Periodontal Inflammation Research Articles

Cytomorphological characteristics of buccal epithelium in patients with undifferentiated connective tissue dysplasia

Relevance. Undifferentiated connective tissue dysplasia (UCTD) is a background condition that reduces the body's adaptive potential and increases the risk and severity of various diseases. The condition of the buccal epithelium reflects systemic homeostasis and its changes under the influence of local and systemic factors. The aim of this study was to assess the cytomorphological characteristics of buccal epithelial cells in patients with UCTD and their alterations in the presence of periodontal inflammation.Materials and methods. The study protocol included an assessment of phenotypic signs of connective tissue dysplasia and an evaluation of periodontal status, based on which four groups were identified: Group I – individuals without signs of UCTD or periodontal inflammation (n = 15); Group II – individuals without UCTD but with periodontitis (n = 20); Group III – individuals with UCTD but without periodontitis (n = 20); and Group IV – individuals with both UCTD and periodontitis (n = 34). A cytomorphological analysis of superficial buccal epithelial cells was performed, including an assessment of microorganism adsorption by epithelial cells.Results. Buccal cytograms of patients with UCTD showed a significantly higher frequency of nuclear aberrations, including micronuclei (10.7-fold increase; p < 0.001), binucleation (3-fold; p = 0.007), perinuclear vacuoles (3.2-fold; p < 0.001), and karyolysis (3.5-fold; p = 0.017). There was also a 3-fold increase in anucleate cells (1.47 ± 0.15%; p < 0.001) and a rise in the cytogenetic index. In patients with both UCTD and periodontitis, the proportion of binucleated cells was 1.3 times lower (p = 0.005) compared to those with UCTD alone. The mean apoptosis index in this group was 17.6 ± 1.1, which was 2.2 times higher than in UCTD patients without periodontitis (p < 0.001) and 1.8 times higher than in patients with periodontitis without UCTD (p < 0.001). The mean cytomorphological coefficient was relatively lower in the UCTD group, although this difference was not statistically significant (p = 0.374).Conclusion. The study identified distinct cytomorphological characteristics of buccal epithelial cells in patients with UCTD, as well as their modifications in the presence of periodontitis.

Ameliorating Effect of Glehnia littoralis Extract on Periodontitis Through Regulation of 11β-Hydroxysteroid Dehydrogenase Type 1 in an Experimental Periodontitis Model

Glehnia littoralis Fr. Schmidt ex Miq. has been cultivated in China for a long time and used as a medicinal plant called “Beishashen” in traditional Chinese medicine and has been traditionally known to have antibacterial and anti-inflammatory effects, but its direct role in periodontitis has not been known. Currently used periodontal treatments require long-term administration, which causes many side effects. Therefore, in this study, we evaluated the effects of G. littoralis extract (GLE) on periodontitis in an experimental periodontitis-induced in vitro and vivo model and understood its potential molecular mechanism. The effect of GLE on periodontitis in vitro was investigated using human periodontal ligament (HPDL) cells mediated by PG-LPS. Additionally, a ligature-induced periodontitis model and a PG-LPS-induced periodontal inflammation model were used to investigate the effect of GLE in vivo. In vitro study results showed that GLE down-regulated the increased inflammatory cytokines and mediators in HPDL cells stimulated with PG-LPS, and simultaneously down-regulated the levels of 11β-HSD1 and glucocorticoid receptor (GR), thereby alleviating periodontal inflammation. At the same time, it restored the lost osteoblast differentiation potential of HPDL cells. In addition, in an in vivo model representatively used for periodontitis research, the periodontal inflammation-alleviating effect and the effect of restoring or protecting damaged periodontal tissue were confirmed. GLE can be considered as a new periodontitis treatment agent through regulating 11β-HSD1.

Resolvin E1 and maresin 1 restore senescence-induced disruption of human periodontal ligament fibroblast function.

