Pathology
The term tendinitis suggests an inflammatory process in the tendon because it ends in -itis. Earlier theoretical models suggested that the problem arose from fiber tearing in the tendon, which led to an inflammatory reaction. Recent investigations into the cellular process of chronic tendon pathologies indicate otherwise. These researchers found a lack of inflammatory cells present and no evidence of fiber-tearing in these conditions. Instead, the problem results from collagen degeneration within the tendon. Therefore, this pathology is more appropriately called tendinosis instead of tendinitis.

While tendinosis is the most common overuse pathology of the Achilles tendon, an inflammatory condition called peritenonitis may affect this tendon as well. A thin membrane called the paratenon, which functions to enhance gliding and protect the tendon, surrounds the Achilles tendon. However, this membrane is not the same as the synovial sheath that surrounds other tendons around the ankle. The synovial sheath reduces friction between the tendon and the binding retinacula surrounding it. There is no retinaculum binding the Achilles tendon.

Peritenonitis is an inflammatory and fibrous reaction between the tendon and the paratenon. It may occur by itself or in conjunction with tendinosis. Tendinosis is more common in the distal region of the tendon, whereas peritenonitis usually occurs proximal to the tendon insertion. It is important to address both tendinosis and peritenonitis when they occur because chronic degeneration could lead to complete tendon ruptures if left untreated.

The potential for developing tendinosis in the Achilles tendon is magnified due to variations in blood supply in different regions of the tendon. Tendinosis is more likely where the blood supply is poor and tissue regeneration is impaired. Adequate blood supply is necessary for proper healing and tissue regeneration. Consequently, the lower portion of the tendon is where degeneration occurs first due to its poor blood supply.

Achilles tendinosis occurs from several factors, such as sudden changes in activity level, like starting a new running program. Since the tendon has not had the opportunity to adapt to the increased tensile load from the new activity, damage from overuse eventually occurs. Other factors that lead to this problem include inadequate stretching; training errors; rigid exercise surfaces, such as concrete; mechanical alignment problems; systemic diseases; or medications.

In addition to the above factors, another biomechanical consideration plays a role in the development of Achilles tendinosis: During normal foot motion there is a whip-like force on the tendon. This action is exaggerated if the person overpronates. Therefore it is important to look at pronation in addition to excessive loads in plantar flexion and dorsiflexion as a cause of tendinosis.

Sometimes Achilles tendinosis will develop without the stress of repetitive motion or biomechanical dysfunction. Recent discoveries have shed light on an unusual cause of this condition: The family of antibiotics called fluoroquinolones causes the same degenerative process to the collagen matrix in the tendon as repetitive overuse. They seem to have the greatest impact on tendons that are under high tensile load. Fluoroquinolones affect the Achilles tendon more than any other tendon in the body. Continued use of these antibiotics has been linked to Achilles tendon ruptures due to chronic long-term degeneration of the tendons. Brand-name examples of fluoroquinolones are Cipro, Levaquin, Floxin, Noroxin and Trovan.

References