The extracellular matrix accounts for about 80% of the total tissue volume, with approximately 30% of its substance being solids and the remaining 70% being water. It consists of fibres and the interfibrillar amorphous ground substance, the substances responsible for supporting and nourishing the cells. The amorphous ground substance also determines the connective tissue’s compliance, mobility and integrity.

The fibrous portion of connective tissue is responsible for determining the tissue’s biomechanical properties. Two major groups of fibres exist: collagen fibres and elastic fibres.

Muscles and tendons are distinct tissues, although they functionally act as one structure, the contractile unit. The tendon cells are derived from the embryonic mesenchyme, the tissue occupying the areas between the embryonic layers, classifying tendon as a connective tissue (Standring 2009). Muscle cells are derived from mesoderm, the intermediate embryonic layer, such that muscle itself belongs to a separate tissue group.

The tendon is an inert structure which does not contract, but as part of the contractile unit it is directly involved in muscle action. Therefore the tendon is assessed by resisted testing via the muscle belly. Active movement does not produce transverse movement within the tendon but its fibrous structure may be moved passively by transverse frictions, to prevent or to mobilize adhesions.

A tendon provides tensile force transmission and storage and release of elastic energy during locomotion – which is particularly important for many sports and activities (Witvrouw et al 2007).

Tendons are exposed to strong, unidirectional forces and to function they require great tensile strength and inelastic properties. They are able to withstand much greater tensile forces than ligaments and are composed of closely packed parallel bundles of collagen micro-fibrils, fibrils and fibres, bound together by irregular connective tissue sheaths into larger bundles (Fig. 2.7). Most fibres are oriented in one direction, parallel to the long axis, which is the direction of normal physiological stress (Alter 2000). Tendons do not usually contain any elastic fibres since their muscle belly acts as an energy damper such that elastic fibres are not required (Akeson 1990). They do have the ability to store and release elastic energy, however, and rehabilitation programmes should aim to increase tendon elasticity. Tendon elasticity has been shown to increase significantly with ballistic stretching (Witvrouw et al 2007).

The fibres are large-diameter type I collagen, well suited to accept tensile forces. The proteoglycans are packed in between the fibres and, because the tendon is so compact, there is little room for the tendon cells or an adequate blood supply. The tendon’s blood vessels lie in the epitenon (adherent to the surface of the tendon) and the endotenon (a division between collagen fibre bundles) (Gelberman et al 1983). The vascularization of tendons is relatively sparse compared with that of muscles (Alfredson et al 2002).

Calcification may occur within the tendon structure that is generated by extracellular organelles known as matrix vesicles. Proteoglycans in the tendon usually suppress the mineralization but ageing and diabetes may alter proteoglycan levels, thus allowing calcification of the normally unmineralized extracellular matrix (Gohr et al 2007).

As mentioned above, tendons are surrounded by a fibroelastic paratenon functioning as an elastic sleeve to facilitate their gliding properties and permitting free movement in the surrounding tissues. Under the paratenon, the entire tendon is surrounded by the thin connective tissue sheath of the epitenon; the two together are sometimes referred to as the peritendon. On its inner surface the epitenon is continuous with the endotenon, which invests each tendon fibre (Józsa & Kannus 1997).

The musculotendinous junction is the area where tension generated in the muscle fibres is transmitted from intra-cellular contractile proteins to extracellular connective tissue proteins. It is a relatively weak area making it susceptible to injury (Józsa & Kannus 1997).

The teno-osseous junction is the point of insertion of the tendon into the bone where the viscoelastic tendon transmits force to the rigid bone. At this point the tendon goes though a transition from tendon to fibrocartilage, mineralized fibrocartilage and finally bone. The mechanism of overuse injuries involving the teno-osseous junction, or enthesis, is not well understood. Benjamin et al (2006) note that bony spurs are well documented at numerous entheses and tend to occur with high levels of physical activity. They are more frequently found in males and occur more commonly with increasing age. They can be compared to osteophytes forming around the articular surfaces in arthritic synovial joints. Some individuals appear to have a greater tendency to form bone than others, both at joint margins and at entheses. Where bony spurs are well documented, e.g. at the attachment of the plantar fascia and the Achilles tendon, osteoarthritis-like degenerative changes have been noted in the enthesis fibrocartilage of the fascia or tendon.

The term tendinopathy is a generic descriptor to indicate clinical conditions affecting tendons. The inflammatory model of tendon pain has been challenged (Khan & Cook 2000, Cook et al 2000) and ‘tendinopathy’ is a more appropriate term since it does not commit to pathology. The terms ‘tendinosis’, ‘paratendinitis’ and ‘tendinitis’ are reserved as histopathological labels. Tendinopathy will be used throughout this text to indicate painful overuse tendon lesions and a discussion on the aetiology and pathological processes associated with tendinopathy is included in Ch. 3.

