuse Solo ECs, ranging from 14 to 36 mg in nicotine content, relative to high- and low-abuse liability comparator products (usual brand combustible cigarettes and nicotine gum, respectively) in a group of 45 EC-naïve smokers. Methods Enrolled subjects’ ratings of subjective effects and nicotine uptake over 6 h were used to measure abuse liability and pharmacokinetics following in-clinic use of each EC. Results Use of Vuse Solo resulted in subjective measures and nicotine uptake that were between those of combustible cigarettes and nicotine gum, although generally closer to nicotine gum. Compared to combustible cigarettes, use of Vuse Solo resulted in significantly lower scores in measures of product liking, positive effects, and intent to use again. These pharmacodynamic findings were consistent with the pharmacokinetic data, showing that cigarettes produced substantially faster and higher levels of nicotine uptake as compared to Vuse Solo and nicotine gum. Vuse Solo resulted in more rapid initial uptake of nicotine compared to nicotine gum, but peak concentration and long-term extent of uptake were not different or were lower with Vuse. Conclusions Collectively, these findings suggest that Vuse Solo likely has an abuse liability that is somewhat greater than nicotine gum but lower than cigarettes. Trial registration ClinicalTrials.gov identifier: NCT02269514

Periodontitis has been implicated as a risk factor for metabolic disorders such as type 2 diabetes, atherosclerotic vascular diseases and non-alcoholic fatty liver disease. Although bacteremias from dental plaque and/or elevated circulating inflammatory cytokines emanating from the inflamed gingiva are suspected mechanisms linking periodontitis and these diseases, direct evidence is lacking. We hypothesize that disturbances of the gut microbiota by swallowed bacteria induce a metabolic endotoxemia leading metabolic disorders. To investigate this hypothesis, changes in the gut microbiota, insulin and glucose intolerance and levels of tissue inflammation were analysed in mice after oral administration of Porphyromonas gingivalis , a representative periodontopathogens. Pyrosequencing revealed that the population belonging to Bacteroidales was significantly elevated in P. gingivalis -administered mice which coincided with increases in insulin resistance and systemic inflammation. In P. gingivalis -administered mice blood endotoxin levels tended to be higher, whereas gene expression of tight junction proteins in the ileum was significantly decreased. These results provide a new paradigm for the interrelationship between periodontitis and systemic diseases.

Oral soft tissue damage can lead to hard tissue damage in the oral cavity, such as periodontal lesions, periapical disorders, cysts, and oral tumors. Cold plasma is known to alleviate inflammation and oxidative stress and promote tissue regeneration, yet the effects of helium plasma on human gingival cells remain poorly understood. In this study, we examined whether helium (He) cold atmospheric pressure plasma (CAP) can induce anti-inflammatory and anti-ferroptotic effects in oral soft tissues by ionizing He gas. Erastin treatment followed by He CAP exposure in human gingival fibroblast-1 (HGF-1) cells reduced the mRNA expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), tumor necrosis factor-α (TNFα), and interleukin-6 (IL-6), which are linked to inflammatory responses. Additionally, He CAP exposure decreased nuclear receptor coactivator 4 (NCOA4) expression and increased glutathione peroxidase 4 (GPX4) expression. Furthermore, mitochondrial membrane potential was restored by increased voltage-dependent anion channel 1 (VDAC1) expression, and reactive oxygen species (ROS) levels in mitochondria and cytoplasm were reduced. These results suggest that He CAP exposure may be associated with modulation of mitochondrial ROS production and reduction of inflammation and ferroptosis, but whether mitochondrial repair contributes to these effects requires further investigation.

Solitary chemosensory cells (SCCs) are epithelial sentinels that utilize bitter Tas2r receptors and coupled taste transduction elements to detect pathogenic bacterial metabolites, triggering host defenses to control the infection. Here we report that SCCs are present in mouse gingival junctional epithelium, where they express several Tas2rs and the taste signaling components α-gustducin (Gnat3), TrpM5, and Plcβ2. Gnat3 −/− mice have altered commensal oral microbiota and accelerated naturally occurring alveolar bone loss. In ligature-induced periodontitis, knockout of taste signaling molecules or genetic absence of gingival SCCs (gSCCs) increases the bacterial load, reduces bacterial diversity, and renders the microbiota more pathogenic, leading to greater alveolar bone loss. Topical treatment with bitter denatonium to activate gSCCs upregulates the expression of antimicrobial peptides and ameliorates ligature-induced periodontitis in wild-type but not in Gnat3 −/− mice. We conclude that gSCCs may provide a promising target for treating periodontitis by harnessing innate immunity to regulate the oral microbiome. Solitary chemosensory cells (SCCs) expressing taste receptors reside in mucosal epithelia including the gingiva. Here the authors show that ablation of taste-sensing by SSCs leads to outgrowth of pathogenic oral bacteria and periodontitis, whereas bitter taste receptor stimulation promotes antimicrobial peptide production and ameliorates periodontitis.

Objectives This study evaluates the efficacy of polyvinylpyrrolidone–sodium hyaluronate (PVP‐SH) gel as a dressing material in enhancing both clinical and patient‐reported outcomes post‐free gingival graft (FGG) harvesting from the hard palate. Material and Methods This randomized clinical trial included 18 patients and spanned from June 2022 to August 2023. Patients received an FGG procedure to manage a lack of attached gingiva. Following graft harvesting, patients were divided into two groups: the control group, which received Coe‐Pak, and the test group, which was treated with PVP‐SH gel. The primary outcome measured was complete epithelialization. Secondary outcomes included the Landry healing scale, post‐operative pain level, and patient willingness to receive the same treatment again. Results The test group reported significantly lower analgesic use (p < 0.001) and reduced pain severity (p < 0.001) compared to the control group. Furthermore, test group patients indicated a higher level of satisfaction regarding the prospect of retreatment. In contrast, the control group showed significantly slower progress in wound healing and epithelization (p < 0.05) compared to the test group. Conclusions The findings of this study suggest that PVP‐SH gel is a superior dressing material post‐FGG harvesting, yielding improved clinical and patient‐reported outcomes relative to Coe‐Pak.

γδT cells are a major component of epithelial tissues and play a role in tissue homeostasis and host defense. γδT cells also reside in the gingiva, an oral tissue covered with specialized epithelium that continuously monitors the challenging dental biofilm. Whereas most research on intraepithelial γδT cells focuses on the skin and intestine epithelia, our knowledge on these cells in the gingiva is still incomplete. In this study, we demonstrate that even though the gingiva develops after birth, the majority of gingival γδT cells are fetal thymus-derived Vγ6⁺ cells, and to a lesser extent Vγ1⁺ and Vγ4⁺ cells. Furthermore, we show that γδT cells are motile and locate preferentially in the epithelium adjacent to the biofilm. Vγ6⁺ cells represent the major source of IL-17–producing cells in the gingiva. Chimeric mice and parabiosis experiments indicated that the main fraction of gingival γδT cells is radioresistant and tissue-resident, persisting locally independent of circulating γδT cells. Notably, gingival γδT cell homeostasis is regulated by the microbiota as the ratio of Vγ6⁺ and Vγ4⁺ cells was reversed in germ-free mice, and their activation state was decreased. As a consequence, conditional ablation of γδT cells results in elevated gingival inflammation and subsequent alterations of oral microbial diversity. Taken together, these findings suggest that oral mucosal homeostasis is shaped by reciprocal interplays between γδT cells and local microbiota.