CHAPTER 1 Healing
The basic processes of soft tissue healing underlie all treatment techniques for sports injuries. We need to know what occurs in the body tissues at each successive stage of healing to be able to select the treatment technique which is most appropriate for that time. A technique aimed at reducing the formation of swelling, for example, would be inappropriate when swelling had stopped forming and adhesions were the problem. Similarly, a manual treatment designed to break up adhesions and mobilize soft tissue would not be helpful when inflammation is still forming and the tissues are highly irritable.
The stages of healing are, to a large extent, purely a convenience of description, since each stage runs into another. The term phasing rather than separate stages may be more suitable. Traditionally, the initial tissue response has been described as inflammation, but some authors see inflammation as a response separate to the processes occurring at the time of injury. Van der Meulen (1982) described both in terms of the ‘reaction phase’, arguing that the classical inflammatory period is preceded by a short (10 minute) period before the inflammatory mechanism is activated. Others (Hunter, 1998), looking at the changes in strength of the healing tissue, have termed the first stage the ‘lag phase’ because tissue strength does not change. In any traumatic injury the initial stage is bleeding which is the precursor for the inflammatory cascade seen as both a vascular and cellular response.
The second stage of healing has been variously called repair, proliferation and regeneration. The tertiary stage has been termed remodelling (Van der Meulen, 1982; Kellett, 1986; Dyson, 1987). The terms injury, inflammation, repair and remodelling will be used in this text.
When describing the stage of healing, the terms acute, subacute and chronic are helpful. The acute stage (up to 48 hours following injury) is the stage of inflammation. The subacute stage, occurring between 14 and 21 days after injury, is the stage of repair. The chronic stage (after 21 days) is the stage of remodelling. The term chronic is also sometimes used to describe self-perpetuating inflammation, where the inflammatory process has restarted due to disruption or persistent irritation of the healing tissues. The total healing process occurs over a continuum, shown in Fig. 1.1.
Figure 1.1 Timescale for healing.
From Oakes, B.W. (1992) The classification of injuries and mechanisms of injury, repair and healing. In Textbook of Science and Medicine in Sport (eds J. Bloomfield, P.A. Fricker and K.D. Fitch). Blackwell Scientific Publications, Melbourne. With permission.
This stage represents the tissue effects at the time of injury, before the inflammatory process is activated. With tissue damage, chemical and mechanical changes are seen. Local blood vessels are disrupted causing a cessation in oxygen to the cells they perfused. These cells die and their lysosome membranes disintegrate, releasing the hydrolysing enzymes the lysosomes contained. The release of these enzymes has a twofold effect. First they begin to break down the dead cells themselves, and second, they release histamines and kinins which have an effect on both the live cells nearby and the local blood capillary network.
The disruption of the blood vessels which caused cell death also causes local bleeding (extravasated blood). The red blood cells break down, leaving cellular debris and free haemoglobin. The blood platelets release the enzyme thrombin which changes fibrinogen into fibrin. The fibrin in turn is deposited as a meshwork around the area (a process known as walling off). The dead cells intertwine in the meshwork forming a blood clot. This network contains the damaged area.
The changes occurring at injury are affected by age (Lachman, 1988). Intramuscular bleeding, and therefore haemorrhage formation, are more profuse in individuals over 30 years of age. The amount of bleeding which occurs will be partially dependent on the vascularity of the injured tissues. A fitter individual is likely to have muscle tissue which is more highly vascularized, and therefore greater bleeding will occur with muscle injury. In addition, exercise itself will affect gross tissue responses. Muscle blood flow is greatly increased through dilatation of the capillary bed, and again bleeding subsequent to injury will be greater.
The next stage in the healing sequence is that of inflammation summarized in Fig. 1.2. This may last from 10 minutes to several days, depending on the amount of tissue damage which has occurred. The inflammatory response to injury is the same regardless of the nature of the injuring agent or the location of the injury itself (Hettinga, 1990). Various agents can give rise to injury, and Evans (1990a) listed physical, thermal, radiational, electrical and chemical causes.
Inflammation is not simply a feature of soft tissue injuries. It occurs when the body is infected, in immune reactions and when infarction stops blood flowing to an area. Some of the characteristics of the inflammatory response have even been described as excessive (Cyriax, 1982) and better suited to dealing with infection, by preventing bacterial spread, than healing injury (Evans, 1990a).
