Cell and cell nucleus deformations have been implicated in the mechanotransduction of mechanical loads acting on tissues. While in situ cell nucleus deformation in response to increasing tissue strains has been examined in articular cartilage this phenomenon has not been investigated in tendons. To examine in situ cell nuclei deformation in tendons undergoing tensile strain rat tail tendons were harvested from adult Sprague-Dawley rats and stained with acridine orange to highlight the cell nuclei. The tendons were mounted on a custom-designed, low-load, tensile testing device affixed to the mechanical stage of a confocal laser microscope. Cells within the tendons were isolated for analysis. Images of individual cells were captured at 0'%1 strain as well as sequentially at 2'%,, 4% and 6'%1 gripto-grip tendon strain. Digital images of the cell nuclei were then measured in the s (length) and y (height) axis and deformation expressed as a percentage of cell nuclei strain. In addition, centroid-to-centroid distances of adjacent cell nuclei within each image were measured and used to calculate local tissue strain. There was a weak (r2 = 0.34) but significant (p < 0.01) correlation between local tissue strain and cell nucleus strain in the x axis. The results of this study support the hypothesis that in situ cell nucleus deformation does occur during tensile loading of tendons. This deformation may play a significant role in the mechanical signal transduction pathway of this tissue.

The effect of stress deprivation and cyclic tensile loading on the mechanical and histologic properties of the canine flexor digitorum profundus tendon was examined using an in vitro system. Stress deprivation resulted in a progressive and statistically significant decrease in the tensile modulus over an 8-week period. Histologically, stress-deprived tendons demonstrated quantitative changes in the morphology and number of cells and in the alignment of collagen. The change in tensile properties was not associated with an alteration in the water content of the tissue, but the change appeared to be dependent on the presence of a viable cell population. Dead (acellular) tendons did not undergo any alteration in tensile modulus in this in vitro system. In vitro cyclic tensile loading of tendons over a 4-week time period resulted in a significant increase in the tensile modulus (93% of the control) compared with that of the stress-deprived tendons (68% of the control). This loading regimen also maintained the normal histologic pattern of the tendons. The results of this study are similar to those previously reported for in vivo studies and suggest that this in vitro model may represent a valid system with which to test the effects of various stress conditions on the tensile properties of tissues.

The use of human tissue-derived autografts and allografts continues to be the gold standard in anterior cruciate ligament (ACL) repair. However, autografts and allografts have their own set of associated risks. Many alternative options, including synthetic replacements, have failed to demonstrate long-term success. In this study, sterile acellular porcine bone-tendon-bone (BTB) xenografts were created using a proprietary process and tested against BTB autografts in goats for 13 and 52 weeks. At 13 weeks, all xenograft-implanted animals ( n = 9) had subjective hind leg motor function (HLMF) that was categorized as either normal (score = 0) or a slight limp (score = 1) compared with two of nine autograft-implanted animals having a moderate limp (score = 2). At 39 weeks, there was HLMF improvement with each autograft-implanted and xenograft-implanted animal having normal HLMF or only a slight limp. At 13 weeks, six of nine animals in each group achieved normal anterior drawer scores, which increased to nine of nine animals in each group by 39 weeks. Both autografts and xenografts exhibited minimal inflammation with excellent integration of the fibrous tendon portion of the graft to host bone, as evidenced histologically by Sharpey’s fiber formation. At 52 weeks, maximum mechanical load at failure for xenografts was 1092.0 ± 586.4 N compared with 1037.0 ± 422.6 N for autografts. These results demonstrate that a sterile acellular porcine BTB xenograft can perform equivalently to BTB autograft in a caprine model of ACL repair.

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