Bei-Min Tian

Objective: Periodontitis treatment centers on three pillars: antibacterial, anti‐inflammatory, and regenerative approaches. This review aims to demonstrate that resveratrol (RSV) simultaneously targets all three core components, positioning it as a multifunctional disease‐modifying agent. Methods: We conducted a narrative review of RSV in periodontitis by searching PubMed and Web of Science from inception to July 2026. Rather than focusing solely on its well‐established antioxidant properties, we comprehensively investigated its multifaceted mechanisms across the three key pathological dimensions. Results: RSV demonstrates broad‐spectrum antibacterial activity by inhibiting biofilm formation, suppressing bacterial ATP synthase, inducing DNA damage, and disrupting efflux pumps to counteract antibiotic resistance. RSV modulates host immune responses through multiple signaling pathways, primarily via SIRT1‐mediated epigenetic regulation. RSV also interacts with immune cells and regulates innate immune memory, thereby reducing the risk of disease recurrence associated with trained immunity‐induced hyperinflammation. Furthermore, RSV orchestrates stem cell recruitment via SDF‐1α signaling and cytoskeletal reorganization, while directing cell differentiation through mitochondrial quality control and epigenetic modifications, thereby promoting endogenous periodontal regeneration. Conclusions: This review provides a comprehensive analysis of the multifaceted roles of RSV in antibacterial action, immunomodulation, and tissue regeneration, highlighting its potential as a multifunctional agent against the complex pathological progression of periodontitis.

P. gingivalis , a keystone periodontal pathogen in periodontitis, is recognized for its capacity to evade host immune clearance. Its intracellular survival leads to both local and systemic infection, thereby increasing the risk of periodontitis and its associated systemic diseases. However, macrophages have limited capacity to clear P. gingivalis , which contributes to disease establishment and progression. Our findings confirmed P. gingivalis presence in periodontitis tissue, with intracellular P. gingivalis mainly located in macrophages. However, P. gingivalis cannot be completely cleared by macrophages and enters the blood circulation through damaged periodontal tissue, leading to systemic infection. Transcriptomic analysis identified mitochondrial calcium uniporter (MCU) as a potential key molecule associated with P. gingivalis immune evasion in macrophages. In vitro functional analyses further confirmed that P. gingivalis infection increased MCU expression and led to both cytosolic and mitochondrial calcium overload, thereby impairing intracellular P. gingivalis clearance in macrophages. Notably, as a natural calcium antagonist, magnesium could inhibit the MCU pathway, reverse calcium overload, and enhance the macrophage‐mediated P. gingivalis clearance. Local administration of magnesium‐containing alginate methacryloyl (AlgMA) hydrogel significantly reduced both local and systemic P. gingivalis infection, relieved inflammation, and alleviated periodontal tissue destruction. Collectively, our findings identify MCU‐mediated calcium overload as a previously unrecognized mechanism by which P. gingivalis evades macrophage immune clearance. Moreover, magnesium‐mediated restoration of Ca ²⁺ homeostasis offers a promising host‐directed immunomodulatory therapy for periodontitis and other infectious diseases.

Outer membrane vesicles (OMVs) derived from Porphyromonas gingivalis (P. gingivalis) exhibit substantially greater pathogenic potential than their parent b

Periodontal ligament stem cells (PDLSCs) are key cells that suppress periodontal damage during both the progression and recovery stages of periodontitis. Although substantial evidence has demonstrated that incubation under an inflammatory condition may accelerate senescence of PDLSCs, whether cellular senescence in response to inflammatory incubation contributes to cell dysfunction remain unexplored. In this study, we first observed inflammation‐caused PDLSC senescence in periodontitis based on comparisons of matched patients, and this cellular senescence was demonstrated in healthy cells that were subjected to inflammatory conditions. We subsequently designed further experiments to investigate the possible mechanism underlying inflammation‐induced PDLSC senescence with a particular focus on the role of long noncoding RNAs (lncRNAs). LncRNA microarray analysis and functional gain/loss studies revealed SLC30A4‐AS1 as a regulator of inflammation‐mediated PDLSC senescence. By full‐length transcriptome sequencing, we found that SLC30A4‐AS1 interacted with SRSF3 to affect the alternative splicing (AS) of TP53BP1 and alter the expression of TP53BP1‐204. Further functional studies showed that decreased expression of TP53BP1‐204 reversed PDLSC senescence, and SLC30A4‐AS1 overexpression‐induced PDLSC senescence was abolished by TP53BP1‐204 knockdown. Our data suggest for the first time that SLC30A4‐AS1 plays a key role in regulating PDLSC senescence in inflammatory environments by modulating the AS of TP53BP1.

This study investigated the perceptions and medical history of third molars (M3s) and assessed the prevalence of visible M3s (V-M3s) among 904 Chinese adul

Third molars, also known as wisdom teeth, are located in the most posterior of the tooth arch

Diabetes mellitus is an established risk factor for periodontal disease that can aggravate the severity of periodontal inflammation and accelerate periodontal destruction. The chronic high glucose condition is a hallmark of diabetes-related pathogenesis, and has been demonstrated to impair the osteogenic differentiation of periodontal ligament stem cells (PDLSCs), leading to delayed recovery of periodontal defects in diabetic patients. Reactive oxygen species (ROS) are small molecules that can influence cell fate determination and the direction of cell differentiation. Although excessive accumulation of ROS has been found to be associated with high glucose-induced cell damage, the underlying mechanisms remain unclear. Nicotinamide adenine dinucleotide phosphate (NADPH) is an important electron donor and functions as a critical ROS scavenger in antioxidant systems. It has been identified as a key mediator of various biological processes, including energy metabolism and cell differentiation. However, whether NADPH is involved in the dysregulation of ROS and further compromise of PDLSC osteogenic differentiation under high glucose conditions is still not known. In the present study, we found that PDLSCs incubated under high glucose conditions showed impaired osteogenic differentiation, excessive ROS accumulation and increased NADPH production. Furthermore, after inhibiting the synthesis of NADPH, the osteogenic differentiation of PDLSCs was significantly enhanced, accompanied by reduced cellular ROS accumulation. Our findings demonstrated the crucial role of NADPH in regulating cellular osteogenic differentiation under high glucose conditions and suggested a new target for rescuing high glucose-induced cell dysfunction and promoting tissue regeneration in the future.

Third molars (M3s) can increase the pathological risks of neighboring second molars (M2s). However, whether the M3 presence affects M2 loss remains unknown. This retrospective study aimed to reveal the reasons for M2 loss and how M2 loss relates to neighboring M3s. The medical records and radiographic images of patients with removed M2(s) were reviewed to analyze why the teeth were extracted and if those reasons were related to adjacent M3s. Ultimately, 800 patients with 908 removed M2s were included. In the included quadrants, 526 quadrants with M3s were termed the M3 (+) group, and the other 382 quadrants without M3s were termed the M3 (−) group. The average age of patients in the M3 (+) group was 52.4 ± 14.8 years and that of the M3 (−) group was 56.7 ± 14.9 years, and the difference between the two groups was statistically significant (p < 0.001). Of the 908 M2s, 433 (47.7%) were removed due to caries and sequelae and 300 (33.0%) were removed due to periodontal diseases. Meanwhile, 14.4% of the M2s with adjacent M3s were removed due to distal caries and periodontitis, which were closely related to the neighboring M3s; this percentage was much lower when M3 were absent (1.8%). Additionally, 42.2% of M3s were removed simultaneously with neighboring M2s. The presence of M3s, regardless of impaction status, was associated with an earlier loss of their neighboring M2s.