The cardinal signs of inflammation are heat (calor), redness (rubor), swelling (tumor) and pain (dolor). These in turn give rise to the so-called fifth sign of inflammation disturbance of function of the affected tissues (functio laesa).
Inflammation is often seen as undesirable. However, inflammation is the first stage of healing and so is a vital step on the road to recovery. The aim should be to prevent excessive inflammation and move the athlete on through the stages of healing towards eventual full function.
Heat and redness take a number of hours to develop, and are due to the opening of local blood capillaries and the resultant increased blood flow. Chemical and mechanical changes, initiated by injury, are responsible for the changes in blood flow.
Chemically, a number of substances act as mediators in the inflammatory process. The amines, including histamine and 5-hydroxytryptamine (5-HT or serotonin) are released from mast cells, red blood cells and platelets in the damaged capillaries and cause vessel dilatation and increased permeability lasting 10–15 minutes (Lachman, 1988). Kinins (physiologically active polypeptides) cause an increase in vascular permeability and stimulate the contraction of smooth muscle. They are found normally in an inactive state as kininogens. These in turn are activated by the enzyme plasmin, and degraded by kininases.
The initial vasodilatation is maintained by prostaglandins. These are one of the arachidonic acid derivatives, formed from cell membrane phospholipids when cell damage occurs, and released when the kinin system is activated. The drugs aspirin and indometacin act to inhibit this change—hence their use as anti-inflammatory agents in sports injury treatment. The prostaglandins E1 and E2 are two of the substances responsible for pain production, and they will also promote vasodilatation, blood vessel permeability and lymph flow (Oakes, 1992).
Aspirin is one of a group of drugs called non-steroidal anti-inflammatory drugs (NSAIDs). These work by affecting prostaglandins, which are also involved in action of the stomach. For this reason NSAIDs may cause gastric irritation and should not be given to those with a history of peptic ulcers.
The complement system, consisting of a number of serum proteins circulating in an inactive form, is activated and has a direct effect on the cell membrane as well as helping to maintain vasodilatation. Various complement products are involved, and these are activated in sequence. Finally, polymorphs produce leukotrienes, which are themselves derived from arachidonic acid. These help the kinins maintain the vessel permeability.
Blood flow changes also occur through mechanical alterations initiated by injury. Normally, the blood flow in the venules, in particular, is axial. The large blood proteins stay in the centre of the vessel, and the plasmatic stream, which has a lower viscosity, is on the outside in contact with the vessel walls. This configuration reduces peripheral resistance and aids blood flow.
In a damaged capillary, however, fluid is lost and so the axial flow slows. Marginalization occurs as the slower flow rate allows white blood cells to move into the plasmatic zone and adhere to the vessel walls. This, in turn, reduces the lubricating effect of this layer and slows blood flow. The walls themselves become covered with a gelatinous layer (Wilkinson and Lackie, 1979), as endothelium changes occur (Walter and Israel, 1987).
Some 4 hours after injury (Evans, 1980) diapedesis occurs as the white cells pass through the vessel walls into the damaged tissue. The endothelial cells of the vessel contract (Hettinga, 1990), pulling away from each other and leaving gaps through which fluids and blood cells can escape (Fig. 1.3). Various substances, including histamine, kinins and complement factors, have been shown to produce this effect (Fox, Galey and Wayland, 1980; Walter and Israel, 1987).
From Evans, D.M.D. (1990a) Inflammation and healing. In Cash’s Textbook of General Medical and Surgical Conditions for Physiotherapists (ed. P.A. Downie), 2nd edn. Faber and Faber, London. With permission.
The normal pressure gradients inside and outside the capillary balance the flow of fluid leaving and entering the vessel (Fig. 1.4). The capillary membrane is permeable to water, and so water will be driven out into the interstitial fluid. However, because the tissue fluids usually contain a small amount of protein, and the blood contains a large amount, an osmotic pressure is created which tends to suck water back from the tissue fluid and into the capillary once more. The magnitude of this osmotic pressure is roughly 25 mmHg. At the arteriole end of the capillary the blood pressure (32 mmHg) exceeds the osmotic pressure and so tissue fluid is formed. At the venous end of the capillary the blood pressure has reduced (12 mmHg) and so, because the osmotic pressure now exceeds this value, tissue fluid is reabsorbed back into the capillary.
During inflammation the capillary bed opens and blood flow increases (heat and redness). The larger blood volume causes a parallel increase in blood pressure. Coupled with this, the tissue fluid now contains a large amount of protein, which has poured out from the more permeable blood vessels. This increased protein concentration causes a substantial rise in osmotic pressure, and this, together with the larger blood pressure in the capillary, forces fluid out into the interstitium, causing swelling.