Aging impairs the mechanisms that regulate inflammation, resulting in low-level chronic inflammation even in the absence of infection and increasing the risk of developing age-related illnesses. Periodontal ligament fibroblasts (PDLF) are responsible for wound healing and periodontal tissue regeneration. Periodontal inflammation disrupts PDLF function, which may be exacerbated by aging. We tested the hypothesis that senescence-induced changes in PDLF will be reversed by specialized mediators of resolution of inflammation-resolvin E1 (RvE1) and maresin 1 (MaR1). Primary human PDLFs were cultured with D-galactose to induce senescence. The senescence was confirmed with a senescence-associated beta-galactosidase assay. The impact of senescence on cell viability, proliferation, wound healing, cell cycle, type I collagen expression, oxidative stress, inflammatory profiles, and growth factor production was evaluated. We measured the specialized pro-resolving mediators (SPM)-mediated effects on senescent PDL fibroblasts by treating them with 100nM RvE1 or 100nM MaR1 or the vehicle. D-galactose treatment significantly increased senescence, oxidative stress, and inflammation while it delayed wound closure and reduced cell viability and proliferation on PDLFs (p<0.05). RvE1 or MaR1 treatment significantly decreased β-galactosidase expression and inflammation, restored cell viability, increased cell proliferation, and accelerated wound closure (p<0.05). MaR1 demonstrated a more potent impact on reversing the senescence and regenerative effect than RvE1. RvE1 and MaR1 reversed the senescence-induced changes in primary PDLFs, restoring wound healing capacity and function. Aging may induce periodontal inflammation, which interferes with the activity of the periodontal ligament fibroblasts (PDLFs). We measured the effect of specific mediators of resolution of inflammation, resolvin E1 (RvE1) and maresin 1 (MaR1), on aging in PDLFs. Treatment with RvE1 or MaR1 significantly reduced inflammation and senescenceand restored cell proliferation, wound closure, and cell viability.

Assessment of periodontal inflammatory burden and radiomorphometric indices in geriatric individuals in Turkey: a retrospective study

BackgroundOral health in older adults is frequently compromised due to a higher prevalence of periodontal disease, tooth loss, and systemic conditions such as osteoporosis. Altough the association between periodontitis and osteoporosis has been explored, further research is warranted to assess the periodontal inflammatory burden in the context of bone health. This study hypothesised that periodontal inflammatory burden, measured by Periodontal Inflamed Surface Area (PISA), may contribute to osteoporotic changes in the mandible. The objective was to evaluate the relationship between periodontal status and mandibular osteoporotic changes by assessing inflammatory burden via PISA and panoramic radiomorphometric indices in geriatric individuals.MethodsThis retrospective study included 149 patients aged ≥ 65 years. Participants were grouped by periodontal health, and PISA values were calculated. Panoramic radiographs were analysed to assess mandibular bone quality using the Mental Index (MI), Panoramic Mandibular Index (PMI), and Mandibular Cortical Index (MCI). Statistical analyses evaluated the associations between periodontal status, PISA values, and radiomorphometric indices.ResultsThe mean participant age was 70 ± 4 years. There were no significant differences in MI, PMI, or MCI among periodontal health groups (p > 0.05). However, PISA values showed substantial correlations with MI (p = 0.024), PMI (p = 0.005), and MCI (p = 0.04), indicating a potential association between periodontal inflammation and mandibular bone structure.ConclusionsTo the best of our knowledge, this is the first study to correlate PISA values with mandibular osteoporotic changes. While the periodontitis stage was not significantly associated with radiomorphometric indices, PISA was. These findings suggest that inflammatory burden, rather than disease severity alone, may influence mandibular bone characteristics. PISA may serve as a valuable indicator of inflammation-related bone changes.

