Nature’s hierarchical materials

Tendon disorders are frequent and are responsible for substantial morbidity both in sports and in the workplace. Tendinopathy, as opposed to tendinitis or tendinosis, is the best generic descriptive term for the clinical conditions in and around tendons arising from overuse. Tendinopathy is a difficult problem requiring lengthy management, and patients often respond poorly to treatment. Preexisting degeneration has been implicated as a risk factor for acute tendon rupture. Several physical modalities have been developed to treat tendinopathy. There is limited and mixed high-level evidence to support the, albeit common, clinical use of these modalities. Further research and scientific evaluation are required before biological solutions become realistic options.

http://health120years.com/cn/pdf/hd_tendonopathy_tendinosis_healing_repair.pdf

Tendon injury and tendinopathy: healing and repair.

Mechanobiology of tendon

Tendon disorders are frequent, and are responsible for much morbidity both in sport and the workplace. Although the presence of degenerative changes does not always lead to symptoms, pre-existing degeneration has been implicated as a risk factor for acute tendon rupture. The term tendinopathy is a generic descriptor of the clinical conditions in and around tendons arising from overuse. The terms "tendinosis" and "tendinitis/tendonitis" should only be used after histopathological examination. Disordered healing is seen in tendinopathy, and inflammation is not typically seen. In acute injuries, the process of tendon healing is an indivisible process that can be categorized into three overlapping phases for descriptive purposes. Tendon healing can occur intrinsically, via proliferation of epitenon and endotenon tenocytes, or extrinsically, by invasion of cells from the surrounding sheath and synovium. Despite remodeling, the biochemical and mechanical properties of healed tendon tissue never match those of intact tendon. Tendon injuries account for considerable morbidity, and often prove disabling for several months, despite what is considered appropriate management. Chronic problems caused by overuse of tendons probably account for 30% of all running-related injuries, and the prevalence of elbow tendinopathy in tennis players can be as high as 40%. The basic cell biology of tendons is still not fully understood, and the management of tendon injury poses a considerable challenge for clinicians. This article describes the structure of tendons, and reviews the pathophysiology of tendon injury and healing.

Biology of tendon injury: healing, modeling and remodeling

Constitutive equations for fibrous connective tissues

A revised morphological model for the crimp structure of tendon is presented. The 300-500 mu diameter tendons of the mature rat tail are comprised of from one to more than ten substructures, called fascicles, of 80-320 mu diameter. Fascicles each possess a "crimp structure" demonstrable in the polarizing microscope and neighboring fascicles within a tendon usually exhibit crimp registry. The fascicle itself is shown to be a cylindrical array of planar-zig-zag crimped 500-5000 A diameter collagen fibrils. The approximate cylindrical symmetry of the fascicle is domonstrated by SEM not equal to and polarizing optical microscopy. A method of replacing native water with other liquids of refractive index near to that of collagen is utilized to reduce or eliminate light diffusion and therby greatly improve OM observations. Small bunches of collagen fibrils removed from the tendon are shown to exhibit the simple planar zig-zag morphology described in previous literature. The planar crimping of collagen fibrils and their assemblage into cylindrically symmetric fascicles is verified by small angle X-ray diffraction.

The Multicomposite Structure of Tendon

A structural mechanical model for tendon crimping.

Mechanical and structural changes in rat tail tendon induced by alloxan diabetes and aging

Tensile behavior over the temperature range 4.2 to 350°K is reported for amorphous polyethylene terephthalate and polycarbonate. Three regimes in tensile behavior are distinguished and the transitions between these regimes are correlated with molecular relaxation processes. The [dtilde]-process at about 50°K is associated with the onset of anelasticity in the stress strain behavior. Below the β-temperature, fracture stresses fall off markedly with decreasing temperature, suggesting that stress concentration effects are active. The effect of the [dtilde]-relaxation on tensile properties is more pronounced in polycarbonate than in polyethylene terephthalate and agrees with the relative relaxation peak intensities. Over the gamma relaxation region, 170 to 200°K, there occurs a broad drop in yield stress in polycarbonate. In polyethylene terephthalate a transition from brittle to yield behavior is observed. Crazing occurs in both polymers over two distinct temperature regimes, one over an approximate...

J. Kastelic

Papers

The Multicomposite Structure of Tendon

A structural mechanical model for tendon crimping.

Mechanical and structural changes in rat tail tendon induced by alloxan diabetes and aging

Crazing, yielding, and fracture in polycarbonate and polyethylene terephthalate at low temperatures

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