Tenosynovitis occurs in ensheathed tendons and involves the synovium rather than the tendon itself. Inflammation of the synovium can produce adhesions between the two layers of the sheath which may produce a palpable crepitus (Cyriax 1982). Adhesion formation interferes with the normal function of the tendon sheath, which is to allow controlled movement of the sheath around the tendon and to facilitate nutrition by forcing synovial fluid into the tendon (Barlow & Willoughby 1992).

Tenovaginitis is a term used to describe thickening of the synovial sheath (Cyriax 1982) and is associated with chronic tenosynovitis, e.g. de Quervain’s stenosing tenosynovitis of the sheath containing the abductor pollicis longus and extensor pollicis brevis tendons.

As with all other connective tissue structures, tendons remodel in response to mechanical demand and they are sensitive and responsive to changes in physical load, a property which may be demonstrated by a difference in structure within one tendon unit. Eccentric exercise programmes affect type I collagen production and tend to increase tendon volume over the long term, an important consideration in the rehabilitation of tendinopathies (Alfredson & Cook 2007).

Merrilees & Flint (1980) looked at the macrostructural features of different regions of the flexor digitorum profundus tendon in the rat. This tendon, in common with most tendons, is subjected to longitudinal stress throughout its length, but it also possesses a sesamoid-like area as it passes under the calcaneus and talus. In this area the tendon is subjected to compressive forces, as well as to the normal longitudinal stress.

In the zone subjected to tension, the collagen fibres were arranged in longitudinal bundles, but in the zone subjected to pressure, the sesamoid-like area took on a form similar to that of fibrocartilage, i.e. a loose weave of collagen fibres and chondrocyte-like cells arranged in columns perpendicular to the main fibre axis.

This illustrates the ability of connective tissue structures to adapt to different functions and to changes in physical loads in a normal situation. In abnormal situations, such as a period of immobility when physical demand is reduced, adaptations in collagen turnover occur. When physical demand is increased, collagen production increases. The turnover (synthesis and lysis) of collagen is a continuing process allowing the remodelling and adaptation of structures to suit demand.

Several factors affect the mechanical forces that act on tendons and influence their adaptation in response. The different types of activity and the location of the tendon in the body induce different levels of force on tendons, since different tendons are subject to different levels of mechanical loading. The relative size between the muscle and the tendon and the level of muscle contraction also affects the stress applied to the tendon, as does the position and movement in the adjacent joints and the activity within the antagonist muscles (Wang et al 2006).

With regard to viscoelasticity, Eliasson et al (2007) set out to observe the effect of disuse on the mechanical properties (primarily creep and hysteresis) in the Achilles tendon. Achilles tendon was harvested at 1 and 6 weeks from 78 rats divided into three experimental groups. Two of the groups were immobilized and the other served to provide loaded controls. The result showed that the tendons lost viscoelasticity (i.e. as shown by the effects on creep and hysteresis) which was possibly more influenced by glycosaminoglycan chains than collagen.

The most marked biochemical change in tendon ageing is decreased tensile strength. Collagen cross-linking increases and alters the mechanical properties of the tendon; the ability to withstand load, the modulus of elasticity and tensile strength all decrease and there is an increase in mechanical stiffness (Kannus et al 2005).

The joint capsule and its supporting ligaments are similar in function, both allowing and restraining movement at the joints. Ligaments can be considered to be a reinforcement of the joint capsule in an area of special stress. As inert tissue structures they are assessed by passive movements, which should be applied at the extremes of range to test function.

The ligaments, together with the fibrous capsule, guide and stabilize the articular surfaces. When excessive stresses are applied to a joint, proprioceptive impulses recruit a muscle response so that the passive stabilizing effect of the ligament is reinforced by dynamic muscle stabilization (Akeson et al 1987).

To meet its functional requirements of resisting shear as well as tensile and compressive forces, the structure of a ligament is different from that of a tendon. The main ligamentous fibres are 70–80% collagen laid down in bundles, which assume a wavy configuration providing an element of elongation and recoil to facilitate movement (Fig. 2.8). Interwoven with these main fibre bundles are 3–5% elastic fibres, to enhance extensibility and elasticity (Akeson et al 1987). When ligaments are put under longitudinal tensile stress, the parallel wavy bundles of collagen straighten out to prevent excessive movement and to provide tensile strength.

Although the joint capsule is similar in function to ligaments, its structure is slightly different. The capsule consists of sheets of collagen fibres which form a fibrous cuff joining opposing bony surfaces. The fibrous structure is predominantly collagen but, rather than a parallel array of fibres, its pattern is more a criss-cross weave, with the fibres becoming more parallel as the capsule is loaded (Fig. 2.9) (Amiel et al 1990, Woo et al 1990). The ability of the fibres to change and straighten depends on them being mobile and able to slide independently of one another. Capsular contractures in the form of disorganized collagen will prevent independent fibre gliding at the nodal intercept points, considerably reducing function and causing pain.

