Tendinosis, sometimes called chronic tendinitis, chronic tendinopathy, or chronic tendon injury, is damage to a tendon at a cellular level (the suffix "osis" implies a pathology of chronic degeneration without inflammation). It is thought to be caused by microtears in the connective tissue in and around the tendon, leading to an increase in tendon repair cells. This may lead to reduced tensile strength, thus increasing the chance of tendon rupture. Tendinosis is often misdiagnosed as tendinitis due to the limited understanding of tendinopathies by the medical community. Classical characteristics of "tendinosis" include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity, and a lack of inflammatory cells which has challenged the original misnomer "tendinitis".
Symptoms can vary from an ache or pain and stiffness to the local area of the tendon, or a burning that surrounds the whole joint around the inflamed tendon. With this condition, the pain is usually worse during and after activity, and the tendon and joint area can become stiffer the following day as swelling impinges on the movement of the tendon. Many patients report stressful situations in their life in correlation with the beginnings of pain, which may contribute to the symptoms.
Tendons are very slow to heal if injured. Partial tears heal by the rapid production of disorganized type-III collagen, which is weaker than normal tendon. Recurrence of injury in the damaged region of tendon is common.
Rehabilitation, rest, and gradual return to the activity in which tendinosis was experienced is a common therapy. There is evidence to suggest that tendinosis is not an inflammatory disorder; anti-inflammatory drugs are not an effective treatment, and inflammation is not the cause of this type of tendon dysfunction. There is a variety of treatment options, but more research is necessary to determine their effectiveness. Initial recovery is usually within 2 to 3 months, and full recovery usually within 3 to 6 months. About 80% of patients will fully recover within 12 months. If the conservative therapy doesn't work, then surgery can be an option. This surgery consists of the excision of abnormal tissue. Time required to recover from surgery is about 4 to 6 months.
Vitamin E has been found to increase the activity of fibroblasts, leading to increased collagen fibrils and synthesis, which seems to speed up the regeneration and increase the regenerative capacity of tendons.
Nitric oxide (NO) also appears to play a role in tendon healing and inhibition of its synthesis impairs tendon healing. The use of a nitric oxide delivery system (glyceryl trinitrate patches) applied over the area of maximal tenderness was tested in three clinical trials for the treatment of tendinopathies and was found to significantly reduce pain and increase range of motion and strength.
Soft tissue mobilization
Augmented Soft Tissue Mobilization (ASTM) is a form of manual therapy that has been shown in studies on rats to speed the healing of tendons by increasing fibroblast activity. One case study showed ASTM resulting in full recovery in the case of an athlete suffering from chronic ankle pain and fibrosis, after an unsuccessful course of surgery and conventional physical therapy.
A promising line of therapy involves eccentric loading exercises involving lengthening muscular contractions.
The use of an inflatable brace (AirHeel) was shown to be as effective as eccentric loading in the treatment of chronic Achilles tendinopathy. Both modalities produced significant reduction in pain scores, but their combination was no more effective than either treatment alone.
Shock-wave therapy (SWT) may be effective in treating calcific tendinosis in both humans and rats. In rat subjects, SWT increased levels of healing hormones and proteins leading to increased cell proliferation and tissue regeneration in tendons. Another study found no evidence that SWT was useful in treating chronic pain in the Achilles tendon.
The future of non-surgical care for tendinosis is likely bioengineering. Ligament reconstruction is possible using mesenchymal stem cells and a silk scaffold. These same stem cells were capable of seeding repair of damaged animal tendons. Autologous tenocyte implantation is currently being tested for tendinosis. There is a large randomized, double-blind, placebo controlled trial being conducted in the Netherlands to test the safety and efficacy of tenocyte therapy. Results from the trial are expected by April 2013.
In other animals
Mesenchymal stem cells, derived from a horse's bone marrow or fat, are currently being used for tendon repair in horses. Bowed tendon is a horseman's term for tendinitis (inflammation) and tendinosis (degeneration), most commonly seen in the superficial digital flexor tendon (SDFT) in the front leg.
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