The Chronically Inflamed Tendon
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mechanobiology
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Abstract Purpose The unique demands of dance technique make dancers more prone to certain pathologies especially of the foot and ankle. Flexor hallucis longus (FHL) tendinopathy, colloquially known as “dancer’s tendinopathy,” is common in dancers and not well studied. The purpose of this study was to assess if morphological alterations in tendon structure occur as an adaptive response to dance activity by comparing the FHL tendon in dancers to non-dancers, and if pathology further alters tendon morphology in dancers clinically diagnosed with tendinopathy. Methods Three groups of ten participants were recruited (healthy non-dancers, healthy dancers, and dancers with FHL tendinopathy). Ultrasound images of the FHL tendons were analyzed for macromorphology by measuring the tendon thickness. The micromorphology was analyzed by determining the peak spatial frequency radius of the tendon. Our study did find increased tendon proper and composite tendon thickness in dancers with tendinopathy but no difference between asymptomatic dancers and non-dancers. Results There was no significant difference in micromorphology found between any of the groups. As expected, dancers with tendinopathy demonstrated increased composite tendon and tendon proper thickness however, there was no evidence of adaptive thickening of the FHL tendon as might be expected for the dance population. There was also no evidence of micromorphological changes in the presence of clinically diagnosed FHL tendinopathy. Conclusion Because of the limited normative data for this pathology, these results can help improve diagnosis and therefore treatment for dancers to decrease the impact of this injury on their careers.
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Purpose. To review the current concepts on tendon damage and reactive oxygen species (ROS). We suggest that tendons are subject to reactive oxygen generated both within the vicinity of the tendon and from the tenocytes themselves.Method. A literature search was conducted to trace relevant literature on tendon damage and ROS.Results. Tendinopathies have a complex aetiology. Tendon physiology and structure may preclude ROS involvement in various aspects of the predisposition to and participation in a failed healing response process and subsequent response to injury. However, given the ubiquitous nature of ROS production and their now accepted involvement in signal transduction, such highly active chemicals may influence signal transduction in the tendon. Therefore, the tendon is continually exposed to ROS during normal and athletic exercise which, in combination with lifestyle and possibly hereditary factors, may influence tendon integrity and orchestrate tendon repair.Conclusions. The production of ROS by tenocytes may be a response to hyperthermia and to repetitive ischaemia/reperfusion, and may influence the development of tendinopathies.
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Summary While there is a significant amount of information available on the clinical presentation(s) and pathological changes associated with tendinopathy, the precise aetiopathogenesis of this condition remains a topic of debate. Classically, the aetiology of tendinopathy has been linked to the performance of repetitive activities (so‐called overuse injuries). This has led many investigators to suggest that it is the mechanobiologic over‐stimulation of tendon cells that is the initial stimulus for the degradative processes which have been shown to accompany tendinopathy. Although several studies have been able to demonstrate that the in vitro over‐stimulation of tendon cells in monolayer can result in a pattern(s) of gene expression seen in clinical cases of tendinopathy, the strain magnitudes and durations used in these in vitro studies, as well as the model systems, may not be clinically relevant. Using a rat tail tendon model, we have studied the in vitro mechanobiologic response of tendon cells in situ to various tensile loading regimes. These studies have led to the hypothesis that the aetiopathogenic stimulus for the degenerative cascade which precedes the overt pathologic development of tendinopathy is the catabolic response of tendon cells to mechanobiologic under ‐ stimulation as a result of microscopic damage to the collagen fibres of the tendon. In this review, we examine the rationale for this hypothesis and provide evidence in support of this theory.
Tenosynovitis
Stimulus (psychology)
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IntroductionThe exact mechanisms leading to tendinopathies and tendon ruptures remain poorly understood while their occurrence is clearly associated with exercise. Overloading is thought to be a major factor contributing to the development of tendon pathologies. However, as animal studies have shown, heavy loading alone won't cause tendinopathies. It has been speculated, that malfunctioning adaptation or healing processes might be involved, triggering tendon tissue degeneration. By analysing the expression of the entirety of degrading enzymes (degradome) in pathological and non-pathological, strained and non-strained tendon tissue, the aim of this study was to identify common or opposite patterns in gene regulation. This approach may generate new targets for future studies.Materials and MethodsRNA was extracted from different tendon tissues: normal (n=7), tendinopathic (n=4) and ruptured (n=4) Achilles tendon; normal (n=4) and tendinopathic (n=4) posterior tibialis tendon; normal hamstrings tendon with or...
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mechanobiology
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Tendon rupture
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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.
Tendinosis
Tendinitis
Tendonitis
Tennis elbow
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Summary Tendon injuries, often called tendinopathies, are debilitating and painful conditions, generally considered to develop as a result of tendon overuse. The aetiology of tendinopathy remains poorly understood, and whilst tendon biopsies have provided some information concerning tendon appearance in late‐stage disease, there is still little information concerning the mechanical and cellular events associated with disease initiation and progression. Investigating this in situ is challenging, and numerous models have been developed to investigate how overuse may generate tendon fatigue damage and how this may relate to tendinopathy conditions. This article aims to review these models and our current understanding of tendon fatigue damage. We review the strengths and limitations of different methodologies for characterizing tendon fatigue, considering in vitro methods that adopt both viable and non‐viable samples, as well as the range of different in vivo approaches. By comparing data across model systems, we review the current understanding of fatigue damage development. Additionally, we compare these findings with data from tendinopathic tissue biopsies to provide some insights into how these models may relate to the aetiology of tendinopathy. Fatigue‐induced damage consistently highlights the same microstructural, biological and mechanical changes to the tendon across all model systems and also correlates well with the findings from tendinopathic biopsy tissue. The multiple testing routes support matrix damage as an important contributor to tendinopathic conditions, but cellular responses to fatigue appear complex and often contradictory.
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