Association between individuals with unilateral and bilateral carotid artery calcifications and periodontal disease: a cross-sectional study

BackgroundThis study investigated the association between unilateral and bilateral carotid artery calcifications (CAC) and periodontal disease severity using panoramic radiographs, and assessed the influence of systemic risk factors such as hypertension, diabetes, and smoking.MethodsA retrospective cross-sectional study analyzed 116 radiographs from 87 females and 29 males with CAC. CAC was identified as radiopaque lesions near the C3–C4 intervertebral space. Participants were categorized into unilateral or bilateral CAC groups. Demographic data, medical histories, and periodontal parameters (plaque index, gingival index (GI), bleeding on probing, probing depth (PD), and clinical attachment loss) were recorded. Participants were classified as healthy, gingivitis, periodontitis stage I–II, or stage III–IV. Binomial logistic regression and independent samples t-tests were used.ResultsAge and gender were not significantly associated with the type of CAC (p > 0.05). Only PD showed a significant association: an increase in PD was linked to higher odds of unilateral CAC and lower odds of bilateral CAC (p < 0.05). Smoking, diabetes, and hypertension were not significantly associated with the type of CAC (p > 0.05). Unilateral CAC was linked to higher GI, PD, and stage III–IV periodontitis, while bilateral CAC was more common in stage I–II (p < 0.05).ConclusionThe findings suggest a differential association between the severity of periodontitis and the type of CAC. Unilateral CAC may be more strongly linked to advanced periodontal inflammation, possibly reflecting an earlier, inflammation-dominant phase of atherosclerosis. Due to the cross-sectional design and use of panoramic radiographs, causal inferences cannot be drawn. Further longitudinal studies using advanced imaging techniques are needed.

The Periodontal-Cardiovascular Axis: Mechanisms, Clinical Implications, and Integrated Management Strategies

A growing body of evidence underscores a significant bidirectional relationship between periodontal disease (PD) and cardiovascular diseases (CVD), particularly atherosclerotic cardiovascular disease (ASCVD) and its interventions. This review synthesizes current knowledge on the pathophysiological mechanisms linking oral dysbiosis and chronic periodontal inflammation to endothelial dysfunction, plaque instability, and adverse cardiovascular events. We examine epidemiological data establishing PD as an independent risk factor for CVD, explore shared inflammatory pathways, and critically evaluate clinical evidence regarding the impact of periodontal treatment on cardiovascular surrogate markers and hard outcomes. Furthermore, we discuss the implications for interdisciplinary care models integrating dentistry and clinical cardiology. A comprehensive literature search of PubMed, Embase, and Cochrane Library databases was conducted, encompassing observational studies, randomized controlled trials (RCTs), systematic reviews, and mechanistic investigations. The evidence strongly supports PD as a contributor to cardiovascular risk via systemic inflammation, bacteremia, and immune dysregulation. While periodontal therapy improves endothelial function and reduces systemic inflammation, large-scale RCTs on hard cardiovascular endpoints are ongoing. Collaborative management strategies between dental and cardiovascular health professionals are crucial for optimizing patient outcomes and warrant broader implementation.

Oral Microbial Dysbiosis Driven by Periodontitis Facilitates Oral Squamous Cell Carcinoma Progression.

