Palatal temporary skeletal anchorage devices (TSADs): What to know and how to do?

OBJECTIVES: Since palatal temporary skeletal anchorage devices (TSADs) have become important tools for orthodontic treatment, this narrative review was aimed to provide an updated and integrated guidelines for the clinical application of palatal TSADs. SETTING AND SAMPLE POPULATION: A narrative review article including researches on palatal TSADs in orthodontics related to anatomy, success rate and clinical application. MATERIALS AND METHODS: The anatomical characteristics, success rate and its consideration factors and clinical application of palatal TSADs based on the direction of tooth movement were evaluated. RESULTS: To improve the stability of TSADs, hard tissue factors such as bone depth, cortical bone thickness, bone density and soft tissue thickness were evaluated. Anatomically risky structures, including the nasopalatine foramen, canal and the greater palatine foramen, nerve, vessel need to be identified before placement. The success rate of palatal TSADs was greater than that of the buccal inter-radicular space. Palatal TSADs have been used for various purposes because they can control tooth movement in all directions and, three-dimensionally; their applications include the retraction of anterior teeth, protraction of posterior teeth, distalization, intrusion, expansion and constriction. They can be applied directly or indirectly to the lingual arch or transpalatal arch. Design modifications using splinted 2 miniscrews have been suggested. CONCLUSION: Palatal TSADs allow clinicians to perform minimally invasive and easy placement with good stability by understanding the anatomical characteristics of the palatal region, and they show good control over 3-dimensional tooth movements in various clinical cases.

Circadian regulation of rice (Oryza sativa L.) CONSTANS-like gene transcripts.

We identified three rice cDNA clones showing amino acid similarity to the Arabidopsis CONSTANS-like proteins from a database search (S12569, S3574, and C60910), to examine if their transcript abundances were under circadian control. Unlike the other two proteins, the protein encoded by the S12569 cDNA contains only one CONSTANS-like zinc finger B box, and a CCT region. We found that the transcript levels of these rice CONSTANS-like (COL) genes were under circadian control. The oscillation phase of the S12569 gene transcript was more or less opposite to those of OsGI (rice GIGANTEA homolog) and Hd1 (rice COSTANS homolog), whereas the phases of the other two gene transcripts were similar to that of the Hd1 transcript. S12569 mRNA started to increase about 3 h after the onset of the dark period, with a peak about 3 h after its end. The S3574 and C60910 genes were expressed to similar extents during the vegetative and reproductive phases, like OsGI. Higher levels of S12569 transcripts, however, like those of Hd1, were detected in the earlier stages of panicle development. Unlike Hd1 transcripts, S12569, S3574, and C60910 transcripts were present at similar levels in the aerial parts of plants and in their roots during the vegetative phase. In conclusion, the rice COL genes showed distinctive expression patterns from the CO and COL genes, as well as Hd1, a rice CO homolog.

Bumetanide, the specific inhibitor of Na+-K+-2Cl- cotransport, inhibits 1alpha,25-dihydroxyvitamin D3-induced osteoclastogenesis in a mouse co-culture system.

The Na(+)-K(+)-2Cl(-) cotransporter (NKCC1) is responsible for ion transport across the secretory and absorptive epithelia, the regulation of cell volume, and possibly the modulation of cell growth and development. It has been reported that a variety of cells, including osteoblasts, contain this cotransporter. In this study, the physiological role of NKCC1 in osteoclastogenesis was exploited in a co-culture system. Bumetanide, a specific inhibitor of NKCC1, reduced the number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. In order to investigate the mechanism by which bumetanide inhibits osteoclastogenesis, the mRNA expressions of the receptor activator of nuclear factor (NF)-kappaB ligand (RANKL) and osteoprotegerin (OPG) were analysed by RT-PCR. Exposure of osteoblastic cells to a medium containing 1 micro M bumetanide reduced RANKL mRNA expression induced by 10 nM 1alpha,25-dihydroxyvitamin D3 (1alpha,25(OH)2D3, in a dose-dependent manner. In addition, RANKL expression was also analysed with enzyme-linked immunosorbant assay (ELISA) using anti-RANKL antibody. The expression of RANKL was decreased with the increase of bumetanide concentration. In contrast, the expression of OPG mRNA, a novel tumour necrosis factor (TNF) receptor family member was increased in the presence of bumetanide. These results imply that bumetanide inhibits osteoclast differentiation by reducing the RANKL/OPG ratio in osteoblastic cells. However, no significant difference in M-CSF mRNA expression was observed when bumetanide was added. Also, we found that the phosphorylation of c-Jun NH2-terminal kinase (JNK), which regulates the activity of various transcriptional factors, was reduced by bumetanide treatment. Conclusively, these findings suggest that NKCC1 in osteoblasts has a pivotal role in 1alpha,25(OH)2D3-induced osteoclastogenesis partly via the phosphorylation of JNK.