RESUMO
Aim One of the major difficulties in orthodontic treatment is the lengthy course of therapy, particularly in situations involving extractions. Hence, various methods for accelerating tooth movement rate had been devised. Flapless corticotomy is one of those methods. This study aimed to evaluate the effects of flapless laser corticotomy (FLC) compared to the conventional retraction (CR) method on the rate of canine retraction. Methods A split-mouth, randomized controlled trial included 56 canines from 14 patients (12 females and two males) with a mean age of 20.4 ± 2.5 years, who were complaining of bimaxillary protrusion requiring extraction of four premolars. All canines were randomly assigned to four groups (maxillary FLC, maxillary control CR, mandibular FLC, and mandibular control CR). Randomization was performed by creating two equal, random computer-generated lists with a 1:1 allocation ratio-one list for the right side and one for the left. The allocation concealment was achieved using opaque sealed envelopes until the time of intervention. FLC was applied on the experimental sides before canine retraction by drilling six holes penetrating 3 mm into the bone on the mesial and distal sides of the canines. Subsequently, all canines were retracted employing closed coil springs to deliver a force of 150 g using indirect anchorage from temporary anchorage devices (TADs). All canines were assessed at T0 (before retraction), T1 (one month after retraction), T2 (two months), and T3 (three months) using three-dimensional (3D) digital models. Additionally, canine rotation, molar anchorage loss assessed using 3D digital models, root resorption assessed using cone beam computed tomography (CBCT), probing depth, plaque, gingival indices, and pulp vitality were all evaluated as secondary outcomes. It was possible to blind only the outcome analysis expert (single-blinded). Results The measurements of canine retraction during the follow-up period from T0 to T3 were 2.46 ± 0.80 mm and 2.55 ± 0.79 mm in maxillary FLC and control groups, respectively, and 2.44 ± 0.96 mm and 2.31 ± 0.95 mm in mandibular FLC and control groups, respectively. The results demonstrated a statistically non-significant difference in the distance of canine retraction between the FLC and control groups at all time points. Moreover, no differences were observed between groups in canine rotation, molar anchorage loss, root resorption, probing depth, plaque, gingival indices, and pulp vitality (p > 0.05). Conclusion In the FLC procedure performed in this study, the rate of upper and lower canine retraction could not be accelerated and no significant differences were observed between FLC and control groups in canine rotation, molar anchorage loss, root resorption, periodontal condition, and pulp vitality.
RESUMO
FGFR1 plays an important role in the development of the nervous system as well as the regulation of the skeletal development and bone homeostasis. Mutations in FGFR1 genes affect skull development, specifically suture and synchondrosis, resulting in craniosynostosis and facial abnormalities. We examined subjects with normal skull morphology for genetic polymorphisms that might be associated with normal craniofacial variations. Genomic DNA was obtained from 216 Japanese and 227 Korean subjects. Four FGFR1 SNPs, namely, rs881301, rs6996321, rs4647905, and rs13317, were genotyped. These SNPs were tested for association with craniofacial measurements obtained from lateral and posteroanterior cephalometries, in which principle component analysis was performed to compress the data of the craniofacial measurements. We observed that SNPs rs13317 and rs6996321 were correlated with the overall head size and midfacial development, indicating that FGFR1 SNPs played crucial roles in the normal variation of human craniofacial morphology. Subjects with the derived alleles of SNPs rs13317 and rs6996321 had a small face and a facial pattern associated with a retruded midface and relatively wide-set eyes. These facial features were similar to but were milder than those of individuals with Pfeiffer syndrome, which is caused by a dysfunctional mutation in FGFR1.
