Tendinopathy (tendinitis, U.S. English) is a type of tendon disorder that results in pain, swelling, and impaired function. It most commonly occurs around larger joints, including the shoulder (rotator cuff tendinitis, biceps tendinitis), elbow (tennis elbow, golfer's elbow), wrist, hip, knee (jumper's knee), or ankle (Achilles tendinitis). Causes may include trauma or repetitive activities. Less common causes include infection, arthritis, gout, thyroid disease, diabetes and the use of quinolone antibiotic medicines. Groups at risk include manual laborers, musicians, and sports participants. Diagnosis is typically based on symptoms, examination, and imaging. Typically, little inflammation remains after a few weeks, assuming that the underlying problem is related to weak or disrupted tendon fibrils. Treatment options include rest, NSAIDs, splinting, and physiotherapy. Steroid injections, surgery, or shockwave therapy may be appropriate. About 80% of overuse tendinopathy patients recover completely within six months. Tendinopathy is relatively common. Older people are most commonly affected.
Signs and symptoms Symptoms include tenderness on palpation, swelling, and pain, often when exercising or with a specific movement.
Cause Causes may include trauma or repetitive activities. Less common causes include infection, arthritis, gout, thyroid disease, and diabetes. Obesity, or more specifically, adiposity or fatness, is linked to increasing incidence of tendinopathy. Quinolone antibiotics are associated with increased risk of tendinitis and tendon rupture. A 2013 review found the incidence of tendon injury among those taking fluoroquinolones to be between 0.08 and 0.2%. Fluoroquinolones most frequently affect large load-bearing tendons in the lower limb, especially the Achilles tendon.
Types Examples include:
Achilles tendinitis Calcific tendinitis Patellar tendinitis (jumper's knee)
Pathophysiology As of 2016, the pathophysiology of tendinopathy was poorly understood. While inflammation plays a role, the relationships among changes to the structure of tissue, the function of tendons, and pain are not understood. Several models are proposed, none of which have been fully validated or falsified. Molecular mechanisms involved in inflammation include release of inflammatory cytokines such as IL-1β which reduce the expression of type I collagen mRNA in human tenocytes and cause extracellular matrix degradation in the tendon. A 2020 review noted that while various inflammatory markers were present in two thirds of the reviewed articles, data heterogeneity and lack of comparable studies prevented any conclusion about a common pathophysiology. Multifactorial theories include tensile overload, tenocyte-related collagen synthesis disruption, load-induced ischemia, neural sprouting, thermal damage, and adaptive compressive responses. The intratendinous sliding motion of fascicles and shear force at interfaces of fascicles could predispose tendons to rupture. The most commonly accepted cause is an overuse syndrome in combination with factors leading to what may be seen as a progressive interference or the failing of the innate healing response. Tendinopathy involves apoptosis, matrix disorganization and neovascularization. Classic characteristics include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity, and a lack of inflammatory cells, which has challenged the misnomer "tendinitis". For chronic tennis elbow, histological findings include granulation tissue, microrupture, degenerative changes, but without traditional inflammation. As a consequence, "lateral elbow tendinopathy or tendinosis" replaces "lateral epicondylitis". Examination of pathologic tennis elbow tissue reveals noninflammatory tissue, elevating the term "angiofibroblastic tendinosis". Cultures from tendinopathic tendons contain increased type III collagen. Longitudinal sonogram of the lateral elbow displays thickening and heterogeneity of the common extensor tendon that is consistent with tendinosis, as the ultrasound reveals calcifications, intrasubstance tears, and marked irregularity of the lateral epicondyle. Although the term "epicondylitis" is frequently used to describe this disorder, most histopathologic findings of studies displayed no evidence of an inflammatory process. Histologic studies demonstrated that this condition is the result of tendon degeneration, which causes normal tissue to be replaced by a disorganized collagen arrangement. Therefore, the disorder is more appropriately referred to as "tendinosis" or "tendinopathy" rather than "tendinitis". Colour Doppler ultrasound reveals structural tendon changes, with vascularity and hypo-echoic areas that correspond to the areas of pain in the extensor origin. Load-induced non-rupture tendinopathy in humans is associated with an increase in the ratio of collagen III:I proteins, a shift from large to small diameter collagen fibrils, buckling of the collagen fascicles in the tendon extracellular matrix, and buckling of the tenocyte cells and their nuclei.
Diagnosis
Symptoms can vary from aches or pains and local joint stiffness, to a burning that surrounds the whole joint around the inflamed tendon. In some cases, swelling occurs along with heat and redness, and there may be visible knots surrounding the joint. With this condition, the pain is usually worse during and after activity, and the tendon and joint area can become stiff the following day as muscles tighten from 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.
Medical imaging 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.
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