Guide to Tendinopathy
Guide to "Tendinopathy":
By the term tendinopathy substantially are described in three pathologies related to tendon:
They are diseases that occur frequently in sportsmen but may involve also sedentary subjects. Often they occur in association with each other creating sometimes complex clinical pictures.
Several factors may contribute to the oneset of a tendonitis. Frequently is the result of an acute event triggered by repetitive microtrauma or functional overload (in athletes often favored by inadequate footwear). Sometimes we tend to generalize the term tendinitis as the term that simply means inflammation of the tendon, which, however, doesn't find an anatomopathologic confirmation; the tendon, being in its inner part not so vascularized shouldn't be the site of inflammatory process. This kind of process concerns the peritenon (the superficial tendon surface).
Entesithis or insertional tendinopathy
Usually associated with peritendinitis, it manifest itself with sharp pain at the tendon insertion. Due to postural defects or functional compensation, the improper solicitation of the distal tendon may, in time, lead to bursitis aggravating the clinical picture.
This is the degeneration of tendon collagen fibers. Tendinosis then is part of the normal aging process. The arrangement of fibrils in collagen fibers that composes the tendon provide strenght to the structure. But over time they can flake and create nodular deformations along the course of the tendon. In severe cases, excessive wear and an asymptomatic clinical picture pose a risk the holding of the tendon, up to a possible partial or total break.
The tendon pathology with fibro-calcific evolution or calcific tendinopathy is often a disease of unknown etiopathology in which multifocal calcific deposits deposit themselves in tendon living tissue. The calcific tendinopathy should be distinguished from dystrophic calcification or enthesopathy, which affects the tendon in its insertion on the bone but not in the central structure of the tendon. The calcific tendinopathy frequently affects the shoulder with an incidence between 2.7% and 7.5%, affecting mainly female with an average age between 40 and 50 years. The etiology of calcific tendinopathy is still controversial; it seems that tissues hypoxia and localized mechanical compression intervene as causal factors. Basically two different mechanisms have been proposed for the formation of calcific deposits. As per the first mechanism, the degeneration of the tendon fibers precedes the formation of calcifications. This theory has been accepted for a long time by different authors. The main cause of the degeneration of the tendon fibers is aging. According to Brewer, with aging, there is a decrease in tendon vascularization associated with changes in the collagen that constitutes the architecture of the tendon. Starting from fourth to fifth decade of life most of the beams undergo thinning and fibrosis, signs of degenerative processes. MacLaughlin described the presence at the level of tendon fibers of small areas of hyaline degeneration which can determine the detachment of the fibrils from normal tendon tissue, thus forming the necrotic fragments that undergo calcification
More recently, according to Bilger and Mohr the process of calcification begins with necrosis of tenocytes and concomitant intracellular accumulation of calcium, often in the form of mikcrospherulites or psammoma bodies. The authors supporting the second mechanism, meanwhile, find that the calcifications are formed in the tendon vital tissue through a process of active cell-mediated. According to Uhthoff the process can be divided into three distinct stages: pre-calcified, calcified and post-calcified. The pre-calcified stage is characterized by the appearance of fibro-cartilaginous metaplasia. The transformation of tenocytes into chondrocytes is accompanied by metachromasia, indicative of proteoglycans elaboration. According to some studies result that the most important condition for the production of cartilaginous metaplasia is represented by the local decrease of oxygen tension, probably associated to mechanical stimulation by compression.
The calcific stadium is divided into three phases:
- formative phase
- state phase
- resorption phase