Achilles Tendon Disorders: Etiology and Epidemiology

Department of Orthopaedic Surgery, Tampere University Hospital, Tampere, Finland.
Foot and Ankle Clinics of North America (Impact Factor: 0.76). 07/2005; 10(2):255-66. DOI: 10.1016/j.fcl.2005.01.013
Source: PubMed

ABSTRACT The Achilles tendon is the strongest tendon in the human body. Because most Achilles tendon injuries take place in sports and there has been a general increase in popularity of sporting activities, the number and incidence of the Achilles tendon overuse injuries and complete, spontaneous ruptures has increased in the industrialized countries during the last decades. The most common clinical diagnosis of Achilles overuse injuries is tendinopathy. The basic etiology of the Achilles tendinopathy is known to be multi-factorial. Although histopathologic studies have shown that ruptured Achilles tendons have clear degenerative changes before the rupture, many Achilles tendon ruptures take place suddenly without any preceding signs or symptoms.

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    • "Achilles tendinopathy, including tendon rupture, occur at a rate of about 250,000 per year in the US alone (Jarvinen et al., 2005; Pennisi, 2002). The mechanism of tendinopathy and rupture is complex and thought to be influenced by tendon geometry, material-strength, sex, disease and genetics. "
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    ABSTRACT: Achilles tendon injuries including rupture are one of the most frequent musculoskeletal injuries, but the mechanisms for these injuries are still not fully understood. Previous in vivo and experimental studies suggest that tendon rupture mainly occurs in the tendon mid-section and predominantly more in men than women due to reasons yet to be identified. Therefore we aimed to investigate possible mechanisms for tendon rupture using finite element (FE) analysis. Specifically, we have developed a framework for generating subject-specific FE models of human Achilles tendon. A total of ten 3D FE models of human Achilles tendon were generated. Subject-specific geometries were obtained using ultrasound images and a mesh morphing technique called Free Form Deformation. Tendon material properties were obtained by performing material optimization that compared and minimized difference in uniaxial tension experimental results with model predictions. Our results showed that both tendon geometry and material properties are highly subject-specific. This subject-specificity was also evident in our rupture predictions as the locations and loads of tendon ruptures were different in all specimens tested. A parametric study was performed to characterize the influence of geometries and material properties on tendon rupture. Our results showed that tendon rupture locations were dependent largely on geometry while rupture loads were more influenced by tendon material properties. Future work will investigate the role of microstructural properties of the tissue on tendon rupture and degeneration by using advanced material descriptions.
    Journal of Biomechanics 10/2014; 47(15). DOI:10.1016/j.jbiomech.2014.10.001 · 2.75 Impact Factor
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    • "Tensile strain is a major mechanical stimulus that tendons are subjected to, and to which tendons can adapt [4], and adaptive advantageous responses to tensile loading have even been demonstrated in healing tendon tissue [5]. Tendon injuries are a frequent problem and in general, the regeneration process of tendon pathologies is poor and often leads to fibrotic changes and inferior function of the tissue [6], [7], [8], [9], [10]. It has remained largely unknown what role the mechanical environment plays in the activation of catabolic changes of human tendon cells, which might explain the development of pathological changes and complication during the regeneration process. "
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    ABSTRACT: Mechanical loading of tendon cells results in an upregulation of mechanotransduction signaling pathways, cell-matrix adhesion and collagen synthesis, but whether unloading removes these responses is unclear. We investigated the response to tension release, with regard to matrix proteins, pro-inflammatory mediators and tendon phenotypic specific molecules, in an in vitro model where tendon-like tissue was engineered from human tendon cells. Tissue sampling was performed 1, 2, 4 and 6 days after surgical de-tensioning of the tendon construct. When tensile stimulus was removed, integrin type collagen receptors showed a contrasting response with a clear drop in integrin subunit α11 mRNA and protein expression, and an increase in α2 integrin mRNA and protein levels. Further, specific markers for tendon cell differentiation declined and normal tendon architecture was disturbed, whereas pro-inflammatory molecules were upregulated. Stimulation with the cytokine TGF-β1 had distinct effects on some tendon-related genes in both tensioned and de-tensioned tissue. These findings indicate an important role of mechanical loading for cellular and matrix responses in tendon, including that loss of tension leads to a decrease in phenotypical markers for tendon, while expression of pro-inflammatory mediators is induced.
    PLoS ONE 01/2014; 9(1):e86078. DOI:10.1371/journal.pone.0086078 · 3.23 Impact Factor
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    • "Inflamm-aging is a component of immunosenescence which is an age associated decline in immune function, whereby the major cell types of the immune system exhibit age-related changes, resulting in a diminished ability to cope with inflammation [37]. Although tendon pathology and incidence of injury are known to increase in aged individuals [18], [38], the effect of age on the ability to resolve tendon inflammation and the contribution of immunosenescence to the development of disease are not understood. The aims of this study were to assess the temporal and differential alterations in prostaglandin and resolving lipid mediators in normal and naturally injured equine tendons throughout the stages of healing and to determine the effect of age and injury stage on the regulation of prostaglandin metabolism. "
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    ABSTRACT: The contribution of inflammation to the pathogenesis of tendinopathy and high prevalence of re-injury is not well established, although recent evidence suggests involvement of prostaglandins. We investigated the roles of prostaglandins and inflammation-resolving mediators in naturally occurring equine tendon injury with disease stage and age. Levels of prostaglandins E2 (PGE2), F2α (PGF2α), lipoxin A4 (LXA4) and its receptor FPR2/ALX were analysed in extracts of normal, sub-acute and chronic injured tendons. To assess whether potential changes were associated with altered PGE2 metabolism, microsomal prostaglandin E synthase-1 (mPGES-1), prostaglandin dehydrogenase (PGDH), COX-2 and EP4 receptor expression were investigated. The ability of tendons to resolve inflammation was determined by assessing FPR2/ALX expression in natural injury and IL-1β stimulated tendon explants. Alterations in the profile of lipid mediators during sub-acute injury included low PGE2 and elevated LXA4 levels compared to normal and chronic injuries. In contrast, PGF2α levels remained unchanged and were three-fold lower than PGE2. The synthetic capacity of PGE2 as measured by the ratio of mPGES-1:PGDH was elevated in sub-acute injury, suggesting aberrations in tendon prostaglandin metabolism, whilst COX-2 and EP4 receptor were unchanged. Paradoxically low tendon PGE2 levels in early injury may be attributed to increased local clearance via PGDH or the class switching of lipid mediators from the prostaglandin to the lipoxin axis. PGE2 is therefore implicated in the development of tendon inflammation and its ensuing resolution. Whilst there was no relationship between age and tendon LXA4 levels, there was an age-associated decline in FPR2/ALX receptor expression with concurrent increased PGE2 levels in injury. Furthermore, uninjured tendon explants from younger (<10 years) but not older horses (≥10 years) treated with IL-1β responded by increasing FPR2/ALX suggesting aged individuals exhibit a reduced capacity to resolve inflammation via FPR2/ALX, which may present a potential mechanism for development of chronic tendinopathy and re-injury.
    PLoS ONE 11/2012; 7(11):e48978. DOI:10.1371/journal.pone.0048978 · 3.23 Impact Factor
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