The joint capsule has two layers: an outer fibrous capsule and an internal synovial membrane. The outer fibrous capsule is strong and flexible but relatively inelastic. It is supported functionally by its ligaments which may be intrinsic, forming an integral part of the joint capsule (e.g. coronary and medial collateral ligaments of the knee), or accessory, being either intracapsular (e.g. the cruciate ligaments) or extracapsular (e.g. lateral collateral ligaments of the knee). The fibrous capsule is perforated by vessels and nerves and contains afferent sensory nerve endings, including mechanoreceptors and nociceptors.

The synovial membrane is mainly a loose connective tissue membrane with a degree of elasticity to prevent its folds and villi becoming nipped during movement. It covers all surfaces within the joint except the articular surfaces themselves and menisci. Adipose fat pads may exist in the joint, acting as shock absorbers, and distinct fringes of synovium may be present, e.g. the plicae of the knee joint. These folds, fringes and villi allow the joints to accommodate to movement.

The synovium is a highly cellular membrane containing synoviocytes, i.e. the synovium-producing cells, and collagen fibres. It has a rich nerve, blood and lymphatic supply. A capillary network is situated on the inner surface of the synovium to produce synovial fluid. Synovial fluid is pale yellow and viscous. It lubricates the ligamentous structures of the joint and nourishes cartilage and menisci through a mechanism of transsynovial flow aided by movement (Akeson et al 1987).

In an arthritis of a joint, the inflammation causes pain and involuntary muscle spasm which prevents full range of movement. The relative immobility causes changes to occur in the connective tissue which lead to capsular contracture, further loss of function and pain. This will be seen clinically as the capsular pattern (see Ch. 1).

Cartilage is a weight-bearing connective tissue displaying a combination of rigidity, which is resistant to compression, resilience and some elasticity. It is relatively avascular and relies on tissue fluid for nourishment. There are three main types:

Elastic cartilage consists of a matrix of yellow elastic fibres and is very resilient. It is found in the external ear, the epiglottis and the larynx.

Fibrocartilage has a large proportion of type I collagen fibres in its matrix, providing it with great tensile strength. Examples are the annulus fibrosus of the intervertebral discs, the menisci of the knee joint, the acetabular and glenoid labra, the articular disc of the acromioclavicular and wrist joints, the lining of the grooves that house tendons, and as a transitional cartilage at the teno-osseous junction of the tendons (Cormack 1987, Palastanga et al 2006, Standring 2009). The annulus fibrosus in the lumbar spine has a unique geometrical pattern of collagen fibres.

Hyaline cartilage is articular cartilage. Its relatively solid gel-like matrix provides a weight-bearing surface which is elastic and resistant to compression. It moulds to the shape of the bones, presenting a smooth articular surface for movement.

Hyaline articular cartilage is composed of scantily deposited chondroblasts and chondrocytes which produce the gel extracellular matrix consisting of type II collagen fibres and amorphous ground substance. The extracellular matrix contains distinctive large super-molecular proteoglycan aggregates which resemble bottle brushes (Fig. 2.10). These provide a network for trapping and retaining water which significantly contributes to the resilience of cartilage (Cormack 1987). The collagen fibres themselves are relatively weak under compression: therefore the water-enhanced matrix compensates for this by providing a resilient weight-bearing surface.

Three separate structural zones exist in hyaline articular cartilage which contribute to its biomechanical functions (Nordin & Frankel 2001). A superficial zone helps to prevent friction between the joint surfaces and to distribute the compressive forces. It consists of fine, tangential, densely packed fibres lying in a plane parallel to the articular surface (Fig. 2.11). In the middle, vertical zone the cells are arranged in vertical columns, perpendicular to the surface, with scattered collagen fibres. The middle layer allows deformation of the collagen fibres absorbing some of the compressive forces. The deep zone forms a transition between the articular cartilage and the underlying calcified cartilage layer; the fibres are arranged in radial bundles. Hyaline articular cartilage has no blood vessels and depends on fluid flow through compressive forces for nutrition. This fluid flow depends on the magnitude and duration of the compressive force and a balance of weight-bearing and non-weight-bearing is important to its health (Levangie & Norkin 2001).

The zonal arrangement of cartilage provides a ‘well-sprung mattress’ arrangement to cope with compression forces. The variation in collagen fibre orientation in each zone enables the articular cartilage to vary its material property with direction of the load.

The fluid content of articular cartilage is responsible for its nutrition as well as its mechanical properties, allowing diffusion of nutrients and products between the cells and the synovial fluid. When cartilage is loaded, the fluid in the ‘sponge’ moves, which is important for the mechanical properties of the cartilage as well as for joint lubrication. Intermittent loading creates a pumping effect but prolonged loading will eventually press fluid out of the cartilage without allowing new fluid to be taken up, leading to degeneration.