Multiscale molecular interactions of tendon

Little, Dianne

doi:10.1080/03008207.2018.1514801

Cited by 1 publication

(1 citation statement)

References 11 publications

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“…This increase has led to definitions of tendinopathy that implicate a wide variety of factors including accumulated damage [2,22,23], altered ECM [15,24], decreased time to heal [2,[25][26][27], and increased cell number and cell rounding [13,28,29]. More recently, research has identified other possible factors, such as metabolic disease [12,30], age [22,31], tendon compression [32,33], tendon location or function [34], and genetics [22] as possible additions to this list. One perspective regarding the reparability of tendon separates tendon into two discrete parts, intrinsic and extrinsic compartments, that perform different, but coordinated functions during tendon healing [12].…”

Section: Introductionmentioning

confidence: 99%

Tendinopathy and tendon material response to load: What we can learn from small animal studies

et al. 2021

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Tendinopathy is a debilitating disease that causes as much as 30% of all musculoskeletal consultations. Existing treatments for tendinopathy have variable efficacy, possibly due to incomplete characterization of the underlying pathophysiology. Mechanical load can have both beneficial and detrimental effects on tendon, as the overall tendon response depends on the degree, frequency, timing, and magnitude of the load. The clinical continuum model of tendinopathy offers insight into the late stages of tendinopathy, but it does not capture the subclinical tendinopathic changes that begin before pain or loss of function. Small animal models that use high tendon loading to mimic human tendinopathy may be able to fill this knowledge gap. The goal of this review is to summarize the insights from in-vivo animal studies of mechanically

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