Järvinen M, Józsa L, Kannus P, Järvinen T L, Kvist M, Leadbetter W
Department of Surgery, University Hospital of Tampere, Finland.
Scand J Med Sci Sports. 1997 Apr;7(2):86-95. 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 a spontaneous tendon rupture is a typical clinical end-state manifestation of 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.
肌腱损伤和其他肌腱疾病是运动医学中常见的诊断和治疗难题，会导致慢性且持久的问题。组织退变是许多与运动相关的肌腱疾病中的常见表现。在绝大多数自发性肌腱断裂中，肌腱断裂部位可见慢性退变改变（1）。全身性疾病以及 specifically deteriorating the normal structure of the tendon（即异物、代谢性、遗传性和感染性肌腱疾病）很少是肌腱病变的原因。遗传性疾病，如各种胶原代谢紊乱且具有特征性病理结构改变的遗传性疾病（埃勒斯 - 当洛综合征、马方综合征、同型胱氨酸尿症（褐黄病）），约占慢性肌腱疾病病因的1%（2），而异物则稍常见一些，在所有慢性肌腱问题中不到10%可发现（1）。类风湿性关节炎和结节病是典型的全身性疾病，可导致肌腱和腱周组织的慢性炎症。总体而言，在对1000多条自发性断裂肌腱的组织学分析中，这些“特定”疾病导致的病理改变不到2%（1, 3, 4）。在该材料中，绝大多数肌腱可见退变改变，表明自发性肌腱断裂是肌腱组织退变过程的典型临床终末表现。过度使用在慢性肌腱损伤和疾病发病机制中的作用尚未完全明确。据推测，当肌腱过度使用时会疲劳并丧失其基本修复能力，重复性微创伤过程因而超过肌腱细胞修复纤维损伤的能力。通常本质上为离心性的高强度重复性活动，可能导致累积性微创伤，进而进一步削弱肌腱的胶原交联、非胶原基质和血管成分。过度使用还被推测通过干扰肌腱的微脉管系统和大脉管系统并导致局部血液循环不足，从而引起慢性肌腱问题。血流减少同时活动增加可能导致局部组织缺氧、营养和能量代谢受损，这些因素共同作用可能在导致肌腱退变的一系列事件中起重要作用（4）。久坐的生活方式被认为是肌腱基础循环不良的主要原因，并且可能至少部分导致偶尔参加高强度体育活动的久坐人群中肌腱问题高发。
