Study On Evaluation Of Salivary Tumor Necrosis Factor-Alpha Level In The Treatment With Fixed Appliances And Clear Aligners
DOI:
https://doi.org/10.64252/w8axkc21Keywords:
TNF-alpha, saliva, fixed orthodontic appliances, clear aligners, inflammation, biomarkerAbstract
Background: Tumor necrosis factor-alpha (TNF-α), a key pro-inflammatory cytokine, plays a significant role in orthodontic tooth movement by mediating periodontal and bone remodeling processes. The level of TNF-α in saliva may serve as a non-invasive biomarker for monitoring inflammatory responses during orthodontic treatment with different appliances.
Objective: This study aimed to evaluate and compare salivary TNF-α levels in patients undergoing orthodontic treatment using fixed appliances and clear aligners over a 3-month treatment period.
Methodology: A total of 60 orthodontic patients aged 18–30 years were recruited and divided into two equal groups: Group A (fixed appliances) and Group B (clear aligners). Unstimulated saliva samples were collected at baseline (T0), 1 week (T1), 1 month (T2), and 3 months (T3) post-application of appliances. TNF-α concentrations were measured using ELISA. Clinical parameters such as plaque index and gingival index were also recorded. Data were analyzed using repeated-measures ANOVA and independent t-tests.
Results: Both groups showed a significant increase in salivary TNF-α at T1 (Group A: 48.2 ± 6.3 pg/mL; Group B: 41.7 ± 5.8 pg/mL; p < 0.001) compared to baseline (Group A: 12.3 ± 2.9 pg/mL; Group B: 11.9 ± 3.1 pg/mL). Levels declined gradually by T3 but remained elevated compared to T0. At all time points, Group A exhibited significantly higher TNF-α levels than Group B (p < 0.05). Plaque and gingival indices were also higher in Group A throughout the study period.
Conclusion: Fixed appliances induce a greater inflammatory response as indicated by elevated salivary TNF-α levels compared to clear aligners. Monitoring salivary TNF-α can be a valuable, non-invasive biomarker for assessing orthodontic treatment-associated inflammation.