So, the tib post tendon connects the tib post muscle, deep in the back of the lower leg, to the bottom of the foot.
It's like a long stiff spring. It absorbs shock, along with several other tendons/springs in the lower leg and foot.
For the tendon to absorb force and spring back, it needs the tib post muscle to contract at exactly the right time, contract/squeeze hard and give the tendon/spring something to anchor to. Two things there: it needs a healthy set of receptors in the foot to send a signal back that it's time to contract/squeeze the tib post muscle; and, it needs a healthy, strong tib post muscle.
In addition to healthy receptors and healthy tib post muscle, the tendon must have structure that tolerates forces that can be from 2 to 10 times your bodyweight.
This structure is like a series of strong cables (collagen fibres) held together by pliable glue (ground substance). Stationed along those cables, within the pliable glue, are tendon cells that are ready to rebuild when necessary.
What can go wrong? First, the health of the receptors is secondary to having mobility in the joints of the foot. When your foot hits the ground, the bones move, the ligaments, tendons and muscles that hold those bones together stretch. Inside the ligaments, tendons and muscles are special tissues that detect lengthening - they send a superfast signal back to the spinal cord that activates a nerve to send a signal back down the leg to the muscles attached to those tendons - they are activated to squeeze and pull back against the stretch of the tissue - this process relies on bones having the ability to subtly move so the movement can be detected. It also relies on not having pain that might interrupt the signal. It also relies on having a healthy nervous system up in the spinal cord, to send a signal back down, and it relies on having foot muscles that have the capacity to squeeze hard enough to counteract the stretching force of 2-10 times your bodyweight.
The difference in force, between 2 and 10 times your bodyweight is because some activities are low shock and others are high shock (like hopping down from a box).
When the muscles contract, it provides a strong anchor for the tendon at one end. At the other end is the bone that's moving - the tendon usually has the flexibility to elongate approximately 2% only of its resting length. So the tibialis posterior tendon is long, very long (from under the foot to up in the middle of the calf area). A 2% lengthening, at most, is not very much. Most of the stretch happens in the muscle attached to it. IF you get a lot of stretch, the whole muscle/tendon length gets longer - this looks like a foot and ankle collapsing forwards and inwards (dorsiflexion and eversion at the ankle and mid-foot). If you don't get a lot of stretch, the ankle collapses much less then springs back. The way to get not a lot of stretch is to have healthy foot receptors to send a signal and a strong tib post muscle to squeeze hard.
Progressively, as our bodyweight increases over our life, and we run and jump and hop, the muscles and tendons get strong and can tolerate those forces. Sometimes physiology gets in the way and it affects load tolerance. Some examples of what might affect it - increased bodyweight (more load than it's used to), periods of inactivity (the body loses some load tolerance), belly fat can affect tendon health, fatigue can affect muscle contraction ability to pre-tension the tendon.
When the body suffers a load that is higher than it cope with, the tendon cells wake up and get to work. Normally, the pliable glue that holds the tendons together contains a protein called Decorin. Most of the pliable glue, called ground substance, is called decorin. Tendon cells that suffer an acute overload might be signalled to produce a different protein called Aggrecans. Aggrecans is a key protein in cartilage and is hydrophilic, meaning it attracts water around it. In cartilage that is beneficial for "plumping" up the structural matrix that gives joint cartilage low friction and shock absorption characteristics. In tendons, a pliable glue/ground substance that has a protein spewed out by tendon cells that attracts water is not good - it causes the tendon to thicken - the ground susbtance thickens and the cable-like collagen fibres get pushed apart, losing connection with other and structural strength. The water that is attracted by aggrecans is not inflammatory fluid, just fluid. It doesn't have inflammatory cells in it. When the tendon suffers an acute overload and the tendon cells spew out aggrecans, the tendon thickens. The goal is to stop them spewing out aggrecans as soon as possible. There are some known substances that inhibit the tendon cells (known as tenocytes) from spewing out aggrecans - they are called tenocyte inhibitors and include three main ones - ibuprofen, green tea and doxycyclin. I think indocid might be another tenocyte inhibitor - I'd have to check that. These substances are primarily used for for other purposes, but interestingly they also inhibit tenocytes. So, ibuprofen is an anti-flammatory that works on tendon cells for a reason not related to inflammation. Green tea inhibits tendon cells from spewing aggrecans in a way that is unrelated to why most people drink green tea. I'm not sure if it's an anti-oxidant process or not. Doxycycline is an anti-biotic but it has an effect on tendon cells like the other two.
The window of opportunity for these three substances to effect the tenocyte is very small - as soon as you have an overload and notice tendon starting to thicken/swell, that's when you have to act. After it's already thickened it's too late. Interestingly, those who've taken these (especially green tea) after the tendon has already thickened tend to get good pain relief anyway so there's clearly some as yet unclear effect of it.
Now, we trust the body to re-model that tendon after the tenocyte has dumped aggrecans into its ground substance and pushed those collagen fibres apart. We trust it to do it, but it needs to happen under a minimum of good conditions. These conditions include not continuing to overload it and cause the tenocytes to keep spewing, and then applying some load to stimulate the collagen fibres to line back up straight. Tendons don't like being unloaded more than a couple of days - they need stimulus to remodel properly.
Now, there's another couple of points of consideration. Sometimes the ability of the tendon to remodel is limited, the damage is done. It can repair up to a point and will tolerate load up to a point. This can be helped by having foot joints that are supple and having a tib post muscle that is very strong.
The other point is that sometimes the tendon is less of a problem than the sheath that surrounds it - it can get irritated, by rubbing against bone and other tissues as the foot/ankle collapses. The irritation can cause the inner lining of the sheath (synovium) to react - this is what leads to sheath inflammation. So, you can have inflammation in the sheath (with inflammatory cells and fluid) and reactive processes inside the tendon itself with fluid that is not inflammatory. In the very early period after acute overload (first 1-2 days) an anti-inflammatory like ibuprofen might work on both the sheath and tendon. After a couple of days, the ibuprofen won't work on the tendon but might work on the sheath. Sheath inflammation is called tenosynovitis. Green tea can work on the tendon early on, and often after the damage is done - in the experience of my clients. A key element is revealing contributing factors - foot/ankle joint mobility dysfunction, tib post strength, and recognition of current state of reactivity of tendon and sheath, and subsequently load tolerance of the whole lower limb.
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