Protein exudation in mild inflammation occurs from the venules only and is probably mediated by histamine (Evans, 1990a). More severe inflammation, as a result of trauma, results in protein exudation from damaged capillaries as well.
During inflammation, lymphatic vessels open up and assist in the removal of excess fluid and protein. The lymph vessels are blind-ending capillaries which have gaps in their endothelial walls enabling protein molecules to move through easily. The lymph vessels lie within the tissue spaces, and have valves preventing the backward movement of fluid. Muscular contraction causes a pumping action on the lymph vessels and the excess tissue fluid is removed to the subclavian veins in the neck.
Pain is the result of both sensory and emotional experiences, and is associated with tissue damage or the probability that damage will occur. It serves as a warning which may cause us to withdraw from a painful stimulus and so protect an injured body part. Unfortunately, pain often continues long after it has ceased to be a useful form of protection. Associated muscle spasm, atrophy, habitual postures, guarding and psychological factors all combine to make chronic pain almost a disease entity in itself.
Pain may be classified as somatogenic (acute or chronic), neurogenic or psychogenic. Chronic pain may be considered as pain which generally lasts for more than 6 weeks, while acute pain is pain of sudden onset which lasts for less than 6 weeks (Donley and Denegar, 1990).
Musculoskeletal pain is not usually well localized—the surface site where the pain is felt rarely correlates directly to injured subcutaneous tissue. Generally, the closer an injured tissue is to the skin surface, the more accurate the athlete can be at localizing it.
Deep pain is normally an aching, ill-defined sensation. It usually radiates in a characteristic fashion, and may be associated with autonomic responses such as sweating, nausea, pallor and lowered blood pressure (Lynch and Kessler, 1990). Pain referral corresponds to segmental pathways, most often dermatomes. The extent of radiation largely depends on the intensity of the stimulus, with pain normally radiating distally, and rarely crossing the mid-line of the body (Cyriax, 1982).
Neurogenic pain is different again. Compression of a nerve root gives rise to ill-defined tingling, especially in the distal part of the dermatome supplied by the nerve. This is a pressure reaction, which quickly disappears when the nerve root is released. Greater pressure causes the tingling to give way to numbness. Compression or tension to the dural sleeve covering the nerve root gives severe pain, generally over the whole dermatome. In contrast, pressure on a nerve trunk usually causes little or no pain, but results in a shower of ‘pins and needles’ as the nerve compression is released. Pressure applied to a superficial nerve distally gives numbness and some tingling, with the edge of the affected region being well defined (Cyriax, 1982).
Irritability may be defined as ‘the vigour of activity which causes pain’ (Maitland, 1991). It is determined by the degree of pain which the patient experiences, and the time this takes to subside, in relation to the intensity of activity that brought the pain on in the first place. The purpose of assessing irritability is to determine how much activity (joint mobilization, exercise, etc.) may be prescribed without exacerbating the patient’s symptoms.
An assessment of irritability may be made at the second treatment session. The amount of movement which the patient was subjected to in the previous session is known, as is the discomfort that he or she feels now. These subjective feelings are then used to determine the intensity of the second treatment session. Similarly, at the beginning of each subsequent treatment session the irritability is again assessed.
Irritability is a measure of the amount of pain a patient experiences as a result of movement (including that of treatment). Irritability should be used to guide the type and intensity of treatment to avoid excessive post-treatment soreness.
Treatment note 1.1 Pain description in examination
During both the subjective examination and the objective examination (see Treatment note 1.5, p. 24) the patient will usually describe pain. Both the type (nature) of pain and its behaviour are important factors in making an accurate clinical diagnosis, and a number of factors should be considered:
The description of pain itself may indicate the structure causing it (see Table 1.1) and the behaviour of the pain on physical examination clarifies the picture.
|Type of pain|
|Cramping, dull, aching, worse with resisted movement||Muscle|
|Dull, aching, worse with passive movement||Ligament, joint capsule|
|Sharp, shooting||Nerve root|
|Sharp, lightning-like, travelling||Nerve|
|Burning, pressure-like, stinging, with skin changes||Sympathetic nerve|
|Deep, nagging, poorly localized||Bone|
|Sharp, severe, unable to take weight||Fracture|
The intensity of pain may be recorded on a visual analogue scale (VAS). The patient is asked to indicate the pain description or number which best represents their pain. Where a 10 cm line is used the distance from the left of the scale to the point marked by the patient may be measured in millimetres and used as a numerical value (Fig. 1.5).
