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Evidence that interfibrillar load transfer in tendon is supported by small diameter fibrils and not extrafibrillar tissue components.

ABSTRACT: Collagen fibrils in tendon are believed to be discontinuous and transfer tensile loads through shear forces generated during interfibrillar sliding. However, the structures that transmit these interfibrillar forces are unknown. Various extrafibrillar tissue components (e.g., glycosaminoglycans, collagens XII and XIV) have been suggested to transmit interfibrillar loads by bridging collagen fibrils. Alternatively, collagen fibrils may interact directly through physical fusions and interfibrillar branching. The objective of this study was to test whether extrafibrillar proteins are necessary to transmit load between collagen fibrils or if interfibrillar load transfer is accomplished directly by the fibrils themselves. Trypsin digestions were used to remove a broad spectrum of extrafibrillar proteins and measure their contribution to the multiscale mechanics of rat tail tendon fascicles. Additionally, images obtained from serial block-face scanning electron microscopy were used to determine the three-dimensional fibrillar organization in tendon fascicles and identify any potential interfibrillar interactions. While trypsin successfully removed several extrafibrillar tissue components, there was no change in the macroscale fascicle mechanics or fibril:tissue strain ratio. Furthermore, the imaging data suggested that a network of smaller diameter fibrils (<150?nm) wind around and fuse with their neighboring larger diameter fibrils. These findings demonstrate that interfibrillar load transfer is not supported by extrafibrillar tissue components and support the hypothesis that collagen fibrils are capable of transmitting loads themselves. Conclusively determining how fibrils bear load within tendon is critical for identifying the mechanisms that impair tissue function with degeneration and for restoring tissue properties via cell-mediated regeneration or engineered tissue replacements. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:2127-2134, 2017.

SUBMITTER: Szczesny SE

PROVIDER: S-EPMC5503823 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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Evidence that interfibrillar load transfer in tendon is supported by small diameter fibrils and not extrafibrillar tissue components.

Szczesny Spencer E SE Fetchko Kristen L KL Dodge George R GR Elliott Dawn M DM

Journal of orthopaedic research : official publication of the Orthopaedic Research Society 20170131 10

Collagen fibrils in tendon are believed to be discontinuous and transfer tensile loads through shear forces generated during interfibrillar sliding. However, the structures that transmit these interfibrillar forces are unknown. Various extrafibrillar tissue components (e.g., glycosaminoglycans, collagens XII and XIV) have been suggested to transmit interfibrillar loads by bridging collagen fibrils. Alternatively, collagen fibrils may interact directly through physical fusions and interfibrillar ...[more]

PMID: 28071819

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Project description:BackgroundShoulder involvement in brachial plexus birth palsy is common, and the adduction, internal rotation contracture deformity often requires some form of surgical treatment. There are very few long-term reports on release of contracted muscles and tendon transfers, especially in older children. We are reporting the single-center results of such a surgery with detailed outcome analysis.MethodsThe prospectively collected data from brachial plexus birth palsy cases who had undergone contracture release and tendon transfer were retrospectively studied and examined. The new Mallet and functional scores were compared with the original data forms and then analyzed. The radiographic evidence of glenoid dysplasia and its correlation with age and functional outcome was assessed.ResultsA total of 82 cases with surgery at mean age of 9.5 ± 5.09 years and a follow-up of 8 ± 3.8 (3-20) years entered the study. Of these, 56% of cases had 7 to 20 years of age at surgery. Fifty-four (66%) patients had only shoulder surgery, and 28 (34%) required additional reconstructive surgeries for hand and wrist. Moderate to severe glenohumeral dysplasia was present in 38%. The preoperative Mallet score of 10.6 ± 2.97 improved to 19.3 ± 3.39 (P < .001). Eighty-one percent of patients showed improvement in "reaching face" functions, 71% in "above head" functions, and 74% in "midline functions." The cases with lack of improvement in midline function mostly belonged to pan-plexus injuries. Noticeable subjective and objective improvement was also observed in cases with glenohumeral dysplasia in their Mallet and functional scores (P < .001). The improvement in function and subjective satisfaction of 92% was observed irrespective of age at surgery.ConclusionSoft-tissue release and tendon transfer for brachial plexus birth palsy shoulder can improve function and limb appearance even in older children and young adults and even in the presence of glenohumeral dysplasia.

Project description:ObjectivesRe-rupture is common after primary flexor tendon repair. Characterization of the biological changes in the ruptured tendon stumps would be helpful, not only to understand the biological responses to the failed tendon repair, but also to investigate if the tendon stumps could be used as a recycling biomaterial for tendon regeneration in the secondary grafting surgery.MethodsA canine flexor tendon repair and failure model was used. Following six weeks of repair failure, the tendon stumps were analyzed and characterized as isolated tendon-derived stem cells (TDSCs).ResultsFailed-repair stump tissue showed cellular accumulation of crumpled and disoriented collagen fibres. Compared with normal tendon, stump tissue had significantly higher gene expression of collagens I and III, matrix metalloproteinases (MMPs), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and insulin-like growth factor (IGF). The stump TDSCs presented both mesenchymal stem and haematopoietic cell markers with significantly increased expression of CD34, CD44, and CD90 markers. Stump TDSCs exhibited similar migration but a lower proliferation rate, as well as similar osteogenic differentiation but a lower chondrogenic/adipogenic differentiation capability, compared with normal TDSCs. Stump TDSCs also showed increasing levels of SRY-box 2 (Sox2), octamer-binding transcription factor 4 (Oct4), tenomodulin (TNMD), and scleraxis (Scx) protein and gene expression.ConclusionWe found that a failed repair stump had increased cellularity that preserved both mesenchymal and haematopoietic stem cell characteristics, with higher collagen synthesis, MMP, and growth factor gene expression. This study provides evidence that tendon stump tissue has regenerative potential.Cite this article: C-C. Lu, T. Zhang, R. L. Reisdorf, P. C. Amadio, K-N. An, S. L. Moran, A. Gingery, C. Zhao. Biological analysis of flexor tendon repair-failure stump tissue: A potential recycling of tissue for tendon regeneration. Bone Joint Res 2019;8:232-245. DOI: 10.1302/2046-3758.86.BJR-2018-0239.R1.

Dataset Information

Evidence that interfibrillar load transfer in tendon is supported by small diameter fibrils and not extrafibrillar tissue components.

Publications

Evidence that interfibrillar load transfer in tendon is supported by small diameter fibrils and not extrafibrillar tissue components.

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