Cytokines and Microbial Levels After Bonding Self-ligating and Conventional Brackets

Objectives: Orthodontic appliance promotes biofilm formation, changes in the homeostasis of the periodontal tissues, and release of chemical mediators in the gingival sulcus. The aims of this study were measuring the cytokines levels in the gingival crevicular fluid (GCF) before and after bonding self-ligating and conventional brackets, and checking the influence of the bracket design in the cytokine releasing. In addition, it was verified the bacterial complex profile, in situ, and their influence on the cytokines expression.
Methods: The sample comprised 20 participants, aged 11 to 15 years (mean age: 13.3 years±1.03), with permanent dentition, proper oral hygiene, and mild tooth crowding, overjet and overbite. A conventional Gemini^TM metallic bracket and two self-ligating brackets InOvation^®R and SmartClip^TM were bonded to the maxillary incisors and canines. GCF was collected, by a standard filter paper strip, before and 60 days after bonding. The cytokine levels (IL-12, IL-1α, IL-1β, IL-6 and TNFα) were performed by the LUMINEX assay. The presence and the levels of the red and orange complexes bacterial species were analyzed by the Checkerboard DNA-DNA hybridization. Data were analyzed statistically using Friedman and Wilcoxon non-parametric tests and Spearman’s correlation coefficient at 5% of significance level.
Results: Sixty days after bonding, increasing of cytokine levels was observed. However, only TNFα (p=0.046) showed a significant difference in relation to SmartClip^TM brackets. The SmartClip^TM brackets presented higher levels of the red complex bacteria when compared to the conventional brackets Gemini^TM (p<0.05). There was a correlation between P. gingivalis and IL-12 in teeth that received Gemini^TM brackets.
Conclusions: The bracket design affected cytokine and the red complex levels. The bracket SmartClip^TM presented the significant alterations, considering that showed the high levels of the pathogenic bacteria from the red complex simultaneously with the increase in the concentration of TNF-α.