Tendinopathy

Anatomy

Tendons are predominately Type I collagen, which consists of tropocollagen chains grouped in a triple helix arrangement. These triple helices are very closely grouped longitudinally in the tendon, with each level of organization being surrounded by an outer covering. The entire tendon is also surrounded by an external covering called the paratenon. In areas where tendons bend at acute angles (e.g., the flexor tendons of the fingers) over bone, the paratenon is usually thicker and lined with synovium, which not only provides mechanical resistance to shearing forces but also produces synovial fluid, lubricating the tendon to decrease frictional injury. This is also commonly referred to as the tendon sheath. It is in these areas that the inflammation can commonly occur, causing synovial fluid production and associated swelling (e.g., intersection syndrome). In the remaining tendon areas, the paratenon is thinner and not lined with synovium.

Causes

As mentioned previously, tendinopathy usually results from chronic overuse microtrauma to a tendon. The precise pathogenesis of tendinopathy is still unknown, but general causative mechanisms [Page 1460]are becoming more clearly understood. Other than paratenonitis, all other categories of tendinopathy have a component of tendinosis or degenerative tendon changes. It is now understood that these changes can occur as early as 3 weeks after the start of the overuse injury.

Table 1 Classification of Tendinopathies

Table 1 Common Tendinopathies

While general aging and tendon underuse can contribute to degenerative tendon changes, most tendinopathy is caused by any combination of excessive repetition, anatomic abnormality (e.g., limb length discrepancy), malalignment (e.g., hyperpronation), muscle imbalance or weakness, improper technique, improper equipment, and incomplete recovery after overuse. These etiologies hold true for competitive and recreational athletes as well as for recreational and vocational laborers.

...