Oral squamous cell carcinoma (OSCC), which accounts for over 90% of all oral malignancies, remains a major global health challenge due to its aggressive clinical course and poor prognosis. Periodontitis, a widespread chronic inflammatory condition affecting the supporting structures of the teeth, has increasingly been implicated as a potential risk factor for the development of various cancers. Emerging evidence suggests that microbial dysbiosis within the oral cavity may contribute to the creation of a pro-tumorigenic microenvironment, thereby promoting tumor initiation and progression. Nevertheless, the precise mechanisms linking periodontitis to OSCC, particularly through alterations in the oral microbiota, remain insufficiently understood. This article seeks to comprehensively analyze the association between periodontitis and OSCC and to elucidate the potential role of oral microbiota dysbiosis in mediating this relationship. In this study, a ligature-induced periodontitis model was established in C57BL/6J mice, and after two weeks, an OSCC model was introduced by the subcutaneous injection of SCC-7 cells to investigate the impact of periodontitis on OSCC progression. The effects of periodontitis on OSCC cell proliferation and invasion were assessed using scratch wound healing assays and CCK-8 proliferation assays. 16S rDNA high-throughput sequencing was conducted to profile the microbial communities present in the oral cavity and OSCC tissues, with particular emphasis on α-diversity indices (including Pielou's evenness and Chao1 richness) and taxonomic composition at both the phylum and class levels. Furthermore, qPCR was utilized to assess the expression levels of cytokines in both periodontal and OSCC tissues, thereby elucidating the inflammatory milieu, potentially linking periodontitis to OSCC progression. Our findings demonstrated that periodontitis significantly promoted OSCC growth and enhanced the invasive potential of OSCC cells. Microbial profiling revealed marked alterations in both the oral and OSCC microbiota, characterized by significant shifts in community composition and increased microbial diversity. Notably, these microbial changes exhibited consistent patterns between the oral cavity and the OSCC microenvironment, suggesting a potential mechanistic link between periodontitis-associated dysbiosis and OSCC progression. Consistently, qPCR analysis revealed elevated expression levels of IL-1β, IL-10, and IL-18 in both periodontal and OSCC tissues, providing evidence that the microbial alterations were accompanied by intensified inflammatory responses, which may contribute to OSCC progression. This study underscores the intricate interplay between periodontitis-induced microbial dysbiosis and the development of oral squamous cell carcinoma (OSCC). The findings suggest that periodontal inflammation, together with associated shifts in the oral microbiota, acts synergistically to drive OSCC progression. The elevated expression of cytokines further supports the role of a pro-inflammatory tumor microenvironment in mediating this interaction. These results offer important insights into the microbial and inflammatory mechanisms underlying the connection between periodontitis and OSCC, highlighting the critical role of maintaining periodontal health in the prevention and management of OSCC.

Dental magnetic resonance imaging for bone loss assessment and disease activity classification in severe periodontitis

ObjectivesTo evaluate the reliability and accuracy of dental MRI (dMRI) for volumetric infrabony and furcation bone loss compared to cone-beam computed tomography (CBCT) and to correlate to clinical signs of inflammation in patients with severe periodontitis.MethodsIn this cross-sectional study nineteen patients with severe periodontitis underwent standardized clinical examination as well as pre-treatment CBCT and 3T-dMRI. Bone lesion volumetry was performed in CBCT, contrast-enhanced-T1-weighting (T1W + C) and T2-weighting (T2W) dMRI. Lesions whose T2W signal significantly exceeded T1W/CBCT margins (indicating excessive edema) were classified as T2W-mismatch. Volumetric data were compared to clinical findings.ResultsTen female and nine male patients with 253 bony lesions were examined. Reliability for bone lesions was highest in CBCT (ICC [95% CI] T1W + C/T2W/CBCT: 0.78 [0.74–0.83]/0.82 [0.77–0.85]/0.87 [0.94–0.89]). Overall, T1W + C and T2W dMRI strongly correlated with CBCT (rs = 0.86 [95% CI: 0.82–0.89], p < 0.001 and rs = 0.91 [95% CI: 0.88–0.93], p < 0.001 respectively) but volume was significantly overestimated by dMRI (median percentage error of T1W + C-T2W: 19–55%). A T2W-mismatch was found in 44.1% and correlated with bleeding (85.8% vs. 70.9%, p = 0.005), giving 47.5% sensitivity and 71.2% specificity.ConclusionsWhile dMRI offers good reliability, T2W- and to a lesser extent T1W + C imaging overestimate infrabony and interradicular periodontal bone lesion volumetry compared to CBCT. While this could increase the risk of overtreatment, dMRI detects periodontal inflammation beyond areas of bone loss, and T2W-mismatch is closely related but not identical to signs of active inflammation in clinical examination. This may provide additional diagnostic information and could serve as a supplemental tool for higher-risk patients.Critical relevance statementDental MRI excels in detecting inflammation beyond bone loss, identifying high-risk tissue. This study assesses reliability in evaluating periodontitis-related bone loss, highlighting its tendency to overestimate lesion volume. A novel “mismatch lesion pattern” was observed, potentially linked to disease activity.Key PointsDental MRI (dMRI) reliably assesses bone loss in periodontitis but overestimates volume vs. cone-beam computed tomography (CBCT).dMRI detects excess bone marrow edema, indicating inflammation beyond visible bone loss.dMRI could aid periodontal diagnosis and guide targeted therapeutic interventions.Graphical

