Background:Hyperuricemia (Hu) is a systemic metabolic disorder implicated in inflammatory conditions and has been epidemiologically associated with an increased prevalence of periodontitis. However, whether Hu is associated with periodontal microbial dysbiosis in experimental periodontitis remains unclear. Objective:This exploratory pilot study aimed to investigate whether Hu is associated with periodontal dysbiosis in experimental periodontitis by characterizing the diversity, taxonomic composition, and predicted functional potential of ligature-associated microbiota using 16S rRNA sequencing. Methods:A mouse model combining potassium oxonate-induced Hu with ligature-induced periodontitis was established. Male C57BL/6 mice were allocated to normouricemia with periodontitis (NuP), hyperuricemia with periodontitis (HuP), and allopurinol-treated hyperuricemia with periodontitis (HuP+Allo) groups. Ligature-associated microbiota were analyzed by 16S rRNA gene sequencing. Correlations between microbial alterations and biochemical parameters were evaluated using redundancy analysis. Results:Hu significantly increased microbial diversity and evenness, as indicated by higher Shannon index (P = 0.007) and Shannoneven index (P = 0.002), but did not affect community richness. At the phylum level, Hu increased the Firmicutes/Bacteroidota ratio and Proteobacteria abundance while decreasing Bacteroidota and Actinobacteriota. At the genus level, Hu enriched potentially pathogenic taxa, including Streptococcus and Escherichia-Shigella. Allopurinol partially reversed these changes. Redundancy analysis revealed that microbial shifts were significantly correlated with serum uric acid (R2  = 0.711, P = 0.040) and creatinine (R2  = 0.695, P = 0.035). Functional prediction suggested that Hu was associated with higher predicted abundances of NOD-like receptor signalling and lower predicted abundance of IL-17 signalling pathways. Conclusion:These exploratory findings suggest that Hu may be associated with dysbiotic remodeling of the periodontal ligature microbiota in experimental periodontitis, linking systemic metabolic disturbance with local microbial imbalance and inflammatory pathway alteration. These alterations were partially reversed by allopurinol and correlated with serum uric acid and creatinine, providing mechanistic insight into how Hu may aggravate periodontal tissue destruction.

BACKGROUND & AIMS:Plant-based diet is growing in popularity throughout the world for various reasons, yet its effect on bone health, especially osteoporosis, remains controversial. This systematic review and meta-analysis aim to investigate the association between plant-based diet and risk of osteoporosis. METHODS:A systematic literature search of observational studies examining the relationship between plant-based diets and osteoporosis risk was performed across PubMed, Embase, Web of Science, Scopus, and ProQuest from inception to June 1, 2024. Two reviewers independently extracted data and assessed study quality using the Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies and the Newcastle-Ottawa Scale. To synthesize effect estimates, a random-effects meta-analysis with inverse variance weighting was applied to pool odds ratios (ORs) and 95 % confidence intervals (CIs). Subgroup analysis and meta-regression were used to explore sources of heterogeneity. RESULTS:This study encompassed 20 original observational studies collectively involving 243,366 participants. Primary analysis revealed that plant-based diet was associated with the risk of osteoporosis at the lumbar spine (OR = 2.44, 95%CI = 1.12-5.33, P = 0.02; τ2 = 1.94; I2 = 91.7 %), compared to omnivorous diet. The association remained directionally consistent although attenuated to non-significant at the femoral neck (OR = 1.91, 95%CI = 0.68-5.42, P = 0.22; τ2 = 3.28; I2 = 94.9 %). Subgroup analysis revealed vegans (FN: OR = 1.79, 95%CI = 0.94-3.54, P = 0.10; LS: OR = 1.45, 95%CI = 1.00-2.12, P = 0.05) and those who followed a plant-based diet for ≥10 y (FN: OR = 1.79, 95%CI = 1.29-2.49, P < 0.01; LS: OR = 1.35, 95%CI = 0.97-1.87, P = 0.07) to exhibit a more pronounced risk of osteoporosis. Heterogeneity was primarily driven by study design. CONCLUSIONS:This systematic review and meta-analysis indicate that adherence to plant-based diet may be associated with an elevated risk of osteoporosis, particularly at the lumbar spine, among individuals following a vegan diet or following a plant-based diet for ≥10 y. However, the heterogeneity observed across studies highlights the need for well-designed prospective studies in future, to clarify this relationship.

