Erosive tooth wear (ETW) has garnered increased attention within the dental community and is now widely recognized by oral health professionals, owing to its rising prevalence and clinical significance. Epidemiological data on ETW in China remain scarce. The aim of this study was to estimate the prevalence, severity and associated factors of erosive tooth wear among 18-39-year-old adults residing in five cities in China. A cross-sectional study was conducted among adults residing in five major cities (Shanghai, Guangzhou, Wuhan, Chengdu and Xi’an) in China. An equal-sized, stratified, multistage sampling was used. ETW was clinically assessed using the Basic Erosive Wear Examination (BEWE) index. Participants were required to complete a self-administered questionnaire, consisting of sociodemographic information, oral health care behavior, dietary habits, and general/oral health history. Statistical analyses included descriptive statistics, univariable logistic regression, and multivariable binary logistic regression to identify factors associated with ETW. A total of 3,405 adults (47.9

This meta-analysis aimed to assess whether oral frailty could be associated with higher odds of physical frailty among older adults. A systematic literature search of observational studies was conducted across PubMed, Web of Science, and Embase from database inception until July 3, 2025. Literature screening, data extraction, and quality assessment were performed independently by two reviewers. Any discrepancies were resolved through discussion or by consultation with a third reviewer. Meta-analysis was performed using STATA 18.0 to calculate pooled odds ratios (ORs) with 95

Backgrounds Erosive tooth wear (ETW) has garnered increased attention within the dental community and is now widely recognized by oral health professionals, owing to its rising prevalence and clinical significance. Epidemiological data on ETW in China remain scarce. The aim of this study was to investigate the prevalence, severity and risk factors of erosive tooth wear among 18-39-year-old urban adults in China. Methods The study was a cross-sectional survey conducted among urban adults from five cities(Shanghai, Guangzhou, Wuhan, Chengdu, Xi’an) in China. An equal-sized, stratified, multistage sampling was used. ETW was clinically assessed using the Basic Erosive Wear Examination (BEWE) index. Participants were required to complete a questionnaire, consisting of sociodemographic information, oral health care behavior, dietary habits, and general/oral health history. Results A total of 3,405 urban young adults (47.9% male), with a mean age of 29.0 years (standard deviation:6.3 years) were included in the oral examination and questionnaire. The prevalence of ETW (BEWE≥2) was 63.7% among 18-39-year-olds. Most of the participants were at a low level for ETW (BEWE score sum ≤8). Severe hard tissue loss (BEWE score sum >13) occurred rarely among participants. Binary Logistic regression analysis showed that sex, age, alcohol and city significantly associated with ETW ( P <0.05). Conclusions Erosive tooth wear is prevalent among urban young adults in China. A better understanding of erosive tooth wear and its associated factors is essential for its prevention and management by dental professionals.

This study aimed to investigate the relationship between oral frailty scores and frailty risk among older adults in Hubei Province, as well as to construct and validate a frailty diagnostic prediction model based on oral frailty scores. A total of 433 elderly individuals were recruited, of whom 384 aged 60 years and above from Hubei Province were ultimately included in the cross-sectional study. Frailty status was assessed using the FRAIL scale. Prior to performing multivariate logistic regression to identify independent associated factors, the data were balanced using the SMOTE-Tomek Links technique. A nomogram prediction model was constructed based on key variables. Its predictive performance and calibration were evaluated using Receiver Operating Characteristic (ROC) curve and calibration curves. Multivariate regression analysis identified age ≥ 80 years, limited physical activity duration, and fewer than 20 remaining teeth as independent associated factors for frailty. ROC curve analysis indicated that both the D-E-N-T-A-L score (AUC = 0.812) and the OFI-8 score (AUC = 0.693) were predictive of frailty status, with the former demonstrating stronger discriminative ability in this sample. The nomogram model integrating age, physical activity level, number of remaining teeth, social interaction, frequency of outings, and the D-E-N-T-A-L score achieved an AUC of 0.838. The nomogram model based on D-E-N-T-A-L oral frailty score demonstrated good discriminative ability for concurrent frailty status in a sample of community-dwelling older adults. It may serve as a potential screening aid for early frailty screening and personalized health management, thereby facilitating early intervention for frailty among older adults.

