Search

Abstract: Oblique facial cleft is an extremely rare disorder, accounting for only 0.24% of facial clefts. Even after initial surgery, depressions of the eyeball and facial surface are formed due to bone defects of the maxilla and orbital floor, and since performing bone reconstruction during infancy and early childhood is difficult, pronounced deformity tends to persist. We report our experience with using an absorbable mesh tray together with particulate cancellous bone and marrow for secondary repair by means of bone reconstruction in a 4-year-old girl, achieving good results at a young age. [Copyright &y& Elsevier]

By producing instability in mouse knee joints, we attempted to determine the involvement of runt‐related transcription factor 2 (RUNX‐2), which is required for chondrocyte hypertrophy, in the development of osteoarthritis (OA).An experimental mouse OA model was created by surgical transection of the medial collateral ligament and resection of the medial meniscus of the knee joints of heterozygous RUNX‐2–deficient (Runx2+/−) mice and wild‐type littermates. Cartilage destruction and osteophyte formation in the medial tibial cartilage were compared by histologic and radiographic analyses. Localization of type X collagen and matrix metalloproteinase 13 (MMP‐13) was examined by immunohistochemistry. Localization of RUNX‐2 was determined by X‐Gal staining in heterozygous RUNX‐2–deficient mice with the lacZ gene insertion at the Runx2‐deletion site (Runx2+/lacZ). Messenger RNA levels of type X collagen, MMP‐13, and RUNX‐2 were examined by real‐time reverse transcriptase–polymerase chain reaction analysis.RUNX‐2 was induced in the articular cartilage of wild‐type mice at the early stage of OA, almost simultaneously with type X collagen but earlier than MMP‐13. Runx2+/− and Runx2+/lacZ mice showed normal skeletal development and articular cartilage; however, after induction of knee joint instability, they exhibited decreased cartilage destruction and osteophyte formation, along with reduced type X collagen and MMP‐13 expression, as compared with wild‐type mice.RUNX‐2 contributes to the pathogenesis of OA through chondrocyte hypertrophy and matrix breakdown after the induction of joint instability. [ABSTRACT FROM AUTHOR]

Because a temporal arrest in the G1-phase of the cell cycle is a prerequisite for cell differentiation, this study investigated the involvement of cell cycle factors in the differentiation of cultured mouse prechondrocyte cell line ATDC5. Among the G1 cell cycle factors examined, both protein and mRNA levels of cyclin-dependent kinase (Cdk6) were downregulated during the culture in a differentiation medium. The protein degradation of Cdk6 was not involved in this downregulation because proteasome inhibitors did not reverse the protein level. When inhibitors of p38 MAPK, ERK-1/2, and PI3K/Akt were added to the culture, only a p38 MAPK inhibitor SB203580 blocked the decrease in the Cdk6 protein level by the differentiation medium, indicating that the Cdk6 inhibition was mediated by p38 MAPK pathway. In fact, p38 MAPK was confirmed to be phosphorylated during differentiation of ATDC5 cells. Enforced expression of Cdk6 in ATDC5 cells blocked the chondrocyte differentiation and inhibited Sox5 and Sox6 expressions. However, the Cdk6 overexpression did not affect the proliferation or the cell cycle progression, suggesting that the inhibitory effect of Cdk6 on the differentiation was exerted by a mechanism largely independent of its cell cycle regulation. These results indicate that Cdk6 may be a regulator of chondrocyte differentiation and that its p38-mediated downregulation is involved in the efficient differentiation. 2005 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]