Types of pain

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

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.

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:

When pain is decreasing the condition is generally resolving, while increasing pain suggests a worsening condition.

Constant pain which does not change with time, alteration of static posture or activities suggests a non-mechanical condition such as chemical irritation, tumours or visceral lesions (Magee, 2002).

Where pain changes (episodic pain), the therapist should try to determine what activities make the pain worse (exacerbation) and what make it better (remission).

The therapist should try to determine if the pain is associated with particular events (e.g. movements, visceral function), or time of day.

Pain with sporting activity which reduces with rest in general suggests a mechanical problem, irritating pain sensitive structures.

Morning pain which eases with movement indicates chronic inflammation which takes time to build up and reduces with movement.

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.

Table 1.1 Pain descriptions and related structures

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
Throbbing, diffuse	Vasculature

Source Magee (2002) and Petty and Moore (2001) with permission.

Recording pain

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).

Figure 1.5 Visual analogue scales (VAS) used in pain description.

From Petty and Moore (2001) with permission.

Red flags

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.

Table 1.2 Red flags in sport examination indicating medical 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
	Dizziness
	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
	Unusual menstruation
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)
	Sudden weakness

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.

Pain production

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.

Articular neurology

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.

Table 1.3 Function of joint receptors

Adapted from Hertling, D. and Kessler, R.M. (1990) Management of Common Musculoskeletal Disorders. JB Lippincott, Philadelphia.

Alteration in the feedback provided by joint receptors is of great importance following sports injury, and is dealt with in the section on proprioceptive training.

Pain pathways

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).

Figure 1.6 Pain pathways.

From Low and Reed (1990) with permission.

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.

Fast pain is registered in the parietal lobe and visceral pain in the insular 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).

Pain relief mechanisms

Three concepts of pain control are generally used within physiotherapy:

The pain gate

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).

Figure 1.7 The pain gate mechanism. Central control—effects caused by higher centre (brain), action system—pain response. SG, substantia gelatinosa.

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.

Descending inhibition

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).

Technique

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.

Figure 1.8 Guide tubes and needles.

Figure 1.9 Use of guide tubes for needle insertion.

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.

Figure 1.10 Oblique and perpendicular needle insertion.

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.

Precautions and contraindications

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.

It is vital that the practitioner using dry needling has a thorough knowledge of underlying anatomy as trauma to body tissues, including the lungs and other organs, has been reported.

Training

Training in dry needling and acupuncture for registered physical therapy practitioners:

Acupuncture Association of Chartered Physiotherapists: www.aacp.uk.com

British Medical Acupuncture Society: www.medical-acupuncture.co.uk

Institute for the Study of Pain (IMS training): www.istop.org

Chronic inflammation

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).

Response to injury

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.

The slight hyperaemia gives way later to alterations of the intimal layer, the total number of layers increasing threefold. If the trauma does not continue, the protein molecules which were released are cleared by the lymphatics and the osmotic pressures return to normal. If mechanical irritation persists, the intimal layer will continue to thicken. The deep synovial cells now show increased activity and protein synthesis escalates.

Alterations occur in the number of type A and type B synoviocyte cells. The number of type A cells reduces as some of these move into the synovial fluid to become macrophages. The synovial lining becomes filled with fibroblasts, which in turn change into type B cells. Neutrophil cells die, releasing proteolytic enzymes which attack the near joint structures. This process can self-perpetuate the synovitis, even in the absence of further trauma, giving rise to a reactive synovitis.

Onset of symptoms following post-traumatic synovitis usually occurs between 12 and 24 hours after injury and can last for between 1 and 2 weeks. Patients complain mainly of joint tightness, with warmth, erythema and pain being encountered less often. The tightness is due to joint effusion, the increased fluid volume causing the normally negative intra-articular pressure to become positive.

The stability of the joint, no longer created by a negative intra-articular pressure, comes from joint distension instead. This places a traction force on the joint capsule and surrounding ligaments. Pressures are greatest in the effused joint in extremes of flexion and extension, and are reduced at about 30° flexion, this being the resting position taken up by the patient. Haemarthrosis is usually present if swelling occurs within 2 hours of injury, and pain is intense.

