Background
The Achilles tendon, named after the seemingly indestructible mythologic Greek warrior, is the largest and strongest tendon in the human body. Achilles tendinitis was the term originally used to describe the spectrum of tendon injuries ranging from inflammation to tendon rupture. Despite this spectrum, through extensive study of the histopathology of Achilles tendinitis, it has been determined that there is no evidence to support primary prostaglandin-mediated inflammation. There are, however, signs of "neurogenic inflammation with presence of neuropeptides like substance P and calcitonin gene related peptide."
Tendon histopathology has been divided into 4 categories[1, 2, 3, 4] : (1) Cellular activation and increase in cell numbers, (2) increase in ground substance, (3) collagen disarray, and (4) neovascularization. Using this as a guide, a histopathologically determined nomenclature has evolved to classify this range of Achilles tendon pathology into 3 stages: (1) paratenonitis, (2), tendinosis, and (3) paratenonitis with tendinosis.
Partial or full tendon ruptures may result from end-stage paratenonitis. Causes of tendon ruptures are associated with multiple factors including overuse, with both extrinsic and intrinsic factors playing a role in increasing susceptibility.[3, 5, 6, 7, 8, 9, 10, 11] Athletes who are poorly conditioned, overtrained, or insufficiently prepared are at the highest risk for this disease process. Repetitive stresses to the tendon, such as prolonged jumping or running, result in chronic pain and tightness along the tendon.[12]
Tendinitis usually develops insidiously after sudden changes in activity or training level, use of inappropriate footwear, or training on poor running surfaces, especially if high-risk factors are present (eg, age, cavus feet, tibia vara, heel and forefoot varus deformities).
For patient education resources, see the Foot, Ankle, Knee, and Hip Center, as well as Tendinitis, Ruptured Tendon, and Achilles Tendon Rupture.
Epidemiology
Frequency
United States
The true incidence of Achilles tendinitis is unknown, although there is a reported incidence of 6.5-18% in runners.
Functional Anatomy
The Achilles tendon (tendo calcaneus) is formed from the tendinous contributions of the gastrocnemius and soleus muscles, coalescing approximately 15 cm proximal to its insertion. Along its course in the posterior aspect of the leg, the tendon spirals 30-150° until it inserts into the calcaneal tuberosity. The tendon's ability to glide is facilitated by the presence of a thin paratenon sheath, which is composed of both a visceral layer and parietal layer, rather than simply a true synovial sheath. The tendon's blood supply arises from the osseous insertion, the musculotendinous junction, and multiple infiltrating mesotenon vessels, which cross the layers of the anterior paratenon.
Various injection and nuclear medicine studies have demonstrated a paucity of mesotenon and intratendinous vessels 2-6 cm proximal to the heel insertion known as the watershed area. Due to the relative lack of blood supply in the watershed area, this region of the tendon is less resilient to repetitive microtrauma and has a higher tendency for irritation, degeneration, and possible rupture than the calcaneal insertion site.[13]
Sport-Specific Biomechanics
The entire gastrocnemius/soleus musculotendinous unit spans the knee joint, tibiotalar (ankle) joint, and talocalcaneal (subtalar) joint. Contracture of this complex flexes the knee, plantar flexes the ankle, and supinates the subtalar joint. During running, forces equaling 10 times the body weight have been measured within the tendon.
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