Metal-Polyphenol Network Coated Bilirubin Nanoparticles for the Alleviation of Periodontitis via Mild Photothermal Therapy and Immunomodulatory Therapy.

At present, the development of nanoplatforms that integrate infection control, inflammation resolution, and tissue repair for the treatment of periodontitis remains an enormous challenge. Based on the intricate pathogenesis of periodontitis and the advantages of mild photothermal therapy (PTT) and nanotherapy, a multifunctional photothermal nanoplatform (designated BR@C3G-Cu) was rationally developed by coating bilirubin nanoparticles (BR NPs) with copper ion coordinated cyanidin-3-O-glucoside metal-polyphenol networks (MPNs) in this study. The synergistic consequences of the photothermal conversion properties and metal-dependent functionality of this MPNs contributed to the effective and persistent elimination of periodontal pathogens under safe and mild conditions, meeting the heterogeneous antibacterial requirements of periodontitis. Further, photothermal BR@C3G-Cu NPs restored the macrophage polarization balance and mitigated periodontal inflammation by countering oxidative stress damage and blocking the cGAS-STING pathway, thereby normalizing the periodontal local osteoimmune microenvironment and promoting the osteogenic differentiation of in situ stem cells. BR@C3G-Cu NPs exposed to near-infrared irradiation also offered beneficial therapeutic outcomes in a mouse periodontitis model, including inhibiting alveolar bone resorption and promoting periodontal tissue remodeling. Overall, this work highlights the potential of MPN-coated engineered NPs (i.e., BR@C3G-Cu) for the treatment of periodontitis through the integration of mild PTT and immunomodulatory therapy to eliminate pathogenic bacteria, alleviate inflammation, and promote regeneration.

1552-P: The Role of PPARα in Modulating Macrophage Polarization during Periodontitis in Diabetes

Introduction and Objective: Periodontitis (PD), a chronic inflammatory condition, is a leading cause of tooth loss and jawbone deterioration and is associated with an increased risk of diabetes. The persistent inflammation in PD results from an imbalance between pro-inflammatory (M1) and anti-inflammatory (M2) macrophages, contributing significantly to tissue destruction. This study investigates the role of peroxisome proliferator-activated receptor alpha (PPARα), a nuclear hormone receptor, in regulating macrophage polarization during PD, particularly in the context of diabetes. Methods: In vivo: PD was induced in diabetic (db/db) mice. PPARα expression levels were analyzed, and the effects of PPARα activation on periodontal inflammation and alveolar bone loss were assessed.In vitro: Macrophages were treated with Porphyromonas gingivalis (P.g.) lipopolysaccharide (LPS) and analyzed for PPARα activity under normal and high-glucose conditions. M1 and M2 macrophage markers, including CD14 and IL-10, were measured following PPARα agonist treatment. Results: PPARα expression was markedly reduced in diabetic animals with PD. Lack of PPARα exacerbated periodontal inflammation and alveolar bone loss in db/db mice, whereas activation of PPARα ameliorated these effects. LPS treatment inhibited PPARα activity in a dose-dependent manner, an effect partially reversed by PPARα agonists. However, the reversal was less effective under high-glucose conditions. PPARα activation reduced M1 macrophage marker expression (CD14) and increased M2 macrophage marker expression (IL-10) in vitro. Conclusion: PPARα plays a critical role in modulating macrophage polarization during PD, particularly in diabetes. Activation of PPARα attenuates inflammation and promotes a shift from pro-inflammatory to anti-inflammatory macrophages, highlighting its therapeutic potential for managing PD and its complications in diabetic individuals. Disclosure A. Hu: None. Y. Chen: None.

