Role of Ossification In Bone Remodeling
Does the mineralization process in bone tissue have any role in remodeling of bone to race appropriate fracture resistance? Having done a fair amount of reading of what's available on the Internet, I'm able to report that, as expected, the process is complex, and that in terms of FR has yet to be looked at in equines or humans.
There are several questions that occur:
1. Is there a certain ideal state of calcification for FR? Another way to pose the question: is bone stronger or weaker due to amount or quality of calcification at the cellular level?
2. If there is a desired calcification or ossification, can this be influenced in any way by what we do with the horse?
Answering these questions requires an amount of technical knowledge, and I will attempt in the next posts to supply some of this for anyone interested. Let me begin this by noting that perhaps when the average horse person considers cannon bone strength and the ability of that bone to withstand the stress of a race, probably what goes through one's mind is that somehow in our training regimen ossification has done its work and we have a stronger bone? But, is this really what happens? Hopefully this question will be answered here shortly.
Begin the discussion by stating two crucial facts: 1. it looks to me as if bone mineralization, which begins in the fetus, reaches a preordained state of maturity, BUT thereafter maintains an equilibrium between construction and destruction. It is this process of maintaining the equilibrium that we need to look at in terms of whether this can be (or is) influenced by concussive stress. 2. The discussion requires an understanding of bone collagen, the qualities of bone collagen, where bone collagen exists within the bone tissue, and, most important, that bone collagen cells actually produce or "excrete" the calcium salts that become the bone matrix!
Before proceeding with this, I'd like to include a few videos which contain info necessary to fully understand what is going on:
x
Training:
Sat: 10/31: riderless fast in deep mud.
Sun: 11/1: riderless fast in deep mud. Both colts were walked under tack for 10 min.
Mon: 11/2: riderless in medium mud for 10 min. Art was trot walked under tack for 1 mile. Rod's front right leg blew up-knee to fetlock. Lot's of swelling. We're concerned about a suspensory pull from the mud.
Tues. 11/3: Art walk-trot-galloped 1.25 miles. Rod's leg is treated with furosome -saran wrap to create heat.
Wed. 11/4: Art trot-galloped 1.6 miles. First time in at least 1.5 months we've been able to use our track. Rod: dodged a bullet as the swelling in front right has completely disappeared. If I looked closely enough at that leg I'd probably see some bite marks. Both horses did a fast pasture romp (which I wanted to avoid), but Rod's injured leg survived!
There are several questions that occur:
1. Is there a certain ideal state of calcification for FR? Another way to pose the question: is bone stronger or weaker due to amount or quality of calcification at the cellular level?
2. If there is a desired calcification or ossification, can this be influenced in any way by what we do with the horse?
Answering these questions requires an amount of technical knowledge, and I will attempt in the next posts to supply some of this for anyone interested. Let me begin this by noting that perhaps when the average horse person considers cannon bone strength and the ability of that bone to withstand the stress of a race, probably what goes through one's mind is that somehow in our training regimen ossification has done its work and we have a stronger bone? But, is this really what happens? Hopefully this question will be answered here shortly.
Begin the discussion by stating two crucial facts: 1. it looks to me as if bone mineralization, which begins in the fetus, reaches a preordained state of maturity, BUT thereafter maintains an equilibrium between construction and destruction. It is this process of maintaining the equilibrium that we need to look at in terms of whether this can be (or is) influenced by concussive stress. 2. The discussion requires an understanding of bone collagen, the qualities of bone collagen, where bone collagen exists within the bone tissue, and, most important, that bone collagen cells actually produce or "excrete" the calcium salts that become the bone matrix!
Before proceeding with this, I'd like to include a few videos which contain info necessary to fully understand what is going on:
x
Training:
Sat: 10/31: riderless fast in deep mud.
Sun: 11/1: riderless fast in deep mud. Both colts were walked under tack for 10 min.
Mon: 11/2: riderless in medium mud for 10 min. Art was trot walked under tack for 1 mile. Rod's front right leg blew up-knee to fetlock. Lot's of swelling. We're concerned about a suspensory pull from the mud.
Tues. 11/3: Art walk-trot-galloped 1.25 miles. Rod's leg is treated with furosome -saran wrap to create heat.
Wed. 11/4: Art trot-galloped 1.6 miles. First time in at least 1.5 months we've been able to use our track. Rod: dodged a bullet as the swelling in front right has completely disappeared. If I looked closely enough at that leg I'd probably see some bite marks. Both horses did a fast pasture romp (which I wanted to avoid), but Rod's injured leg survived!
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