It is important for the therapist to appreciate when pain and other symptoms may suggest serious pathology which requires medical investigation—so called ‘red flags’ (Table 1.2). Where the patient has persistent pain and is generally unwell, the indication is that a pathology other than a musculoskeletal condition exists. In addition, changes in bladder and bowel habits, alteration in vision or gross changes in gait all require further investigation.
|System/possible pathology||Pain behaviour|
|Cancer||Persistent night pain|
|Constant (25 hour) pain|
|Unexplained weight loss (e.g. 4–6 kg in 10 days)|
|Loss of appetite|
|Unusual lumps or growths|
|Sudden persistent fatigue|
|Past history of carcinoma|
|Cardiovascular||Shortness of breath|
|Pain or feeling of heaviness in the chest|
|Pulsating sensations in the body|
|Discolouration in the feet|
|Persistent swelling with no history of injury|
|Gastrointestinal/genitourinary||Frequent or severe abdominal pain|
|Frequent heartburn or indigestion|
|Frequent nausea or vomiting|
|Change in bladder or bowel habits|
|Neurological||Changes in hearing|
|Frequent or severe headache|
|Problems in swallowing or changes in speech|
|Gait disturbance, or problems with balance/ coordination|
|Drop attacks (fainting)|
Source Magee (2002) and Waddell, G., Feder, G. and Lewis, M. (1997) Systematic reviews of bed rest and advice to stay active for acute low back pain. British Journal of General Practice, 47, 647–652. With permission.
Free or ‘bare’ nerve endings (type IV) respond to painful stimuli and are termed nociceptors. They are largely unresponsive to normal stimuli, but have a low threshold to mechanical and thermal injury, anoxia and irritation from inflammatory products. Tissues vary in the intensity of pain they will produce when stimulated. The joint capsule and periosteum are the most sensitive to noxious stimuli. Subchondral bone, tendons and ligaments are the next in line in terms of sensitivity, followed by muscle and cortical bone, the synovium and cartilage being largely insensitive.
The pain receptors are supplied by a variety of different nerve fibres. Skin receptors are supplied by thinly myelinated (A delta) fibres which carry ‘fast’ pain and respond to strong mechanical stimuli and heat above 45°C (Low and Reed, 1990). They give the initial sharp well-localized pain feeling (pinprick). The function of fast pain is to help the body avoid tissue damage and it often provokes a flexor withdrawal reflex.
Impulses from free nerve endings found in deeper body tissues are carried by non-myelinated C fibres. This is ‘slow’ pain, which tends to be aching and throbbing in nature, and poorly defined. Its onset is not immediate, and the sensation it produces persists after the pain stimulus has gone. The function of slow pain seems to be to enforce inactivity and allow healing to occur and it is therefore often associated with muscle spasm. The C fibres respond to many different types of stimuli and, as such, are said to be ‘polymodal’. However, they are most sensitive to chemicals released as a result of tissue damage. Histamine, kinins, prostaglandins E1 and E2, and 5-HT have all been implicated in this type of pain production during inflammation (Walter and Israel, 1987; Lachman 1988).
It can be seen that the pain experienced as a result of sporting injury will usually be either mechanical or chemical in nature. Mechanical pain is the result of forces which deform, or damage the nociceptive nerve endings, and so may be caused by stretching contracted tissue or by fluid pressure. This type of pain is influenced by movement. Chemical pain, on the other hand, results from irritation of the nerve endings, and is less affected by movement or joint position, but will respond to rest.
In addition to pain receptors (type IV), three other joint receptors are important. Type I receptors are located in the superficial layers of the joint capsule. They are slow adapting, low-threshold mechanoreceptors, which respond to both static and dynamic stimulation. These receptors provide information about the static position of a joint, and contribute to the regulation of muscle tone and movement (kinaesthetic) sense. The type I receptors sense both the speed and direction of movement.
Type II receptors are found mainly in the deeper capsular layers and within fat pads. These are dynamic receptors with a high threshold, and they adapt quickly. They respond to rapid changes of direction of joint movement.
