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Background. Oral lichen planus (OLP) is a relatively common chronic inflammatory disease of unknown etiology, which might be caused by oxidative stress and impaired antioxidant defense. Objective. To systematically investigate the markers of oxidative stress and antioxidant systems in the saliva and blood from OLP patients and healthy controls. Methods. The PubMed, Cochrane Library, and Embase were systematically queried to collect data from studies in which oxidative stress/antioxidant markers from OLP and healthy subjects had been evaluated until March 10, 2021. Results. A total of 28 studies fulfilled inclusion criteria, and 25 of them, having 849 OLP patients and 1,052 control subjects and analyzing 12 oxidative stress and antioxidant state marker levels, were subjected to meta-analysis. We found a significant decrease in total antioxidant capacity (TAC) and uric acid (UA) and a significant increase in malondialdehyde (MDA) and nitric oxide (NO) levels in the saliva and serum/plasma of OLP patients. Moreover, a significant elevation of 8-hydroxy-deoxyguanosine (8-OHdG) and advanced oxidation protein product (AOOP) level and a decrease in vitamin C were also observed in the saliva of the OLP group. In contrast, salivary vitamin A, zinc, glutathione peroxidase (GPx), vitamin E, and nitrite were not significantly different between the two groups. In single studies, markers of oxidative stresses such as superoxide dismutase (SOD) and 8-isoprostanelevels were elevated in OLP, and antioxidant parameters such as glutathione (GSH) and total protein (TP) levels were dysregulated. Conclusion. This meta-analysis helps to clarify the profile of oxidative stress and antioxidant state markers in OLP patients although existing evidence is rather heterogeneous and many studies are affected by several limitations. Larger and more standardized studies are warranted to ascertain whether these markers are potential causes or effects of OLP and whether antioxidant therapy improving oxidative stress will be useful.

The role of autoimmune diseases (ADs) in temporomandibular disorders (TMDs) has been emphasized in observational studies. However, whether the causation exists is unclear, and controversy remains about which specific disorder is destructive in TMDs. This Mendelian randomization (MR) study aims to estimate the causal effect of common ADs on TMDs. Genetic data from published genome-wide association studies for fourteen common ADs, specifically multiple sclerosis (MS, N = 15,283), ankylosing spondylitis (AS, N = 22,647), asthma (N = 408,422), celiac disease (N = 15,283), Graves' disease (N = 458,620), Hashimoto thyroiditis (N = 395,640), primary biliary cirrhosis (PBC, N = 11,375), primary sclerosing cholangitis (PSC, N = 14,890), psoriasis vulgaris (N = 483,174), rheumatoid arthritis (RA, N = 417,256), systemic lupus erythematosus (SLE, N = 23,210), Type 1 diabetes (T1D, N = 520,580), inflammatory bowel disease (IBD, N = 34,652), and Sjogren's syndrome (SS, N = 407,746) were collected. Additionally, the latest summary-level data for TMDs (N = 228,812) were extracted from the FinnGen database. The overall effects of each immune traits were assessed via inverse-variance weighted (IVW), weighted median, and MR-Egger methods, and performed extensive sensitivity analyses. Finally, 731 immune cell phenotypes (N = 3,757) were analyzed for their mediating role in the significant causality. Univariable MR analyses revealed that genetically predicted RA (IVW OR: 1.12, 95% CI: 1.05-1.19, < 0.001) and MS (IVW OR: 1.06, 95% CI: 1.03-1.10, = 0.001) were associated with increased risk of TMDs. Two out of 731 immune cell phenotypes were identified as causal mediators in the associations of RA with TMDs, including \"CD25++ CD8+ T cell % CD8+ T cell\" (mediation proportion: 6.2%) and \"CD3 on activated CD4 regulatory T cell\" (5.4%). Additionally, \"CD127 on granulocyte\" mediated 10.6% of the total effect of MS on TMDs. No reverse directions, heterogeneity, and pleiotropy were detected in the analyses ( > 0.05). This MR study provides new evidence regarding the causal impact of genetic predisposition to RA or MS on the increased risk of TMDs, potentially mediated by the modulation of immune cells. These findings highlight the importance for clinicians to pay more attention to patients with RA or MS when consulting for temporomandibular discomfort. The mediating role of specific immune cells is proposed but needs further investigation.