Surgical removal of the synovial membrane (synovectomy) may be performed in a number of inflammatory joint disorders. With time the synovium will regrow, and the use of continuous passive motion (CPM) may be used to assist this process (Salter, 1990). Without mechanical stimulation synovial membrane will degenerate through the loss of proteoglycan, so movement is vital to its effective healing.

Types

Bone is essentially a fibrous matrix impregnated with mineral salts (mainly calcium phosphate), and it therefore combines the properties of both elasticity and rigidity. It is a living tissue, which is continually remodelled, and subject to hormonal control. Bone injury within sport is assessed using x-ray, see Treatment note 1.4.

Treatment note 1.4 Diagnostic imaging

Diagnostic imaging is used to support a thorough examination and should not be relied upon as the only means of clinical diagnosis. In some cases physical examination will be superior to imaging, a situation recognized, for example, with ankle injury (see Ottawa ankle rules, Chapter 12).

Imaging types

There are several imaging types used within the management of sports injuries. Reflective imaging includes ultrasound (US) and magnetic resonance imaging (MRI).

With this type of imaging energy is passed into the tissues and reflected back to form an image. Ionizing radiation imaging includes standard x-rays (plain films) and computed tomography (CT). X-rays use radiation which passes through the tissues onto film to cause an image, whereas CT again uses radiation but converts the radiation into digital units to create slices (3 mm minimum) through the body. Emission imaging (bone scan) uses a radiopharmaceutical agent injected into the blood. This is taken up by areas of the body with increased metabolic activity and these show up as images.

Standard x-rays

X-rays pass through the tissues at different rates depending on tissue density. Air is the least dense (radiolucent) and metal the most dense (radio-opaque). X-rays pass easily through air creating the darkest image on x-ray film. The lungs, airways and colon therefore appear black. Fat is the next densest tissue and so appears as very dark grey and is found throughout the body. Fluid absorbs more of the x-rays than air or fat, giving a whiter image. Bone is the most dense naturally occurring tissue, appearing white on x-ray film. This may be either bone itself or where tissues have calcified, for example in myositis ossificans or calcific tendon pathology. Metal completely blocks x-rays and so metal implants are easily visualized on plain film as totally white.

Because x-rays pass through the body in a straight line, they create a planar image, that is one structure superimposed on another. Two images are therefore used lying at 90° to one another, most commonly anteroposterior (AP) and lateral (lat.). X-rays obey the laws of light, and so body positioning is important. The closer the body area to be imaged is to the x-ray film (further from the x-ray beam) the clearer the image will be.

X-ray analysis

A systematic analysis of x-rays may be made using the ABCs mnemonic, standing for Alignment, Bone density, Cartilage and Soft tissue (Table 1.4).

Alignment is assessed by comparing the contour of one bone to that of the adjacent bone. This is normally assisted by drawing a mental line along the edge of the bones. Changed alignment suggests altered stability through soft tissue changes and/or fracture.

Bone is assessed for changes in both density and dimension. In long bones the shaft should appear uniform with increased density towards the edge and less density within the medullary canal. The periosteum should not be lifted and the edge of the bone continuous. At the bone ends the trabeculae of the cancellous bone should be uniform. Bone dimension is compared to neighbouring segments, for example within the spine to the vertebrae above and below to identify wedging.

Cartilage evaluation includes both hyaline cartilage across the joint surface and menisci or labral cartilage within a joint. An arthrogram is required to identify cartilage damage, but when cartilage is changed bone alignment alteration and bone density change normally follow.

Table 1.4 A systematic analysis of x-rays, using the ABCs mnemonic

References

Davis F.A., Magee D.J. Orthopedic Physical Assessment, fifth ed. Saunders/Elsevier; 2008.

Swain J., Bush K.W. Diagnostic Imaging for Physical Therapists. Saunders/Elsevier; 2009.