To evaluate the synergistic effect of a novel Hydroxyapatite (HAP)-Citrate complex toothpaste on dentinal tubule occlusion and the relief of dentine hypersensitivity (DH). For the in vitro study, thirty bovine dentin discs were randomly divided into three groups with ten specimens each: group A, a test toothpaste (HAP, potassium citrate and NaF), group B, a control toothpaste (HAP and NaF), and group C, a placebo toothpaste (NaF only). After 3 and 7 days of simulated brushing, tubule occlusion and mineralized layer formation was assessed using Scanning electron microscopy (SEM). A 12-week, double-blind, randomized trial involving 129 subjects compared the test toothpaste to a bioactive glass-based positive control toothpaste and a placebo. The severity of DH, indicated by Schiff (air) and Yeaple (tactile), was evaluated at baseline, 2, 6, 8, and 12 weeks, with the last 4 weeks being a washout period. Data were analyzed using ANOVA to compare differences between groups, with a significance level set at p < 0.05. In the in-vitro study, the HAP-Citrate complex toothpaste demonstrated rapid and effective occlusion. After 3 and 7 days, it achieved a dentinal tubule occlusion rate of 96.0 ± 2.1

Metabolic disorders and accompanying complications pose considerable risks to systemic organ health. Clinical studies have revealed a significant correlation between nonalcoholic steatohepatitis (NASH) and increased severity of periodontitis. However, directed mechanistic insights remain limited. This study aimed to elucidate the direct impact of NASH on periodontitis progression and to investigate the underlying mechanisms using both in vivo and in vitro models. In mice, a NASH diet induced severe liver damage and steatosis compared with chow-fed controls. Furthermore, NASH significantly exacerbated ligature-induced periodontitis, as evidenced by enhanced alveolar bone loss, inflammatory infiltration, and osteoclast activity. Notably, NASH was associated with elevated macrophage NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation in periodontitis relative to lean controls. Mechanistic in vitro experiments revealed that metabolic stimuli, palmitic acid and cholesterol, synergistically promoted NLRP3 inflammasome activation in Porphyromonas gingivalis, P. gingivalis lipopolysaccharide, as well as Escherichia coli lipopolysaccharide-conditioned macrophages. Importantly, macrophage conditioned medium generated with the combination of palmitic acid and cholesterol markedly potentiated osteoclast differentiation and function, as evidenced by enhanced osteoclastogenesis, F-actin ring assembly, and bone resorptive activity in receptor activator of NF-κΒ ligand-stimulated bone marrow-derived macrophages. This study suggests that NASH exacerbates experimental periodontitis by priming periodontal macrophages through the metabolic activation of the NLRP3 inflammasome. These collective data uncover a novel mechanism linking systemic metabolic dysregulation and osteoimmune responses, providing important insights into the comorbidity of inflammatory diseases.

Background and Objective: People living with dementia typically have poor oral health. However, studies of caries status in this population have revealed different results. This systematic review aimed to assess caries status in old adults with dementia. Method: The PubMed, Web of Science, Embase, and Scopus databases were searched from inception to 13 February 2025. The Newcastle-Ottawa Scale (NOS) was used to assess the risk of bias in case-control studies, and the Joanna Briggs Institute (JBI) Critical Appraisal Checklist was used to assess the risk of bias in cross-sectional studies. Caries status was measured by the decayed, missing, filled teeth (DMFT) index, decayed, missing, filled surfaces (DMFS) index, or the component of DMFT/S. A random effects model was used to pool the included data. The weighted mean difference (WMD) and 95% confidence interval (CI) were calculated to analyze the effect of dementia on caries. Results: A total of 5363 studies were retrieved, and 20 studies were included in this study. Meta-analysis showed the DMFT index (WMD: 3.76, p < 0.0001; 13 studies), decayed teeth (DT) index (WMD: 0.40, p < 0.0001; 10 studies), and missing teeth (MT) index (WMD: 3.67, p = 0.04; 7 studies) values were higher in the dementia group than the control group. There were no differences in the filled teeth (FT) index (WMD: -0.66, p = 0.09; 9 studies) between the dementia group and the control group. Conclusions: Caries status was poorer in people with dementia than the controls. These findings suggest that medical staff and caregivers need to pay more attention to the oral health of dementia patients.