In order to assess the association between urinary heavy metals and early childhood caries (ECC), a survey of deciduous tooth decay and urinary heavy metal concentrations of 408 children was conducted in a typical industrial and mining area. The results indicated that urinary heavy metal concentrations were ranked as Zn > Fe > Cu > Pb > Ni > Cd > As > Cr > Mn > Hg. The zero-inflated negative binomial model identified Hg as a significant risk factor for ECC (P25 P75, OR = 3.499; > P75, OR = 3.184). Bayesian kernel machine regression further revealed that Pb, Cd, and Hg were positively correlated with ECC. Additional analysis using the Wilcoxon rank sum test and restricted cubic splines confirmed a positive correlation between the urinary concentrations of Pb, Cd, As, and Hg and the number of ECC (p < 0.05). Moreover, Bayesian kernel function regression and weighted quantile sum regression indicated that combined exposure to heavy metals was positively associated with ECC, with Hg (0.420) being the most dominant contributor, followed by As, Pb, and Cd. In conclusion, this study demonstrated a significant positive correlation between urinary heavy metals and both the occurrence and severity of ECC, with Hg identified as the most influential factor. It was recommended to minimize children’s exposure to heavy metals to protect their dental health.

ABSTRACT Aim To investigate the effects of hyperuricemia on periodontitis and the underlying mechanisms by establishing combined animal and cell models. Methods A hyperuricemia mouse model was established by potassium oxonate injection, with sodium carboxymethylcellulose treatment serving as controls. Both models were treated with or without periodontitis induction ( n = 10/group). RAW264.7 macrophages and THP‐1‐derived macrophages were stimulated with Porphyromonas gingivalis ‐lipopolysaccharide in the presence of normal or excessive concentrations of uric acid. Allopurinol intervention was applied to both animal and cell models. Periodontal destruction was measured by micro‐computed tomography and histology. The immune response and oxidative stress in the periodontium and macrophages were assessed using various methods including immunohistochemistry, quantitative PCR, western blotting, flow cytometry and multiplex cytokine assays. Results Potassium oxonate successfully induced hyperuricemia without affecting serum glucose/lipid levels or xanthine oxidoreductase activity. In mice with periodontitis, hyperuricemia exacerbated alveolar bone loss and the presence of osteoclasts and M1 macrophages. Mechanistically, hyperuricemia promoted NLRP3 inflammasome activation, disrupted the inflammatory cytokine response and exacerbated oxidative stress both in the periodontium and in vitro. Allopurinol treatment reversed all relevant changes in both mice and macrophages. Conclusion Hyperuricemia exacerbates periodontitis possibly via uric acid‐induced periodontal inflammation and oxidative stress.

To explore the association between hyperuricemia and having periodontitis. A representative cross-sectional dataset of 10,158 adults was extracted from the National Health and Nutrition Examination Survey (NHANES) 2009–2014. The association between hyperuricemia (the primary exposure) and having periodontitis (outcome) were evaluated using weighted logistic regression models. Serum uric acid (UA) levels and the UA to creatinine (UA/Cr) ratio were used as secondary exposures. Their associations with the diagnosis periodontitis were analyzed using weighted logistic regression or restricted cubic spline regression. The prevalence of Stages III/IV periodontitis was 47.7

Background and ObjectiveClinical studies found high levels of hepatocyte growth factor (HGF) expression in patients with periodontitis. Studies suggest that HGF plays an important role in periodontitis, is involved in inflammation, and modulates alveolar bone integrity in periodontitis. This study aims to investigate the effects and mechanisms of HGF in the progression of experimental periodontitis.MethodsWe used silk thread ligation to induce periodontitis in HGF-overexpressing transgenic (HGF-Tg) and wild-type C57BL/6J mice. The effects of HGF overexpression on alveolar bone destruction were assessed by microcomputed tomography imaging at baseline and on days 7, 14, 21, and 28. We analyzed the cytokines (IL-6 and TNF-alpha) and lymphocytes in periodontitis tissues by enzyme-linked immunosorbent assay and flow cytometry. The effects of HGF on alveolar bone destruction were further tested by quantifying the systemic bone metabolism markers CTXI and PINP and by RNA sequencing for the signaling pathways involved in bone destruction. Western blotting and immunohistochemistry were performed to further elucidate the involved signaling pathways.ResultsWe found that experimental periodontitis increased HGF production in periodontitis tissues; however, the effects of HGF overexpression were inconsistent with disease progression. In the early stage of periodontitis, periodontal inflammation and alveolar bone destruction were significantly lower in HGF-Tg mice than in wild-type mice. In the late stage, HGF-Tg mice showed higher inflammatory responses and progressively aggravated bone destruction with continued stimulation of inflammation. We identified the IL-17/RANKL/TRAF6 pathway as a signaling pathway involved in the HGF effects on the progression of periodontitis.ConclusionHGF plays divergent effects in the progression of experimental periodontitis and accelerates osteoclastic activity and bone destruction in the late stage of inflammation.

