Introduction Orthodontic relapse occurs after orthodontic treatment and shifting of teeth to unfavorable positions. Bisphosphonates’ effects on bone resorption and relapse prevention have been extensively investigated. However, topical administration, which results in local effect, is still a problem. Objective This study aimed to investigate the effect of risedronate with gelatin hydrogel as a carrier to prevent relapse movement by inhibiting osteoclast activity. Methods Lower incisors of 75 guinea pigs were moved distally using an orthodontic appliance until ±3 mm length. Gelatin hydrogel was fabricated to obtain a semisolid controlled release of 250 (Bis-CR250) and 500 mmol/L risedronate (Bis-CR500) and then applied intrasulcularly into the mesial subperiosteal area of 50 guinea pigs (25 in each group) every 3 days; the rest were the control (Bis-CR000). After 14 days of stabilization, the apparatus was removed. The distance decrease between incisors and the osteoclast number with TRAP staining at 0, 3, 7, 14, and 21 days were measured. ANOVA was used to determine the differences among the different time and experimental groups. Results Both treatments showed significantly less relapse movement compared to the control (p < 0.05) at 14 and 21 days. Bis-CR500 more effectively inhibited the relapse movement than Bis-CR250 on day 21, indicating a dose dependency in the inhibition. Both treatments showed less osteoclast numbers than control (p < 0.05). Conclusion Controlled release of bisphosphonate risedronate with a topically administered gelatin hydrogel has shown to be effective in decreasing the tooth relapse movement and osteoclast activity.

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.

Background: Osteoblast and osteoclast are the important factor in periodontal tissue remodeling for the orthodontic treatment success. Resorption process takes place in compression area by osteoclast and apposition in the tension

The aim of this study was to determine whether treatment with fish oil may alter the periapical bone resorption following pulp exposure in rats. Untreated and pulp-exposed animals served as the negative and positive control, respectively. Other pulp-exposed animals were orally treated with fish oil at different concentrations and frequencies. Periapical tissue sections were stained with tartrate-resistant acid phosphatase (TRAP), and then the numbers of both periapical osteodasts and preosteoclasts were determined. The levels of bone resorption were assessed using the osteoclast-bone interface (OBI) index. The results showed that no differences between the numbers of both osteoclasts and preosteoclasts in the fish oil-treated animals and the negative control at day 14 could be found. Similarly, the periapical bone resorption in the animals treated with fish oil for 14 days significantly reduced to the levels of that in the negative control. The results of the present study, therefore, suggest that oral treatment with fish oil may inhibit bone resorption following pulp exposure in rats and hence, may have a therapeutic modality for inflamed periradicular tissue.

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