Histopathological findings in chronic tendon disorders

Abstract

Tendon injuries and other tendon disorders represent a common diagnostic and therapeutic challenge in sports medicine, resulting in chronic and long‐lasting problems. Tissue degeneration is a common finding in many sports‐related tendon complaints. In the great majority of spontaneous tendon ruptures, chronic degenerative changes are seen at the rupture site of the tendon (1). Systemic diseases and diseases specifically deteriorating the normal structure of the tendon (i.e. foreign bodies, and metabolic, inherited and infectious tendon diseases) are only rarely the cause of tendon pathology. Inherited diseases, such as various hereditary diseases with disturbed collagen metabolism and characteristic pathological structural alterations (Ehlers‐Danlos syndrome, Marfani syndrome, homocystinuria (ochronosis)), represent approximately 1% of the causes of chronic tendon complaints (2), whereas foreign bodies are somewhat more common and are found in less than 10% of all chronic tendon problems (1). Rheumatoid arthritis and sarcoidosis are typical systemic diseases that cause chronic inflammation in tendon and peritendinous tissues. Altogether, these ‘specific’disorders represented less than 2% of the pathological alterations found in the histological analysis of more than 1000 spontaneously ruptured tendons (1, 3, 4). In this material, degenerative changes were seen in a great majority of the tendons, indicating that aspontaneous tendon rupture is a typical clinical end‐state manifestationof a degenerative process in the tendon tissue. The role of overuse in the pathogenesis of chronic tendon injuries and disorders is not completely understood. It has been speculated that when tendon is overused, it becomes fatigued and loses its basal reparative ability, the repetitive microtraumatic processes thus overwhelming the ability of the tendon cells to repair the fiber damage. The intensive repetitive activity, which often is eccentric by nature, may lead to cumulative microtrauma which further weakens the collagen cross‐linking, non‐collagenous matrix, and vascular elements of the tendon. Overuse has also been speculated to cause chronic tendon problems, by disturbing the micro‐ and macrovasculature of the tendon and resulting in insufficiency in the local blood circulation. Decreased blood flow simultaneous with an increased activity may result in local tissue hypoxia, impaired nutrition and energy metabolism, and together these factors are likely to play an important role in the sequence of events leading to tendon degeneration (4). A sedentary lifestyle has been proposed as a main reason for poor basal circulation of the tendon, and presumably is at least partly responsible for the high number of tendon problems in people with a sedentary lifestyle who occasionally take part in high physical activity sports events.

Loss of Homeostatic Strain Alters Mechanostat “Set Point” of Tendon Cells In Vitro

“…The cell nuclei became more ovoid and there was less intimate contact between adjacent cells. Similar alterations in tenocyte morphology have been reported in clinical cases of tendinopathy [26,31,37,50]. In our study, these changes coincided with a progressive loss of intimate contact between the cells and their pericellular matrix.…”

“…Indeed, in vitro experimental studies have demonstrated that loss of homeostatic tendon strain can produce a pattern of catabolic gene expression [5,[33][34][35][36]41], apoptosis [3,17], and degenerative histological changes [5,21] similar to those seen in clinical cases of tendinopathy [1,2,5,19,24,26,28,30,31,38,39,40,45,50,54,60,61]. However, the effect of these catabolic changes on the subsequent mechanoresponsiveness of tendon cells is unknown.…”

Expression profiling of metalloproteinases and tissue inhibitors of metalloproteinases in normal and degenerate human achilles tendon

“…Tendon "overuse" has been proposed as a destructive mechanism that precedes overt pathologic development, implying that repeated strains below the injury threshold induce changes in the tendon-matrix composition and organization (28,30). Since metalloproteinase expression in tendon cells is known to be modulated by mechanical loading (31)(32)(33)(34), it is possible, given the absence of inflammation in most specimens, that at least some of the changes in gene expression described herein are induced by an altered mechanical environment.…”

“…Eight of the 11 cadaver tendons showed a mostly normal histologic appearance, although there were some variations in cell shape and density. The sections consisted of mostly longitudinally oriented fibrous matrix, and the majority of cells were long, thin, and aligned with the collagen fibers, essentially as described elsewhere (1)(2)(3)28). Some cell and matrix abnormalities were observed in 3 cadaver tendon specimens (27%), such as an increased proportion of rounded cells, some loss of matrix organization, loss of crimp, increased amounts of interfascicular loose connective tissue, and increased staining for matrix glycosaminoglycans.…”

Eccentric training as a new approach for rotator cuff tendinopathy: Review and perspectives

“…In conclusion, higher rates of turnover in the nonruptured supraspinatus may be Among the most common sites of tendinopathy are the Achilles tendon, the patellar tendon, the wrist extensors tendon and the supraspinatus tendon [7,13,54,55] . The degenerative changes found in these tendons are associated with old age and with the high physical demands (strain, compression or shear forces) at the neighboring joints [6,56] with high rates of matrix turnover [50] .…”