Objectives To explore the relationship between hyperuricemia and the risk of developing periodontitis. Materials and Methods A representative dataset of 10,158 adults was extracted from the National Health and Nutrition Examination Survey (NHANES) 2009–2014. The relationship between hyperuricemia (the primary exposure) and the risk of periodontitis (outcome) were evaluated using weighted logistic regression models. Serum uric acid (UA) levels and the UA to creatinine (UA/Cr) ratio were used as secondary exposures. Their associations with the risk of periodontitis were analyzed using weighted logistic regression or restricted cubic spline regression. Results The prevalence of moderate/severe periodontitis was 56.7% among individuals with hyperuricemia and 44.8% among those without. After adjustment, individuals with hyperuricemia had a 26.9% higher risk of developing moderate/severe periodontitis compared to those without hyperuricemia (adjusted OR = 1.269, 95% CI = 1.080 to 1.492, P = 0.006). This increased risk could be explained by a linear relationship with the serum UA/Cr ratio and a U-shaped relationship with serum UA levels. Each unit increase in the serum UA/Cr ratio was associated with a 4.6% higher risk of developing moderate/severe periodontitis (adjusted OR = 1.046, 95% CI = 1.008 to 1.086, P = 0.021). Additionally, each 1 mg/dL increase in serum UA was associated with a 10.2% higher risk (adjusted OR = 1.102, 95% CI = 1.008 to 1.206, P = 0.035) of developing moderate/severe periodontitis when UA levels were greater than 5.5 mg/dL, but a 10.6% lower risk when UA levels were 5.5 mg/dL or lower (adjusted OR = 0.894, 95% CI = 0.800 to 0.998, P = 0.046). Sensitivity analyses validated the robustness of the findings. Conclusions This study provides the first direct evidence that hyperuricemia is associated with an increased risk of developing periodontitis, especially the moderate and severe forms. Clinical Relevance Individuals with hyperuricemia may represent a subgroup of the population susceptible to periodontitis. It may be prudent to initiate timely systemic and periodontal interventions in patients with hyperuricemia to halt the progression of periodontitis.

BackgroundUric acid, a formerly-known antioxidant that has recently been linked to numerous inflammatory diseases as a pro-inflammatory and -oxidative mediator in pathological conditions. It is imperative to reassess the association between periodontitis and uric acid locally and systematically. The aim of this systematic review was to systemically evaluate the association between periodontitis and the uric acid (UA) levels in blood, saliva and gingival crevicular fluid (GCF).MethodsRelevant clinical studies up to January 28, 2023 were identified and retrieved from electronic databases including PubMed, Scopus, EMBASE and Web of Science, with periodontitis, uric acid, hyperuricemia and gout as the keywords. The weighted (WMD) or standardized mean difference (SMD) was calculated using fixed- or random-effect models. Methodological heterogeneity was assessed.ResultsSixteen eligible observational studies and one RCT were enrolled, which included 1354 patients with periodontitis and 989 controls. Three sample types for UA detection were involved, including blood (n = 8), saliva (n = 9) and GCF (n = 1). Meta-analysis demonstrated an enhanced plasma UA concentration (WMD = 1.00 mg/dL, 95% CI 0.63 to 1.37, P < 0.001) but a decreased salivary UA level (SMD = -0.95, 95% CI -1.23 to -0.68, P < 0.001) in periodontitis versus control. Statistical heterogeneity among the plasma- and saliva-tested studies were moderate (I-2 = 58.3%, P = 0.066) and low (I-2 = 33.8%, P = 0.196), respectively.ConclusionsWithin the limitations of the enrolled studies, it seems that there is an association between periodontitis and increased blood UA and decreased salivary UA. (Registration no. CRD42020172535 in Prospero).

