Tendon Tertiary fibre bundle

Secondary fibre bundle (fascicle)

Primary fibre bundle (subfascicle)

Collagen fibre

Collagen fibril

Epitenon Endotenon ANATOMY

The Achilles tendon is the largest and strongest tendon in the human body (Fig. 1.). It is formed by the merging of the deep and superficial fasciae of the triceps surae and it inserts into the posterior aspect of the calcaneum where a deep retrocalcaneal bursa is frequently present (8).

The Achilles tendon lacks a true tendon sheath and is enveloped by paratenon, a double-layered membrane. The tendon itself consists of longitudinally orientated collagen fibrils interspersed with fibroblasts (Fig. 2.). These collagen fibrils are bundled into fascicles, containing vasculo–neural and lymphatic systems, all of which are separated by connective tissue septations known as endotenon. These fascicles are then grouped together by epitenon, which in turn is surrounded

INTRINSIC FACTORS

Gender

Biomechanical abnormalities (e.g. poor gastroc– soleus flexibilty,

over-pronation of foot during heel strike)

Aberrant gene regulation of

cellular and matrix interactions

Altered expression of protein mRNA (e.g. MMP3 and collagen

EXTRINSIC FACTORS

Patterns of training

Poor training techique

Faulty equipment

Environmental malfunctions

Excessive loading of

tendons during vigorous physical training

Figure 2: The hierarchical structure of tendon. Groups of fibres form the fascicles, which are surrounded by the endotenon, a loose connective tissue layer. The tertiary bundles of fascicles are surrounded by another connective tissue layer, the epitenon, and a double-layered covering, the paratenon (not shown)

by peritenon. This epitenon and peritenon constitute the layers of the paratenon membrane (8,9). Around 90–95% of the cellular element of the tendon consists of tenocytes and tenoblasts, while the extracellular matrix consists of collagen, elastin fibres, proteoglycans and organic components such as calcium (10). Type 1 collagen fibres are the most abundant, followed by type 2. Together these collagen fibres account for 65–80% of the dry mass of the tendon, while elastin fibres only comprise 1–2% of this (11).

Figure 3: Aetiological factors in Achilles tendinopathy 24

In general, blood to the Achilles tendon is supplied by the posterior tibial and peroneal arteries. Both have an input to three vascular territories: the midsection (supplied by the peroneal artery) and the proximal and distal sections (supplied by the posterior tibial artery) (12). The posterior tibial artery contributes the most to the vascular supply, which is why the midsection of the Achilles tendon is usually more hypervascular than the rest of the tendon (12,13). The nervous supply of the Achilles tendon mainly originates from surrounding muscles and the branches of the cutaneous nerves. Although they mainly terminate on the superficial aspect of the tendon, some nerves follow the vascular channels within the long axis of the tendon (14). Nerve endings of myelinated fibres function as specialised mechanoreceptors, detecting pressure and tension, while the unmyelinated nerve endings act as nociceptors, detecting pain (15).

AETIOLOGY As mentioned before, the aetiology of Achilles tendinopathy is not completely understood, although the cause can be classified as either intrinsic or extrinsic. Extrinsic factors include changes in training patterns, poor technique, and equipment and environmental malfunctions (10,15,16). However, excessive loading of tendons during vigorous physical training is considered to be the main pathological stimulus for tendon degeneration. Tendons respond to repetitive overloading beyond the physiological threshold by inflammation of the tendon sheath, degeneration of the tendon body, or both (15). Common intrinsic causes include biomechanical abnormalities, genetic factors and gender differences (14). Among the biomechanical factors are poor gastroc–soleus flexibility and over-pronation of the foot during heel strike. Thus over-pronation results in excessive motion of the hindfoot in the frontal plane and is thought to cause a ‘whipping’ action on the Achilles tendon, hence predisposing to tendinopathy (10,17). A prospective cohort study on male cadet officers identified that the strength of the plantar flexors and the amount of dorsiflexion excursion were significant predictors of an Achilles tendon overuse injury (18). The genetic influence involves changes in the expression of genes regulating cell–cell and cell–matrix interactions, with downregulation of MMP3 mRNA in tendinopathic Achilles tendon samples. In addition, type 1 and type 3 collagen mRNAs have been found at higher levels in tendinopathic samples than in normal samples (19). While appreciating the interplay of both extrinsic and intrinsic factors, in general it is the extrinsic factors that tend to cause acute Achilles tendon trauma, but a combination of both intrinsic and extrinsic factors is responsible for chronic tendinopathy (15).

HISTOPATHOLOGY

The histopathology can be classified as peritendinous or intratendinous (14) (see Fig. 4). Histologically, Achilles tendinopa- thy is characterised by non-inflammato- ry intratendinous collagen degeneration and a failed healing response. There is also scattered vascular ingrowth, hypercellularity, and increased levels of interfibrillar glycosaminoglycans (20,21).

sportEX medicine 2010;45(Jul):23-30