Makroskopik anatomy tendon Achilles

The 2 muscle bellies of the gastrocnemius muscle join the deeper soleus muscle in an aponeurosis roughly 12-15 cm from the insertion of the tendon into the os calcis, although the soleus can remain independent until insertion. The length of the tendon is variable, and the tendon spirals about 90 prior to its insertion, with most of the rotation occurring in the last 5-6 cm.[6] The rotation is thought to aid in elastic recoil of the tendon.[7] The tendon inserts into the posterior-superior aspect of the calcaneal tuberosity with the bursa lying anteriorly. Running concurrently with the tendon is the plantaris, which crosses the soleus to run medial to the Achilles tendon and which also inserts into the calcaneus. Like the palmaris longus in the forearm, it is absent in about 7-10% of individuals. The tendon is covered by a paratenon. This is a double-layered sheath of synovial cells. The inner layer is in contact with the tendon itself, and the outer layer is continuous with the subcutaneous tissue and ventral mesotendon and its rich blood supply. The paratenon can become inflamed and enlarged, usually in runners, with acute crepitus felt over the fusiform swelling, which can originate from the paratenon or the tendon itself. Just anterior to the Achilles tendon lies the retrocalcaneal bursa. This can become inflamed, leading to pain anterior to the tendon, especially on dorsiflexion of the foot. It is important to differentiate this type of pain from paratenon inflammation or tendinosis. An enlarged bony prominence at the posterosuperolateral aspect of the calcaneus, called the Haglund process, may be associated with retrocalcaneal bursitis but also with insertional tendinitis as well. This is a reason why plain radiography still has value in diagnosis and management. The blood supply to the Achilles tendon is derived mainly from vessels traversing the mesotendon. The main blood supply is derived from the vincula, both long and short, via the paratenon and especially from the ventral mesotendon. Small longitudinal supplies from the muscle bellies and the distal insertion are also present. However, blood supply is also derived directly from the muscle bellies themselves and distally from bone where the tendon inserts into the calcaneus. Microvascular Doppler flow studies have shown that flow is distributed evenly throughout the tendon, but it is less at the insertion.[8] Studies have also demonstrated higher resting blood flow rates in individuals with tendinosis than in healthy control subjects.[9] Cadaveric studies have shown a relative decrease in both the frequency and the total area of vessels in the mid portion of the Achilles tendon.[10] Dynamic studies have refuted the oncepopular historical theory that the pathology is related mainly to a hypovascular zone at the mid tendon. However, the relative lack of blood vessels in the area that usually ruptures has led to the term watershed area, which is still used today. As discussed below, the blood supply is a factor in Achilles tendinosis, but whether it is causative or reactive is still under debate.

Achilles Tendon Rupture Overview

The Achilles tendon, or tendon calcaneus, is a large ropelike band of fibrous tissue in the back of the ankle that connects the powerful calf muscles to the heel bone (calcaneus). Sometimes called

the heel cord, it is the largest tendon in the human body. When the calf muscles contract, the Achilles tendon is tightened, pulling the heel. This allows you to point your foot and stand on tiptoe. It is vital to such activities as walking, running, and jumping. A complete tear through the tendon, which usually occurs about 2 inches above the heel bone, is called an Achilles tendon rupture.

Achilles Tendon Rupture Causes

The Achilles tendon can grow weak and thin with age and lack of use. Then it becomes prone to injury or rupture. Certain illnesses (such as arthritis and diabetes) and medications (such as corticosteroids and some antibiotics) can also increase the risk of rupture.

Rupture most commonly occurs in the middle-aged male athlete (the weekend warrior who is engaging in a pickup game of basketball, for example). Injury often occurs during recreational sports that require bursts of jumping, pivoting, and running. Most often these are tennis, racquetball, basketball, and badminton. The injury can happen in these situations.
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You make a forceful push-off with your foot while your knee is straightened by the powerful thigh muscles. One example might be starting a foot race or jumping.

You suddenly trip or stumble, and your foot is thrust in front to break a fall, forcefully overstretching the tendon. You fall from a significant height.

Pathology

Microscopic pathology
Adult tendons are composed of large-diameter type I collagen fibrils. These are 150 nm in diameter, tightly packed with type III collagen, and dispersed in an aqueous gel containing proteoglycan and elastic fibers.[17] The actin and myosin bundles are arranged helically. In healthy tendons, 95% of the collagen is type I.[18] Degenerate tendons have less type I collagen and significantly more type III collagen. The same changes are also seen during the natural aging process, although to a lesser extent. This may be why the tendon is less elastic in older individuals and more prone to rupture.[19] Type III collagen seems to be the major collagen synthesized in the healing tendon after injury. This observation again suggests that the tendon degeneration in tendinosis is an incomplete repair process. Animal testing has shown that tendons can stretch by 4% of their original length before damage occurs. If stretched more than 8%, rupture is likely.[20]

Systemic pathology affecting the Achilles tendon

A number of systemic or external factors appear to be linked to tendon degeneration and rupture. As has been mentioned, age is a factor. Other factors that affect the Achilles tendon include the following:

Steroids: Whether taken systemically or injected around the tendon, steroids appear to increase the rate of acute rupture.[21, 22] Quinolones: Numerous case reports appear to link the administration of quinolone antibiotics to tendon rupture. These drugs may have a toxic effect on the tenocytes, leading to tendon degeneration.[23, 24] Chronic renal failure: This systemic illness may be a factor.[25, 26] Rheumatoid arthritis and systemic lupus erythematosus (SLE): Both have been implicated in tendinosis. Other systemic illnesses: Collagen deficiencies, infectious diseases, thyroid disorders, parathyroid disorders, and diabetes mellitus have been implicated as having association with Achilles tendinosis or rupture. Other associations: In general, another factor associated with an increased incidence of Achilles rupture and Achilles tendinosis is blood group O.[27, 28]

Intrinsic pathology of tendinosis

Histologic changes in the Achilles tendon include changes to the extracellular and intracellular matrices. These include collagen degeneration, fiber disorientation, and increased mucoid ground substance, but no increase in inflammatory cells occurs. Focal hypercellularity and vascular proliferation are usually present. The number and morphologic variations of tenocytes increases.[29] Also increased is the number of apoptotic (dead) cells, both in the degenerate and in the ruptured tendon.[30] The proportion of type III collagen is also increased in the degenerate tendon. Pathologically, Achilles degeneration has been described as lipoid or mucoid.[31] In mucoid degeneration, the tendon becomes more brown or gray, with mucoid patches and vacuoles. Lipoid degeneration involves increased lipid content in the tendon tissue.[32] Other studies have shown an increase of type I and type III collagen mRNA. Also, glutamate concentrations increase in the painful degenerate tendon.[33] Neovascularization is often a feature of the degenerate tendon. It is associated with painful tendinosis.[34] Eccentric training leading to good clinical results is associated with a reduction and/or absence of neovascularization, and conversely, poor results are associated with continuing neovascularization.[35, 36] Tendon rupture is almost always the terminal event in the ongoing degenerative process of the tendon, as confirmed in histologic studies of ruptured tendons.[37]