Association between periodontitis and uric acid levels in blood and oral fluids: a systematic review and meta-analysis.

BACKGROUND: Uric 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). METHODS: Relevant 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. RESULTS: Sixteen 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 (I2 = 58.3%, P = 0.066) and low (I2 = 33.8%, P = 0.196), respectively. CONCLUSIONS: Within 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).

Untargeted and targeted gingival metabolome in rodents reveal metabolic links between high-fat diet-induced obesity and periodontitis.

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.

[A triple-wavelength visible spectroscopic method for determination of iron content in lignocellulosic materials].

The present paper described a triple-wavelength visible spectroscopic method for the determination of iron content in lignocellulosic materials. After the sample was pretreated with acidic hydrolysis method under selected conditions, the color agent, 1, 10-phenanthroline monohydrate, was added in the filtrate and then measured by a triple-wavelength spectroscopic method at wavelengths of 416, 510 and 700 nm, from which the iron contents of the sample can be calculated. The results showed that this method can efficiently deduct the influences of acidic soluble lignin and furfural compounds generated during the sample pretreatment and baseline drift caused by the tiny particles in the filtrates. It not only has a good measurement precision but also is accurate, in which the relative differences of the results obtained by the present method and ICP-OES method is less than 5%. The method is simple and practical, and suitable for industrial applications.

[Establishment and application of an intact natural model of human dental plaque biofilm].

PURPOSE: Human dental plaque is implicated in a number of oral diseases. Collection of its undisturbed intact structure facilitates observing the formation and the effect of treatment. This study established a model in vivo to collect intact natural dental plaque biofilm, and observed the features and evaluated the immediate penetration and bactericidal effect of an essential oil (EO) mouthrinse on it at different periods. METHODS: Three 500 microm wide grooves were cut into hydroxyapatite (HA) discs. The discs were worn by six volunteers for 6, 24 and 48 hours, then broken into halves, one served as control, while the other received a one-minute extra-oral EO mouthrinse treatment. 5, 15 and 30 minutes later, the plaque was visualized with a vitality staining technique to observe the sustained changes of biofilm structure in situ and the effect of EO on intact biofilm. The biofilm thickness and fluorescent density of vital and total bacteria were obtained through diagram analysis, assessing the percentage of thickness and fluorescent density of vital to total bacteria. All data analysis was performed using SPSS 13.0 software package. One-way ANOVA and Student-Neuman-Keuls tests were used. RESULTS: The thickness of 6h, 24h and 48 h biofilm was (11.92 + or - 4.63) microm, (18.63 + or - 4.66)microm, (27.55 + or - 6.35) microm, respectively, which increased significantly within 48 hours (P<0.05), especially those within 6 hours. The percentages of thickness and fluorescent density of vital to total bacteria at different periods showed no significant changes (P>0.05). For 6-hour samples, plaque vitality for thickness and fluorescent density decreased significantly within 5 minutes after exposure to the EO (P<0.05). Meanwhile, for 24, 48-hour samples, plaque vitality decreased significantly within 15 minutes (P<0.05). CONCLUSIONS: This study successfully establishes a model for collecting natural undisturbed plaque biofilm in situ, showing the changes constantly within 48 hours. EO mouthrinse has an immediate penetration and antimicrobial effect on the sustained dental plaque biofilm, especially 15 minutes later.