Two types of bone are generally described, cancellous or spongy bone and compact bone, and important differences exist in both their mechanical properties and methods of healing. Cancellous bone is found at a number of sites, including the bone ends, and is arranged in a system of trabeculae aligned to resist imposed stresses. The shaft of a long bone consists of a ring of compact bone surrounding a hollow cavity. This structure in turn is surrounded by a further layer of compact bone. The bone cavity contains marrow. In infants the bone marrow is red, but this is gradually replaced by yellow bone marrow until, by puberty, only the cancellous bone cavities at the ends of the long bones contain red marrow. With age the bone marrow in these cavities too is replaced, but red bone marrow may still be found in the vertebrae, sternum and ribs, as well as the proximal ends of the femur and humerus.

The bone is enclosed in a dense membrane called the periosteum, which is absent in the region of the articular cartilage. The periosteum is highly vascular and responsible for the nutrition of the bone cortex which underlies it. The deep layers of periosteum contain bone-forming cells (osteoblasts). These lay down successive layers of bone during growth, and so the periosteum is responsible for alterations in the bone width; in addition these cells play an important part in bone healing. In contrast, the bone cavity is lined by bone-destroying cells (osteoclasts) which erode the inner surface of the bone. A direct blow to the bone which produces bleeding beneath the periosteum will lift it, causing bone deposition by the osteoblasts. This is a common problem over the anterior tibia in footballers and hockey players.

Bone may be further classified into four major types. The long bones are found within the limbs, and consist of a shaft and two enlarged ends. Short bones have a block-like appearance such as those of the carpals, and are mainly cancellous bone. Flat bones are thinner, and consist of two layers of compact bone sandwiching a thin layer of cancellous bone; examples are the skull vaults and the ribs. Finally, irregular bones consist of a thin layer of compact bone surrounded by cancellous bone; examples are the vertebrae.

Development

Skeletal development begins with loosely arranged mesodermal cells which are mostly converted to hyaline cartilage. Between the seventh and twelfth intrauterine week a primary ossification centre appears within the shaft of the long bone, and spreads towards the bone ends. The centre of the shaft is hollowed out and filled with red bone marrow, and the whole shaft is called a diaphysis. At the end of the bone, secondary centres of ossification appear, usually after birth. Gradually the main part of the cartilage is replaced, leaving only the articular cartilage, and a cartilage plate (growth plate, or physis) between the shaft and end of the bone.

The growth plate is of great importance in paediatric sports medicine. This cartilage layer is responsible for the increase in bone length. As the cartilage grows it becomes thicker, and its upper and lower surfaces are converted to bone. Eventually the cartilage stops growing, but its ossification continues so that the cartilage becomes thinner, until it eventually disappears. At this point the diaphysis and epiphysis are united, and growth in length of the bone is no longer possible. The point at which this occurs may be influenced by a number of factors, including impact stresses (see below).

Intramembranous ossification occurs in the mandible, clavicle and certain bones of the skull (Palastanga, Field and Soames, 1989). Here, the intermediate stage of cartilage formation is omitted and the bone ossifies directly from connective tissue.

Epiphyseal injury

Two types of epiphysis are found. Pressure epiphyses are found at the end of long bones, and are interarticular. They are subjected to compression stress with weight bearing, and are responsible for changes in bone length. Traction epiphyses (apophyses) occur at the insertion of major muscles. They experience tension stress as the muscles contract, and alter bone shape.

The growth plate itself forms a weak link in the immature skeleton, and shearing or avulsion stresses can cause it to be dislodged. Because the epiphyses are weaker than the major joint structures, injuries which in the adult would cause dislocation or tendon rupture may cause epiphyseal injury in a child.

Five types of injury have been described (Salter and Harris, 1963), as shown in Fig. 1.15. The type I lesion involves horizontal displacement of the growth plate while with the type II lesion the fracture line runs through to the adjacent metaphysis. In the type III and IV fractures the joint surface is involved, so the complication rate is higher (Watson, 1992). Gentle manipulation under anaesthetic is normally used to realign the epiphysis in the first fracture types. Crush injuries and those through the growth plate may cause more severe problems of growth disturbance. When a fracture crosses the growth plate, bone may fill the gap formed, giving unequal growth. Crush injuries may lead to premature closure of the plate with associated deformities of shortening and altered bony angulation.