Assessment of pulpal changes in periodontitis patients using CBCT: a volumetric analysis

IntroductionEvidence suggests that periodontal disease can lead to inflammation and degeneration within dental pulp, highlighting the need for dental professionals to understand this association better.ObjectiveThe objective for this study was to establish a correlation between pulp volume and periodontal disease using Cone-Beam Computed Tomography (CBCT) imaging.MethodsA cross-sectional study design was employed for the collected data from 148 patients aged 39.51 years using dental images obtained by CBCT and analyzed by medical software to create three-dimensional (3D) images. Pulp-volume analysis was performed using Amira software and measurements were derived using bio-models generated from CBCT images. Obtained data was analyzed using SPSS-27 statistical software.ResultsThe mean pulp volume between healthy and teeth with periodontitis showed certain differences. The mean low and largest pulp volumes of 9.15 ± 3.3 mm3 and 15.24 ± 4.2 mm3 were observed involving teeth # 41 and teeth # 13, respectively. Furthermore, a higher mean of pulp volume was observed in healthy teeth than in periodontitis-diagnosed teeth except for teeth # 33 and 43. The significant difference (p < 0.05) was easily detected involving teeth # 22, 23, 11, and 13. However, the lowest difference, with non-significant difference (p > 0.05), involving teeth # 43, 31, and 33 was observed.DiscussionThe study's findings underscore a significant correlation between periodontitis and reduced pulp volume, suggesting that periodontal inflammation may influence pupal remodeling.

In vitro models of periodontitis: research progress

Due to the high prevalence of periodontitis, the control of periodontal inflammation, as well as the regeneration and repair of periodontal tissues have attracted extensive attentions. To better understand the mechanism of periodontal diseases, in vivo and in vitro models are usually required. With the rapid development of tissue engineering, in vitro models with the advantages of easy observation, high controllability, low cost, and high efficiency has become a unique choice for current research. In vitro models of periodontitis are no longer limited to cellular models, researchers are increasingly inclined to develop simple, effective, and realistic models to simulate the periodontal microenvironment. This article reviews in vitro models of periodontitis that have been successfully established, aiming to provide researchers with new ideas to simulate the human periodontitis microenvironment in vitro, which is helpful to explore the pathogenesis of periodontitis.

Impact of Sympathetic Nervous System Activation and Inflammatory Response on Periodontitis Severity

The sympathetic nervous system (SNS) is crucial for stress response regulation and immune modulation. Prolonged SNS activation, often induced by stress exposure, disrupts immune homeostasis and intensifies inflammatory processes, contributing to periodontal disease progression. This study investigates the relationship between SNS activity and periodontitis severity, utilizing salivary biomarkers chromogranin A (CgA) and alpha-amylase (sAA) alongside pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-6 (IL-6). Saliva samples from 67 patients, categorized by periodontitis severity (Stages I/II and III/IV), were analyzed using enzyme-linked immunosorbent assay (ELISA). The results revealed significantly higher median levels of CgA (9.45 vs. 3.93 pmol/mL) and IL-1β (257.81 vs. 220.11 pg/mL) in patients with Stage III/IV periodontitis compared with those with Stage I/II, indicating heightened SNS activity and inflammatory response. Correlations between these biomarkers and clinical periodontal parameters, such as probing depth and clinical attachment loss, further support these findings. Despite elevated sAA levels in severe cases, statistical significance was not achieved. IL-6 levels also showed no significant variation across disease stages, although trends aligned with increased severity. This study highlights the interplay between SNA activation and periodontal inflammation, as evidenced by elevated salivary levels of CgA and IL-1β in patients with advanced periodontitis. By integrating neuroendocrine and inflammatory biomarkers into the diagnostic process, clinicians may be able to better identify patients at increased risk for periodontal breakdown and to consider adjunctive interventions such as stress management, thereby supporting more personalized approaches to periodontitis treatment.

