No abstract

From the above results, the expression of OPG, RANKL, and RANK during the osseointegration of the dental titanium implant was observed within bone tissue. The application of the LLL influenced the expression of OPG, RANKL, and RANK, and resulted in the expansion of metabolic bone activity and increased the activity of bone tissue cells.

The purpose of this study was to compare treatment outcome and relapse between maxillary advancement surgery with LeFort I osteotomy and maxillary distraction osteogenesis in patients with cleft lip and palate with maxillary hypoplasia. The sample consisted of a maxillary advancement surgery with LeFort I osteotomy group (group 1, N= 14, mean age, 21.7 years) and a maxillary distraction osteogenesis group (group 2, N = 11, mean age, 16.3 years). Lateral cephalograms were taken and traced at presurgery (T0), postsurgery (T1), and postretention (T2). Nine hard and four soft tissue cephalometric variables were measured. Differences in measurements at each stage, treatment outcome (T1-T0), and relapse (T2-T1) were compared between groups with independent t test. Because the amount of surgical movement could affect the amount of relapse, a difference in relapse between two groups was compared by analysis of covariance with the amount of surgical movement as a covariant. Although the amounts of forward movements of A point (P < 0.01), upper incisor (P < 0.001), and upper lip (P < 0.001) during T1-T0 were greater in group 2, there were no significant differences in the amounts of relapse (T2-T1) between the two groups. During T1-T0, counterclockwise rotation of the palatal plane was observed in group 2 as a result of downward movement of posterior nasal spine (PNS) at T1, whereas group 1 had clockwise rotation of palatal plane at T1 because of downward movement of anterior nasal spine (ANS). The amounts of relapse (T2-T1) in vertical movements of PNS and upper incisor were significantly different between the two groups (P < 0.05). The amount of required maxillary advancement, vector control of palatal plane, and vertical position of upper incisor would be important factors when planning a surgical treatment in patients with cleft lip and palate with midface hypoplasia.

No abstract

The aim of this study was to examine the effects of human umbilical cord blood-derived CD34-positive endothelial progenitor cells (CD34+ EPCs) on osteoblastic differentiation of cultured human periosteal-derived osteoblasts (POs). CD34+ cells from human umbilical cord blood were sorted to purify more EPCs in characterization. These sorted cells showed CD31, VE-cadherin, and KDR expression as well as CD34 expression and formed typical tubes in Matrigel. These sorted cells were referred to as human cord blood-derived CD34+ EPCs. In in vivo bone formation using a miniature pig model, the newly formed bone was clearly examined in defects filled with polydioxanone/pluronic F127 (PDO/Pluronic F127) scaffolds containing either human umbilical cord blood-derived CD34+ EPCs and POs or human umbilical vein endothelial cells (HUVEC) and POs; however, the new bone had the greatest density in the defect treated with CD34+ EPCs and POs. Osteoblastic phenotypes of cultured human POs using ALP activity and von Kossa staining were also more clearly found in CD34+ EPC-conditioned medium than CD34-negative (CD34-) cell-conditioned medium, whereas HUVEC-conditioned medium had an intermediate effect. PCR array for common cytokines and growth factors showed that the secretion of interleukin (IL)-1β was significantly higher in CD34+ EPCs than in HUVEC, followed by level in CD34- cells. In addition, IL-1β also potently and dose dependently increased ALP activity and mineralization of POs in culture. These results suggest that human umbilical cord blood-derived CD34+ EPCs stimulates osteoblastic differentiation of cultured human POs. The functional role of human umbilical cord blood-derived CD34+ EPCs in increasing the osteogenic phenotypes of cultured human POs may depend on IL-1β secreted from human umbilical cord blood-derived CD34+ EPCs.