|Classification and external resources|
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".
- 1 Diagnosis
- 2 Treatment
- 3 Research
- 4 Other animals
- 5 See also
- 6 References
- 7 External links
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.
Swelling in a region of micro damage or partial tear may be detected visually or by touch.
Ultrasound imaging can be used to evaluate tissue strain, as well as other mechanical properties.
Ultrasound-based techniques are becoming more popular because of its affordability, safety, and speed. Ultrasound can be used for imaging tissues, and the sound waves can also provide information about the mechanical state of the tissue.
Tendinosis of the common extensor tendon of the elbow (“tennis elbow”) is a common cause of elbow pain for adults. Longitudinal ultrasound of the lateral elbow shows thickening and heterogeneity of the common extensor tendon that is consistent with tendinosis. There are intrasubstance tears, marked irregularities, and calcifications of the lateral epicondyle.
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.
Both eccentric loading and extracorporeal shockwave therapy are currently being researched as possible treatments for tendinosis. One study found both modalities to be equally effective in treating tendinosis of the Achilles tendon and more effective than a 'wait and see' approach. Other treatments for which research is on-going includes vitamin E, vitamin B6, nitric oxide, and stem cell injections.
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.
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.
Autologous tenocyte injection
A study investigated autologous tenocyte injection for the treatment of severe, chronic resistant lateral epicondylitis. A needle biopsy was used on the patellar tendon, and the extracted tendon cells were expanded by in vitro culture. The autologous tenocytes were sorted and purified by real-time polymerase chain reaction, and amplified by flow cytometry. The tenocytes were then injected into the injured tendinopathy site, which was the origin of the extensor carpi radialis brevis tendon, under the guidance of an ultrasound. After the autologous tenocyte injection treatment, patients with chronic lateral epicondylitis showed improved clinical function and structural repair at the origin of the common extensor tendon.
Nonbulbar dermal sheath cells
RepliCel has planned a Phase 2 Achilles tendinosis clinical trial using fibroblasts that are isolated from the nonbulbar dermal sheath cells of a hair follicle. The tendon treatment will be tested in approximately 90–120 subjects in a Phase 2 trial, and will start in Q3 2014. Nonbulbar dermal sheath cells are used because they produce more type I collagen than fibroblasts that are derived from adipose tissue. Type I collagen is the primary collagen in tendons. Nonbulbar dermal sheath cells will be replicated, and then reintroduced into the wounded tendons with ultrasound. After the injections, subjects will be assessed for pain, safety, and function, as well as changes in interstitial tears, tendon thickness, echotexture, and neovascularity.
Allogenic adipose-derived mesenchymal stem cells
As of November 2013, researchers at the Seoul National University Hospital will be looking to recruit participants into a clinical trial to evaluate the efficacy of allogenic adipose-derived mesenchymal stem cells (ALLO-ASC) for the treatment of a lateral epicondylitis tendon injury where the duration of the symptoms is over six months. Adipose-derived mesenchymal stem cells will be administrated to the patients with lateral epicondylitis (tennis elbow) by an ultrasonographic-guided injection.
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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