Figure 1.15 Epiphyseal injuries.

After Salter and Harris (1963) with permission.

Osteochondrosis

Osteochondrosis affects the pressure epiphyses during their growth period, and are the most common overuse injuries seen in children. There is an interference with the epiphyseal blood supply, causing an avascular necrosis to the secondary ossification centre. The bone within the epiphysis softens, dies and is absorbed (Fig. 1.16). Because the cap of articular cartilage surrounding the epiphysis receives nutrition from the synovial fluid, it remains largely unaffected. The combination of softening bone contained within an intact articular cap leads to flattening of the epiphysis. Gradually the dead bone is replaced by new bone by a process of ‘creeping substitution’. Trauma may be one factor which initiates the ischaemic process, either through direct injury or vascular occlusion as a result of traumatic synovitis (Gartland, 1987).

Figure 1.16 Stages of osteochondritis. (A) Normal epiphysis. (B) The bony nucleus undergoes necrosis, loses its normal texture and becomes granular. (C) The bony nucleus becomes fragmented during the process of removal of dead bone. (D) If subjected to pressure the softened epiphysis becomes flattened. (E) Re-ossification with restoration of normal bone texture, but deformity may persist. The whole process takes 2–3 years.

From Gartland (1987) with permission.

The osteochondroses may be categorized into four groups (Pappas, 1989):

Any pressure epiphysis may be affected by osteochondrosis, the condition taking the name of the person who first described it in that region. The most common conditions are shown in Table 1.5, and details of these are given in the relevant clinical chapters in Section II of this book.

Table 1.5 The osteochondroses

Healing

Bone healing is governed by a number of factors, including the type of tissue which is damaged, the extent of the damage and position of the bony fragments, the amount of movement present at the fracture site as healing progresses and the blood supply. In a long bone, healing may be divided into five stages, as shown in Fig. 1.17 (Crawford-Adams, 1978; Apley and Solomon, 1988).

Figure 1.17 Stages of fracture healing. (A) Haematoma. Tissue damage and bleeding occur at the fracture site, the bone ends die back a few millimetres. (B) Inflammation. Inflammatory cells appear in the haematoma. (C) Callus. The cell population changes to osteoblasts and osteoclasts, dead bone is mopped up and woven bone appears in the fracture callus. (D) Consolidation. Woven bone is remodelled to resemble the normal structure (E).

From Apley and Solomon (1988) with permission.

The rate of healing is dependent on a number of factors. The type of bone is important, cancellous bone healing far more quickly than cortical bone. Also, the fracture type will dictate the speed of healing, with a spiral fracture healing more quickly than a transverse type. If the blood supply has been compromised at the time of injury, or if the fracture has occurred in an area with a poor blood supply, the healing rate will be slower. The age and health of the patient are other determining factors, with fractures in children healing almost twice as fast as those in adults. In general terms, callus may be visible radiographically within 2–3 weeks of injury, with firm fracture union taking about 4–6 weeks for upper limb fractures and 8–12 weeks for those in the lower limb. Full consolidation may take as much as 8 and 16 weeks for upper and lower limb fractures, respectively.

In contrast to long bone, cancellous bone remains fairly immobile when fractured, and heals by ‘direct repair’ with a minimum of callus formation. The main difference occurs because there is no medullary canal in cancellous bone, and the area of contact between the two injured bone fragments is much greater. Following haematoma formation, new blood vessels and osteogenic cells penetrate the area and meet similar tissue from the opposite bone fragment. The intercellular matrix which is laid down by osteoblasts is calcified into woven bone. This type of healing also occurs when internal fixation is used.

Mechanical properties

Bone responds to mechanical stress in similar ways to other connective tissue, but at a considerably slower rate. Its ability to adapt its structure, size and shape depends on the mechanical stresses placed upon it. When stress is reduced, by prolonged bed rest for example, mineral reabsorption occurs and the bone reduces in strength. Raising stress to an optimal level, by exercise, leads to an increase in bone strength.