Background Observational studies have shown that body mass index (BMI) is highly correlated with the occurrence of temporomandibular disorders (TMDs). However, these studies failed to present a causal relationship. Thus, we aimed to performed a Mendelian randomization (MR) study to investigate causality between BMI and TMDs. Methods We performed a two-sample bidirectional MR analysis using large-scale genome-wide association studies (GWAS). Data were obtained from a large-scale BMI dataset (N = 322,154), TMDs dataset (N = 134,280). The causal effects were estimated with inverse-variance weighted (IVW) method, MR Egger, weighted median. Sensitivity analyses were implemented with Cochran’s Q test, MR-Egger intercept test, MR-PRESSO, leave-one-out analysis and the funnel plot. Results In the forward MR analysis, a genetic prediction of low BMI was causally associated with a higher risk of TMDs (IVW OR: 0.575, 95% CI: 0.415–0.798, p : 0.001). Similar results were obtained using other complementary methods (MR Egger OR: 0.270, 95% CI: 0.104–0.698, p : 0.009; weighted median OR: 0.496, 95% CI: 0.298–0.826, p : 0.007). In the reverse MR results, TMDs was shown to have no significant effect on BMI (all p  > 0.05). No pleiotropy and heterogeneity were detected in the bidirectional analysis ( p  > 0.05). Conclusion A lower BMI might be causally associated with increased risk of TMDs, supporting the importance of weight control for the prevention of TMDs. Clinicians should pay more attention to the low-BMI patients among those seeking medical advice due to temporomandibular joint discomfort.

Background Observational studies suggest a link between diabetes and oral potentially malignant disorders (OPMDs), such as oral lichen planus (OLP) and oral leukoplakia (OLK). The causal relationship, as well as the type of diabetes that promotes OPMDs development, remains unclear. This Mendelian randomization (MR) study estimated the causal effects of diabetes-related traits on OPMDs. Methods Large-scale genome-wide association study data on type 1 diabetes (T1D), type 2 diabetes (T2D), fasting glucose (FG), fasting insulin (FI), glycated hemoglobin (HbA1c), OLP, OLK, and actinic cheilitis (AC) were used. Causal effects were assessed using inverse-variance weighted (IVW), weighted median, and MR–Egger methods. Multivariable MR analyses evaluated the independent roles of these traits, with extensive sensitivity analyses. Results Genetic susceptibility to T1D (IVW OR = 1.09, 95% CI 1.02–1.17, P  = 0.007) and T2D (IVW OR = 0.91, 95% CI 0.86–0.97, P  = 0.002) showed protective effects against AC. T1D was associated with an increased risk of OLP (IVW OR = 1.09, 95% CI 1.02–1.17, P  = 0.007). The effect of T1D on AC and OLP remained robust after adjusting for FI, FG, and HbA1c, while T2D's effect on AC was not significant when considering these glycemic traits. No potential pleiotropy was detected ( P  > 0.05). Conclusions T1D may have a causal role in the development of OLP independent of glycemic traits, emphasizing the need for routine oral examinations in T1D patients. Conversely, genetically predicted T1D and T2D are significantly associated with a reduced risk of AC, challenging previous assumptions and offering new insights into the relationship between diabetes and OPMDs. Further extensive investigations are required to address the limitations of this study and to clarify these associations. Graphical abstract

Background Oral candidiasis is a common opportunistic fungal infection caused by the genus Candida that primarily affects immunocompromised individuals. However, the clinical application of antifungal agents still faces frequent side effects and antifungal resistance, highlighting the urgent need for alternative therapeutic options. This systematic review aimed to synthesize RCT evidence up to February 2025, comprehensively comparing clinical outcomes across various probiotic regimens, in order to assess the efficacy of probiotics for oral candidiasis. Methods A literature search was conducted to identify randomized clinical trials (RCTs) comparing probiotic regimens (multi-strain combinations or strain-specific interventions) with control groups. Thirteen RCTs were analyzed, using a classical frequentist meta-analysis model. Outcomes focused on the odds ratio (OR) of oral candidiasis (defined as CFU/mL > 10 3 or 10 4 ) and heterogeneity across studies. The analysis integrated evidence up to February 2025 to comprehensively assess clinical outcomes. Results The meta—analytic OR was 0.38 (95% confidence interval (95%CI): 0.22, 0.68), indicating a beneficial effect of treatment; the I 2 index was 60.3%. Focusing on participants diagnosed with oral candidiasis or related diseases, the OR was 0.40 (95% CI, 0.23, 0.70), with an I 2 index of 18.2%. Conclusion The treatment effect in the susceptible populations appeared to have lower heterogeneity and more stable outcomes, indicating that the application of probiotics is beneficial for oral candidiasis, and the effects vary according to the population characteristics and sample size. Owing to the small sample size and high-risk studies, the results should be interpreted with caution.

