Preventing Tendon Injury in the Horse
By: Mila Bon, July, 2014
It is generally agreed that tendons sustain cumulative microdamage for undefined periods of time prior to rupture, implying that there is a ‘window of opportunity’ for intervention as stated by Patterson-Kane et al. (2012).
#1 Physical stress, #2 hyperthermia and #3 hypoxia (reduced oxygen supply, in this case due to reduced perfusion) are listed as the main factors in initial tendon injury.
In vitro studies and cultured studies differ in the fact that the number of tenocytes (tendon cells) in cultured systems does not change while the more stress is put on a tendon in vivo, the more it is indiced to replicate tenocytes and grow stronger to adjust to the stresses (Patterson-Kane et al., 2012), as healthy living tissue tends to do under favourable circumstances.
Under normal circumstances tenocytes are subjected to cyclical strain, but mechanical overstimulation of tenocytes initiates micro-damage (Patterson-Kane et al., 2012). The 'continuum of tendon pathology' proposed by Cook and Purdam (2009) shows the progression of the tendon pathology which starts as a healthy tendon adapting to the stresses put upon until tenocytes are no longer able to react appropriately and progress from dysrepair to irreversible degeneration and weaken the tendon matrix.
On the other side, as noted in Paterson-Kane (2012) stress deprivation has been shown to have similar effect and results in inappropriate cellular degradative activity in response to reduced mechanical stimulation. So does understimulation, for instance due to uneven loading.
Somewhere in the middle must lay the answer to how tendons adapt to cyclic stresses. According to the Patterson-Kane (2012) review, this is not only different per tendon location, it also relates to the age of the animal (or human for that matter), the degree of strain, whether is is uniaxial (one direction) or biaxial (two directions) etc. Type I Collagen synthesis is consistent with tenocyte activity. But excessive strain in rabbit tendons has been shown to make tendon specific stem-cells or progenitor cells (TSPCs) enriched for markers of adipocytes, chondrocytes or osteocytes (instead of tenocytes!), which would explain the calcification and mucinous matrix formation which changes the tendon matrix.
Apoptosis (programmed cell death*) has been detected in mechanical over and under stimulation, which precedes rupture. Tendon microdamage usually lacks inflammatory cells. Paterson-Kane (2012) attributes that to failure to see the very earliest lesions, but if phagocytic cells are able to destroy apoptic bodies without causing an inflammatory reaction then to me that would be a better explanation.
*During apoptosis, a cell triggers a process that will allow it to "commit suicide." In this process, the cell undergoes a reduction in size as its cellular components break down and condense. Bubble shaped balls called blebs appear on the surface of the cell. The cell then breaks down into smaller fragments called apoptotic bodies. These fragments are enclosed in membranes so as not to harm near-by cells. Other cells, known as phagocytic cells, engulf and destroy the apoptotic bodies without causing an inflammatory reaction (about.biology.com).
This makes me wonder if at this point enough rest would still be sufficient and what happens if apoptosis occurs due to mechanical understimulation, would exercise still be able to reverse the damage? or is apoptosis irreversible? Which wouldn't necessarily mean that further damage would occur, I guess it makes it more likely that it will occur sometime in the future?
By: Mila Bon
References:
about.biology.com, page available at: http://biology.about.com/cs/cellbiology/a/aa031204a.htm
Cook, J.L., Purdam, C.R., (2009). Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British Journal of Sports Medicine, 43, 409e416.
Patterson-Kane, J.C., Becker, D.L., Rich, T., 2012. The Pathogenesis of Tendon Microdamage in Athletes: the Horse as a Natural Model for Basic Cellular Research. Journal of Comparative Pathology, 2012, Vol.147(2-3), pp.227-247
It is generally agreed that tendons sustain cumulative microdamage for undefined periods of time prior to rupture, implying that there is a ‘window of opportunity’ for intervention as stated by Patterson-Kane et al. (2012).
#1 Physical stress, #2 hyperthermia and #3 hypoxia (reduced oxygen supply, in this case due to reduced perfusion) are listed as the main factors in initial tendon injury.
In vitro studies and cultured studies differ in the fact that the number of tenocytes (tendon cells) in cultured systems does not change while the more stress is put on a tendon in vivo, the more it is indiced to replicate tenocytes and grow stronger to adjust to the stresses (Patterson-Kane et al., 2012), as healthy living tissue tends to do under favourable circumstances.
Under normal circumstances tenocytes are subjected to cyclical strain, but mechanical overstimulation of tenocytes initiates micro-damage (Patterson-Kane et al., 2012). The 'continuum of tendon pathology' proposed by Cook and Purdam (2009) shows the progression of the tendon pathology which starts as a healthy tendon adapting to the stresses put upon until tenocytes are no longer able to react appropriately and progress from dysrepair to irreversible degeneration and weaken the tendon matrix.
On the other side, as noted in Paterson-Kane (2012) stress deprivation has been shown to have similar effect and results in inappropriate cellular degradative activity in response to reduced mechanical stimulation. So does understimulation, for instance due to uneven loading.
Somewhere in the middle must lay the answer to how tendons adapt to cyclic stresses. According to the Patterson-Kane (2012) review, this is not only different per tendon location, it also relates to the age of the animal (or human for that matter), the degree of strain, whether is is uniaxial (one direction) or biaxial (two directions) etc. Type I Collagen synthesis is consistent with tenocyte activity. But excessive strain in rabbit tendons has been shown to make tendon specific stem-cells or progenitor cells (TSPCs) enriched for markers of adipocytes, chondrocytes or osteocytes (instead of tenocytes!), which would explain the calcification and mucinous matrix formation which changes the tendon matrix.
Apoptosis (programmed cell death*) has been detected in mechanical over and under stimulation, which precedes rupture. Tendon microdamage usually lacks inflammatory cells. Paterson-Kane (2012) attributes that to failure to see the very earliest lesions, but if phagocytic cells are able to destroy apoptic bodies without causing an inflammatory reaction then to me that would be a better explanation.
*During apoptosis, a cell triggers a process that will allow it to "commit suicide." In this process, the cell undergoes a reduction in size as its cellular components break down and condense. Bubble shaped balls called blebs appear on the surface of the cell. The cell then breaks down into smaller fragments called apoptotic bodies. These fragments are enclosed in membranes so as not to harm near-by cells. Other cells, known as phagocytic cells, engulf and destroy the apoptotic bodies without causing an inflammatory reaction (about.biology.com).
This makes me wonder if at this point enough rest would still be sufficient and what happens if apoptosis occurs due to mechanical understimulation, would exercise still be able to reverse the damage? or is apoptosis irreversible? Which wouldn't necessarily mean that further damage would occur, I guess it makes it more likely that it will occur sometime in the future?
By: Mila Bon
References:
about.biology.com, page available at: http://biology.about.com/cs/cellbiology/a/aa031204a.htm
Cook, J.L., Purdam, C.R., (2009). Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British Journal of Sports Medicine, 43, 409e416.
Patterson-Kane, J.C., Becker, D.L., Rich, T., 2012. The Pathogenesis of Tendon Microdamage in Athletes: the Horse as a Natural Model for Basic Cellular Research. Journal of Comparative Pathology, 2012, Vol.147(2-3), pp.227-247