physical trauma changes the normal composition of the underlying architecture. Connective tissue becomes denser and more irregular, and the number of plump fibroblasts increases (24). The defined lines of demarcation of the epimysium can become obliterated, resulting in loss of effective sliding movement (25). In scarred fascia, the following physical changes were

discovered compared with normal fascia (26): n an increase in collagen solubility n an increase in the ratio of collagen type III to type I n an increase in total glycosaminoglycan types (chondroitin, dermatan and heparin sulfates). Collagen type III is more extensible than, contains thinner

fibrils than, and is not as strong as type I collagen; therefore, the reduction in the type I/type III ratio gives rise to a fascia with reduced mechanical strength. Similarly, changes in collagen and glycosaminoglycan (GAG) content result in conditions observed in hypertrophic scars (27). McCombe and colleagues showed that the structurally

defined interface of fascia and muscle creates an effective plane for sliding motion, but scarred fascia can disrupt the planes and limit motion (24). This scar may also prove to be the source of pain for some considerable time after its formation as a result of local nociceptive stimulation.

TISSUE HEALING During the inflammatory phase, the tensile strength of the tissue is significantly reduced and remains at its weakest for the first five days post-injury (17,28,29). The temporary fibrin is extremely fragile and needed to curtail haemorrhage of the injured tissue (10,28). Additionally, the vascular system of the newly forming tissue is delicate and liable to tear easily with stretch or pressure (28,30). It is widely agreed that inflammation is imperative to normal tissue healing and, as such, should not be unduly interrupted or shortened (28,30,31). On the other hand, excessive inflammation leads to excessive scar formation (30), pain, oedema, secondary tissue ischemia, loss of motion and weakness, all of which are harmful to the final outcome (31).

The tensile strength of the healing tissue remains relatively low initially, since the ECM and collagen fibres

still lack the organisation and orientation of mature tissue. However, organisation improves as healing progresses (32), so that by day 18, fibroblasts and collagen fibrils are mostly oriented in the longitudinal axis and consolidated into densely packed bundles (8). During the last stage of proliferation, the contraction of the wound occurs, which is due to the centripetal movement of pre-existing tissue (33); this reduces the wound’s size and causes a decrease in the mobility of the scar tissue (28). Approximately three to four weeks after injury, the intra- and intermolecular cross-linkages begin to establish between the collagen fibres. These add tensile strength, lead to the creation of adhesions, and restrict the mobility of the scar (28). The proliferation stage begins as the inflammatory phase subsides, at about three to five days post-injury, and extends to roughly day 21 of the healing process (11,30). Depending on the degree of damage, however, this stage has been noted to last for approximately 6–10 weeks (34) or 12 weeks (32) after injury. Collagen turnover peaks during this phase and remains greater than normal throughout (7,32). Synthesis of type I collagen, which is of high tensile strength, predominates over that of type III (28,34).

TREATMENT DTFs, championed by Cyriax (35), are recommended during the proliferation stage of healing (10). These are thought to apply movements to the damaged tissue in imitation of its normal movement, to limit adhesion formation (that cause continuous irritation and inflammation), to cause an increase in local blood flow and to decrease pain (35). It is also theorised that DTFs transmit a tensile stress to the tissue via a “bowstring” effect (1). Friction massage may have a beneficial effect on all three phases of repair.

It has been suggested that a less strongly applied

version of DTF (gentle transverse frictions) applied in the early inflammatory phase enhances the mobilisation of tissue fluid and therefore increases the rate of phagocytosis (36). During maturation, the scar tissue is modified and strengthened by removing, reorganising and replacing cells and matrix (37). It is now generally recognised that internal

SOURCE OF PAIN FOR SOME CONSIDERABLE TIME

22

THE SCAR MAY ALSO PROVE TO BE THE

sportEX dynamics 2009;22(Oct):21-24