Clinical Features Associated With Periodontal Case Misclassification by an Active Matrix Metalloproteinase-8 Point-of-Care Oral Rinse Test.

The diagnostic performance of active matrix metalloproteinase-8 (aMMP-8) point-of-care oral rinse test (POC-ORT) for periodontitis needs to be improved because of its relatively low sensitivity. This study attempted to identify the clinical features associated with the misclassification of periodontal cases by the test. This work consisted of two cross-sectional diagnostic accuracy studies involving a representative cohort in Hong Kong, China, and a convenience sample of subjects in Shanghai, China. The outcomes of the aMMP-8 POC-ORT (index test) were compared to the case definitions of the 2017 World Workshop on the classification of periodontal health status (reference test). The analysis reports the diagnostic accuracy parameters, the Youden index and correlations between the aMMP-8 test outcomes and clinical features. In this study, 384 and 390 subjects were enrolled in Hong Kong and Shanghai, respectively. The conventional 20 ng/mL threshold failed to detect more than 50% of early-stage (I/II) cases. The positive POC-ORT results were significantly correlated with the number of sites with bleeding on probing (BOP), probing pocket depth (PPD) ≥ 4 mm, PPD ≥ 5 mm, PPD ≥ 4 mm and BOP, PPD ≥ 5 mm and BOP and clinical attachment loss. The adjusted odds ratio (OR) for a positive test increased with the number of sites with PPD ≥ 5 mm: 1.092 (95% CI: 1.063-1.127, p < 0.001) for the Hong Kong sample and 1.074 (95% CI: 1.050-1.100, p < 0.001) for the Shanghai sample, suggesting a higher likelihood of a positive result with each additional pocket ≥ 5 mm. The same was observed for PPD ≥ 5 mm with BOP: 1.093 (95% CI: 1.064-1.129, p < 0.001) and 1.077 (95% CI: 1.052-1.105, p < 0.001). Notably, the false-negative cases were characterised by a significantly smaller number of periodontal pockets, BOP percentages and bleeding pockets than the true-positive ones. The false-negative cases, which are responsible for the observed low sensitivity of the POC-ORT, showed morelocalised periodontal inflammation and pocketing. As the oral rinse test measures the overall level of aMMP-8 cleared by the gingival crevicular fluid from various lesions throughout the whole dentition, localised periodontitis appears moredifficult to detect. Additional studies are needed to optimise the sampling strategy and set the cut-off value of a positivetest. The study was approved by the Institutional Review Board of the University of Hong Kong/Hospital Authority Hong Kong West Cluster (IRB Approval: UW22-132; trial registration: NCT03928080) and the Shanghai Ninth People's Hospital Ethics Committee (IRB Approval: SH9H-2021-T408-3; trial registration: NCT05513599).

Toll-like receptor engaged in activation and osteoimmuno-cytokines production by unswitched memory B cells during periodontitis.

Previous research has established that memory B cells contribute to osteoclastogenesis by producing RANKL. However, the phenotypic and functional alterations of switched (CD27 + IgD-) and unswitched (CD27 + IgD +) memory B cells during periodontitis were not fully understood. This study aims to elucidate the specific role of unswitched memory B cells in periodontitis. We analyzed the distribution and function of both memory B cell subsets using flow cytometry to assess their frequency and phenotype. The production of cytokines RANKL, TNF-α, and IL-6 was evaluated using ELISA and PCR. Additionally, cell culture experiments were performed to investigate the impact of TLRs on cytokine production by memory B cells and their capacity to induce osteoclastogenesis. Our findings revealed a higher proportion of switched memory B cells and a lower proportion of unswitched memory B cells in the gingival tissues of periodontitis patients compared to healthy individuals (p < 0.05). Periodontal inflammation was associated with increased TNF-α mRNA levels in switched memory B cells and elevated IL-6 mRNA levels in unswitched memory B cells, with TLR9 and TLR7/8 playing roles in these processes. Furthermore, TLR4 enhanced the ability of memory B cells to produce RANKL and promote osteoclastogenesis. These results suggest a novel mechanism by which unswitched memory B cells contribute to periodontal inflammation and alveolar bone resorption, independent of antibody secretion, and highlight the potential role of TLRs in exacerbating local inflammation during periodontitis.

