Impact of Medication-Induced Salivary Hypofunction and Sjögren’s Disease on Saliva pH: a clinical study

Abstract

ABSTRACT Background: Salivary hypofunction is a major etiological factor of xerostomia and is associated with an increased risk of oral diseases. However, the precise relationship between reduced salivary flow and corresponding alterations in salivary pH and buffering capacity remains incompletely understood. Elucidating the association between salivary quantity, pH, and buffering capacity is essential for the accurate clinical evaluation of patients with xerostomia and hyposalivation. Methods: We conducted a single-center observational cross-sectional study with healthy controls, participants experiencing medication-induced salivary hypofunction, and diagnosed Sjögren’s disease. Standardized protocols were used to collect unstimulated and stimulated whole saliva. The flow rates of saliva were measured by weight. Both a calibrated digital electrode and colorimetric test strips were performed to measure the pH of saliva. Standardized clinical assays to measure the buffering capacity was utilized. Validated instruments were used to measure both subjective and clinical xerostomia severity. Statistical analysis included descriptive statistics and group comparisons using ANOVA or Kruskal–Wallis tests, as appropriate. Adjusted analyses were performed using ANCOVA and multivariable regression, controlling for age, sex, and buffering capacity. Exploratory analyses assessed correlations between number of medications and Sjögren’s disease duration. Results: Compared with healthy controls, both medication-induced salivary hypofunction and Sjögren’s disease groups showed significantly reduced unstimulated salivary flow, with the greatest reduction in Sjögren’s disease (p ≤ 0.001). Stimulated salivary flow was also significantly lower in Sjögren’s disease compared with both other groups (p < 0.001), while no difference was observed between healthy and medication groups. No significant differences were found among groups in unstimulated or stimulated salivary pH or buffering capacity (p > 0.05). Xerostomia-related outcomes (Xerostomia Inventory, Challacombe, and VAS scores) were significantly higher in both disease groups than in controls (p < 0.05). In multivariable analyses, stimulated buffering capacity was the strongest independent predictor of salivary pH (β = 0.135, p < 0.001), whereas disease group was not significant after adjustment. ANCOVA confirmed no group differences in stimulated pH after controlling for buffering capacity, flow, age, and sex (p > 0.05). Reliability between methods was moderate to good (ICC = 0.67–0.74, p < 0.001). Exploratory analyses showed increased xerogenic medication burden reduced stimulated buffering capacity (β = −0.703, p = 0.023), while disease duration showed no significant associations with salivary parameters (p > 0.05). Conclusions: Salivary hypofunction substantially affects quantitative salivary flow and patient- reported xerostomia without significantly altering salivary pH. These findings suggest that oral acid–base homeostasis is primarily maintained by buffering mechanisms rather than salivary volume alone. Therefore, the clinical evaluation of xerostomia should emphasize comprehensive assessment of salivary quality and associated symptoms rather than relying solely on quantitative salivary flow rates and pH measurements.