The type III fibres are found in the joint ligaments, and are again high threshold dynamic mechanoreceptors, but are slow adapting. These receptors monitor the direction of movement, and have a ‘braking’ effect on muscle tone if the joint is moving too quickly or through too great a range of motion. The type IV receptor is the nociceptor described above. Table 1.3 provides a synopsis of the various movement categories to which the receptors respond.
|Static position||Type I|
|Speed of movement||Type I|
|Change in speed||Type II|
|Direction of movement||Types I and II|
|Postural muscle tone||Type I|
|Tone at initiation of movement||Type II|
|Tone during movement||Type II|
|Tone during harmful movements||Type III|
Adapted from Hertling, D. and Kessler, R.M. (1990) Management of Common Musculoskeletal Disorders. JB Lippincott, Philadelphia.
Three categories or ‘orders’ of neurone make up the pain pathways. First order neurones travel from the pain receptors to the spinal cord, second order neurones travel within the cord to the brainstem and third order neurones travel from the brainstem to the higher centres of the cerebral cortex.
Seventy percent of the C fibres (slow pain) enter the spine via the dorsal root, while 30% of the fibres enter via the ventral root. The C fibres synapse with second order neurones in the substantia gelatinosa (SG) of the cord and these neurones ascend in the anterolateral funiculus on the opposite side of the cord (Fig. 1.6). From here they travel via the reticular formation to the intralaminar nuclei of the thalamus. The neurones synapse here once more and travel to the prefrontal region of the cerebral cortex. Some of the C fibres travel to the limbic system (cingulate gyrus) and generate emotional responses to pain (described as anxiety, fear and dread). C fibre pain is therefore poorly localized with a large emotional effect (White, 1999).
The A delta fibres (fast pain), on the other hand, synapse in the outer part of the posterior horn of the cord and cross to ascend in the spinothalamic tract to the ventrobasal nuclei in the thalamus, and then to the postcentral gyrus of the cortex.
With more major injuries both fibres will produce a pain effect. The response to an ankle sprain, for example, will be an intense, well-defined stabbing sensation (A delta) followed by a dull ache accompanied by an emotional response (C fibre).
The pain gate theory (Melzack and Wall, 1965) proposed that pain perception was regulated by a ‘gate’ which could be opened or closed. When stimulated, mechanoreceptors in the skin send impulses via A beta fibres to the posterior horn of the cord. Here, collateral branches are given off. These collaterals affect A delta and C pain fibres in the substantia gelatinosa (SG), reducing their excitability by presynaptic inhibition. Stimulation of A delta fibres by low intensity, high frequency transcutaneous electrical nerve stimulation (TENS) (100–200 Hz) will therefore reduce pain through this gating mechanism (Fig. 1.7).
From Melzack, R. and Wall, P.D. (1965) Pain mechanisms: a new theory. Science, 150, 197. American Association for the Advancement of Science. With permission.
Interneurones within the substantia gelatinosa are able to produce endogenous (made in the body) opioid peptides, which have similar effects to opioids such as morphine, heroin and codeine, which are some of the most powerful analgesics known. These opioids inhibit C fibre cells. Collateral branches of A delta fibres in the posterior horn connect to the interneurones and stimulate them to produce opioids.
The opioids, including enkephalins and endorphins, are produced in various areas of the central nervous system (CNS) including the limbic system and thalamus, pituitary gland, substantia gelatinosa and nerve terminals. These substances inhibit transmission in the A delta and C fibre pathways and so block pain before it reaches sensory levels. Stimulation of the A delta fibres with high intensity low frequency TENS (2–10 Hz) will damp down C fibre activity and reduce pain through this method.
Descending inhibition occurs when A delta fibres activate a chain of neurones which travel down the length of the spinal cord. Two separate systems are generally said to be involved (White, 1999), one involving serotonin, the other noradrenaline (norepinephrine). In the first, fibres from the periaqueductal grey matter (PAG) of the midbrain travel to the nucleus raphe magnus and then to the stalked cells in the dorsal horn of the spinal cord. In these cells, serotonin is released, which in turn causes the release of enkephalin to inhibit the cells of the SG. In the second system, the arcuate nucleus of the hypothalamus activates nuclei in the brainstem. Descending fibres in turn release noradrenaline (norepinephrine) into the dorsal horn of the cord to again inhibit the SG. Stimulation at frequencies above 50 Hz may affect this system (De Domenico, 1982).