AIM:Early childhood caries (ECC) remains a significant global health challenge. While fluoride-based treatments are the standard, bioactive glass (BAG) has emerged as a promising alternative for caries prevention. This clinical trial aimed to evaluate the effectiveness of a fluoride-free BAG-based toothpaste compared to a fluoride toothpaste in preventing ECC. METHODS:This double-blinded, multicentre, randomized controlled trial enrolled 1063 children aged 3 to 4 years from 12 kindergartens in Hubei, China. Participants were randomly assigned to either the test (fluoride-free toothpaste containing 7.5% (w/w) BAG) or the control (fluoride toothpaste containing 800 ppm F) group. The primary outcomes were caries increment, measured as changes in decayed, missing, and filled teeth (dmft) and surfaces (dmfs) scores, and caries incidence after 27 months. Secondary outcomes included caries increment and incidence assessed at 12 months of follow-up. RESULTS:Baseline characteristics were well balanced between the test and control groups. Both groups demonstrated progressive increases in caries measures during the follow-up periods, though no statistically significant differences emerged between the interventions. At 27 months, caries increment and incidence were comparable between the test and control groups (P > .05 for all comparisons). Similar patterns were observed at 12 months, with both groups showing equivalent caries progression. No adverse events were reported during the study period. CONCLUSIONS:This trial revealed that fluoride-free toothpaste containing 7.5% (w/w) BAG exhibited comparable efficacy to 800 ppm fluoride toothpaste in preventing ECC over 27 months. However, both interventions were associated with substantial caries progression (mean dmft increment >2.0), indicating limited effectiveness in preschool children.

Aim or purpose: This double-blind randomized controlled clinical trial aimed to use an evaporative (air) stimulus and a tactile stimulus to investigate the desensitizing efficacy of hydroxyapatite (HAP) containing toothpaste through a 12-week clinical observation. Materials and methods: After a 2-week washout period, 129 subjects were enrolled and randomly assigned to three groups in parallel: (1) test group (a commercial Repair & Protect Toothpaste containing HAP, potassium citrate and NaF); (2) a commercially available anti-sensitivity positive control toothpaste (with Bioglass and NaF); (3) a placebo control toothpaste (without HAP and potassium nitrate, with NaF). Subjects daily used the assigned toothpaste for 2 minutes each time and conducted OST examination and hypersensitivity evaluation at 2, 6, 8 and 12 weeks. Results: After 6 weeks of use, the Schiff index of the test toothpaste group and the positive control group was significantly improved compared with the placebo control group (p<0.05), the improvement was 21.52% and 28.70%, respectively. After 8 weeks of use, the Yeaple index of the test toothpaste group and the positive control group was significantly improved compared with the placebo control group (p<0.05), the improvement value was 17.22 and 12.33, respectively. After 8 weeks’ evaluation, all subjects switched to ordinary commercially available fluoride toothpaste, the Schiff index of the test toothpaste group continued to improve after 4 weeks evaluation. Conclusions: The clinical results showed hydroxyapatite containing toothpaste can effectively relieve hypersensitivity in 6 weeks’ usage, and the effect lasts for 4 weeks after discontinuation.

BACKGROUND:Overactivation of osteoclasts plays a key driver of bone loss in osteolytic diseases, including periodontitis. Although current antiresorptive agents are clinically effective, their long-term safety and economic burden limit widespread use, highlighting the need for novel, mechanism-based therapeutic strategies. OBJECTIVE:This study aims to evaluate the impact of the natural flavonoid neobavaisoflavone (NBIF), on osteoclast function and periodontitis progression, and explore its underlying molecular mechanisms. METHODS:In vitro, osteoclast differentiation and resorptive activity were assessed using TRAP staining, F-actin ring formation, and scanning electron microscopy. Mechanistic studies employed transcriptomic analysis, molecular docking, and cellular thermal shift assays (CETSA). The therapeutic efficacy and safety of NBIF were further evaluated in a ligature-induced periodontitis mouse model. RESULTS:NBIF markedly inhibited osteoclast differentiation, F-actin ring formation, and bone resorption in vitro. Mechanistic investigations revealed that NBIF directly binds Keap1, stabilizes Nrf2, and promotes its nuclear translocation, leading to upregulation of the iron exporter FPN1, reduction of intracellular iron levels, and suppression of ferroptosis signaling and senescence. In vivo, NBIF significantly mitigated alveolar bone loss, improved trabecular bone architecture, and exhibited favorable safety profiles. CONCLUSION:NBIF shows strong therapeutic potential for osteolytic diseases by suppressing osteoclast formation and bone resorption through the KEAP1-NRF2-FPN1 axis, highlighting the iron metabolism-senescence pathway as a promising therapeutic target and providing a new paradigm for drug development in osteoclast-related bone loss.

