Abstract

Relapse is considered a significant failure after orthodontic treatment. In response to relapse, RANKL expressions will increase, while OPG expressions will decrease. CHA is thought to be one of an ideal candidate for enhancing bone formation. Moreover, a-PRF is a source high levels of growth factors that play a central role in the bone remodeling. This research was intended to investigate the effect of hydrogel CHA-aPRF in preventing relapse. Hydrogel-CHA was initially designed, with its degradation profile and FTIR (Fourie’s Transform Infrared) spectra were investigated as the basis to find out optimum formulation before incorporated with aPRF. Hydrogel-CHA microspheres were prepared in 3 different compositions: those were encoded 30-CHA, 40-CHA, and 50-CHA. After the hydrogel formulation and characterization were completed, 10 mL blood samples were collected, then centrifuged at 1500 rpm for 14 min. At the end of the centrifugation process, the aPRF clot was isolated and then pressed to obtain their releasate. The releasate aPRF was then loaded into the best formulation candidate of hydrogel CHA. The hydrogel incorporated aPRF was then gently injected on the mesial side of incisor gingival sulcus of the rabbit after orthodontic tooth movement. The FTIR analysis showed that carbonated apatite was successfully developed during the fabrication process of hydrogel-CHA microspheres. It was also known that degradation profile of 30-CHA was considered ideal compared to the other compositions. The application of CHA-aPRF (group C) was proven to significantly prevent relapse, indicated by lowest percentage of relapse 21 days after debonding (29.95±3.91%) compared to control group. Furthermore, it has been found that expressions of RANKL were significantly lowest (p<0.05) in group C on day 0, 3, and 7, while OPG expressions showed significantly highest (p<0.05) in group C on day 14 and 21 after debonding. These results indicate that incorporation of hydrogel-CHA has potential effect to enhance alveolar bone remodeling and prevent orthodontic relapse by stimulates OPG expression and suppresses RANKL expression.

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