Treatment note 1.2 Dry needling
Dry needling is an acupuncture technique which involves using a solid (no bore) atraumatic needle inserted into the body tissues. Pain relief has been described through both the pain gate mechanisms and diffuse noxious inhibitory control. In addition, according to Oriental medicine pain can be a result of a blockage and/or stagnation of acupuncture energy (qi) and acupuncture is designed to increase the flow of qi energy to stimulate healing and pain relief.
Both painful points (trigger points) and classic acupuncture points may be used. Classic acupuncture points are needled to specific depths described in acupuncture literature (see Norris, 2001). Trigger points may be either needled superficially to a depth of 0.5 cm (Baldry, 1998) or up to 8–10 cm (Gunn, 1996), depending on the mechanism being used. Superficial needling is said to activate A delta nerve fibres responsible for acupuncture pain relief, while deep needling is said to reduce pain but also induce healing through the production of platelet derived growth factor (PDGF) to stimulate new collagen formation (Gunn, 1996).
It should be noted that dry needling carries risks, and requires postgraduate training. Deep needling of the type used in intramuscular stimulation (IMS) in particular is a technique which involves highly specialist training (see Training section at the end of this box).
Acupuncture needles used for musculoskeletal conditions are of pre-sterilized disposable stainless steel construction and they vary from 0.22 mm to 0.45 mm in diameter and may be up to 4 inches in length. The patient’s skin should be cleaned prior to the treatment and the practitioner’s hands should be washed and sterilized with an alcohol-based sanitizer before treatment.
The needles are normally inserted using a plastic guide tube which is slightly shorter than the needle (Fig. 1.8). The guide tube is placed on the skin with the needle within it and the needle inserted through the skin surface with a small, brisk tap. Once the needle is inserted the guide tube is removed, and the needle pressed in further to the required depth (Fig. 1.9). Throughout this procedure, sterile practice must be maintained. To guard against infection, each needle is only used once and the shaft of the needle should not be touched.
The needle is often manipulated by rotation, scraping or flicking to increase the sensation felt by the patient—known as sensory propagation along channels or deqi in Oriental medicine. The needle may be inserted perpendicular to the skin or at oblique and transverse angles (Fig. 1.10). Once the needle is withdrawn the acupuncture point may be pressed with a cotton bud or probe to reduce the likelihood of bruising.
Needles are in general inserted for between 10 and 15 minutes, though shorter insertion techniques may be used to directly stimulate the muscle through intramuscular stimulation (IMS). In addition to muscular treatment, the periosteum of the bone itself may be used as a form of treatment, particularly for joint degeneration. The aim is to strike the periosteum, and the sensation felt is a dull ache rather than the immediate pain of a tissue needle.
Patients who are on anticoagulant therapy and those who have haemophilia should not be treated with dry needling. Diabetic patients should be closely monitored if they are to have needles inserted into hands and feet. Patients with prosthetic or damaged heart valves should be treated with caution. Epileptic patients should not be treated if they have had a fit during the last 3 months. Points on the lower abdomen and the lumbar sacral region should be used with caution during the first trimester of pregnancy. Following needling, it is common for patients to feel drowsy and they should be warned about this.
The effects of acute inflammation can be reduced by slowing the body’s response represented by the cardinal signs. Redness and heat are therefore treated by trying to reduce localized bleeding through the use of cold or ice and compression. Swelling is similarly managed by the use of compression to contain local oedema, and gentle movement to assist lymphatic drainage. By reducing the chemical and mechanical effects of the three inflammatory signs above, pain is also reduced.
Inflammation is the beginning phase in the healing process. Ordinarily tissues progress through the healing process sequentially to restore full function. However, in certain cases injuries remain in the inflammatory period, like a computer program that has become stuck in a loop. This is then termed chronic inflammation and occurs because macrophages have been unable to completely clear (debride) the area of foreign substances. This material may be dead cells, extracellular blood, or sand or dirt in some cases. Either way, the material is surrounded by collagen to isolate it from the body. This mass of encapsulating scar is called a granuloma.
Chronic inflammation has been shown to have a low concentration of growth factors and a high concentration of protease (Hom, 1995). Adding growth factor to a chronic wound has been shown to improve healing in a number of soft tissues. Platelet derived growth factor has been used to treat ligaments and tendons in general (Evans, 1999) whilst insulin like growth factor (IGF-1) has been used with the achilles tendon (Kurtz, Loebig and Anderson, 1999) and articular cartilage (Nixon, Fortier and Williams, 1999).
