Tendinosis vs. Tendonitis

The tendon is one of the most frequently injured sites in overuse sports injuries, especially in sports requiring endurance and power. We usually think of the tendon as inert tissue that mainly transmits force from muscle to bone, resulting in joint movement; but tendons store elastic energy; allowing elastic recoil and longitudinal movement.

The tendon is covered by the epitenon, which is a loose connective tissue sheath containing the vascular, lymphatic, and nerve elements.  Those tendons that rub over a bony protuberance have a paratenon that covers the epitenon. Tendons with a paratenon can develop a paratenonitis, as in De Quervain’syndrome (condition affecting where the thumb meets the wrist). In a paratenitis, after a few days, a fibrinous exudate fills the tendon sheath and causes the inflammation and crepitus that is clinically evident.

Histopathologic examination of symptomatic Achilles (unless it is the paratenon), patellar, rotator cuff, and elbow tendons do not show inflammatory cells. If chronic inflammatory cells (lymphocytes and macrophage-type cells) show up in tendons, they are due to traumatic repair and include granulation of scar tissue.

Most tendon problems relate to the body of the tendon rather than the paratenon, however, and this pathology is described as the tendinosis. Tendinosis refers to collagen degeneration with separation and disorganization of the fibers and nonfunctional vascular elements. Changes in the collagen fiber structure and arrangement and leads to granulation-like tissue known as angiofibroblastic tendinosis.

Because tendinosis is considered a degeneration rather than an inflammation, the question arises as to the role of the corticosteroid injection, iontophoresis, or nonsteroidal anti-inflammatory drugs (NSAIDSs). It is known that corticosteroid injection into tendon tissue leads to cell death and tendon atrophy; even if the injection is around the tendon it will inhibit collagen synthesis.  The effect of corticosteroids on healing may have nothing to do with the steroids. It is possible that the soft tissue trauma and bleeding caused by the injection might be the stimulus for extrinsic healing of the tendon. This also explains why certain manual techniques that can initiate an ecchymosis, such as friction massage and Graston Technique, may have a healing effect on tendinosis.

Fibroblastic proliferation produces collagen and proteoglycans. For healing to occur, a fibroblast-driven process is necessary to integrate old and new collagen in order to contribute the final stability of the matrix. It appears that manual soft tissue and rehabilitative techniques that stimulate fibroblastic proliferation and therefore new collagen and proteoglycans will have the ability to alter tendinosis-type tissue. There is some evidence that laser and high-voltage galvanic stimulation can stimulate collagen synthesis in the laboratory setting. Eccentric exercise may stimulate the mechanoreceptors in tenocytes to produce collagen, helping to reverse the tendinosis cycle.

It has been recommended that the term tendinopathy instead of tendonitis or tendinosis as a general clinical descriptor of tendon injuries in sport because inflammation is not common. In order for tendinitis to occur, vascular disruption is necessary to help create inflammatory repair response (see tabke 5C2-1). A vascular response is related to a macrotrauma, which is hardly as common as overuse microtrauma that occurs over time. Seldom does a tennis elbow or patella tendon lesion present as a mactrotrauma. Inflammation is associated mostly with tendon ruptures or involvement of the paratenon.

*Topic of the Week referenced by "Conservative Management of Sports Injuries" by Thomas E. Hyde, Marianne S. Gengenbach