The tendon is the part of a muscle that attaches muscle to bone. Ligaments attach bone to bone.
Before attaching onto a bone, the muscle fibres slowing transition from being the contractile, moving proteins that allow muscles to shorten, into densely packed and parallel arranged collagen fibres. Collagen is the most abundant protein in the body, has incredible tensile strength, and can adapt, and grow (or shrink) to response to
the load it experiences. More force = thicker and strong tendon, less force = weaker tendon predisposed to injury
Between the type one collagen fibres that make up the tendon, there is a small amount of water, other material called “ground substance” and a host of tendon cells conveniently called tenocytes (teno= tendon, cytes = cells)
Itis= denotes inflammation of the tendon
Osis = denotes abnormal tendon structure and pathology but without inflammation
Tendon injury is called tendinopathy because it acknowledges the current understanding that these injuries exists on a continuum between inflammation and degenerative non-inflammatory tendon changes. We have moved away from the word tendonitis because inflammation is not the main cause. The tendons are not red, hot and swollen . While inflammation appears to be part of most tendinopathies in terms of its progression and promoting certain tissue changes, the core pathological changes lean towards the non-inflammatory end of the continuum.
With tendinopathy the once nicely, parallel organization of dense and strong collagen fibres, becomes tangled, poorly organized like a ball or yarn, and less able to withstand stress. New tendon cells begin to form and produce massive amounts of disorganized collagen actually producing thickening visible on MRI and ultrasound. There is an increase in the water content of the tendon with more ground substance and non-tensile proteins. Inflammatory cells and chemicals have been found in minute amounts and seem to help to perpetuate these conditions, produce the new growth of nerves, blood vessels and cells, and potentially cause pain.
The growth of blood vessels and nerves into the tendon is what is believed to be the primary cause of pain with tendinopathy. These changes in the structure of the tendon that make it more sensitive to pain (nerves) promote the chronicity of this conditions and make them a challenge to treat.
Over-use, and a failure to allow proper healing and adaptation time is the cause of the majority of tendinopathies. In short, the tendon’s load-bearing capacity is exceeded; molecular and structural changes occur, which reduces subsequent load bearing capacity of the tendon – To much force, too often, too soon, not enough time to heal –
It is suspected that in response to this overload on the tendon, the body undergoes a failed healing response that results in the aforementioned pathological changes.
In some cases, it is believed that under-loading of the tendon, called stress-shielding, results in reactive inflammation, weakening and subsequent injury. In these cases, parts of the tendon, often close to the bone, do not experience tensile force or even compressed. This causes the tendons to swell, enlarge and undergo the aforementioned pathological changes that are visibly the same on MRI and US are those exposed to too much force.
Determining why your tendons are being overloaded with force or experiencing stress-shielding is the key to
stoping the tendinopathy for expediting your care and stop the problem from returning. In most cases, weakness in other muscles around a joint, can result in compensation, directing too much force through a particular muscle. Over time, a failure of other muscles to help can result in overload of the tendon and subsequent injury.
In the case of tennis elbow, a tendinopathy of the common extensor tendon, a combination of improper lifting, weakness of the forearm muscles and even poor stabilization at the shoulder blade and shoulder, can overload the tendon yielding an injury. Until all these issues are corrected, this condition will often be perpetuated.
Any tendon can be subject to tendinopathy and injury. They most commonly happen at the end of the tendon as it inserts into the bone, though they can occur as in the case of mid-substance Achilles tendinopathy
The treatment of a tendon injury is specific to the location of the injury. Nonetheless, some basic principles apply for treatment of these injuries
If you need help with a chronic tendon injury, would like to book a free consultation or have any questions, please leave an inquiry for Dr. Ritza here.
Cook, J. L., and Craig R. Purdam. “Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy.” British journal of sports medicine 43.6 (2009): 409-416.
Rees, Jonathan D., Matthew Stride, and Alex Scott. “Tendons–time to revisit inflammation.” British journal of sports medicine (2013): bjsports-2012.
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