Periodontitis is associated with abnormal purine metabolism, which is manifested by increased uric acid in host blood and increased expression of the purine-degrading enzyme, xanthine oxidoreductase (XOR), in periodontal tissues. Both XOR and uric acid are pro-oxidative and pro-inflammatory mediators under pathological conditions. Animal studies have found that injection of uric acid promotes the progression of periodontitis and that febuxostat (an XOR inhibitor) improves tissue destruction in periodontitis. Therefore, blocking the source of uric acid may be a therapeutic strategy to control the progression of periodontitis. In this article, the rationality of XOR inhibitors as potential therapeutic drugs for periodontitis is reviewed. The literature review results suggest that XOR inhibitors show antioxidative, anti-inflammatory, and anti-osteoclastic effects, and XOR inhibitors show clinical efficacy in the treatment of infectious, inflammatory and osteolytic diseases. Although there is no direct evidence to support the finding that XOR inhibitors can ameliorate periodontal microecological dysbiosis, these drugs can modulate intestinal microflora dysbiosis, and there is indirect evidence to support a beneficial effect of XOR inhibitors on periodontal microecological dysbiosis. In conclusion, XOR inhibitors may be used as immunomodulators for the adjuvant treatment of periodontitis by inhibiting inflammation, oxidative stress and anti-osteoclast effects.

Obesity and periodontitis constitute mutual risk factors in respiratory disorders; this study aimed to explore the pulmonary immune response to periodontal infection using combined animal models with diet-induced obesity (DIO). Thirty-two C57 BL/6J mice were randomly divided into low-fat (LF) or high-fat (HF) diet groups and fed an LF diet as a control or an HF diet to induce obesity. The 30-week mice in the diet group were divided into periodontal ligation group (10 days using Porphyromonas gingivalis ATCC 33277) or sham-ligation group. The expressions of the macrophage-specific maker (F4/80), macrophage chemotactic protein1 (MCP1), and inflammatory cytokines in lung tissues were analyzed. The mRNA and protein levels of F4/80, MCP1, interleukin (IL)-1β, and IL-6 expressions were significantly upregulated by obesity in lung tissues. However, the mRNA and protein levels of F4/80, MCP1, and IL-6 were downregulated by periodontitis in DIO mice relative to that of the HF control group. Periodontitis increased tumor necrosis factor-α level of lung tissues under LF, while IL-10 was not affected by obesity regardless of periodontitis. Periodontitis may aggravate pulmonary immune response in obese rodents. This may relate to the imbalance of the pro- and anti-inflammatory cytokine status of lung lesions, which tends to attenuate the infiltration of alveolar macrophages.

Objective Establish a murine model for hyperuricemia (HU) and periodontitis to explore whether there is correlation between them and provide a basis for periodontal treatment. Methods Fourteen male KM mice were divided into 2 groups; the HU group (n=7) was fed food supplemented with potassium oxonate and uric acid, the NC group (n=7) was fed standard food, and the induction period was 35 days. On the 25th day, the molars on one side were ligated to induce periodontitis (P side), while the opposite was true for the control (C side). Baseline and terminal serum uric acid (UA) levels were detected, and alveolar bone resorption was analyzed by micro-CT. Results The serum UA level of HU mice was (112.94 ± 26.82 )mol/L, that of the NC group was (72.21 ± 19.95) μmol/L, and the difference in UA level was statistically significant (P < 0.05). The P side bone volume fractions of the HU and NC groups were( 29.01 ± 11.09)% and (29.56 ± 15.27)%, respectively, which were not significantly different (t=-0.072, P=0.944). The P side bone mineral densities of the HU and NC groups were(0.53 ± 0.16) g/cm3 and (0.52 ± 0.14) g/cm3, respectively, which were not significantly different (t=0.038, P=0.970). Additionally, there was no correlation between HU or serum UA and alveolar bone resorption (P > 0.05). Conclusion This research established a murine model for HU and periodontitis, but based on micro-CT analysis of alveolar bone, no relationship between HU or UA levels and periodontitis was found.