In addition to changes in total mineral content, bone varies its strength according to the direction of the imposed stress. At bony attachment sites such as tubercles, alignment of collagen fibres is parallel to the direction of the imposed force. In the shaft of a long bone, fibre orientation is along the bone axis, indicating that this part of the bone is designed to resist tension and compression forces. In cancellous bone at the epiphysis, shear stresses are maximal and so fibre alignment is in the direction of the shearing forces.

A number of mechanisms have been proposed to explain how the bone remodels to imposed stress. Bassett (1965) argued that, in theory, mechanical stresses on bone create electrical charges (piezoelectric effect). Areas of compression were said to develop negative charges while those subjected to tensile stress are more positive. The suggestion is that bone deposition by osteoblasts occurs in negatively charged areas, while reabsorption by osteoclasts takes place in regions of positive excitation. Experiments with dogs (Bassett and Pawlick, 1964) have shown that new bone is laid down at an implanted cathode site, although other authors have described bone deposition at both negative and positive sites (Hert and Zalud, 1971) so the effects of polarity are still uncertain.

Electrical fields formed in bone as a result of imposed stresses have been shown to stimulate protein synthesis in frog osteogenic cells (Becker and Murray, 1970), and increased rate of bone formation has been shown as a result of direct current (d.c.) administered through implanted electrodes (Becker, Spadaro and Marino, 1977).

Bone trabeculae subjected to maximum stress will be strengthened by bone deposition, in the direction of the imposed force. Regions of high stress have denser trabeculae, aligned to minimize the bending effect on a bone. Where a bone is subjected to an unbalanced force, which would tend to bend it, remodelling occurs as a result of changes in surface strain (Reigger, 1990). On the convex surface of the bone, osteoclastic activity leads to bone reabsorption, while on the concave surface the reverse occurs and bone deposition is seen. Bone therefore moves towards the concavity which has been induced through loading of the shaft, to minimize the bending effect, a process known as flexural drift. The stress imposed on the bone causes an increase in the calcium concentration found within the interstitial fluid, as a result of changes in bone crystal solubility.

Osteoporosis

Osteoporosis (bone mineral loss) has now reached epidemic proportions in the Western world (Carbon, 1992). The condition involves a progressive decrease in bone mineral density (BMD), due to an imbalance between bone formation and bone reabsorption. Bone mass reaches its peak in the third and fourth decade, and loss occurs normally in both sexes with ageing, but this rate is increased markedly with osteoporosis. Normal bone loss of 3% per decade may increase to as much as 10% per decade for trabecular bone. This leads to a reduction per decade in ultimate stress of 5%, ultimate strain of 9% and energy absorption of 12% (Behiri and Vashishth, 2000).

Osteoporosis may be either primary, governed by age and sex, or secondary as a result of disease. The most common primary types are postmenopausal osteoporosis and senile osteoporosis.

The loss of mass makes the bone susceptible to fracture, particularly as a result of microtrauma. Common fracture sites include the distal radius and vertebrae for postmenopausal osteoporosis, and the proximal femur for senile osteoporosis. Fracture of the distal radius presents as a Colles’ fracture, while vertebral wedging gives rise to an increased thoracic kyphosis or ‘dowager’s hump’.

There is a marked increase in the risk of fracture once bone density reduces below a certain level (known as the fracture threshold, Fig. 1.18). The incidence of hip and vertebral fractures rises with age (Fig. 1.19), but the rise in hip fracture incidence in men occurs some 5 years later than that in women (Wolman and Reeve, 1994), an indication of the effect of postmenopausal osteoporosis.

Figure 1.18 Changes in bone density with age.

From Wolman, R.L. and Reeve, J. (1994) Exercise and the skeleton. In Oxford Textbook of Sports Medicine (eds M. Harries et al.). Reprinted with permission of Oxford University Press, Oxford.

Figure 1.19 Incidence of common osteoporotic fractures.

