Periodontitis, a dysbiotic disease caused by an imbalanced oral microbiota, poses a significant threat to tooth-supporting tissues, often resulting in irreversible periodontal degradation and tooth loss. Early detection, prevention, and treatment are crucial for managing this disease. In this study, we optimized methods for processing saliva to achieve accurate and reproducible quantification of five key bacterial species associated with periodontitis—Porphyromonas gingivalis (Pg), Fusobacterium nucleatum (Fn), Prevotella intermedia (Pi), Streptococcus mutans (Sm), and Aggregatibacter actinomycetemcomitans (Aa)—as well as total bacterial load, total DNA, and total protein. We analyzed the saliva of 44 periodontitis patients in different disease stages. Our results revealed the significant correlations between bacterial abundance and disease severity. Aa, an early colonizer linked to immune evasion, had a higher load in early-stage periodontitis (6.8–7.5 log cells/mL) but has dropped in advanced stages (6.9–6.4 log cells/mL, P < 0.001). In contrast, Pg, a keystone pathogen involved in tissue destruction, increased significantly from healthy (6.0–6.7 log cells/mL) to severe periodontitis (7.5–8.2 log cells/mL, P < 0.0001). Similarly, Fn and Pi, which produce biofilms and are linked to inflammation, showed progressive increases from healthy (5.9–6.5 log and 6.2–6.9 log cells/mL) to severe stages (7.4–8.0 log and 7.7–8.3 log cells/mL, P < 0.0001 and P < 0.0002, respectively). Sm, associated with acid production, increased in early stages (6.6–7.2 log cells/mL) but plateaued later (6.8–7.4 log cells/mL). On the other hand, total bacterial load significantly increased with disease severity (P < 0.05). In contrast, total DNA concentration and total protein concentration did not show significant differences (P > 0.05). Ongoing efforts are focused on correlating sensor-derived data with clinical measurements to enhance diagnostic accuracy. These findings will offer valuable insights for advancing non-invasive diagnostic tools and personalized treatment approaches for periodontitis.

Rathnayake A. Rathnayake

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