Pexidartinib Inhibits Macrophage Senescence Through Glycolysis in Periodontitis Microenvironment

Pexidartinib Inhibits Macrophage Senescence Through Glycolysis in Periodontitis Microenvironment

Molecular detection of toxigenic Clostridioides difficile in subgingival biofilm of severe periodontitis.

Molecular detection of toxigenic Clostridioides difficile in subgingival biofilm of severe periodontitis.

A Chitosan-based Hydrogel to Modulate Immune Cells and Promote Periodontitis Healing in the High-Fat Diet-induced Periodontitis Rat Model.

Periodontitis is a multifactorial inflammatory disease driven by prolonged, dysregulated inflammation between dysbiotic microbiota and the host immune system. Risk factors such as metabolic syndrome exacerbate periodontitis progression through systemic inflammation. Current treatments primarily focus on removing pathogenic dental plaque, but subsequent healing relies mainly on the host immune response. Modulating the local immune environment, particularly dendritic cells (DCs) and T-cells, in periodontitis complicated by metabolic syndrome could enhance the healing process. The objective of this study is to develop a biomaterial-based adjuvant therapy to immunomodulate DCs and T-cells and promote healing in periodontitis complicated by metabolic syndrome. We developed and characterized a chitosan-based thermosensitive injectable self-assembled hydrogel (TISH), which exhibited an interconnected porous structure conducive to cell migration and adhesion. TISH was loaded with granulocyte-macrophage colony-stimulating factor (GM-CSF) and resveratrol (TISH(GR)), enabling sustained release over time. Mechanistically, TISH(GR) suppressed inflammatory signalling pathways (MAPKs and NF-κB) downstream of Toll-like receptor-4 in DCs. In a high-fat diet-induced periodontitis rat model, TISH(GR) administered as an adjuvant to SRP significantly alleviated periodontal inflammation and tissue destruction compared to SRP alone. TISH(GR) treatment was associated with decreased TH17 cell infiltration and elevated expression of the Tregs-associated cytokine IL-10 in the periodontium. In conclusion, TISH(GR) was developed and optimized as an injectable immunomodulatory hydrogel targeting DCs and T-cells. It demonstrated promising potential to attenuate inflammation and enhance periodontal healing, particularly in immunocompromised patients with metabolic syndrome. STATEMENT OF SIGNIFICANCE: Current treatments for periodontitis primarily focus on dental plaque removal, with healing heavily dependent on the host immune system. However, metabolic diseases can dysregulate the local immune response, exacerbating periodontal inflammation and impairing post-treatment healing. In this study, we developed a chitosan-based hydrogel designed to immunomodulate dendritic cells and T-cells, polarizing them toward an anti-inflammatory phenotype that promotes tissue repair. When administered as an adjuvant to scaling and root planing, this combination therapy significantly enhanced periodontal healing and reduced tissue damage in a high-fat diet complicated periodontitis model. These findings highlight the clinical potential of this hydrogel formulation to improve treatment outcomes, particularly in challenging clinical cases involving metabolic comorbidities.

USP7 - A novel target for controlling periodontal inflammation through modulation of macrophage polarization.

USP7 - A novel target for controlling periodontal inflammation through modulation of macrophage polarization.

Triggering mouth-resident antiviral CD8+ T cells potentiates experimental periodontitis.

Triggering mouth-resident antiviral CD8+ T cells potentiates experimental periodontitis.