AIM:To characterize gingival metabolome in high-fat diet (HFD)-induced obesity in mice with/without periodontitis.METHODS:HFD-induced obesity mouse model was established by 16-week feeding, and a lean control group was fed with low-fat diet (n = 21/group). Both models were induced for periodontitis on the left sides by molar ligation for 10 days, whereas the right sides were used as controls. Gingival metabolome and arginine metabolism were analysed by non-targeted/targeted liquid chromatography-mass spectrometry.RESULTS:Of 2247 reference features, presence of periodontitis altered 165 in lean versus 885 in HFD mice; and HFD altered 525 in absence versus 1435 in presence of periodontitis. Compared with healthy condition, periodontitis and HFD had distinct effects on gingival metabolome. Metabolomic impacts of periodontitis were generally greater in HFD mice versus lean controls. K-medoids clustering showed that HFD amplified the impacts of periodontitis on gingival metabolome in both intensity and extensity. Ten metabolic pathways were enriched, including 2 specific to periodontitis, 5 specific to HFD and 3 shared ones. Targeted validation on arginine metabolism confirmed the additive effects between HFD and periodontitis.CONCLUSION:The obese population consuming excessive HFD display amplified metabolic response to periodontitis, presenting a metabolic susceptibility to exacerbated periodontal destruction.

Background. Few studies have explored the relationship between the level of physical activity and the occurrence or prevalence of obesity and hypertension among people residing in urbanised areas. Method. A cross-sectional study involving a sample of 1,001 adults was conducted. Descriptive statistics were used to describe sociodemographic variables, physical activity levels, body mass index (BMI), and prevalence of hypertension. Logistic regression models were adopted to investigate the relationship between these factors. Results. A total of 939 respondents who provided valid responses were included. Among them, 56.5% of the participants reported engaging in high levels of physical activity. However, 40.4% of the respondents were classified as overweight or obese, and 31.9% had diagnosed hypertension. After adjusting for sociodemographic factors, logistic regression analysis revealed that physical activity levels were negatively correlated with the prevalence of BMI (OR = 0.564, 95% CI: 0.352–0.905; OR = 0.583, 95% CI: 0.375–0.907) and hypertension (OR = 0.556, 95% CI: 0.348–0.888). Conclusions. Our study confirms recent evidence regarding the amount of physical activity that is associated with lower prevalence of obesity and hypertension in Pingshan District. Furthermore, different physical activities of various intensity levels had different effects on hypertension. Residents should be encouraged to engage in physical activities and maintain a healthy weight to improve their quality of life.

Disturbance in the proteolytic process is one of the malignant signs of tumors. Proteolysis is highly orchestrated by cysteine cathepsin and its inhibitors. Cystatin-B (CSTB) is a general cysteine cathepsin inhibitor that prevents cysteine cathepsin from leaking from lysosomes and causing inappropriate proteolysis. Our study found that CSTB was downregulated in both oral squamous cell carcinoma (OSCC) tissues and cells compared with normal controls. Immunohistochemical analysis showed that CSTB was mainly distributed in the epithelial structure of OSCC tissues, and its expression intensity was related to the grade classification. A correlation analysis between CSTB and clinical prognosis was performed using gene expression data and clinical information acquired from The Cancer Genome Atlas (TCGA) database. Patients with lower expression levels of CSTB had shorter disease-free survival times and poorer clinicopathological features (e.g., lymph node metastases, perineural invasion, low degree of differentiation, and advanced tumor stage). OSCC cell models overexpressing CSTB were constructed to assess the effects of CSTB on malignant biological behaviors and upregulation of CSTB inhibited cell proliferation, migration, and invasion in vitro . Weighted gene correlation network analysis (WGCNA) and gene set enrichment analysis (GSEA) were performed based on the TCGA data to explore potential mechanisms, and CSTB appeared to correlate with squamous epithelial proliferation-differentiation processes, such as epidermal cell differentiation and keratinization. Moreover, in WGCNA, the gene module most associated with CSTB expression (i.e., the brown module) was also the one most associated with grade classification. Upregulation of CSTB promoted the expression levels of markers (LOR, IVL, KRT5/14, and KRT1/10), reflecting a tendency for differentiation and keratinization in vitro . Gene expression profile data of the overexpressed CSTB cell line were obtained by RNA sequencing (RNA-seq) technology. By comparing the GSEA enrichment results of RNA-seq data (from the OSCC models overexpressing CSTB) and existing public database data, three gene sets (i.e., apical junction, G2/M checkpoint, etc.) and six pathways (e.g., NOTCH signaling pathway, glycosaminoglycan degradation, mismatch repair, etc.) were enriched in the data from both sources. Overall, our study shows that CSTB is downregulated in OSCC and might regulate the malignant characteristics of OSCC via the epithelial proliferation/differentiation program.

