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WIREs Syst Biol Med
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A conceptual framework for computational models of Achilles tendon homeostasis

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Computational modeling of tendon lags the development of computational models for other tissues. A major bottleneck in the development of realistic computational models for Achilles tendon is the absence of detailed conceptual and theoretical models as to how the tissue actually functions. Without the conceptual models to provide a theoretical framework to guide the development and integration of multiscale computational models, modeling of the Achilles tendon to date has tended to be piecemeal and focused on specific mechanical or biochemical issues. In this paper, we present a new conceptual model of Achilles tendon tissue homeostasis, and discuss this model in terms of existing computational models of tendon. This approach has the benefits of structuring the research on relevant computational modeling to date, while allowing us to identify new computational models requiring development. The critically important functional issue for tendon is that it is continually damaged during use and so has to be repaired. From this follows the centrally important issue of homeostasis of the load carrying collagen fibrils within the collagen fibers of the Achilles tendon. Collagen fibrils may be damaged mechanically—by loading, or damaged biochemically—by proteases. Upon reviewing existing computational models within this conceptual framework of the Achilles tendon structure and function, we demonstrate that a great deal of theoretical and experimental research remains to be done before there are reliably predictive multiscale computational model of Achilles tendon in health and disease. WIREs Syst Biol Med 2013, 5:523–538. doi: 10.1002/wsbm.1229

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Diagram to illustrate interaction of cells and association with collagen fiber bundles (cylinders); two cells are shown longitudinally (lower cells), and two laterally. Collagen bundles are enclosed by lateral cell processes and passed from cell to cell longitudinally.
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Confocal microscope image of a fluorescein‐stained surface from a mature New Zealand white rabbit Achilles tendon, which has been cut through with a sharp scalpel and imaged. White arrows show collagen fibers, while the faintly visible lines within the collagen fibers are comprised of groups of collagen fibrils. Image size: width and height 750 µm. (Confocal image by Dr. Ping Wu)
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The organization of tendon structure from collagen fibrils to the entire tendon. Note that collagen fibrils are comprised of polymerized tropocollagen mers.
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View of a section of an aggregate generated with rods composed of a single elastomeric domain of length 20 units and diameter 1 unit, using KT = 20 and X = 1000. Orange arrows indicate the direction of lateral surface diffusion for a newly accreted rod (red) that drive the minimization of exposed hydrophobic surface.
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Decorin interacts with collagen and regulates collagen fibrillogenesis in vivo. (a) Three‐dimensional model of decorin interacting with a triple helix of collagen (yellow). The concave surface of decorin is lined by charged residues with basic and acidic amino acid residues in blue and red, respectively. (b) Electron micrograph showing abnormal collagen fibers from the dermis of a decorin null mouse. Notice the variability in cross‐sectional diameter and the irregular contours because of abnormal lateral fusion of small fibrils into larger ones along their major axes.
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Schematic diagram of damage mechanism that underlies tendon fatigue. Initial fatigue loading lengthens the fibers from the crimped (a) to the uncrimped (b) state. Continued loading causes stretching of a local population of fibers into their plastic range of deformation (c, dashed line), resulting in the formation of kinked fiber deformation patterns. Further loading leads to rupture of the plastically deformed fibers (d, dotted line). Subsequently, loading is assumed by the surviving, intact fibers with longer lengths and/or higher fatigue quality (dashed line).
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(a) Untransformed model; (b) planar crimp model; (c) helically transformed model; and (d) helically transformed model combined with planar crimp. The top models show the full mesh while bottom models show just the fibrils with the matrix material removed.
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Examples of the three morphological tenocyte types reported in equine digital tendons: (a) type 1 cells with long, spindle‐shaped nuclei; (b) type 2 cells with plump, cigar‐shaped nuclei; and (c) chondrocyte‐like type 3 cells, typically found in ‘wrap around’ regions of tendons where the matrix is fibro‐cartilaginous. Stain haematoxylin and eosin (magnification ×400).
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Blanche Capel

Blanche Capel

earned her Ph.D. at the University of Pennsylvania and has been at Duke University since 1993. She earned her endowed professorship, the James B. Duke Professor of Cell Biology, for the meaningful discoveries she has made since her postdoctoral work in genetics at the National Institute for Medical Research in London. The broad goal of the research in Dr. Capel’s laboratory is to characterize the cellular and molecular basis of morphogenesis – how the body forms. She uses gonadal (gender/sex) development in the mouse as her model system and investigates a gene she helped discover, Sry, the male sex determining gene. Gonad development is unique in that a single rudimentary tissue can be induced to form one of two different organs, an ovary or testis, and she is learning all she can about this central mystery of biology.

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