Periodontitis is a prevalent chronic inflammatory disease closely associated with various systemic disorders. Conventional therapies, including mechanical debridement and antibiotics, are often insufficient to fully resolve inflammation or restore bone homeostasis. Sulforaphene (LFS) is abundant in radish seed oil and Lai Fu-zi, a traditional Chinese herbal medicine and has been recognized for its anti-inflammatory potential. Here, we show that LFS markedly attenuates the secretion of pro-inflammatory cytokines (IL-1β, IL-6, and IL-8) from human gingival fibroblasts and inhibits osteoclast differentiation even under IL-1β-induced inflammatory conditions, without compromising the osteogenic capacity of periodontal ligament cells (PDLC). Mechanistically, LFS activates the NRF2 pathway and its protective effect against alveolar bone loss was evident in Nrf2 +/+ mice but not Nrf2 -/- mice. Notably, LFS was also found to inhibit the growth, virulence, and biofilm formation of P. gingivalis in vitro, and reduced its abundance within the subgingival microbiota in vivo. Together, these findings identify LFS as a potent NRF2-dependent modulator, offering a promising therapeutic strategy for the prevention and treatment of periodontitis.

Alzheimer’s disease (AD) is characterized by progressive cognition and behavior impairments. Diagnosing AD early is important for clinicians to slow down AD progression and preserve brain function. Biomarkers such as tau protein and amyloid-β peptide (Aβ) are used to aid diagnosis as clinical diagnosis often lags. Additionally, biomarkers can be used to monitor AD status and evaluate AD treatment. Clinicians detect these AD biomarkers in the brain using positron emission tomography/computed tomography or in the cerebrospinal fluid using a lumbar puncture. However, these methods are expensive and invasive. In contrast, saliva collection is simple, inexpensive, non-invasive, stress-free, and repeatable. Moreover, damage to the brain parenchyma can impact the oral cavity and some pathogenic molecules could travel back and forth from the brain to the mouth. This has prompted researchers to explore biomarkers in the saliva. Therefore, this study provides an overview of the main finding of salivary biomarkers for AD diagnosis. Based on these available studies, Aβ, tau, cholinesterase enzyme activity, lactoferrin, melatonin, cortisol, proteomics, metabolomics, exosomes, and the microbiome were changed in AD patients’ saliva when compared to controls. However, well-designed studies are essential to confirm the reliability and validity of these biomarkers in diagnosing and monitoring AD.

As bone-resorbing cells rich in mitochondria, osteoclasts require high iron uptake to promote mitochondrial biogenesis and maintain a high-energy metabolic state for active bone resorption. Given that abnormal osteoclast formation and activation leads to imbalanced bone remodeling and osteolytic bone loss, osteoclasts may be crucial targets for treating osteolytic diseases such as periodontitis. Isobavachin (IBA), a natural flavonoid compound, has been confirmed to be an inhibitor of receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclast differentiation from bone marrow-derived macrophages (BMMs). However, its effects on periodontitis-induced bone loss and the potential mechanism of its anti-osteoclastogenesis effect remain unclear. Our study demonstrated that IBA suppressed RANKL-induced osteoclastogenesis in BMMs and RAW264.7 cells and inhibited osteoclast-mediated bone resorption in vitro. Transcriptomic analysis indicated that iron homeostasis and reactive oxygen species (ROS) metabolic process were enriched among the differentially expressed genes following IBA treatment. IBA exerted its anti-osteoclastogenesis effect by inhibiting iron accumulation in osteoclasts. Mechanistically, IBA attenuated iron accumulation in RANKL-induced osteoclasts by inhibiting the mitogen-activated protein kinase (MAPK) pathway to upregulate ferroportin1 (Fpn1) expression and promote Fpn1-mediated intracellular iron efflux. We also found that IBA inhibited mitochondrial biogenesis and function, and reduced RANKL-induced ROS generation in osteoclasts. Furthermore, IBA attenuated periodontitis-induced bone loss by reducing osteoclastogenesis in vivo. Overall, these results suggest that IBA may serve as a promising therapeutic strategy for bone diseases characterized by osteoclastic bone resorption.

