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Abstract Succinate receptor GPR91 is one of the G protein-coupled receptors (GPCRs) that interacts with various proteins to regulate diverse cellular functions such as cell morphology, apoptosis, and differentiation. In this study, we investigated whether the GPR91-mediated signaling pathway regulates mineralization in Porphyromonas gingivalis (P. gingivalis)-treated osteoblasts and to determine its potential role in osteoclast differentiation. Primary mouse osteoblasts from wild-type (WT) and GPR91 knockout (GPR91-/-) mice infected with P. gingivalis were used for in vitro experiments. The results showed that inhibition by 4C, a specific inhibitor, and GPR91 knockout promoted mineralization in P. gingivalis-infected osteoblasts. Surprisingly, GPR91 knockdown decreased the migration ability of osteoblasts. Moreover, compared with P. gingivalis-infected WT osteoblasts, GPR91-/- osteoblasts exhibited decreased RANKL production, and conditioned media (CM) from bacteria-infected GPR91-/- osteoblasts suppressed the formation of osteoclast precursors. Moreover, P. gingivalis mediated the role of GPR91 in osteoblast mineralization by activating the NF-κB pathway. These findings suggest that GPR91 activation reduces mineralization of P. gingivalis-infected osteoblasts and promotes osteoclastogenesis in macrophages. Therefore, targeting GPR91 may mitigate the loss of alveolar bone during bacterial infection.

Abstract Background This study aimed to investigate the potential associations between alveolar bone thickness, bucco-palatal inclination of maxillary lateral incisors, and lateral incisor root resorption in patients with unilateral maxillary impacted canines (UMICs). Methods A total of three hundred and five subjects (120 males, 185 females; mean age, 16.39 years; standard deviation, 4.04) with UMICs were included. Canine position and root resorption were assessed using CBCT. UMICs were divided into palatal, buccal and mid-alveolus groups (PICs, BICs and MAICs), with 117, 137 and 51 subjects, respectively. Alveolar bone thickness and bucco-palatal inclination of lateral incisors were measured using the Dolphin software. Results The prevalence of lateral incisor root resorption was significantly lower in the BICs (13.9%) than MAICs (29.4%) and PICs (29.1%). Alveolar bone thickness of the apical area was smaller in UMICs with lateral incisor root resorption than no resorption in both PICs (8.33 ± 1.64 vs 10.53 ± 2.55 mm) and BICs (8.94 ± 1.85 vs 10.76 ± 2.28 mm). Furthermore, lateral incisors on the impacted side were more buccally inclined in PICs with lateral incisor root resorption than no resorption, while in both BICs and MAICs, there was no statistical difference between lateral incisor root resorption than no resorption. Moreover, alveolar bone thickness of the apical area, rather than bucco-palatal inclination of lateral incisors, was significantly correlated with lateral incisor root resorption both in PICs and BICs. Conclusions Lateral incisor root resorption is less common in BICs. Thinner alveolar bone thickness at the apical area of lateral incisors can be considered as a potential risk factor for lateral incisor root resorption in UMICs.

Macrophages are important for maintaining tissue homeostasis and defending against pathogens in periodontal tissues. However, these tissues are often vulnerable to damage due to local inflammatory responses within the host tissues. This study aimed to investigate the role of G protein-coupled receptor 91(GPR91) during the inflammatory response to Porphyromonas gingivalis (P. gingivalis) in bone marrow-derived macrophages (BMDMs). To this end, we examined expression levels of GPR91 genes in human periodontal tissues affected by periodontitis. Utilizing primary mouse BMDMs from wild-type (WT) and GPR91 knockout (GPR91−/−) mice infected with P. gingivalis, we demonstrated that GPR91 accumulates in inflamed gingival tissues. Additionally, P. gingivalis can induce intercellular succinate accumulation, inflammatory mediator generation, reactive oxygen species (ROS) production, lipid peroxidation, and superoxide dismutase activity in WT-BMDMs. Moreover, inhibition of GPR91 by the specific inhibitor 4C as well as knockdown of GPR91 reduced inflammation and oxidative stress in P. gingivalis-infected BMDMs. Furthermore, we discovered that GPR91-mediated inflammation in P. gingivalis-infected BMDMs is activated via the Erk/Nuclear Factor-κB pathway. These findings provide new insights into the metabolic pathogenesis of periodontal inflammation.