Background The relation between neighbourhood built environment and obesity has been described as both nuanced and complex. Aim The objective of this study was to examine the relationship between the built environment, physical activity, and obesity in a rapidly urbanised area of China. Subjects and methods This is a cross-sectional study. Descriptive statistics were used to describe the socio-demographic variables, physical activity levels and BMI status. Multivariable logistic regression models were used to examine the association between neighbourhood environment, the likelihood of engaging in different types of physical activity, and BMI. Results A total of 842 respondents completed the questionnaires and were included (84.1% response rate). Among them, 56.4% reported meeting high physical activity levels, while 40.7% were overweight or obese. Multivariable regression analysis showed that better road conditions (beta = 0.122, t = 2.999, p = 0.003) and access to physical activity facilities (beta = 0.121, t = 3.193, p = 0.001) were significantly associated with higher levels of physical activity. Physical activity levels were inversely associated with the likelihood of being overweight (OR = 0.565, 95%CI: 0.3 4 9-0.917) or obese (OR = 0.614, 95%CI: 0.3 9 0-0.966). Conclusion The built environment has an important impact on physical activity. However, the direct impact of leisure physical activity on BMI is not significant. This research provides a summary of recent evidence in Pingshan District on built environments that are most favourable for physical activity and obesity.

Objectives The systematic review and meta-analysis were performed to summarize the available evidence and assess the efficacy of telemedicine for urinary incontinence in women. Methods PUBMED, EMBASE, Web of Science, The Cochrane Library, CBM, CNKI, WanFang, and VIP databases were electronically searched to identify eligible studies updated to February 2020 to collect RCTs regarding the efficacy of telemedicine for urinary incontinence in women. Two reviewers independently screened the literature, extracted data, and assessed the risk of bias of included studies with the Cochrane Handbook for Systematic Reviews of Interventions. A meta-analysis was performed using RevMan 5.3. Results Seven studies involving a total of 836 patients were included in the systematic review and meta-analysis. The results of the meta-analysis showed that compared with usual care, telemedicine intervention significantly reduced the UI severity (SMD = −0.90, 95% CI, −1.73 – −0.07, P = 0.003) and improved QOL (SMD = 0.71, 95% CI, 0.21–1.20, P = 0.005). The results of the descriptive analysis indicated that telemedicine intervention can also reduce the patients’ anxiety and depression, improving patients’ self-efficacy and their impression of improvement. Conclusion The systematic review and meta-analysis demonstrate that telemedicine can reduce the UI severity and anxiety and depression, improving QOL, self-efficacy, and impression of improvement for women with urinary incontinence. Due to the limited quality and quantity of the included studies, rigorous studies with adequate sample sizes are required to conclude with more confidence.

This study conducted scientific evidence linking neighbourhood built environment to adults' leisure-time physical activity (LTPA) among adults in China. Data were obtained from a questionnaire survey conducted from April to July 2017 among 1002 adults aged 18-69 years old in Pingshan District, Shenzhen, China. Chinese Walkable Environment Scale for urban community residents and International Physical Activity Questionnaire were used to measure participants' neighbourhood built environment and leisure-time physical activity, which was categorised into leisure-time walking (LTW) and leisure-time moderate-to-vigorous physical activity (LTMVPA). A total of 986 participants (mean age = 40.7 years, 53.3% females) were included in this research. Descriptive statistics were used to describe the socio-demographic variables, LTW and LTMVPA by sex. Multivariable logistic regression models were used to examine the association between neighbourhood environment characteristics and the likelihood of engaging in active LTW and LTMVPA. Only 20.7% of participants engaged in active LTW and 17.8% active LTMVPA. Better road condition was associated with higher likelihood of active (at least 150 min/week) LTW and LTMVPA. High perceived esthetic was positively associated with LTW and LTMVPA. Active LTW was related to better perception of traffic condition as well. The improvement of the neighbourhood environment characteristics can promote active LTPA among adults living in Shenzhen, China. Our findings support the importance of considering population health effects in urban planning and development.