Periodontitis is a widely prevalent oral disease around the world characterized by the disruption of the periodontal ligament and the subsequent development of periodontal pockets, as well as the loss of alveolar bone, and may eventually lead to tooth loss. This research aims to assess the suppressive impact of Eupatilin, a flavone obtained from Artemisia argyi, on osteoclastogenesis in vitro and periodontitis in vivo. We found that Eupatilin can efficiently obstruct the differentiation of Raw264.7 and bone marrow-derived macrophages (BMDMs) induced by RANKL, leading to the formation of mature osteoclasts. Consistently, bone slice resorption assay showed that Eupatilin significantly inhibited osteoclast-mediated bone resorption in a dose-dependent manner. Eupatilin also downregulated the expression of osteoclast-specific genes and proteins in Raw264.7 and BMDMs. RNA sequencing showed that Eupatilin notably downregulated the expression of Siglec-15. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses identified significantly enriched pathways in DEGs, including MAPK signaling pathway. And further mechanistic investigations confirmed that Eupatilin repressed MAPKs/NF-κBsignaling pathways. It was found that Siglec-15 overexpression reversed the inhibitory impact of Eupatilin on the differentiation of osteoclasts. Furthermore, activating MAPK signaling pathway reversed the downregulation of Siglec-15 and the inhibition of osteoclastogenesis by Eupatilin. To sum up, Eupatilin reduced the expression of Siglec-15 by suppressing MAPK signaling pathway, ultimately leading to the inhibition of osteoclastogenesis. Meanwhile, Eupatilin suppressed the alveolar bone resorption caused by experimentalperiodontitis in vivo. Eupatilin exhibits potential therapeutic effects in the treatment of periodontitis, rendering it a promising pharmaceutical agent.

BACKGROUND:To verify the validity of diagnosing initial caries on occlusal surface of permanent posterior teeth by laser fluorescence instrument DIAGNOdent pen. METHODS:Patients from School of Stomatology in Wuhan University were selected and their posterior teeth were examined using DIAGNOdent pen and the International Caries Detection and Assessment System (ICDAS II) by an experienced dentist. After teeth extraction, histological criteria were used to determine the severity of the lesions. The sensitivity, specificity, accuracy, the area under the curve (AUC), and correlation of DIAGNOdent pen and ICDAS II were analyzed compared with histological criteria. Examiners' agreement was measured. RESULTS:The sensitivity range was 0.440-1 while that of specificity was 0.750-0.994. The accuracy and AUC were above 80% and 0.7 respectively. Consistency of examiners' kappa values of ICDAS II, DIAGNOdent pen, and histological criteria were ranged from 0.629 to 0.840. CONCLUSIONS:ICDAS II and DIAGNOdent pen can be effectively used in tandem or independently for the assessment of initial caries.

Background and purpose: Inflammatory disorders have been found to induce bone loss through sustained and persistent activation of osteoclast differentiation, leading to heightened bone resorption. The current pharmacological interventions for combating bone loss to harbor adverse effects or contraindications. There is a pressing need to identify drugs with fewer side effects. Experimental approach: The effect and underlying mechanism of sulforaphene (LFS) on osteoclast differentiation were illustrated in vitro and in vivo with RANKL-induced Raw264.7 cell line osteoclastogenesis and lipopolysaccharide (LPS)-induced bone erosion model. Key results: In this study, LFS has been shown to effectively impede the formation of mature osteoclasts induced from both Raw264.7 cell line and bone marrow macrophages (BMMs), mainly at the early stage. Further mechanistic investigations uncovered that LFS suppressed AKT phosphorylation. SC-79, a potent AKT activator, was found to reverse the inhibitory impact of LFS on osteoclast differentiation. Moreover, transcriptome sequencing analysis revealed that treatment with LFS led to a significant upregulation in the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and antioxidant-related genes. Then it's validated that LFS could promote NRF2 expression and nuclear translocation, as well as effectively resist oxidative stress. NRF2 knockdown reversed the suppression effect of LFS on osteoclast differentiation. In vivo experiments provide convincing evidence that LFS is protective against LPS-induced inflammatory osteolysis. Conclusion and implications: These well-grounded and promising findings suggest LFS as a promising agent to addressing oxidative-stress related diseases and bone loss disorders.

