Despite the fact that saliva contains measurable concentrations of urea and creatinine, it is not widely used in clinical nephrology. One of the reasons is the high inter‐ and intra‐individual variability in the salivary markers of kidney function. We hypothesized that gingival bleeding in patients with periodontitis could contribute to this variability by increasing the concentration of salivary urea or creatinine. Samples were collected from 25 patients with periodontitis and 29 healthy controls. In addition, saliva samples from five healthy volunteers were artificially contaminated with blood. The concentration of urea, but not that of creatinine, was more than twice as high in patients with periodontitis than in controls. Artificial contamination of saliva with blood did not affect the salivary concentration of creatinine. Salivary urea increased only with very high levels of contamination (≥2.5% blood in saliva), but that did not occur in patients. In conclusion, periodontitis increases the concentration of salivary urea, but this is not likely to be a result of contamination with blood. Future studies should investigate the composition of the oral microbiome, specifically regarding how it affects the concentration of salivary urea. Salivary creatinine seems to be a more robust non‐invasive marker of renal functions than salivary urea.

Extracellular DNA (ecDNA) is a potential marker and predictor in several inflammatory diseases. Periodontitis, a chronic inflammatory disease, is associated with epithelial cell death and could lead to release of DNA. Our aim was to analyze salivary DNA concentration and deoxyribonuclease (DNase) activity in periodontitis patients. We hypothesized that salivary ecDNA will be higher than in controls and could serve as a marker of periodontitis severity. Samples of saliva were collected from 25 patients with chronic periodontitis and 29 age-matched controls. DNA was quantified fluorometrically in whole saliva, as well as in supernatants after centrifugation (depletion of cells at 1600× g) and in double-centrifuged supernatants (depletion of cell debris at 1600× g and 16,000× g). The subcellular origin of ecDNA was assessed using real-time PCR. In comparison to controls, patients with periodontitis had twofold higher salivary DNA (p < 0.01), higher mitochondrial DNA in centrifuged supernatants (p < 0.05) and lower nuclear ecDNA in double-centrifuged samples (p < 0.05). No correlations were found between salivary DNA and oral health status, but mitochondrial DNA positively correlated with papillary bleeding index in centrifuged samples. Salivary DNase activity was comparable between the groups. In conclusion, we proved that salivary DNA is higher in periodontitis. The source of the higher mitochondrial DNA in cell-free saliva and the causes of lower nuclear ecDNA remain to be elucidated. Further studies should focus on the role of mitochondrial DNA as a potential driver of inflammation in periodontitis.