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The meta-analysis observed an enhanced plasma uric acid concentration in patients with periodontitis when compared with controls.
Despite the potential limitations of the included clinical studies, investigators observed an association between periodontitis and increased blood uric acid (UA) as well as decreased salivary UA, according to a study published in BMC Oral Health.1
Periodontitis, a chronic inflammatory condition that affects almost a quarter of the global population, causes tooth decay, negatively impacts quality of life, and creates an enormous socioeconomic burden.2
“UA is a formerly-known antioxidant that has recently been linked to numerous inflammatory diseases as a pro-inflammatory and -oxidative mediator in pathological conditions,” a team of international investigators stated. “It is imperative to reassess the association between periodontitis and uric acid locally and systematically.”
To evaluate the association between periodontitis and UA levels in gingival crevicular fluid (GCF), saliva, and blood, investigators identified studies from electronic databases such as EMBASE, Scopus, PubMed, and Web of Science. Relevant keywords included uric acid, hyperuricemia, gout, and periodontitis. Eligible studies were cohort, cross-sectional, case-controlled, or randomized/non-randomized controlled trials. The weighted mean difference (WMD) and standardized mean difference (SMD) were calculated using fixed- or random-effect models.
In total, 16 observational studies and 1 randomized controlled trial were included in the analysis, comprised of 1354 patients with periodontitis and 989 controls. Of these, 10 studies were conducted in Asia, 3 in Europe, 2 in South America, and 2 in Africa. Blood UA levels were assessed in 8 studies (725 patients with periodontitis vs 1201 controls), saliva UA was assessed in 9 studies (233 patients with periodontitis and 174 controls), and GCF was assessed in 1 study (78 patients with periodontitis vs 50 controls).
The meta-analysis observed an enhanced plasma UA concentration (WMD = 1.00 mg/dL, 95% confidence interval [CI] 0.63 to 1.37, P < 0.001) in patients with periodontitis when compared with controls. However, a decrease in salivary UA level was observed (SMD = -0.95, 95% CI -1.23 to -0.68, P < 0.001). The statistical heterogeneity among the plasma-tested studies was moderate (I2 = 58.3%, P = 0.066) and the heterogeneity among the saliva-tested studies was low (I2 = 33.8%, P = 0.196).
Although periodontitis appears to be linked to an increased blood UA concentration regarding normouricemia, investigators could not determine whether there is an association between periodontitis and hyperuricemia/gout.
A mandatory analysis with Egger’s test reported no publication bias in studies involving blood UA (P = 0.118, n = 8). However, a potential bias in studies evaluating salivary UA was observed (P = 0.012, n = 9).
Investigators noted that the number and sample size of studies ultimately included were limited, specifically in studies evaluating saliva and GCF. Therefore, results should be interpreted with caution until further large-scale studies are performed. Another limitation was that most findings were originated from retrospective studies, which need to be confirmed by high-quality prospective and interventional studies. Finally, potential confounding variables, such as body mass index, smoking status, and age, were unavailable in some studies. Effects on the findings are unknown and may contribute to statistical heterogeneity in the current meta-analysis.
“In contrast to the change of UA in the blood, the amount of UA in saliva and GCF seems to be decreased in the presence of periodontitis,” investigators concluded. “The potential mechanisms underlying the reversal of changes require additional investigations.”