Elevated blood uric acid (UA) levels have been positively associated with the severity of periodontitis. It thus brings out a hypothesis that hyperuricemia, a pathological elevation of blood UA, might be a risk factor for periodontitis. Namely, periodontitis individuals with Hu might acquire more severe periodontal destruction compared to those without Hu. To support the hypothesis, four aspects of evidences are proposed. First, hyperuricemia and periodontitis share many metabolic and inflammatory comorbidities such as metabolic syndrome, diabetes and cardiovascular diseases which are commonly related to elevated UA levels and gout. Second, observational and interventional studies have found altered UA levels in blood and saliva in periodontitis patients or after periodontal treatment, suggesting an epidemiological connection between hyperuricemia and periodontitis. Third, plausible immuno-metabolic mechanisms by which hyperuricemia might promote the progression of periodontitis are suggested, such as impaired immune response, oxidative stress, pathological bone remodeling and dysbiosis. The last, our empirical data exhibited elevated UA levels in gingival tissue in periodontitis mice compared to controls. If the hypothesis is true, given the high prevalence of the two conditions, hyperuricemia would be a significant risk factor increasing the global burden of periodontal diseases. Evidences on a directional correlation between hyperuricemia and periodontitis are sparse. Longitudinal and experimental studies would be necessary to determine the magnitude of periodontal risk, if any, exacerbated by hyperuricemia and the underlying mechanisms.

Background : To evaluate whether oral lichen planus (OLP) is a risk factor for peri-implant diseases (PIDs) with a systematic review and meta-analysis. Methods : Five electronic databases including Medline, Embase, Web of Science, the Cochrane Library and Scopus were searched. The included studies are observational human studies written in English. The population of interest included those with/without OLP who received dental implant treatment. The follow-up time after implantation was from one month to 20 years. The quality of the included articles regarding risk of bias and methodology were assessed with the Newcastle-Ottawa Scale or the Agency for Healthcare Research and Quality. The data involving exposure (OLP), primary outcomes (implants having PIDs) and secondary outcomes (probing depth/PD, bleeding on probing/BOP and bone loss/BL) and potential confounders were extracted. Heterogeneity was assessed by I² test. Dichotomous data are expressed as the risk ratio (RR) and 95% confidence interval (CI) which were calculated with a fixed effect model. Results : Of the 66 articles, two studies were enrolled and evaluated as high quality, which totally contained 68 participants receiving 222 (OLP vs. non-OLP, 112 vs. 110) implants with 12 to 120-month follow-up time. Proportions of implants with PIDs between OLP and non-OLP groups were as follows: 19.6% (22/112) vs. 22.7% (25/110) for PIM and 17.0% (19/112) vs. 10.9% (12/110) for PI. The meta-analysis revealed no recognizable difference in number of implants with PIDs (PI: RR = 1.49, 95% CI 0.77-2.90, P = 0.24; PIM:RR = 0.88, 95% CI 0.53 -1.46, P = 0.61; PIDs: RR = 1.08, 95% CI 0.75 -1.55, P = 0.68) or BOP (RR = 0.90, 95% CI: 0.70-1.15, P = 0.40) between OLP and non-OLP groups. Conclusions : Available articles regarding the effects of OLP on PIDs remains very limited. Existing evidence does not support OLP as a suspected risk factor for PIDs. Large-scale prospective trials are required to validate the findings.

Background: Randomized controlled trials (RCTs) provide the highest level of evidence and are likely to influence clinical decision-making. This study evaluated the reporting quality of RCT abstracts on drug therapy of periodontal disease and assessed the associated factors. Material and Methods: The Pubmed database was searched for periodontal RCTs published in Science Citation Indexed (SCI) dental journals from 2010/01/01 to 2019/07/17. Information was extracted from the abstracts according to a modified Consolidated Standards of Reporting Trials (CONSORT) guideline checklist. The data was analyzed using descriptive statistical analysis and the statistical associations were examined using the linear regression analysis (P<0.05). Results: This study retrieved 1715 articles and 249 of them were finally included. The average overall CONSORT score was 15.6 +/- 3.4, which represented 40.9% (+/- 0.6) of CONSORT criteria filling. The reporting rate of some items (trial design, numbers analyzed, confidence intervals, intention-to-treat analysis or per-protocol analysis, harms, registration) was less than 30%. The adequate reporting rate of some items (participants, randomization, numbers analyzed, confidence intervals, intention-to-treat analysis or per protocol analysis) was no more than 4%. None of the abstracts reported funding. According to the multivariable linear regression results, number of authors (P=0.030), word count (P<0.001), continent (P=0.003), structured format (P<0.001), type of periodontal disease (P<0.001) and international collaboration (P=0.023) have a significant association with reporting quality. Conclusions: The quality of RCT abstracts on drug therapy of periodontal disease in SCI dental journals remained suboptimal. More efforts should be made to improve RCT abstracts reporting quality.