The purpose of this study was to evaluate the effect of reverse pull headgear (RPHG) in the treatment of Class III malocclusions in the late mixed and early permanent dentition and its long-term stability at the time when facial growth was close to completion. The treatment group comprised 22 subjects (12 males and 10 females, mean age: 11.38 ± 0.69 years). The control group included 17 subjects (7 males and 10 females, mean age: 11.54 ± 1.07 years). The mean RPHG treatment time was 1.5 ± 0.95 years and the observation time for the control group was 1.75 ± 0.83 years. For each subject, lateral cephalograms were obtained before (T1) and after (T2) treatment or observation. These cephalograms were traced and analyzed and the differences between T1 and T2 values were examined with paired t-tests. Of the 22 treated cases, 10 patients were followed up until at the mean age of 16.18 years (T3). Since there was no relapse in anterior crossbite, the long-term effects of RPHG were evaluated by measuring the maxillary and mandibular skeletal changes. The follow-up patients were divided into two groups based on the change in ANB: a stable group (decrease in ANB < 2 degrees) and an unstable group (decrease in ANB > 2 degrees). The skeletal effects of RPHG in treating Class III anomalies just before or at the beginning of the pubertal growth spurt include protraction of the maxilla and dentition and inhibition of forward growth of the mandible. With regard to the long-term change, a slight alteration in the position of the maxilla and in the position and growth direction of the mandible resulted in a slight decrease in ANB in the stable group. The slight retrusion in the maxilla, combined with the significant protrusion in the mandible and the more horizontal mandibular growth direction, resulted in a decrease in ANB in the unstable group. This indicated that the maxilla remained relatively stable and that the unstable factor was continuing mandibular growth during the pubertal and post-pubertal period. For patients with an excessive mandible, orthopaedic therapy should start at the beginning of pubertal growth and orthodontic fixed appliance should follow immediately after RPHG so that mandibular growth in the sagittal direction during puberty or even after pubertal growth may be effectively inhibited.
Background/Aims: RECQL1, a member of the human RECQ helicase family, participates in DNA repair. Recent reports showed that RECQL1 silencing in cancer cells resulted in mitotic catastrophe, which prevented tumor growth in murine models. However, its therapeutic potential has never been examined in tongue squamous cell carcinoma (SCC). Methods: To explore the role of RECQL1 in the development of tongue SCC, we used RNA interference technology to silence RECQL1 in SCC-9 and SCC-15 human tongue SCC cell lines, and to subsequently evaluate its effects both in vitro and in vivo. Results: After RECQL1 was silenced in SCC cells by siRNA, we observed downregulation of RECQL1 mRNA and protein in cancer cells. RECQL1 is one of the predicted miR-203 targets, and we found that miR-203 downregulated the expression of RECQL1 at the post-transcriptional level. RECQL1-shRNA or miR-203 overexpression inhibited SCC-9 cell growth. In addition, there was accumulation of cells in the sub-G1 fraction and increased apoptosis 72 h post-transfection. In addition, knockdown of RECQL1 led to a strong anticancer effect, as the tumorigenicity of SCC-9 cells was inhibited in vivo. Moreover, we found that two immunosuppressive factors were also significantly downregulated upon RECQL1 knockdown or miR-203 overexpression in vitro. Conclusion: Collectively, these results indicate that RECQL1 plays an important regulatory role in cancer cell proliferation and tumor progression.
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