[Show abstract][Hide abstract] ABSTRACT: Embryonic development of articular cartilage has not been well understood and the role of doublecortin (DCX) in determination of chondrocyte phenotype is unknown. Here, we use a DCX promoter-driven eGFP reporter mouse model to study the dynamic gene expression profiles in mouse embryonic handplates at E12.5 to E13.5 when the condensed mesenchymal cells differentiate into either endochondral chondrocytes or joint interzone cells. Illumina microarray analysis identified a variety of genes that were expressed differentially in the different regions of mouse handplate. The unique expression patterns of many genes were revealed. Cytl1 and 3110032G18RIK were highly expressed in the proximal region of E12.5 handplate and the carpal region of E13.5 handplate, whereas Olfr538, Kctd15, and Cited1 were highly expressed in the distal region of E12.5 and the metacarpal region of E13.5 handplates. There was an increasing gradient of Hrc expression in the proximal to distal direction in E13.5 handplate. Furthermore, when human DCX protein was expressed in human adipose stem cells, collagen II was decreased while aggrecan, matrilin 2, and GDF5 were increased during the 14-day pellet culture. These findings suggest that DCX may play a role in defining chondrocyte phenotype.
International Journal of Molecular Sciences 04/2014; 15(4):6941-60. DOI:10.3390/ijms15046941 · 2.86 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Objectives. The objective of this study was to compare the damage to the rotator cuff tendons caused by four different anchor systems. Methods. 20 cadaveric human shoulder joints were used for transtendon insertion of four anchor systems. The Healix Peek, Fastin RC, Bio-Corkscrew Suture, and Healix Transtend anchors were inserted through the tendons using standard transtendon procedures. The areas of tendon damage were measured. Results. The areas of tendon damage (mean ± standard deviation, n = 7) were 29.1 ± 4.3 mm(2) for the Healix Peek anchor, 20.4 ± 2.3 mm(2) for the Fastin RC anchor, 23.4 ± 1.2 mm(2) for the Bio-Corkscrew Suture anchor, 13.7 ± 3.2 mm(2) for the Healix Transtend anchor inserted directly, and 9.1 ± 2.1 mm(2) for the Healix Transtend anchor inserted through the Percannula system (P < 0.001 or P < 0.001, compared to other anchors). Conclusions. In a cadaver transtendon rotator cuff repair model, smaller anchors caused less damage to the tendon tissues. The Healix Transtend implant system caused the least damage to the tendon tissues. Our findings suggest that smaller anchors should be considered when performing transtendon procedures to repair partial rotator cuff tears.
[Show abstract][Hide abstract] ABSTRACT: Bupivacaine and supraphysiologic temperature can independently reduce cell viability of articular chondrocytes. In combination, these 2 deleterious factors could further impair cell viability.
Hyaluronan may protect chondrocytes from death induced by bupivacaine at supraphysiologic temperatures. Study Design: Controlled laboratory study.
Bovine articular chondrocytes were treated with hyaluronan at physiologic (37°C) and supraphysiologic temperatures (45°C and 50°C) for 1 hour and then exposed to bupivacaine for 1 hour at room temperature. Cell viability was assessed at 3 time points: immediately after treatment, 6 hours later, and 24 hours later using flow cytometry and fluorescence microscopy. The effects of hyaluronan on the levels of sulfated glycosaminoglycan in the chondrocytes were determined using Alcian blue staining.
(1) Bupivacaine alone did not induce noticeable chondrocyte death at 37°C; (2) bupivacaine and temperature synergistically increased chondrocyte death, that is, when the chondrocytes were conditioned to 45°C and 50°C, 0.25% and 0.5% bupivacaine increased the cell death rate by 131% to 383% in comparison with the phosphate-buffered saline control group; and (3) addition of hyaluronan reduced chondrocyte death rates to approximately 14% and 25% at 45°C and 50°C, respectively. Hyaluronan's protective effects were still observed at 6 and 24 hours after bupivacaine treatment at 45°C. However, at 50°C, hyaluronan delayed but did not prevent the cell death caused by bupivacaine. One-hour treatment with hyaluronan significantly increased sulfated glycosaminoglycan levels in the chondrocytes.
Bupivacaine and supraphysiologic temperature synergistically increase chondrocyte death, and hyaluronan may protect articular chondrocytes from death caused by bupivacaine.
This study provides a rationale to perform preclinical and clinical studies to evaluate whether intra-articular injection of a mixture of bupivacaine and hyaluronan after arthroscopic surgery may protect against bupivacaine's chondrotoxicity.
The American Journal of Sports Medicine 03/2012; 40(6):1375-83. DOI:10.1177/0363546512439025 · 4.36 Impact Factor