Consecutive use of mini-implants in the palate to treat skeletal maxillary constriction and Class II malocclusion in an adult case.

This report describes the successful use of two multifunctional mini-implants that were inserted into the palate in the treatment of an 18-year-old woman in whom the maxilla was skeletally narrowed and the molars have migrated mesially on both sides. Three different appliances were used in sequence in the course of treatment: first, an appliance supported by bone and teeth (hybrid hyrax) for surgically-assisted rapid maxillary expansion (SARME); second, a distalization device supported by mini-implants to achieve molar distalization; and third, a transpalatal arch (TPA) stabilized by mini-implants to allow indirect anchorage during retraction of the incisors. The mini-implants in the palate led to a reduction in the adverse effects of the SARME procedure and made treatment with cervical headgear unnecessary. TPA stabilized by the mini-implant was also used to retract the anterior teeth en masse, with no need for alterations in the treatment mechanism and using routine orthodontic methods.

Novel ENAM mutation responsible for autosomal recessive amelogenesis imperfecta and localised enamel defects.

The genetic basis of non-syndromic autosomal recessive forms of amelogenesis imperfecta (AI) is unknown. To evaluate five candidate genes for an aetiological role in AI. In this study 20 consanguineous families with AI were identified in whom probands suggested autosomal recessive transmission. Family members were genotyped for genetic markers spanning five candidate genes: AMBN and ENAM (4q13.3), TUFT1 (1q21), MMP20 (11q22.3-q23), and KLK4 (19q13). Genotype data were evaluated to identify homozygosity in affected individuals. Mutational analysis was by genomic sequencing. Homozygosity linkage studies were consistent for localisation of an AI locus in three families to the chromosome 4q region containing the ENAM gene. ENAM sequence analysis in families identified a 2 bp insertion mutation that introduced a premature stop codon in exon 10. All three probands were homozygous for the same g.13185_13186insAG mutation. These probands presented with a generalised hypoplastic AI phenotype and a class II openbite malocclusion. All heterozygous carriers of the g.13185_13186insAG mutation had localised hypoplastic enamel pitting defects, but none had AI or openbite. The phenotype associated with the g.13185_13186insAG ENAM mutation is dose dependent such that ARAI with openbite malocclusion segregates as a recessive trait, and enamel pitting as a dominant trait.

The effects of the FR-3 appliance on the transversal dimension.

The purpose of this study was to examine the effects of the FR-3 appliance on the transversal dimension. The treatment group consisted of 20 patients with Class III malocclusion, who were treated with the FR-3 appliance. The control group consisted of 19 patients with Class III malocclusion. Posteroanterior radiographs and study models were taken at the beginning and at the end of the study in both groups. The results suggested that although FR-3 appliance therapy does not increase the width of the nasal cavity and does not stimulate the growth of the maxillary apical base, it does cause an increase in the intermolar and interpremolar distances in the maxilla both in the dental and the alveolar areas.

The effects of the Fränkel's function regulator on the Class III malocclusion.

The material of this investigation consisted of 40 functional Class III malocclusion subjects. Each treatment and control group consisted of 20 Class III cases (10 boys and 10 girls). The mean age of the subjects in the function regulator, FR-3, group was 9.5 years at the beginning of the treatment, and in the control group 9.3 years at the beginning of the observation period. The mean treatment period of the FR-3 group was 1.9 years and the mean observation period of the control group is 1.8 years. In this study, as a result of FR-3 appliance therapy in the functional Class III malocclusion group, the negative overjet that was present at the beginning of the treatment has been converted into a positive overjet by an average increase of 3.8 mm at the end of the treatment. The sum of downward and backward rotation of the mandible, the decrease in the SNB angle with a subsequent increase of the ANB angle, and the retrusion of the lower incisors were effective in the increase of the overjet. The increase in the SNA angle and the protrusion of the upper incisors were found to be insignificant. The overbite decreased due largely to the downward and backward rotation of the mandible.