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Periodontitis and diabetes mellitus exhibit a bidirectional relationship. This narrative review descriptively outlines the role of chlorhexidine in the periodontal treatment of diabetic patients, focusing on its antimicrobial mechanisms against microbial communities and its antiplaque effects. Although chlorhexidine is proven to be effective in combating microbial presence and improving gingivitis with substantial supporting evidence, its impact on glycemic control and insulin resistance in diabetic patients remains contentious. Additionally, the effectiveness of chlorhexidine as an adjunctive chemotherapeutic in the periodontal treatment of gestational diabetes has not yet been studied, highlighting a gap in research that necessitates further prospective studies and randomized controlled trials. Considering the interconnection between periodontal inflammation and glycemic levels, this article finally advocates for collaborative care between dental and medical professionals to manage periodontitis in diabetic patients effectively., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.)

Objectives: Changes of macrophage in the local immune microenvironment of periodontitis cause alveolar bone resorption. This study aims to investigate the effect of a new drug delivery method of aspirin on the immune microenvironment of periodontitis to promote alveolar bone repair, and to explore mechanism of aspirin's effect on macrophage., Methods: We isolated extracellular vesicles (EVs) from periodontal stem cells (PDLSCs) and loaded with aspirin by sonication, and then evaluated the treatment efficacy of aspirin-loaded vesicles (EVs-ASP) in periodontitis model in mice. In vitro, we explored the role of EVs-ASP in the regulation of LPS-induced macrophages. The underlying mechanism by which EVs-ASP regulates phenotypic remodeling of macrophages in periodontitis was further investigated., Results: EVs-ASP inhibited the inflammatory environment of LPS-induced macrophage, and promoted anti-inflammatory macrophages formation both in vivo and in vitro, and reduced bone loss in periodontitis models. Moreover, EVs-ASP enhanced oxidative phosphorylation and suppressed glycolysis in macrophages., Conclusions: Consequently, EVs-ASP improves the periodontal immune microenvironment by enhancing oxidative phosphorylation (OXPHOS) in macrophages, resulting in a certain degree of regeneration of alveolar bone height. Our study provides a new potential strategy for bone repair in periodontitis therapy., Competing Interests: Declaration of competing interest All authors have seen and approved the final version. The authors have declared that no competing interest exists., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Periodontitis is one of the most prevalent dental diseases, and the patients with periodontitis often suffer from refractory periodontitis or recurrence of disease due to improper or inadequate treatment. In clinical practice, the early and accurate assessment of post-treatment prognosis in periodontitis patients is always very important in order to implement timely interventions. In this study, a pre-treatment saliva SERS based prognostic protocol was explored to predict the prognosis of periodontal non-surgery therapy in periodontitis patients. According to the biomolecular analysis, significant differences in the levels of ascorbic acid, uric acid and glutathione are observed between good prognosis group and poor prognosis group, which are expected to serve as potential prognostic markers. Furthermore, high accuracy, sensitivity and specificity can also be achieved by using the proposed prognostic model. The excellent performance of the proposed method has demonstrated its potential for fast, accurate, and non-invasive prognostic prediction of periodontal non-surgery therapy in periodontitis patients, even at the time before implementing treatment, thus is expected to benefit timely and rational guidance on clinical interventions., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Inflammatory microenvironment causes the change of epigenetic modification in periodontal ligament stem cells derived from periodontitis tissues (P-PDLSCs), which results in defective osteogenic differentiation compared to cells from healthy tissues. It's urgent to explore therapeutic strategies aimed at epigenetic targets associated with the regenerative ability of PDLSCs. Osthole, a small-molecule compound extracted from Chinese herbs, has been documented to promote osteogenesis and cell sheets formation of healthy PDLSCs. However, whether osthole shows same effect on P-PDLSCs and the mechanism of promotive effect is still unknown. The purpose of this study was to determine whether Osthole could restore defective osteogenic differentiation of P-PDLSCs via epigenetic modification. We demonstrated that 10 -7  Mol/L of Osthole was the best concentration for osteogenic differentiation and proliferation of P-PDLSCs. Mechanistically, we also found that Osthole upregulated MOZ and MORF, histone acetylases that specifically catalyze acetylation of Histone3 lisine9 (H3K9) and Histone3 lisine14 (H3K14), which are key regulators in osteogenic differentiation of P-PDLSCs. Furthermore, Osthole treatment improved cell sheet formation and enhanced the bone formation of PDLSC sheets in animal models of periodontitis. Our study suggests that Osthole is a promising drug to cure periodontitis via regulating epigenetic modification in cell sheets engineering.

The association between inflammation and endoplasmic reticulum (ER) stress has been described in many diseases. However, if and how chronic inflammation governs the unfolded protein response (UPR) and promotes ER homeostasis of chronic inflammatory disease remains elusive. In this study, chronic inflammation resulted in ER stress in mesenchymal stem cells in the setting of periodontitis. Long-term proinflammatory cytokines induced prolonged ER stress and decreased the osteogenic differentiation of periodontal ligament stem cells (PDLSCs). Interestingly, we showed that chronic inflammation decreases the expression of lysine acetyltransferase 6B (KAT6B, also called MORF), a histone acetyltransferase, and causes the upregulation of a key UPR sensor, PERK, which lead to the persistent activation of the UPR in PDLSCs. Furthermore, we found that the activation of UPR mediated by MORF in chronic inflammation contributes to the PERK-related deterioration of the osteogenic differentiation of PDLSCs both in vivo and in vitro. Taken together, our results suggest that chronic inflammation compromises UPR function through MORF-mediated-PERK transcription, which is a previously unrecognized mechanism that contributes to impaired ER function, prolonged ER stress and defective osteogenic differentiation of PDLSCs in periodontitis.

