Histopathological findings in chronic tendon disorders

• Published in: Scandinavian journal of medicine & science in sports 1997-04, Vol.7 (2), p.86-95
• Main Authors: Järvinen, M., Józsa, L., Kannus, P., Järvinen, T. L. N., Kvist, M., Leadbetter, W.
• Format: Article
• Language: English
• Subjects: chronic; degeneration; disorder; histopathology; human; Humans; Inflammation - pathology; paratenonitis; tendinitis; Tendinopathy - pathology; tendinosis; tendon; Tendon Injuries - etiology; Tendon Injuries - pathology; Tendon Injuries - physiopathology; tendon rupture; Tendons - pathology; Tendons - ultrastructure
• ISSN: 0905-7188; 1600-0838
• DOI: 10.1111/j.1600-0838.1997.tb00124.x

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 importa