Inflammation may continue for 5 days, but with minor trauma it is usually complete by the third day after injury (Evans, 1980). Following this, tissue repair can take place. Repair is by resolution, organization or regeneration, depending on the severity of the injury and the nature of the injured tissues. A minor injury will result in acute inflammation as described above, and the phagocytic cells will clear the area. If there is little tissue damage, the stage of resolution will result in a return to near normal (Lachman, 1988). True resolution rarely occurs with soft tissue injuries, but is more common with inflammatory tissue reactions such as pneumonia.
On the periphery of the injured area, macrophages and polymorphs are active because they can tolerate the low oxygen levels present in the damaged tissue. Cellular division by mitosis is seen in the surrounding capillaries about 12 hours after injury. During the next 3 days capillary buds form and grow towards the lower oxygen concentration of the injured area. These capillaries form loops and blood begins to flow through them. This new capillary rich material is known as granulation tissue. Plasma proteins, cells and fluid pour out of these highly permeable vessels. The gradually increasing oxygen supply to the previously deoxygenated area means phagocytosis can now begin.
New lymphatic vessels bud out from the existing lymphatics, linking to form a renewed lymphatic drainage system. As this process is occurring, fibroblast cells multiply and move towards the injured tissue. By the fifth day after injury they begin to lay down fibrils of collagen, a process requiring adequate amounts of vitamin C.
The individual fibrils form into parallel bundles lying in the direction of stress imposed on the tissue. If no movement occurs to stress the collagen bundles, they are laid down in a haphazard and weaker pattern (Cyriax, 1982). Controlled movement causes the fibrils to align lengthways along the line of stress of the injured structure (Burri, Helbing and Spier, 1973). Variation in longitudinal fibre alignment will determine the stress–strain response of the tissue to loading (Fig. 1.11). Where fibre alignment is parallel to the tissue body, the steep stress–strain curve (C) indicates that less deformation will occur for a given tissue loading. The tissue is therefore ‘stronger’.
From Oakes, B.W. (1992). The classification of injuries and mechanisms of injury, repair and healing. In Textbook of Science and Medicine in Sport (eds J. Bloomfield, P.A. Fricker and K.D. Fitch). Blackwell Scientific Publications, Melbourne. With permission.
It becomes clear that external mechanical factors, and not the previous organization of the tissue, dictate the eventual pattern of fibril arrangement. Total rest during this stage of healing is therefore contraindicated in most cases.
External mechanical factors have a positive influence on tissue healing and can dictate the eventual strength of the healing tissues. Long periods of total rest are therefore rarely required when treating sports injuries.
In some tissue full regeneration occurs, damaged cells being replaced by functioning normal tissue. Fractured bone exhibits this property, as do torn ligaments and peripheral nerves providing conditions are suitable (Evans, 1990b).
The remodelling stage overlaps repair, and may last from 3 weeks to 12 months (Kellett, 1986). During this stage, collagen is modified to increase its functional capacity. Remodelling is characterized by a reduction in the wound size, an increase in scar strength, and an alteration in the direction of the collagen fibres (Van der Meulen, 1982).
Contraction of granulation tissue will occur for as long as the elasticity of the fibres will allow (Van der Meulen, 1982). Fibroblast cells transform into myofibroblasts which then form intercellular bonds. These contain contractile proteins (actomyosin) and behave much like smooth muscle fibres.
Three weeks after injury, the quantity of collagen has stabilized (Van der Meulen, 1982) but the strength of the fibres continues to increase. Strength increases are a result of an expansion in the number of cross-bonds between the cells, and the replacement collagen cells themselves. There is a continuous turnover of collagen, a process influenced by a number of factors, including the age of the patient, the type of tissue injured, the quantity of scar tissue present, the site and direction of the scar and external forces (Van der Meulen, 1982; Frank et al., 1983).
Final collagen fibre alignment should match the tissue function (Fig. 1.12). Fibres within a ligament will respond to a range of motion exercises which tense the ligament rhythmically. This may cause mild discomfort (VAS 2−3) but not pain (VAS 7−8). Pain is an indication of tissue damage indicating that the healing process has reverted back from the remodelling stage to the inflammatory stage. Fibres within muscle respond similarly, but to force transmission encountered by active and light resisted exercise during rehabilitation.
The tensile strength of injured soft tissue will reduce substantially after injury due to mechanical damage to the tissues. By the first postinjury day, tensile strength may have reduced by some 50%. Although healing begins immediately, collagen is not laid down until the fifth postinjury day (Garrett, 1990). The period between injury and the beginning of collagen synthesis has been described as the ‘lag phase’ (Fig. 1.13). Manual therapy techniques applied in this period should be aimed at pain resolution and oedema reduction. Only when collagen synthesis begins should therapy aim to prevent adhesions and align collagen fibres in the direction of stress.
