Basic Science and Clinical Aspects of Achilles Tendinopathy

Department of Trauma and Orthopaedic Surgery, University Hospital Wales, Heath Park Cardiff, UK.
Sports medicine and arthroscopy review (Impact Factor: 1.68). 10/2009; 17(3):190-7. DOI: 10.1097/JSA.0b013e3181b37eb7
Source: PubMed


Achilles tendinopathy is one of the common disorders seen in athletes. It is a degenerative rather than an inflammatory, condition. There is a lifetime risk of 52% in former elite male distance runners. This condition is difficult to manage and up to 29% of Achilles tendinopathy patients may require surgery. It often results in chronic pain and discomfort along with failure to regain full function. It can be complicated by partial tears or complete rupture causing long-term burden on healthcare system and making treatment quite difficult.

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Available from: Nicola Maffulli, Apr 03, 2014
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    • "In the knee area a typical formation of patellofemoral syndrome known as " runner's knee " or patellar tendinitis known as " jumper's knee " and some forms of bursitis could occur. In the shank and foot area we could find a presence of medial tibial stress syndrome and frequent injuries of Achilles tendon (Alfredson, 2003; Järvinen, Kannus, Maffulli, & Khan, 2005; Maffulli, Sharma, & Luscombe, 2004; Zafar, Mahmood, & Maffulli, 2009). For example de Vos et al. (2010) found out that up to 52% of endurance runners hurt their Achilles tendon sometime during their career. "
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    Procedia - Social and Behavioral Sciences 05/2015; 186:618-623. DOI:10.1016/j.sbspro.2015.04.039
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    • "Despite some advancements in the management of acute and chronic tendinopathies, several aspects related to the pathophysiology of human tendons remain largely unclear [1]–[3]. Tendon cells, residing between fibril components mainly represented by collagens and proteoglycans, synthetize extracellular matrix (ECM) [4]–[6]. "
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    ABSTRACT: In vitro models of human tenocytes derived from healthy as well as from ruptured tendons were established, characterized and used at very early passage (P1) to evaluate the effects of Extracorporeal Shock Wave Treatment (ESWT). The molecular analysis of traditional tenocytic markers, including Scleraxis (Scx), Tenomodulin (Tnm), Tenascin-C (Tn-C) and Type I and III Collagens (Col I and Col III), permitted us to detect in our samples the simultaneous expression of all these genes and allowed us to compare their levels of expression in relationship to the source of the cells and treatments. In untreated conditions, higher molecular levels of Scx and Col I in tenocytes from pathological compared to healthy samples have been detected, suggesting - in the cells from injured tendon - the natural trigger of an early differentiation and repairing program, which depends by Scx and requires an increase in collagen expression. When ESWT (at the dose of 0.14 mJ/mm(2)) was applied to cultured tenocytes explanted from injured source, Scx and Col I were significantly diminished compared to healthy counterpart, indicating that such natural trigger maybe delayed by the treatment, in order to promote cellular repair. Herein, we show for the first time that ESWT enhances in vitro functional activities of ruptured tendon-derived tenocytes, such as proliferation and migration, which could probably contributes to tendon healing in vivo.
    PLoS ONE 11/2012; 7(11-11):e49759. DOI:10.1371/journal.pone.0049759 · 3.23 Impact Factor
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    • "In one study of 785 male former elite athletes, their cumulative incidence of AT degeneration or rupture before the age of 45 was five to eight times that of the control population; however, for AT rupture it was up to 15 times that of controls in sprinters specifically (Kujala et al., 2005). Up to 29% of patients with AT injuries may require surgery (Zafar et al., 2009); time for a return to activity varies from 6 weeks to almost 10 months depending on the complexity and chronicity of the injury, and rerupture rates of 2e12% have been reported (Molloy and Wood, 2009; Saxena et al., 2011). The functional equivalence of the SDFT and AT is largely due to their pivotal role in saving energy during high-speed locomotion, by reducing muscular work (Biewener, 1998; Malvankar and Khan, 2011). "
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    ABSTRACT: The equine superficial digital flexor tendon (SDFT) is a frequently injured structure that is functionally and clinically equivalent to the human Achilles tendon (AT). Both act as critical energy-storage systems during high-speed locomotion and can accumulate exercise- and age-related microdamage that predisposes to rupture during normal activity. Significant advances in understanding of the biology and pathology of exercise-induced tendon injury have occurred through comparative studies of equine digital tendons with varying functions and injury susceptibilities. Due to the limitations of in-vivo work, determination of the mechanisms by which tendon cells contribute to and/or actively participate in the pathogenesis of microdamage requires detailed cell culture modelling. The phenotypes induced must ultimately be mapped back to the tendon tissue environment. The biology of tendon cells and their matrix, and the pathological changes occurring in the context of early injury in both horses and people are reviewed, with a particular focus on the use of various tendon cell and tissue culture systems to model these events.
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