Abstract Background Gingival recession and post-operation discomfort are still a problem for patients receiving the periodontal regeneration surgery for intra-bony defects. To further reduce the trauma and the post-operation gingival recession, a novel periodontal endoscopy-aided non-incisional regeneration technique (NIT) was proposed in the treatment of intra-bony defects. Methods Retrospective analysis of 21 subjects treated with NIT and 21 subjects with periodontal endoscopy-aided scaling and root planing (PSRP) at baseline and 1-year evaluation was conducted. After removing the subgingival calculus and granulation tissue, bone grafting materials were placed into intrabony defects with the assistance of a gingival retractor in the NIT group. Probing depth (PD), gingival recession (GR), clinical attachment level (CAL), as well as the distance between bone crest (BC) level and base of the defect (BD) (intrabony defect depth, IBD) were evaluated at baseline and 1 year after treatment. Results At 1-year follow-up, the value of CAL, PD and IBD were statistically significant different compared with baseline in both two groups (p

This study aimed to investigate correlation between mitochondrial reactive oxygen species and Porphyromonas gingivalis in the process of cementoblast pyroptosis. Lactate dehydrogenase activity assay, enzyme-linked immunosorbent assay, western blotting and flow cytometry analysis were utilized to explore whether Porphyromonas gingivalis triggered pyroptosis in cementoblasts. Reactive oxygen species and mitochondrial reactive oxygen species were detected using flow cytometry and fluorescence staining. The effect of mitochondrial reactive oxygen species on the Porphyromonas gingivalis-induced pyroptosis of cementoblasts was assessed by Mito-Tempo, mitochondrion-targeted superoxide dismutase mimetic. Phosphorylation levels of p65 were measured by western blotting. SC75741, a nuclear factor-kappa B inhibitor, was added to block the nuclear factor-kappa B in the Porphyromonas gingivalis-infected cementoblasts. Porphyromonas gingivalis triggered pyroptosis of cementoblasts, and an elevation in reactive oxygen species generation in the mitochondria was observed. Inhibition of mitochondrial reactive oxygen species reduced pyroptosis and nuclear factor-kappa B signaling pathway mediated the pyroptotic cell death in Porphyromonas gingivalis-infected cementoblasts. Together, our findings demonstrate that mitochondrial reactive oxygen species increased by Porphyromonas gingivalis participated in the pyroptosis of cementoblasts. Targeting mitochondrial reactive oxygen species may offer therapeutic strategies for root surface remodeling or periodontal regeneration.

Abstract Background To evaluate the incidence and severity of open gingival embrasures (OGEs) in adult patients treated with clear aligners and fixed appliances. Methods Two hundred non-extraction adult subjects with less than 5 mm of crowding (mean age, 24.6 ± 3.8 years) were enrolled in this retrospective study. The subjects were divided into the clear aligner (n = 100) and fixed appliance group (n = 100). The intraoral photographs were utilized to determine the incidence of OGEs in the upper arch between maxillary central incisors, as well as the lower arch between mandibular central incisors. Crown overlap, crown shape, posttreatment root angulation, the distance from the interproximal contact point (ICP) to the alveolar bone crest (ABC) after treatment and interproximal enamel reduction (IPR) were determined in the two groups. Results The incidence of OGEs between maxillary and mandibular central incisors after orthodontic treatment was 35.0% and 38.0% in the clear aligner group, respectively, significantly higher than that (18.0% and 24.0%) in the fixed appliance group (P

Abstract Objective This retrospective study aimed to analyze the clinical efficacy of two regenerative surgical methods — Bio-Oss granules combined with barrier membranes and Bio-Oss Collagen alone — and to help clinicians achieve better periodontal regeneration outcomes in the specific periodontal condition. Methodology Patients who underwent periodontal regeneration surgery from January 2018 to April 2022 were retrospectively screened, and their clinical and radiographic outcomes at 6 months postoperatively were analyzed. The probing depth (PD), clinical attachment level (CAL), bleeding on probing (BOP), gingival recession (GR), distance from the cemento-enamel junction to the bottom of the bone defect (CEJ-BD), and depth of intrabony defects (INFRA) were recorded before the operation (T0) and 6 months after it (T1), and subsequently compared. Results In total, 143 patients were included — 77 were placed in the Bio-Oss group and 66 were placed in the Bio-Oss Collagen group. All indicators, including PD and CAL at T1, showed significant differences compared to baseline, for both groups (P

Abstract Background When infected with Porphyromonas gingivalis, gingival fibroblasts undergo metabolic reprogramming, and rely on aerobic glycolysis rather than oxidative phosphorylation for rapid energy replenishment. Hexokinases (HKs) are catalysts for glucose metabolism, and HK2 constitutes the major HK inducible isoform. The objective of this study is to determine whether HK2-mediated glycolysis promotes inflammatory responses in inflamed gingiva. Methods Levels of glycolysis-related genes were assessed in normal and inflamed gingiva. Human gingival fibroblasts were harvested and infected with Porphyromonas gingivalis in order to mimic periodontal inflammation. 2-deoxy-d-glucose, an analogue of glucose, was used to block HK2-mediated glycolysis, while small interfering RNA was used to knock down HK2 expression. The mRNA and protein levels of genes were analyzed by real-time quantitative PCR and western blotting, respectively. HK2 activity and lactate production were assessed by ELISA. Cell proliferation was assessed by confocal microscopy. The generation of reactive oxygen species was assessed by flow cytometry. Results Elevated expression of HK2 and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 was observed in the inflamed gingiva. P. gingivalis infection was shown to promote glycolysis in human gingival fibroblasts, as evidenced by increased gene transcription of HK2 and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3, cell glucose consumption, and HK2 activity. Inhibition and knockdown of HK2 resulted in reduced cytokine production, cell proliferation, and reactive oxygen species generation. Furthermore, P. gingivalis infection activated the hypoxia-inducible factor-1α signaling pathway, thus promoting HK2-mediated glycolysis and proinflammatory responses. Conclusions HK2-mediated glycolysis promotes inflammatory responses in gingival tissues, and therefore glycolysis can be targeted in order to inhibit the progression of periodontal inflammation.

