Objective. The process of N-glycosylation is involved in the pathogenesis of various diseases. However, little is known about the contribution of changes in N-glycans in osteoarthritis (OA). The aim of this study was to identify the alterations in N-glycans in human OA cartilage, to characterize the messenger RNA (mRNA) expression of N-glycan biosynthesis enzyme genes (N-glycogenes) in mouse articular chondrocytes during cartilage degradation, and to analyze the relationship between altered N-glycan patterns and mechanisms of cartilage degradation.Methods. Alterations in N-glycans were analyzed in human OA cartilage and degraded mouse cartilage by high-performance liquid chromatography and mass spectrometry. N-glycogene mRNA expression in mouse chondrocytes was measured using reverse transcription-polymerase chain reaction. To assess the relationship between the altered N-glycans and degradation of mouse cartilage, experiments involving either knockdown or overexpression of N-glycogenes were performed in mouse articular chondrocytes.Results. Alterations in high-mannose type N-glycans were observed in both human OA cartilage and degraded mouse cartilage. The expression of 1,2N-acetylglucosaminyltransferase I (GlcNAc-TI) mRNA, which converts high-mannose type N-glycans, was significantly increased in degraded mouse cartilage. Mouse chondrocytes with suppressed GlcNAc-TI expression had reduced levels of matrix metalloproteinase 13 (MMP-13) and ADAMTS-5 (aggrecanase 2) mRNA following stimulation with interleukin-1␣ (IL-1␣). In contrast, mouse chondrocytes overexpressing GlcNAc-TI had increased levels of MMP-13 and ADAMTS-5 mRNA following stimulation with IL-1␣.Conclusion. These findings indicate that alterations in high-mannose type N-glycans and N-glycogenes in chondrocytes correlate with the release of MMP-13 and ADAMTS-5 during cartilage degradation. These findings suggest that N-glycans play a crucial role in the initiation and progression of OA.Osteoarthritis (OA), the most common joint disease, is characterized by the degradation of articular cartilage, which frequently leads to disability in older persons, particularly in performing daily activities. Chondrocytes are the only cells in cartilage responsible for the synthesis and degradation of the extracellular matrix (ECM). Chondrocyte metabolism is regulated by genetic and environmental factors, such as the composition of the ECM, soluble mediators, and mechanical factors. A breakdown in the balance of this metabolism results in cartilage degradation. Elucidation of the pathogenesis of OA requires a better understanding of the mechanism of cartilage degradation. Despite the large number of biomechanical and biochemical studies performed to clarify the mechanisms of cartilage degradation (1-7), these mechanisms remain unclear.Glycobiology, the study of the biologic functions of sugar chains bound to proteins and lipids, was recently applied to molecular-based studies in the biomedical field (8-11). The majority of glycans attached to proteins
These results indicate that changes in the expression of N-glycans are correlated with OA in an animal model. Understanding mechanisms underlying changes in N-glycans seen in OA may be of therapeutic value in treating cartilage deterioration.
The supraspinatus tendon consists morphologically of two sub-regions, anterior and posterior. The anterior sub-region is thick and tubular while the posterior is thin and strap-like. The purpose of this study was to compare the structural and mechanical properties of the anterior and posterior sub-regions of the supraspinatus tendon. The supraspinatus tendons from seven human cadaveric shoulders were morphologically divided into the anterior and posterior sub-regions. Length, width, and thickness were measured. A servo-hydraulic testing machine (MTS Systems Corporation, Minneapolis, MN) was used for tensile testing. The maximal load at failure, modulus of elasticity and ultimate tendon stress were calculated. Repeated measures were used for statistical comparisons. The mean anterior tendon cross-sectional area was 47.3 mm(2) and the posterior was 32.1 mm(2) . Failure occurred most often at the insertion site: anterior (5/7) and posterior (6/7). All parameters of the anterior sub-region were significantly greater than those of the posterior sub-region. The moduli of elasticity at the insertion site were 592.4 MPa in the anterior sub-region and 217.7 MPa in the posterior (P = 0.01). The ultimate failure loads were 779.2 N in the anterior sub-region and 335.6 N in the posterior (P = 0.003). The ultimate stresses were 22.1 MPa in the anterior sub-region and 11.6 MPa in the posterior (P = 0.008). We recognized that the anterior and posterior sub-regions of the SSP tendon have significantly different mechanical properties. In a future study, we need to evaluate how best to repair an SSP tendon considering these region-specific properties.
We have carried out a replacement of the lunate in 12 patients with advanced Kienböck's disease, with excision of the lunate and insertion of an iliac bone flap wrapped into palmaris longus. The aims of this study were to determine the effect of this procedure for advanced Kienböck's disease. At a mean follow-up period of 45.3 months, the mean clinical score was excellent in all cases. Radiographically, progression of osteoarthritis (OA) in the radiocarpal joint was found in two patients. At follow-up, the X-ray findings indicated a reduced of osseous core in four patients. On the other hand, carpal height ratio showed no significant change at follow-up. Excision arthroplasty using a tendon ball with osseous core for advanced Kienböck's disease leads to OA progression in some cases. However, clinical results were excellent in all cases. Therefore, this current study provides effective therapeutic procedure for advanced Kienböck's disease.
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