A severe skeletal Class III malocclusion treated with Le Fort I combined with sagittal split ramus osteotomy, mandibular body ostectomy and tongue reduction surgery. A case report

This case report describes the orthodontic-orthognathic management of a 17-year-old male patient with extremely severe skeletal Class III malocclusion due to a marked mandibular protrusion with a small and narrowed upper jaw which increased the remarkable concave facial profile. Dental articulation was entirely lacking, resulting in great difficulty in masticating food. A two-jaw surgery combined with mandibular body ostectomy was performed to correct mandibular asymmetry and the severe sagittal skeletal discrepancy (Wits appraisal –36.5 mm and ANB angle –14.3°). Bi-maxillary surgery was performed in two-stages; the first surgery consisted of maxillary advancement with Le Fort I osteotomy followed by a second surgery where a combination of sagittal split ramus osteotomy (SSRO) and mandibular body ostectomy was performed to correct the severe mandibular prognathism. A partial glossectomy was also carried out to address macroglossia. After a total treatment time of 32 months, a Class I occlusion with a favorable facial profile and lip competence were obtained. The occlusion was made approximately ideal, and mastication improved remarkably. Three years after retention, the occlusion was stable and no relapse was observed. The patient’s complaints and orthodontic problems were completely resolved. Therefore, a combination of two-jaw surgeries with Le Fort I maxillary osteotomy, mandibular SSRO, mandibular ostectomy, and glossectomy may be a viable option in the correction of extremely severe anteroposterior skeletal discrepancy

Repair of root resorption 2 to 16 weeks after the application of continuous forces on maxillary first molars in rats: a 2- and 3-dimensional quantitative evaluation.

INTRODUCTION: Root resorption is a side effect of orthodontic treatment that occurs with the removal of hyalinized tissue. Studies have shown that a reparative process in the periodontium begins when the applied orthodontic force is discontinued or reduced below a certain level. However, quantitative 3-dimensional evaluation of root resorption repair has not been done. The aim of this study was to quantitatively assess the 2- and 3-dimensional changes of root resorption craters after 2 weeks of continuous mesially applied orthodontic forces of 50 g on rat molars and 2- to 16-week retention periods. METHODS: We used 60 male Wistar rats (10 weeks old). Nickel-titanium closed-coil springs were used to apply 50-g mesial forces for 2 weeks to move the maxillary left first molars. The rats were randomly allocated to 6 groups. Those in the zero-week retention group were killed after force application. In the remaining 5 groups, the interdental spaces between the maxillary first and second molars were filled with resin to retain the molars. The molars were extracted after periods of retention from 2 and 16 weeks. The maxillary right molars were used as the controls. Mesial and distal roots (distobuccal and distopalatal) were examined by using scanning electron and 3-dimensional scanning laser microscopes. The surface area, depth, volume, and roughness of the root resorption craters were measured. RESULTS: The area, depth, and volume of the craters decreased gradually and showed similar trends over the retention time, approaching a plateau at the 12th week. After 16 weeks of retention, the volumes of the resorption craters of the distobuccal and distopalatal roots reached recovery peaks of 69.5% and 66.7%, respectively. Small pits on the mesial roots showed recovery of 62.5% at the 12th week. The healing patterns in distal roots with severe resorption and mesial roots with shallow resorption had no significant differences. CONCLUSIONS: The resorption and repair processes during the early stages of retention are balanced, and most of the reparative process occurs after 4 weeks of passive retention after the application of orthodontic force. Frequent orthodontic reactivations should be avoided to allow recovery and repair of root surface damage

ゾレドロン酸を全身投与した卵巣摘出ラットにおける矯正的歯の移動と歯根吸収

長崎大学学位論文 [学位記番号]博（医歯薬）甲第612号 [学位授与年月日]平成25年9月19

High Extracellular Ca2+ Stimulates Ca2+-Activated Cl− Currents in Frog Parathyroid Cells through the Mediation of Arachidonic Acid Cascade

