Tendinopathy: Difference between revisions
(Created page with "This is a page about tendinopathy") |
No edit summary |
||
| Line 1: | Line 1: | ||
This is a | ==Pathology== | ||
[[File:Reactive on degenerative tendinopathy.jpg|thumb|right|‘Reactive-on-degenerative’ tendinopathy.{{#pmid:27127294|cook2016}}]] | |||
There are profound changes in tendon structure in tendinopathy. In tendinopathy there is loss in capacity to take load through an area of degeneration. This leads to difficulty in stimulating any reparative response. | |||
It isn't possible to tear normal collagen. With tendon rupture there is rupture of highly degenerative tendon without much normal tissue. Therefore without a collagen tearing response, there is no bleeding response, and without bleeding there is no inflammatory response. | |||
inflammation occurs in tendinopathy, however it is low grade. There are a few inflammatory cells peri-vascularly, and also some inflammatory mediators that are possibly produced by tenocytes and visiting cells. Inflammation is unlikely to be the prime driver of pathology or pain, and in the past when management was directed at this, outcomes were poor. While with rupture or bleeding in a tendon, inflammation ''is'' a prime driver. | |||
The tendon cells, called tenocytes, are intimately connected to collagen and are sensitive and responsive to matrix load. The mechano-set point of the cell is dependent on the load that is placed on it, and this can be up- or down-regulated, with positive and negative responses. | |||
Degenerative tendinopathy is a terminal state and cannot be recovered. In early stages of tendon pathology it is reversible, however once the tissue is in a non-load bearing state, there is no capacity to repair. A tendon with degeneration will also have an area of normal tendon. So with rehabilitation when there is overload placed only on the normal tendon, a reactive change occurs in the normal tendon. This is called reactive on degenerative tendinopathy. | |||
==Further Reading== | |||
*Open access article on the continuum model of tendon pathology by Cook et al.<ref name="cook2016"/> | |||
[[Category:Tendinopathies]] | |||
Revision as of 15:52, 28 June 2021
Pathology
There are profound changes in tendon structure in tendinopathy. In tendinopathy there is loss in capacity to take load through an area of degeneration. This leads to difficulty in stimulating any reparative response.
It isn't possible to tear normal collagen. With tendon rupture there is rupture of highly degenerative tendon without much normal tissue. Therefore without a collagen tearing response, there is no bleeding response, and without bleeding there is no inflammatory response.
inflammation occurs in tendinopathy, however it is low grade. There are a few inflammatory cells peri-vascularly, and also some inflammatory mediators that are possibly produced by tenocytes and visiting cells. Inflammation is unlikely to be the prime driver of pathology or pain, and in the past when management was directed at this, outcomes were poor. While with rupture or bleeding in a tendon, inflammation is a prime driver.
The tendon cells, called tenocytes, are intimately connected to collagen and are sensitive and responsive to matrix load. The mechano-set point of the cell is dependent on the load that is placed on it, and this can be up- or down-regulated, with positive and negative responses.
Degenerative tendinopathy is a terminal state and cannot be recovered. In early stages of tendon pathology it is reversible, however once the tissue is in a non-load bearing state, there is no capacity to repair. A tendon with degeneration will also have an area of normal tendon. So with rehabilitation when there is overload placed only on the normal tendon, a reactive change occurs in the normal tendon. This is called reactive on degenerative tendinopathy.
Further Reading
- Open access article on the continuum model of tendon pathology by Cook et al.[1]