Treatment note 1.3 Influencing the mechanical properties of healing tissue
The use of deep transverse frictional massage (DTF) has been claimed to assist soft tissue healing. By applying shear and gliding movements to an injured tendon, ligament or muscle, tensile strength of the healing scar may be improved and adhesions reduced. Gentle DTF applied in the acute phase of healing could increase the rate of phagocytosis by inducing agitation of tissue fluid. In the chronic stage of healing the therapeutic movement produced by DTF is said to soften and mobilize adhesions (Kesson and Atkins, 1998).
Specific soft tissue mobilization (SSTM) is a technique pioneered by Hunter (1998). The procedure involves tensioning the tissue using physiological joint movement and accessory joint movement and adding a dynamic soft tissue mobilization. In the acute phase of healing, SSTM is claimed to influence the mechanical properties of healing tissue by altering collagen and ground substance synthesis.
A sustained load of five repetitions of a 30-second hold is used in a treatment session and the patient performs home exercise by self-stretching for three repetitions of a 30-second hold every 3–4 hours. Using the Achilles tendon as an example (Fig. 1.14), the mobility of the tendon is assessed by subjecting it to shearing forces, beginning distally and moving proximally. The aim is to fix the proximal segment of the tendon with the fingers and then move the tendon in the opposite direction with the fingers of the other hand. The shearing motion is moved up the tendon progressively, assessing range and quality of movement.
Eccentric loading has been used extensively for rehabilitation of the Achilles tendon. It is claimed that the controlled lengthening of the tendon during eccentric actions increases the tensile strength of the tendon (Stanish, Rubinovich and Curwin, 1986; Kannus, 1997) and allows for more storage of elastic energy in the stretch shorten cycle. In addition, eccentric loading may prepare the tendon for rapid unloading. The sudden release of force in this way produces shearing forces within the tendon which could conceivably break up adhesions within the Achilles itself (Curwin, 1994).
In this section we will look at the responses of the individual tissues to injury, and the effects these have upon subsequent rehabilitation. Aspects of tissue structure relevant to sports injury are discussed.
The synovium consists of two layers, the intima, or synovial lining, and the subsynovial (subintimal) tissue. The intimal layer is made up of specialized cells known as synoviocytes, arranged in multiple layers. Two types of synoviocytes are present, type A cells, which are phagocytic, and type B cells, which synthesize the hyaluronoprotein of the synovial fluid. The two types are not distinct, however, and appear to be functional stages of the same basic cells (Hettinga, 1990).
The subsynovial tissue lies beneath the intima as a loose network of highly vascular connective tissue. Cells are interspaced with collagen fibres and fatty tissue. The subsynovial tissue itself merges with the periosteum of bone lying within the synovial membrane of the joint. Similar merging occurs with the joint cartilage through a transitional layer of fibrocartilage.
The blood vessels of the joint divide into three branches, one travelling to the epiphysis, the second to the joint capsule and the third to the synovial membrane (Paget and Bullough, 1981). From here the vessels of the subsynovium are of two types. The first is thin walled and adapted for fluid exchange, and the second thick walled and capable of gapping to allow particles, especially nutrients, to pass through.
Once free of the vessels, any material must pass through the synovial interstitium before entering the synovial fluid itself. The passage of this material is by diffusion on the whole, but by active transport for glucose molecules.
The synovium must adapt to movement with normal function of the joint. Rather than stretching, the synovium unfolds to facilitate flexion. The synovium is well lubricated by the same hyaluronate molecules found within the synovial fluid itself, and so the various layers slide over each other. Since the synovium must alter shape within the confines of the joint capsule, the process of synovial adaptation is at its best when the fluid volume of the joint is at a minimum.
Synovial fluid plays a significant role in joint stability. The negative atmospheric pressure within the joint creates a suction effect, which, aided by the surface tension of the synovial fluid, draws the bony surfaces of the joint together.
With minor trauma the synovium is not microscopically disturbed, but will instead suffer a vasomotor reaction (Hettinga, 1990). The synovium will dilate and fluid filtration increases. Protein leaks into the interstitium, changing the osmotic pressure and causing local oedema and joint exudation. This process constitutes a post-traumatic synovitis.