From Wolman, R.L. and Reeve, J. (1994) Exercise and the skeleton. In Oxford Textbook of Sports Medicine (eds M. Harries et al.). Reprinted with permission of Oxford University Press, Oxford.

Assessment of osteoporosis

Changes in BMD is the standard objective measure for osteoporosis, but low bone density in itself is asymptomatic. It is only when a fracture occurs or they develop pain or substantial postural changes that individuals seek help. Assessment of BMD may be made by direct examination of x-rays. Cortical index measures the thickness of the bone cortex in comparison to the bone shaft. The combined width of the two cortices should be 50% of the total width of the bone at mid-shaft (Apley and Solomon, 1993). Trabecular index is a method of assessing bone mass from the radiographic pattern of bone trabeculae in the proximal femur or calcaneus. A more accurate measure of BMD is obtained by dual energy x-ray absorpiometry (DXA). The amount of radiation used is relatively small, representing no more than 3% of the natural background radiation in a large city (Lewis, Blake and Fogelman, 1994; Huda and Morin, 1996). Measurement is taken yearly, and only changes greater than 2–3% are significant (Bennell, Khan and McKay, 2000). Results are expressed as BMD in g/cm², as a Z score which compares the value to an age matched group, or as a T score which compares the obtained value to a young healthy population. The World Health Organization has classified degrees of BMD loss as shown in Table 1.6.

Table 1.6 Classification of osteoporosis

BMD expressed as standard deviations (SD) below the mean of a young adult (T score). World Health Organization (1994) Assessment of Fracture Risk and its Application to Screening for Osteoporosis. Report of WHO study group. World Health Organization, Geneva. With permission.

Subjective assessment includes elements such as family history, fracture status, history of falls, menstrual history, smoking and dietary habits, and exercise status. Objective examination is of posture, pain and functional limitation (CSP, 1999; Bennell, Khan and McKay, 2000).

Three main factors are important in the development of osteoporosis: diet, oestrogen level and physical activity.

Diet

Modern diet can fail to provide an adequate daily intake of calcium. Recommended requirements as high as 1500 mg of calcium and 400 IU of vitamin D have been made for postmenopausal women (MacKinnon, 1988), but many women may consume as little as 300 mg of calcium (McArdle, Katch and Katch, 1986), placing themselves in negative calcium balance. Excess salt or caffeine, and a large intake of meat promote calcium loss in the urine, and an excessive intake of fibre and alcohol can bind calcium in the gut, preventing its absorption (Deakin and Brotherhood, 1992).

Calcium deficiency in animals has been shown to produce osteoporosis (Martin and Houston, 1987), but effects in man are less clear. Studying early postmenopausal women, Nilas, Christiansen and Rodbro (1984) gave a 500 mg calcium supplement over a 2-year period and assessed bone density in the distal radius, while Ettinger, Genant and Cann (1987) gave a 1000 mg supplement and assessed the lumbar vertebrae. Both of these studies failed to show any significant differences between the treatment and non-treatment groups. However, in late postmenopausal women calcium supplementation may be more beneficial (MacKinnon, 1988). However, the effect of calcium supplementation on the incidence of fractures remains unproven (Evans, 1990b).

Adequate calcium is clearly necessary for health, and those individuals who show a deficiency in their calcium intake may need dietary supplementation. Others should receive advice on good diet to enable them to maintain an adequate intake of calcium and vitamin D, remembering that excessive vitamin D intake can be toxic.

Exercise

Weight-bearing exercise creates bone stress and acts as a stimulus for maintaining bone mass. Loss of bone mass has been reported both as a result of prolonged bed rest (Donaldson, Hulley and Vogel, 1970) and following weightlessness (Mazess and Whedon, 1983). Similarly, athletes have been shown to have greater bone density than non-athletes (Nilsson and Westlin, 1977), and tennis players have been shown to have a greater bone density in their dominant arm (Huddleston, Rockwell and Kuland, 1980).

