As of 2016 the pathophysiology of<unk>  is poorly understood. While inflammation appears to play a role, the relationships among changes to the structure of tissue, the function of tendons, and pain are not understood and there are several competing models, none of which have been fully validated or falsified. Molecular mechanisms involved in inflammation includes release of inflammatory cytokines like IL-1β which reduces the expression of type I collagen mRNA in human tenocytes and causes extracellular matrix degradation in the tendon. There are multifactorial theories that could 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 be an important mechanical factor for the development of<unk>  and predispose tendons to rupture. Obesity, or more specifically, adiposity or fatness, has also been linked to an increasing incidence of<unk> . The most commonly accepted cause for this condition however is seen to be an overuse syndrome in combination with intrinsic and extrinsic factors leading to what may be seen as a progressive interference or the failing of the innate healing response.<unk>  involves cellular apoptosis, matrix disorganization and neovascularization. Classic 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". Histological findings include granulation tissue, microrupture, degenerative changes, and there is no traditional inflammation. As a consequence, "lateral elbow<unk>  or tendinosis" is used instead of "lateral epicondylitis". Examination of tennis elbow tissue reveals noninflammatory tissue, so the term "angiofibroblastic tendinosis" is used. Cultures from<unk> c tendons contain an increased production of 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 have displayed no evidence of an acute, or a chronic inflammatory process. Histologic studies have demonstrated that this condition is the result of tendon degeneration, which causes normal tissue to be replaced by a disorganized arrangement of collagen. Therefore, the disorder is more appropriately referred to as "tendinosis" or<unk> " 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<unk>  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.
Tendinopathy
Compartment syndrome
Myopathy
Shin splints
Lumbar enlargement
Olecranon bursitis
Muscle atrophy
Xiphodynia