Periodontal ligament stem cells (PDLSCs) from periodontitis patients showed defective osteogenic differentiation. However, the mechanism of impaired osteogenic differentiation of PDLSCs in inflammatory microenvironments is still unclear. In this study, we found that inflammation in the microenvironment resulted in downregulation of histone acetyltransferase GCN5 expression and lack of GCN5 caused decreased osteogenic differentiation of PDLSCs. Previous study showed activated Wnt/β-cateinin pathway of PDLSCs resulted in defective osteogenic differentiation. Here we found knockdown of GCN5 decreased the expression of DKK1, an inhibitor of Wnt/β-cateinin pathway, thus activated Wnt/β-catenin pathway of PDLSCs. Mechanistically, GCN5 regulated DKK1 expression by acetylation of Histone H3 lysine 9 (H3K9) and Histone H3 lysine 14 (H3K14) at its promoter region. Interestingly, we found that in vivo injection of aspirin rescued the periodontitis of rats through inhibiting inflammation and upregulating GCN5 expression. Furthermore, aspirin treatment of PDLSCs upregulated GCN5 expression and increased osteogenic differentiation of PDLSCs. In conclusion, GCN5 plays a protective role in periodontitis through acetylation of DKK1 and applying drugs targeting GCN5, such as aspirin, could be a new approach for periodontitis treatment.

Introduction: Periodontitis is initiated and sustained by bacteria. However, the mechanism of bacteria induced periodontitis is still unknown. We hypothesized that bacterial components can affect the functions of stem cells in the periodontium. In this study, we comparatively investigated the influence of Lipopolysaccharide (LPS) on the osteogenesis potential of human periodontal ligament stem cells (PDLSCs) and bone marrow mesenchymal stem cells (BMMSCs)., Methods: Human PDLSCs and BMMSCs were harvested and mineralized nodule formation was assessed by alizarin red S staining. Expression level of osteogenic related gene was detected by quantitative RT-PCR (qRT-PCR). The expression of Toll-like receptor 4 (TLR4) and its downstream signaling pathway were examined by western blot. The role of TLR4 and related signaling pathway in LPS impairing the osteogenic potential of human PDLSCs and BMMSCs were also studied by alizarin red S staining and qRT-PCR. Experimental periodontitis was induced in adult Sprague-Dawley rats and the alveolar bone loss was measured by micro computed tomography analysis. The expression of alkaline phosphatase (ALP) was assessed by immunohistochemistry and the number of osteoclasts was shown by Tartrate-resistant acid phosphatase (TRAP) staining., Results: LPS decreased the osteogenic differentiation of human PDLSCs through TLR4 regulated nuclear factor (NF)-κB pathway, but not for BMMSCs. Blocking TLR4 or NF-κB signaling partially reversed the decreased osteogenic potential of PDLSCs and prevented the alveolar bone loss caused by LPS experimental periodontitis in rats. The ALP expression in the periodontal ligament was elevated after treatment with anti-TLR4 antibody or pyrrolidinedithiocarbamate, whereas there was no statistical significance among groups for the number of osteoclasts., Conclusions: These data suggest that LPS can activate TLR4 regulated NF-κB pathway of human PDLSCs, thus decreasing their osteogenic potential. Blockage of TLR4 or NF-κB pathway might provide a new approach for periodontitis treatment.

Periodontitis is a chronic inflammatory disease caused by a variety of microbial ecological disorders, which is associated with cardiovascular disease. The possible biological mechanism is that inflammatory mediators released by periodontitis enter the bloodstream and cause systemic low-grade chronic inflammation. Periodontal pathogens are closely related to the occurrence of hypertension and atherosclerosis, which further leads to the development of cerebral infarction. Periodontal pathogens are closely related to the occurrence, development and prognosis of cerebral infarction. This paper describes the relationship between periodontitis and cerebral infarction, and probes into the possible mechanism of periodontal pathogenic bacteria affecting cerebral infarction, which brings consideration to the further study of the interaction between periodontitis and cardiovascular and cerebrovascular diseases. [ABSTRACT FROM AUTHOR]

Periodontal disease combined with inflammatory bowel disease (IBD) is a common disease in the department of stomatology. Both of them are affected by the imbalance of microbiota and immune reaction in the process of onset, forming a pathological mutual promotion, leading to the gradual deterioration of the disease. Recent studies have shown that there is a close relationship between periodontal disease and IBD, including direct and indirect pathways. The direct pathway is the translocation of pro-inflammatory microorganisms from the oral cavity to the intestine, and the stimulation of intestinal immunity. Indirect pathways include systemic immune activation and may be accompanied by non-specific immune function.This paper reviewes the microbial/immune interaction between periodontal disease and IBD in recent years, and summarizes the complex pathogenic relationship between periodontal disease and IBD, providing guidance for the treatment of Periodontal disease with IBD. [ABSTRACT FROM AUTHOR]

(D) Protein expression of Runx2, ALP and Osterix in H-PDLSCs, P-PDLSCs and P-PDLSCs with 10-7 Mol/L Osthole as assayed by Western blot. (E) qRT-PCR showed gene expression of fifteen histone acetylases in P-PDLSCs and P-PDLSCs with 10-7 Mol/L Osthole measured by qRT-PCR. (C) Gene expression of Runx2, ALP and Osterix in H-PDLSCs, P-PDLSCs and P-PDLSCs with 10-7 Mol/L Osthole as assayed by qRT-PCR. [Extracted from the article]