Effect of Moringa oleifera leaf extract on orthodontic relapse: an in vivo study with bioinformatic analysis of miRNA–EGFR interaction

Background Orthodontic relapse remains a major challenge, primarily due to incomplete alveolar bone remodeling. This study aimed to apply bioinformatics analysis to identify potential microRNAs regulating the EGFR an important factor in osteoblast differentiation and evaluate the effect of Moringa oleifera leaf extract on relapse in vivo study. Methods An in silico analysis was conducted using miRTarBase, miRWalk, and TargetScan databases to identify miRNAs targeting the EGFR gene. The in vivo experiment was performed on ten New Zealand white rabbits, after 14 days of mandibular central incisor movement, the animals were divided into two groups: group A (saline) and group B (MO extract at 75 mg/kg/day). Relapse distance was measured every 2 days over 14 day period using 3D models obtained from a Medit Scan i700 scanner. After 28 days, the animals were euthanized for histological evaluation of alveolar bone using H&E staining as well as assessment of hepatic and renal toxicity. Results Bioinformatics analysis identified four miRNAs including hsa-miR-138-5p, hsa-miR-133b, hsa-miR-7-5p, and hsa-miR-875-5p. Among these, hsa-miR-7-5p was prioritized due to stronger evidence support and the identification of two binding sites on EGFR, with a high cumulative total binding affinity (− 39.9 kcal/mol). In vivo study, group B showed significantly greater relapse in the early phase (p = 0.004), but significantly reduced relapse in the late phase (p = 0.018) compared to the control group. Histological analysis revealed a significant decrease in osteoclast numbers among group B (p = 0.0367). No histopathological abnormalities were observed in the liver or kidneys of MO-treated group. Conclusion Moringa oleifera extract may reduce late-phase orthodontic relapse by promoting alveolar bone remodeling and decreasing osteoclast activity. This effect may be associated with the regulation of the PI3K–AKT signaling pathway via hsa-miR-7-5p–mediated inhibition of EGFR.