The Effect of Concomitant Arthroscopic Lateral Retinacular Release on Postoperative Patellar Position and Orientation in Open Wedge High Tibial Osteotomy

PURPOSE: The purpose of this study was to evaluate the effect of concomitant arthroscopic lateral release (LR) in open wedge high tibial osteotomy (OWHTO) by comparing the pre- and postoperative radiological parameters of patellar position and orientation. MATERIALS AND METHODS: The study was comprised of 19 knees undergoing OWHTO and concomitant LR and 18 knees undergoing OWHTO alone. Radiological parameters for patellar position and orientation included the Caton-Deschamps index (CDI), Blackburne-Peel index (BPI), patellar tilting angle (PTA), patellar lateral shift (PLS), and patellofemoral distance (PFD), which were evaluated in the preoperative period and at one year after surgery. RESULTS: Patellar height was significantly reduced after surgery as indicated by the decrease in BPI (p=0.03) in the OWHTO/LR group, and decrease in CDI (p=0.03) and BPI (p=0.04) in the OWHTO alone group. PTA and PLS were significantly reduced after the combined OWHTO/LR procedure (p=0.04 and p=0.04, respectively). By contrast, no significant changes were detected when isolated OWHTO was performed. CONCLUSIONS: OWHTO induced a postoperative decrease in patellar height in both groups. Regarding the change in patellofemoral alignment, concomitant LR in OWHTO significantly decreased lateral patellar tilt and shift, while no significant difference in those parameters were noted in the OWHTO alone knees.

Back out of Locking Pin with Hinge Fracture after High Tibial Osteotomy

Low-profile fixation devices for medial opening wedge high tibial osteotomy (OWHTO) were developed in order to avoid skin irritation and additional invasion. However, the low-profile system is associated with additional risks. We report three cases of locking pin back out with the low-profile locking plate system for medial OWHTO.

Regulation of Cartilage Development and Diseases by Transcription Factors

Genetic studies and molecular cloning approaches have been successfully used to identify several transcription factors that regulate the numerous stages of cartilage development. Sex-determining region Y (SRY)-box 9 (Sox9) is an essential transcription factor for the initial stage of cartilage development. Sox5 and Sox6 play an important role in the chondrogenic action of Sox9, presumably by defining its cartilage specificity. Several transcription factors have been identified as transcriptional partners for Sox9 during cartilage development. Runt-related transcription factor 2 (Runx2) and Runx3 are necessary for hypertrophy of chondrocytes. CCAAT/enhancer-binding protein β (C/EBPβ) and activating transcription factor 4 (ATF4) function as co-activators for Runx2 during hypertrophy of chondrocytes. In addition, myocyte-enhancer factor 2C (Mef2C) is required for initiation of chondrocyte hypertrophy, presumably by functioning upstream of Runx2. Importantly, the pathogenic roles of several transcription factors in osteoarthritis have been demonstrated based on the similarity of pathological phenomena seen in osteoarthritis with chondrocyte hypertrophy. We discuss the importance of investigating cellular and molecular properties of articular chondrocytes and degradation mechanisms in osteoarthritis, one of the most common cartilage diseases.

Transcriptional Network Controlling Endochondral Ossification

Endochondral ossification is the fundamental process of skeletal development in vertebrates. Chondrocytes undergo sequential steps of differentiation, including mesenchymal condensation, proliferation, hypertrophy, and mineralization. These steps, which are required for the morphological and functional changes in differentiating chondrocytes, are strictly regulated by a complex transcriptional network. Biochemical and mice genetic studies identified chondrogenic transcription factors critical for endochondral ossification. The transcription factor sex-determining region Y (SRY)-box 9 (Sox9) is essential for early chondrogenesis, and impaired Sox9 function causes severe chondrodysplasia in humans and mice. In addition, recent genome-wide chromatin immunoprecipitation-sequencing studies revealed the precise regulatory mechanism of Sox9 during early chondrogenesis. Runt-related transcription factor 2 promotes chondrocyte hypertrophy and terminal differentiation. Interestingly, endoplasmic reticulum (ER) stress-related transcription factors have recently emerged as novel regulators of chondrocyte differentiation. Here we review the transcriptional mechanisms that regulate endochondral ossification, with a focus on Sox9.