Objective The objective of the study was to determine the anti-osteoclastogenic potential of ginsenoside Rb3 for the treatment of periodontitis. Methods The anti-osteoclastogenic effect was determined using RANKL-induced RAW264.7 cells and murine bone marrow-derived macrophages followed by TRAP and phalloidin staining. Expression of osteoclastogenesis-related genes and proteins were examined by qPCR and WB. Activation of signaling pathways was detected by WB and IHC techniques. Experimental periodontitis rat model was built up by gingival injections of P. gingivalis LPS. After 21 days of Rb3 treatment, rats were sacrificed for micro-CT, IHC, H&E, and TRAP staining analyses. Results Rb3 dramatically inhibits RANKL-induced osteoclastogenesis. Nfatc1, Mmp9, Ctsk, Acp5 mRNA, and MMP9, CTSK proteins were dose-dependently downregulated by Rb3 pretreatment. WB results revealed that Rb3 suppressed activations of p38 MAPK, ERK, and p65 NF-kappa B, and the inhibition of ERK was most pronounced. Consistently, IHC analysis revealed that p-ERK was highly expressed in alveolar bone surface, blood vessels, odontoblasts, and gingival epithelia, which were notably suppressed by Rb3 treatment. H&E staining and micro-CT analyses showed that Rb3 significantly attenuated gingivitis and alveolar bone resorption in rats. Conclusion Rb3 inhibits RANKL-induced osteoclastogenesis and attenuates P. gingivalis LPS-induced gingivitis and alveolar bone resorption in rats via ERK/NF-kappa B signaling pathway.

目的 探讨口腔医学专业本科生临床前期手卫生理论教学和实践训练模式.方法 将同一年级口腔医学专业本科生分为2组,试验组学生通过教师课堂教学形式学习手卫生知识后参加理论考试和洗手考核,对照组未经课堂学习手卫生知识直接进行理论考试和洗手考核.洗手采样和结果评价按照GB15982-2012《医院消毒卫生标准》,洗手训练采用PDCA循环管理体系进行监测.结果 2组学生在性别和学制上成绩比较,差异均有统计学意义(P＜0.05).试验组学生知晓洗手、卫生手和外科手的概念和指征、手卫生消毒的标准均明显高于对照组,差异均有统计学意义(P＜0.05).但2组学生手卫生具体方法上的知晓率比较,差异无统计学意义(P＞0.05).2组学生在性别和学制上比较,第3次明显高于第1次,差异有统计学意义(P＞0.05).结论 口腔医学专业本科生临床前期纳入手卫生学习和训练很有必要,应将手卫生原则和指征进行重点教学,手卫生训练需经PDCA循环反复实践才能达到理想的效果.

Signal transducer and activator of transcription 3 (STAT3), a cytokine-responsive transcription factor, is known to play a role in immunity and bone remodeling. However, whether and how STAT3 impacts macrophage NLR family pyrin domain containing 3 (NLRP3) inflammasome activation associated with inflammatory bone loss remains unknown. Here, STAT3 signaling is hyperactivated in macrophages in the context of both non-sterile and sterile inflammatory osteolysis, and this was highly correlated with the cleaved interleukin-1β (IL-1β) expression pattern. Strikingly, pharmacological inhibition of STAT3 markedly blocks macrophage NLRP3 inflammasome activation in vitro, thereby relieving inflammatory macrophage-amplified osteoclast formation and bone-resorptive activity. Mechanistically, STAT3 inhibition in macrophages triggers PTEN-induced kinase 1 (PINK1)-dependent mitophagy that eliminates dysfunctional mitochondria, reverses mitochondrial membrane potential collapse, and inhibits mitochondrial reactive oxygen species release, thus inactivating the NLRP3 inflammasome. In vivo, STAT3 inhibition effectively protects mice from both infection-induced periapical lesions and aseptic titanium particle-mediated calvarial bone erosion with potent induction of PINK1 and downregulation of inflammasome activation, macrophage infiltration, and osteoclast formation. This study reveals the regulatory role of the STAT3/mitophagy axis at the osteo-immune interface and highlights a potential therapeutic intervention to prevent inflammatory bone loss. © 2022 American Society for Bone and Mineral Research (ASBMR).