A number of authors have demonstrated the beneficial effects of weight-bearing exercise in slowing bone loss. Smith, Smith and Ensign (1984) assessed the effects of exercise (45 minutes, 3 days per week) on bone loss in postmenopausal women and showed a 1.4% increase in bone mass during the second and third years of their study. Krolner, Toft and Nielsen (1983) studied the effects of exercise (1 hour, twice per week) on postmenopausal women. They showed a 3.5% increase in bone mineral content of the lumbar spine for the exercising group compared to 2.7% for their control.

High impact exercise which generates a ground reaction force greater than twice body weight is likely to create bone remineralization (Heinonen, Kannus and Sievanen, 1996). Exercise should be performed at least three times per week at intensities beginning with 40–60% maximal oxygen uptake (VO₂ max) and progressing to as much as 80% VO₂ max, even in the elderly (ACSM, 1998). Strength (weight) training at 70% 1 RM has been shown to maintain hip and spine BMD, but programmes must be given progressively, taking clinical history into account. A flowchart to guide exercise prescription is shown in Fig. 1.20.

Figure 1.20 Exercise prescription for osteoporosis.

Adapted from Bennell, Khan and McKay (2000), with permission.

Clearly, regular weight-bearing exercise is important for the prevention and management of osteoporosis. However, the increased risk of fracture in this group means that caution must be shown. Repeated spinal rotation or flexion should be avoided, and high impact activities should be limited at the early stages of treatment, especially where osteoporosis already exists.

Hormone replacement therapy

The use of low dosage oestrogen in hormone replacement therapy (HRT) to slow or even halt bone loss in postmenopausal women is widely recommended. HRT is used to make up for the decline in oestrogen levels seen during the menopause. Oestrogen plays an important part in calcium absorption by the body. Secreted by the ovaries and corpus luteum, oestrogen (a steroid hormone) stimulates regeneration of the endometrium, increases mucus output from the cervical glands, and promotes epiphyseal closure and growth of the bones and skeletal muscle.

HRT has been linked with an increased risk of endometrial carcinoma, although the risk is reduced when oestrogen is combined with progesterone (Hedlund and Gallagher, 1988).

Transient osteoporosis

Transient osteoporosis most commonly affects the hip, where it is termed idiopathic transient osteoporosis of the hip (ITOH) (Harrington et al., 2000). It is a relatively rare condition which must be differentiated from both stress fracture and avascular necrosis. The condition was first described in women during late pregnancy (Curtiss and Kincaid, 1959). However, the main group to suffer from this condition are middle-aged (40–70 years) men, who represent over 70% of cases (Lakhanpal, Ginsburg and Luthra, 1987). ITOH is a self-limiting condition which demonstrates bone marrow oedema and slight bone cortex thinning. There is no evidence of the focal subchondral bone defect of the femoral head seen in avascular necrosis (Harrington et al., 2000). Joint fluid is sterile (non-infected) and only mild synovial thickening is present (McCarthy, 1998).

Subjective examination reveals progressive unilateral hip pain referred into the groin and anterior thigh. Pain is exacerbated with weight bearing and eased with rest (contrast with malignancy which gives pain at rest). Typically pain is worse 4–8 weeks after onset, and enforced rest may show disuse atrophy of the quadriceps and gluteal muscles. The joint and greater trochanter may be tender to palpation and the FABRE test positive.

Management is by protected weight-bearing (crutches) and non-weight-bearing or partial weight-bearing exercise to pain tolerance (pool/walking/jogging). Non-steroidal anti-inflammatory drugs (NSAIDs) may be of use, and protracted cases have responded to core decompression of the femur (Apel, Vince and Kingston, 1994).

Injury

Articular cartilage is to a great extent protected from injury by the elasticity of other joint structures, and the neuromuscular reflexes. Reflex muscular contraction and soft tissue ‘give’ will largely dampen shock before it reaches the cartilage. However, unexpected loading (such as trauma) which occurs too rapidly to invoke reflex protection will cause injury, but this is more frequently bony fracture rather than damage to the cartilage itself.