Background The role of thyroid health in temporomandibular disorders (TMDs) has been emphasized in observational studies. However, whether the causation exists is unclear, and controversy remains about which specific disorder, such as hypothyroidism or hyperthyroidism, is destructive in TMDs. This study aims to investigate the overall and specific causal effects of various thyroid conditions on TMDs. Methods Mendelian randomization (MR) studies were performed using genetic instruments for thyrotropin (TSH, N  = 119,715), free thyroxine (fT4, N  = 49,269), hypothyroidism ( N  = 410,141), hyperthyroidism ( N  = 460,499), and TMDs ( N  = 211,023). We assessed the overall effect of each thyroid factor via inverse-variance weighted (IVW), weighted median, and MR-Egger methods, and performed extensive sensitivity analyses. Additionally, multivariable MR was conducted to evaluate the direct or indirect effects of hypothyroidism on TMDs whilst accounting for TSH, fT4 and hyperthyroidism, and vice versa. Results Univariable MR analyses revealed a causal effect of hypothyroidism on an increased risk of TMDs (IVW OR: 1.12, 95% CI: 1.05–1.20, p  = 0.001). No significant association between genetically predicted hyperthyroidism, TSH, or fT4 and TMDs. In the multivariable MR analyses, the effects of hypothyroidism on TMDs occurrence remained significant even after adjSusting for TSH, fT4 and hyperthyroidism (multivariable IVW OR: 1.10, 95% CI: 1.03–1.17, p =  0.006). No pleiotropy and heterogeneity were detected in the analyses ( p  > 0.05). Conclusions Hypothyroidism might causally increase the risk of TMDs through a direct pathway, highlighting the critical role of managing thyroid health in the prevention of TMDs. Clinicians should give heightened attention to patients with hypothyroidism when seeking medical advice for temporomandibular discomfort. However, caution is warranted due to the potential confounders, pleiotropy, and selection bias in the MR study.

Background The epigenetic-age acceleration (EAA) represents the difference between chronological age and epigenetic age, reflecting accelerated biological aging. Observational studies suggested that oral disorders may impact DNA methylation patterns and aging, but their causal relationship remains largely unexplored. This study aimed to investigate potential causal associations between dental traits and EAA, as well as to identify possible mediators. Methods Using summary statistics of genome-wide association studies of predominantly European ancestry, we conducted univariable and multivariable Mendelian randomization (MR) to estimate the overall and independent effects of ten dental traits (dentures, bleeding gums, painful gums, loose teeth, toothache, ulcers, periodontitis, number of teeth, and two measures of caries) on four EAA subtypes (GrimAge acceleration [GrimAA], PhenoAge acceleration [PhenoAA], HannumAge acceleration [HannumAA] and intrinsic EAA [IEAA]), and used two-step Mendelian randomization to evaluate twelve potential mediators of the associations. Comprehensive sensitivity analyses were used to verity the robustness, heterogeneity, and pleiotropy. Results Univariable inverse variance weighted MR analyses revealed a causal effect of dentures on greater GrimAA (β: 2.47, 95% CI: 0.93–4.01, p =  0.002), PhenoAA (β: 3.00, 95% CI: 1.15–4.85, p =  0.001), and HannumAA (β: 1.96, 95% CI: 0.58–3.33, p =  0.005). In multivariable MR, the associations remained significant after adjusting for periodontitis, caries, number of teeth and bleeding gums. Three out of 12 aging risk factors were identified as mediators of the association between dentures and EAA, including body mass index, body fat percentage, and waist circumference. No evidence for reverse causality and pleiotropy were detected ( p  > 0.05). Conclusions Our findings supported the causal effects of genetic liability for denture wearing on epigenetic aging, with partial mediation by obesity. More attention should be paid to the obesity-monitoring and management for slowing EAA among denture wearers.

The presence of the impurity element Fe significantly influences the overall performance of recycled aluminum alloy. This study aims to elucidate the impact of Fe content on the microstructure and tensile properties of friction-stir-welded (FSW) joints in recycled cast A356 aluminum alloy. Three samples with varying Fe content were prepared for FSW joints. The quality of the weld zone was meticulously assessed through macrostructure and microstructure analyses. The tensile strengths of the joints were carefully evaluated and correlated with the microhardness and microstructure of the weld zone. The research findings reveal that, among the three fabricated joints, the one with an Fe content of 0.3 wt.% demonstrates the most favorable tensile performance. This particular joint exhibits the highest tensile strength of 153 MPa, commendable yield strength of 90 MPa, and a favorable elongation of 5.7%. The mechanisms responsible for grain refinement in the weld nugget zone involve plastic deformation and dynamic recrystallization. Significantly, the disruptive effects of friction-stir action on eutectic silicon phases and rich iron phases emerge as crucial factors contributing to the enhanced performance of the weld nugget zone in the welded joint.