Skeletal Class III malocclusion with unilateral congenitally missing maxillary incisor treated by maxillary protractor and edgewise appliances.

This case report describes the orthodontic treatment of a 10-year-old female patient with a combination of Angle Class III malocclusion, a missing maxillary right lateral incisor, a supernumerary tooth with a short root on the lingual side of the maxillary incisor, a skeletal Class III jaw base relationship caused by a diminutive maxilla, and retroposition of the maxilla. We chose to close the space of the missing tooth, as well as the space created by extraction of the maxillary lateral incisor, by forward movement of the canine and premolars using a maxillary protractor with edgewise appliances. As a result, both the maxillary premolars and the molars were moved mesially, and a Class II molar relationship with tight interdigitation was achieved. Our results suggest that the combination of maxillary protractor and nontorque brackets was effective not only for correcting skeletal Class III malocclusion, but also for forward movement of the maxillary posterior teeth.

IGF2 modulates the microenvironment for osteoclastogenesis.

We previously reported that hypoxic stress enhanced osteoclast differentiation via increasing insulin-like growth factor 2 (IGF2) production. However, the mechanisms underlying IGF2 stimulation remains unknown. In this study, we investigated the molecular mechanisms of osteoclastogenesis by IGF2 treatment. Primary mouse bone marrow cells were cultured with IGF2. Total RNAs were applied to a DNA microarray analysis, and quantitative RT-PCR was then used to confirm the microarray data and clarify which cells expressed the relative genes. The most interesting findings were the upregulations of CXC chemokine ligand 7 (CXCL7) expression in stromal cells and stromal cell-derived factor 1 (SDF1) expression in osteoblastic cells with IGF2 treatment. The addition of exogenous SDF1 to CXCL7 increased the number of osteoclasts and promoted the formation of giant osteoclasts. These results suggest that IGF2 modulates the microenvironment around osteoclast precursor cells. SDF1 together with CXCL7 may promote the formation of giant osteoclasts.

Hypoxic stress enhances osteoclast differentiation via increasing IGF2 production by non-osteoclastic cells.

Development of bone depends on a continuous supply of bone-degrading osteoclasts. Although several factors such as cytokines and integrins have been shown to be important for osteoclast recruitment, their mechanism of action is poorly understood. In this study, we demonstrated the enhancement of osteoclast formation by hypoxia and investigated the molecular mechanisms involved. Primary mouse bone marrow cells were cultured in normoxic and hypoxic conditions, and RNA was prepared from each group of cells. Total RNAs were applied to a DNA microarray analysis and then RT-PCR was performed to confirm the microarray data. The most interesting finding of our microarray analysis was upregulation of insulin-like growth factor 2 (IGF2) and stromal cell-derived factor 1 (SDF1) under hypoxic conditions. RT-PCR analysis revealed that IGF2 expression was markedly upregulated in the non-osteoclastic cells. The addition of exogenous IGF2 increased the number of osteoclastic TRAP-positive multinuclear cells formed under normoxic conditions, whereas the addition of exogenous SDF1 did not change osteoclast formation. These results suggest that the upregulation of IGF2 derived from non-osteoclastic cells might be a crucial factor for osteoclast differentiation.