Evaluation of the success rate of single- and dual-thread orthodontic miniscrews inserted in the palatal side of the maxillary tuberosity.

BACKGROUND: Recent studies have reported that the placement of miniscrews for orthodontic anchorage in maxillary tuberosity is anatomically safe and can aid in achieving efficient tooth movement mechanically. However, the success rate of miniscrews placed on the palatal aspect of the maxillary tuberosity has not yet been elucidated. This study aimed to evaluate the success rate of single- and dual-thread miniscrews inserted in the palatal aspect of the maxillary tuberosity. METHODS: A total of 101 miniscrews (17 single-thread miniscrews: diameter 2.0 mm, length 10 mm; 84 dual-thread miniscrews: diameter 2.0 mm, length 12 mm) placed in 61 patients (6 males, 55 females; mean age = 30.9 ± 8.66 years) were retrospectively examined. Miniscrews that could be maintained for orthodontic anchorage for more than 6 months were considered successful. The direction of placement, bone-miniscrew contact (BMSC) rate, and survival of miniscrews were measured using cone-beam computed tomography. RESULTS: The overall success rate of single-thread miniscrews was 82.4% and that of dual-thread miniscrews was 94.0%. There was no significant difference in the overall clinical success rate between the two designs. Sex, mandibular plane angle, and malocclusion type did not significantly affect the success rate in both groups. CONCLUSIONS: Both single- and dual-thread miniscrews placed on the palatal aspect of the maxillary tuberosity showed high success and BMSC rates. However, there were no significant differences in the overall success rate and BMSC rate between the two miniscrew designs.

The Damon System and release of substance P in gingival crevicular fluid during orthodontic tooth movement in adults.

Metabolism by peptidases plays an important role in modulating the levels of biologically active neuropeptides. One of these neuropeptides, substance P (SP), a component of gingival crevicular fluid (GCF), may exponentiate the inflammatory process during orthodontic tooth movement. The aim of this study was to investigate the GCF levels of SP in patients using different bracket systems. Subjects were 10 patients (four males, six females; mean age, 25.1 ± 4.4 years) undergoing orthodontic movement (leveling) in the maxilla. Conventional brackets were placed on the left side, while the teeth on the right received self-ligating brackets. The teeth on the mandibular left side without any orthodontic attachments served as controls. GCF was sampled at 0, 1, 24, and 168 hours after initiation of treatment. Prevention of plaque-induced inflammation allowed assessment of the dynamics of mechanically stimulated SP levels in the GCF, which was determined using commercially enzyme-linked immunoabsorbent assay (ELISA) kits. GCF levels of SP for the Damon System sites were significantly lower than for the teeth with conventional brackets at 24 hours. This result indicates that the Damon System inhibited an increase in the amount of SP in the GCF. Thus, the Damon System is useful to reduce the inflammation and pain resulting from orthodontic forces.

Protection from inactivation of the adenine nucleotide translocator during hypoglycaemia-induced apoptosis by mitochondrial phospholipid hydroperoxide glutathione peroxidase.

We demonstrated that mitochondrial phospholipid hydroperoxide glutathione peroxidase (PHGPx) first suppressed the dissociation of cytochrome c (cyt c) from cardiolipin (CL) in mitochondrial inner membranes and then apoptosis caused by the hypoglycaemia by the prevention of peroxidation of CL [Nomura, Imai, Koumura, Arai and Nakagawa (1999) J. Biol. Chem. 274, 29294-29302; Nomura, Imai, Koumura, Kobayashi and Nakagawa (2000) Biochem. J. 351, 183-193]. The present study shows the involvement of peroxidation of CL in the inactivation of adenine nucleotide translocator (ANT) and the opening of permeability transition pores by using the system of ANT-reconstituted liposome and isolated mitochondria. ANT activity appeared in dioleoyl phosphatidylcholine proteoliposome containing 10% (mol/mol) CL or phosphatidylglycerol (PG), but not other classes of phospholipids. ANT activity was competitively inhibited by the addition of cardiolipin hydroperoxide (CLOOH) in reconstituted liposomes containing CL. However, phosphatidylcholine hydroperoxide failed to inactivate the activity of ANT. The activity of ANT in reconstituted liposomes, including CLOOH, recovered when CLOOH in reconstituted liposome was reduced to hydroxycardiolipin by incubation with PHGPx. The activity of ANT was determined in rat basophil leukaemia RBL2H3 cells after their exposure to 2-deoxyglucose. ANT activity decreased to 50% of the control level by 4 h in response to apoptosis. In parallel, cyt c and apoptosis-inducing factor (AIF) were released from mitochondria. Suppression of the accumulation of CLOOH by overexpression of PHGPx in mitochondria effectively prevented the inactivation of ANT, the opening of permeability transition pores and the release of cyt c and AIF from mitochondria in hypoglycaemia-induced apoptotic cells. These findings suggest that mitochondrial PHGPx might be involved in the modulation of the activity of ANT and the opening of pores for the release of cyt c via the modulation of levels of CLOOH in the mitochondria.