Periodontitis is associated with impaired olfactory function: A clinical study.

AIM: To explore the association between periodontitis and olfactory disorders. METHODS: Clinical data were collected from 198 individuals between the ages of 18 and 60 years living in Denmark. The exposure was periodontitis, and the outcome was olfactory function (Threshold, Discrimination, Identification - TDI score), both measured clinically. Covariates included sex, age, education level, income, usage of nasal spray, tongue coating, halitosis, xerostomia, smoking, and history of COVID-19. Structural equation modeling was used to estimate the association between periodontitis and olfactory function. Periodontitis was defined using the AAP/EFP classification and dichotomized into "no" (healthy subjects) and "yes" (Stages I, II, and III). Olfactory function was treated as a one-factor latent variable, including the different olfactory scores. In addition, extra models were performed considering each olfactory component as a separate outcome and the TDI Global Score. RESULTS: The results showed that periodontitis was associated with a lower olfactory function [standardized coefficient (SC) -0.264, 95% CI -0.401, -0.118]. Additionally, periodontitis was also associated with a lower olfactory Threshold (odorant concentration required for detection) (SC -0.207, 95% CI -0.325, -0.089), Discrimination (ability to discriminate between odorants) (SC -0.149, 95% CI -0.270, -0.027), Identification (ability to identify odorants) scores (SC -0.161, 95% CI -0.277, -0.045), and TDI Global Score (SC -0.234, 95% CI -0.370, -0.099). CONCLUSIONS: This study suggests that periodontitis is associated with olfactory impairment.

Development of a nomogram for identifying periodontitis cases in Denmark.

Although self-reported health outcomes are of importance, attempts to validate a clinical applicable instrument (e.g., nomogram) combining sociodemographic and self-reported information on periodontitis have yet to be performed to identify periodontitis cases. Clinical and self-reported periodontitis, along with sociodemographic data, were collected from 197 adults. Akaike information criterion models were developed to identify periodontitis, and nomograms developed based on its regression coefficients. The discriminatory capability was evaluated by receiver-operating characteristic curves. Decision curve analysis was performed. Smoking [OR 3.69 (95%CI 1.89, 7.21)], poor/fair self-rated oral health [OR 6.62 (95%CI 3.23, 13.56)], previous periodontal treatment [OR 9.47 (95%CI 4.02, 22.25)], and tooth loss [OR 4.96 (95%CI 2.47, 9.97)], determined higher probability of having "Moderate/Severe Periodontitis". Age [OR 1.08 (95%CI 1.05, 1.12)], low educational level [OR 1.65 (95%CI 1.34, 2.23)], poor/fair self-rated oral health [OR 3.57 (95%CI 1.82, 6.99)], and previous periodontal treatment [OR 6.66 (95%CI 2.83, 15.68)] determined higher probability for "Any Periodontitis". Both nomograms showed excellent discriminatory capability (AUC of 0.83 (95%CI 0.75, 0.91) and 0.81 (95% CI 0.74, 0.88), good calibration, and slight overestimation of high risk and underestimation of low risk. Hence, our nomograms could help identify periodontitis among adults in Denmark.

Effect of Sample Storage Conditions on Measurements of Salivary Cotinine Levels.

Information on smoking exposure obtained with self-reports may be inaccurate. Cotinine has a large half-life and its salivary levels correlate well with plasmatic levels. The influence of storage conditions on the validity and precision of salivary cotinine assessments has rarely been evaluated. Here, smokers donated saliva samples, which were sent for immediate analysis, mail posting, storage at 4 °C for 30 or 90 days, or storage at -20 °C for 30 or 90 days. Cotinine levels were determined using enzyme-linked immune-sorbent assay. Agreement of cotinine level measurements was assessed using Bland-Altman analyses. Average age (years), duration of smoking (years) and number of cigarettes smoked (/day) were 55.4 (±SD 9.4), 35.1 (±SD 11.3), and 15.3 (±SD 7.6). The mean immediate cotinine level was 457 ng/mL (range 11.3 to 1318 ng/mL). Mean cotinine levels in samples analyzed after delay ranged between 433 ng/mL (-20 °C 30 days) and 468 ng/mL (4 °C 30 days). A dose-response gradient was observed in the relationship between salivary cotinine level and self-reported smoking status. A good agreement between cotinine levels for all storage conditions compared with immediate analysis was observed, with average differences ranging from -11 to 24 ng/mL. Cotinine levels remained stable regardless of the tested condition. The stability of salivary cotinine may enable samples to be obtained in difficult-to-reach areas, reduce study costs, and improve the validity of the information on exposure to smoking.