Achilles tendinopathy is classified as both an insertional and non-insertional phenomenon, depending on whether it occurs at the osteotendinous junction or more proximally. It is a problem that is progressively increasing at both professional and amateur sporting levels. It is a disabling condition whose etiology is not yet fully understood, except for intrinsic and extrinsic factors, including biomechanical anomalies and functional overloads. It is a disorder widely present in runners, basketball players and other athletes who practice jumping sports but can also be found among non-athletes.
Attention is now drawn to two specific terms: tendonitis and tendinosis. The first term is usually associated with forms in which the tendon shows ONLY inflammatory components. Tendinosis, on the other hand, indicates a histopathological entity that affects all components of the tendon, including collagen fibers, tenocytes and the extracellular matrix.
Anatomy of the Achilles tendon
The Achilles tendon is the largest and strongest tendon in the human body. It is composed of the emergence of the superficial and deep bands of the triceps surae and is inserted at the posterior surface of the calcaneus, where there is a deep retrocalcaneal bursa. The Achilles tendon lacks a true tendon sheet and is instead surrounded by the paratendon, a double-layered membrane. The tendon itself consists of longitudinally oriented collagen fibers interspersed with fibroblasts. These collagen fibers are grouped into fascicles containing vascular-nervous and lymphatic systems, each of which is separated by septa of connective tissue called endotendons. These fascicles are then bundled together by an epitendin which in turn is wrapped by the peritendin. The epitendin and the peritendin constitute the two layers of the paratendinous membrane. Approximately 90-95% of the cellular elements of the tendon are tenocytes and tenoblasts, while the extracellular matrix is composed of collagen, elastic fibers (elastin), proteoglycans and organic components such as calcium. Type I collagen fibers are the most numerous, followed by Type II ones. Together, these collagen fibers make up 65-80% of the dry mass of the tendon while the elastin fibers make up only 1-2%.
The blood supply to the Achilles tendon is provided by the posterior tibial and peroneal arteries which divide into three territories: the intermediate portion is supplied by the peroneal artery and the proximal and distal portion are supplied by the posterior tibial artery.
The innervation originates mainly from the surrounding muscles and from the branches of the cutaneous nerves. Almost all innervations end in the superficial layer of the tendon, and some nerves follow the vascular channels, along the major axis of the tendon. The nerve endings of myelinated fibers serve as mechanoreceptors specialized in sensing pressure and tension while the unmyelinated endings serve as nociceptors, pain detectors.
Etiology
As already mentioned, the specific causes are not yet clear, although there is a tendency to highlight intrinsic and extrinsic pseudo-causes. Extrinsic factors can be correlated to defects in training, quality of training, equipment (shoes) and terrain. Excessive tendon overload during training is considered the main pathological stimulus for tendon degeneration. The tendon responds to repeated overloads with different levels of inflammation that can affect the peritendinous layer, the tendon body or both. The most common intrinsic causes include biomechanical abnormalities and genetic factors. The main biomechanical anomalies are poor gastro-soleal flexibility and hyperpronation of the foot during heel support. Overpronation involves excessive mobility of the hindfoot on a frontal plane. A study carried out on walkers highlighted that excessive strength of the plantar flexors associated with a high number of dorsiflexions of the foot was a clear factor in tendon overload. Genetic influence instead involves changes in the expression of genes that regulate cell-cell and cell-matrix interactions with a downregulation in mRNA samples in the pathological Achilles tendon.
Generally, however, it is extrinsic factors that cause acute trauma to the Achilles tendon while a combination of intrinsic and extrinsic factors creates chronic tendinopathy.
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