If cartilage injury does occur, it is most likely due to slip or shear. Three injury stages have been described (Hettinga, 1990): first, splitting of the cartilage layer at the tidemark between the calcified and uncalcified tissue; second, cartilage depression into the subchondral bone; and third, fissuring of the cartilage and underlying bone.

Partial thickness injuries, limited to the articular cartilage alone, heal poorly. The healing which does take place is by proliferation and invasion from soft tissue, and the further away from this tissue the injured area is, the poorer the healing. Full thickness defects, extending through the subchondral bone, heal by superficial tissue bridging the break. Blood vessels grow into the uncalcified cartilage. Osteogenic cells and granulation tissue from the base of the break invade the area, resulting in the formation of fibrous tissue, bony trabeculae and fibrocartilage. There is obvious demarcation of the region into zones, a chondrin-free ring surrounding the uninjured tissue. The healed defect appears as a slightly discoloured roughened area of fibrous tissue.

Cartilage repair

Several surgical techniques may be used to aid repair of injury to articular cartilage (Table 1.7). The joint surface may be debrided (scraped) and the joint itself washed out (lavaged) to remove fragments of cartilage or subchondral bone. Damaging enzymes produced through cartilage degeneration are also removed. New cartilage cells may be introduced into the damaged area to stimulate healing. Osteochondral grafts of this type may be taken from the patient (autografts) or from cadaveric donors (allografts). A number of tissues have been used for autografts including rib perichondrial cells, periosteum and chondrocytes themselves. The technique involves two surgical procedures. First the cells must be removed, then allowed to grow in a laboratory, and finally the cells must be replanted into the damaged cartilage. Allograft techniques can result in high degrees of rejection as a complication (Wroble, 2000) but only involve a single surgical procedure.

Table 1.7 Management of articular cartilage degeneration

Drilling, abrasion and microfracture all work by penetrating the subchondral bone and stimulating cell regrowth. The aim is to allow a conduit for clot formation containing mesenchymal stem cells capable of forming repair tissue (Steadman, Rodkey and Singleton, 1997). Unfortunately fibrocartilage rather than renewed hyaline cartilage is produced by these procedures. Further details of cartilage repair and rehabilitation are given in Chapter 9.

Myositis ossificans traumatica

Myositis ossificans traumatica (MOT) is soft tissue ossification of muscle resulting in the formation of non-neoplasmic bone (Booth and Westers, 1989). It usually occurs in the proximal limb muscles, and is seen most commonly following contusion of the quadriceps femoris musculature (Jackson, 1975), although other regions include the elbow flexors and hip abductors.

Several aetiological theories have been suggested (Booth and Westers, 1989). Calcification of a muscle haematoma can occur following fibrosis, or intramuscular bone formation may result from periosteal detachment. Rupture of the periosteum may lead to the proliferation of osteoblasts and their escape into the surrounding muscle. Intramuscular connective tissue may undergo metaplasia into bone, and Urist et al. (1978) demonstrated that certain skeletal muscle cells, known as inducible osteogenic precursor cells (IOPC), have the capability of differentiating into osteoblasts. Certain individuals have been shown to have a predisposition to the condition (Rothwell, 1982).

Clinically, the patient presents with severe post-traumatic pain and limitation of movement. There is local swelling and erythema, with the area being warm and tender to palpation. Tenderness usually becomes more pronounced with time, and tissue signs do not respond to conservative management. The factor which should alert the practitioner to the possibility of MOT is a reduction in movement range over time. Normally, an increasing range would be expected as a condition resolves. Radiological evidence of ossification is usually seen within 2 months following injury, and other investigations, including computed tomography (Vas et al., 1981) and ultrasound scanning (Kramer et al., 1979) have been used.

Management of MOT is aimed at lessening any disability rather than affecting the bone mass. Initially, the soft tissue response to trauma, especially bleeding, is limited by the use of such regimens as rest, ice, compression and elevation (RICE). Rehabilitation is slower than with a normal muscle haematoma, isometric exercises being used 7–14 days following injury, but active exercises (within the pain-free range) are not used until 2–4 weeks after injury (Booth and Westers, 1989).