Background Microtubule dynamics plays a crucial role in the spatial arrangement of cell organelles and activation of the NLRP3 inflammasome. Purpose This study aimed to explore whether microtubule affinity regulating kinase 4 (MARK4) can be a therapeutic target of periodontitis by affecting microtubule dynamics and NLRP3 inflammasome-mediated pyroptosis in macrophages. Materials and Methods The NLRP3 inflammasome-related genes and MARK4 were measured in the healthy and inflamed human gingival tissues. Bone marrow-derived macrophages (BMDMs) were infected with Porphyromonas gingivalis, while the MARK4 inhibitors (OTSSP167 and Compound 50) and small interference RNA were utilized to restrain MARK4. Apoptosis-associated speck-like protein (ASC) speck was detected by confocal, and levels of interleukin-1β (IL-1β), as well as IL-18, were assessed by ELISA. Results Increased staining and transcription of MARK4, NLRP3, ASC, and Caspase-1 were observed in the inflamed gingiva. P. gingivalis infection promoted MARK4 expression and the NLRP3 inflammasome in BMDMs. Inhibition of MARK4 decreased LDH release, IL-1β and IL-18 production, ASC speck formation, and the pyroptosis-related genes transcription. Furthermore, MARK4 inhibition reduced microtubule polymerization and acetylation in P. gingivalis-infected BMDMs. Conclusions MARK4 promoted NLRP3 inflammasome activation and pyroptosis in P. gingivalis-infected BMDMs by affecting microtubule dynamics. MARK4 inhibition might be a potential target in regulating the NLRP3 inflammasome during periodontitis progress.

The damage monitoring and identification of arch bridges provide an important means to ensure the safe operation of arch bridges. At present, many methods have been developed, and the applicability and effectiveness of these methods depend on the damage type, structural configuration and available data. To guide the practical application of these methods, a systematic review is implemented in this paper. Specifically, the damage monitoring and identification methods of arch bridges are divided into the damage monitoring of local diseases and damage identification of overall performance. Firstly, the research on the damage monitoring of the local diseases of arch bridges is reviewed. According to the disease type, it is divided into four categories, including suspender inspection, void monitoring, stress detection and corrosion detection. For each disease, this paper analyzes the principles, advantages and shortcomings of various methods. Then, the damage identification methods of the overall performance of arch bridges are reviewed, including masonry arch bridges, steel arch bridges, reinforced concrete arch bridges and concrete-filled steel tubular arch bridges. And the commonly used damage indexes of damage identification methods are summarized. This review aims to help researchers and practitioners in implementing existing damage detection methods effectively and developing more reliable and practical methods for arch bridges in the future.

Graphene, with its excellent properties and unique structure, has been extensively studied in the context of modifiable cement-based materials. However, a systematic summary of the status of numerous experimental results and applications is lacking. Therefore, this paper reviews the graphene materials that improve the properties of cement-based materials, including workability, mechanical properties, and durability. The influence of graphene material properties, mass ratio, and curing time on the mechanical properties and durability of concrete is discussed. Furthermore, graphene’s applications in improving interfacial adhesion, enhancing electrical and thermal conductivity of concrete, absorbing heavy metal ions, and collecting building energy are introduced. Finally, the existing issues in current study are analyzed, and the future development trends are foreseen.

Hereditary gingival fibromatosis (HGF) is the most common genetic form of gingival fibromatosis which is featured as a localized or generalized overgrowth of gingivae. Currently two genes (SOS1 and REST), as well as four loci (2p22.1, 2p23.3–p22.3, 5q13–q22, and 11p15), have been identified as associated with HGF in a dominant inheritance pattern. Here, we report 13 individuals with autosomal-dominant HGF from a four-generation Chinese family. Whole-exome sequencing followed by further genetic co-segregation analysis was performed for the family members across three generations. A novel heterozygous missense mutation (c.2812G > A) in zinc finger protein 862 gene (ZNF862) was identified, and it is absent among the population as per the Genome Aggregation Database. The functional study supports a biological role of ZNF862 for increasing the profibrotic factors particularly COL1A1 synthesis and hence resulting in HGF. Here, for the first time we identify the physiological role of ZNF862 for the association with the HGF.