Elevation of extracellular Ca2+ concentration induces intracellular Ca2+ signaling in parathyroid cells. The response is due to stimulation of the phospholipase C/Ca2+ pathways, but the direct mechanism responsible for the rise of intracellular Ca2+ concentration has remained elusive. Here, we describe the electrophysiological property associated with intracellular Ca2+ signaling in frog parathyroid cells and show that Ca2+-activated Cl− channels are activated by intracellular Ca2+ increase through an inositol 1,4,5-trisphophate (IP3)-independent pathway. High extracellular Ca2+ induced an outwardly-rectifying conductance in a dose-dependent manner (EC50∼6 mM). The conductance was composed of an instantaneous time-independent component and a slowly activating time-dependent component and displayed a deactivating inward tail current. Extracellular Ca2+-induced and Ca2+ dialysis-induced currents reversed at the equilibrium potential of Cl− and were inhibited by niflumic acid (a specific blocker of Ca2+-activated Cl− channel). Gramicidin-perforated whole-cell recording displayed the shift of the reversal potential in extracellular Ca2+-induced current, suggesting the change of intracellular Cl− concentration in a few minutes. Extracellular Ca2+-induced currents displayed a moderate dependency on guanosine triphosphate (GTP). All blockers for phospholipase C, diacylglycerol (DAG) lipase, monoacylglycerol (MAG) lipase and lipoxygenase inhibited extracellular Ca2+-induced current. IP3 dialysis failed to induce conductance increase, but 2-arachidonoylglycerol (2-AG), arachidonic acid and 12S-hydroperoxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12(S)-HPETE) dialysis increased the conductance identical to extracellular Ca2+-induced conductance. These results indicate that high extracellular Ca2+ raises intracellular Ca2+ concentration through the DAG lipase/lipoxygenase pathway, resulting in the activation of Cl− conductance

Severe Dental Open Bite Malocclusion With Tongue Reduction After Orthodontic Treatment

We treated a 21-year-old woman with a severe open bite and macroglossia with a standard edgewise appliance and without partial glossectomy. This was followed by retention using a Begg-type plate retainer for the upper dental arch and a fixed canine-to-canine for the lower arch. A crib was added to the upper plate retainer for suppression of a tongue thrust. The lower arch relapsed during the retention period, with a widening of the intermolar distance, flaring of the anterior teeth, and increased mobility of the teeth. We chose tongue reduction to resolve these problems and one-third of the middle dorsal part of the tongue was excised. After the tongue reduction, the patient experienced no functional problem in mastication, swallowing, and gustation, but she complained of mild speech difficulty and slight pain on the dorsal portion of her tongue. These symptoms disappeared 6 months after surgery. At this time, the mandibular dental arch was markedly improved. The flared lower dental arch had returned to an upright position and the tooth mobility reduced to normal. No appliance was used after surgery. Most of the recovery changes occurred within 4 months. This case highlights the importance of the teeth tending to move toward a balance between the tongue pressure from the inside and labio-buccal pressure from the outside

Molecular analysis of RANKL-independent cell fusion of osteoclast-like cells Induced by TNF-α, lipopolysaccharide, or peptidoglycan

Focusing on the final step of osteoclastogenesis,we studied cell fusion from tartrate-resistant acid phosphatase (TRAP)-positive mononuclear cells into multinuclear cells. TRAP-positive mononuclear cells before generation of multinuclear cells by cell fusion were differentiated from RAW264.7 cells by treatment with receptor activator of nuclear factor kappa B ligand (RANKL), and then the cells were treated with lipopolysaccharide (LPS), followed by culturing for further 12 h. LPS-induced cell fusion even in the absence of RANKL. Similarly, tumor necrosis factor (TNF)-α and peptidoglycan (PGN) induced cell fusion, but M-CSF did not. The cell fusion induced by RANKL, TNF-α, and LPS was specifically blocked by osteoprotegerin (OPG), anti-TNF-α antibody, and polymyxin B, respectively. LPS- and PGN-induced cell fusion was partly inhibited by anti-TNF-α antibody but not by OPG.When TRAP-positive mononuclear cells fused to yield multinuclear cells, phosphorylation of Akt, Src, extracellular signal-regulated kinase (ERK), p38MAPK (p38), and c-JunNH2-terminal kinase (JNK) was observed. The specific chemical inhibitors LY294002 (PI3K), PP2 (Src), U0126 (MAPK-ERK kinase (MEK)/ERK), and SP600125 (JNK) effectively suppressed cell fusion, although SB203580 (p38) did not. mRNA of nuclear factor of activated T-cells c1 (NFATc1) and dendritic cell-specific transmembrane protein (DC-STAMP) during the cell fusion was quantified, however, there wasno obvious difference among the TRAP-positive mononuclear cells treated with or without M-CSF,RANKL, TNF-α, LPS, or GN. Collectively, RANKL,TNF-α, LPS, and PGN induced cell fusion of osteoclasts through their own receptors. Subsequent activation of signaling pathways involving PI3K, Src, ERK, and JNK molecules was required for the cell fusion. Although DC-STAMP is considered to be a requisite for cell fusion of osteoclasts, cell fusion-inducing factors other than DC-STAMP might be necessary for the cell fusion