Aetiology
The aetiology of tendinopathy is not clear.[7][8][9] While multiple factors including age, genetics, body weight, dysregulated metabolism, individuals prone to pro-inflammatory states, and muscle weakness are believed to be involved, repetitive mechanical loading of tendons is considered to be the major risk factor in the development of tendinopathy.[16][17][18]
Tendons serve several functions including mechanical force transmission, joint stabilisation, and shock absorption to limit muscle damage. Tendons consist of collagens, proteoglycans, glycoproteins, water, and cells. They are able to alter their structure and composition in response to mechanical loads. While appropriate mechanical loading of tendons is beneficial, over-use (chronic, repetitive mechanical loading placed on tendons) may result in pathological changes.[4][16][19]
Pathophysiology
The pathogenesis of tendinopathy continues to be debated. Mechanical over-use most probably results in tendon degeneration and leads to cell phenotype changes and neovascularisation. Changes in cell phenotype are characterised by an increased number of round cells that produce more type III collagen than type I collagen. Type III collagen is thinner and less capable of forming bundles than type I collagen. There is also an increase in the larger proteoglycans such as aggrecan.
This combination leads to tendon structure disruption and a reduction in the ability of the tendon to absorb mechanical loads. Neovascularisation represents a healing process of injured tendons. However, the newly generated vessels and nerves may be a source of pain related to tendinopathy.[20][21][22] The loss of matrix integrity, tendon disruption, and neovascularisation support the hypothesis that tendinopathy is a failed healing process resulting in a painful, vascularised, and biomechanically inferior tendon.[5] Certain patients with dysregulated metabolisms or who are prone to pro-inflammatory states, such as those with type 2 diabetes, may be subject to increasingly impaired tendon healing and higher rates of tendinopathy.[18]
In summary, tendon degeneration is characterised by collagen fragmentation, loss of collagen orientation, alterations in the biochemical composition, increased levels of proteoglycans, and decreased enzyme activity.
Classification
Shoulder
Rotator cuff tendinopathy
Elbow
Lateral epicondylitis
Medial epicondylitis
Knee
Patellar tendinopathy:
Stage 1: pain after activity
Stage 2: pain at the beginning of activity that disappears after warm-up
Stage 3: constant pain during activity
Stage 4: tendon rupture.
Quadriceps tendinopathy
Ankle
Achilles' tendinopathy
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