Many common locomotor problems are short-lived and self-limiting or settle with a course of simple analgesia and/or physical treatment; for example, physiotherapy or osteopathy. Nonetheless, they represent 20-30% of the workload of the primary care physician. Recognition and appropriate early treatment of many painful rheumatic conditions may help reduce the incidence of chronic pain disorders. Early recognition and subsequent treatment of inflammatory arthritis by specialist multidisciplinary teams leads to better symptom control and prevents long-term joint damage and disability. A wide selection of pamphlets offer helpful advice for patients, and their use should be encouraged. Most of the musculoskeletal diseases are seen world-wide, although the prevalence of individual conditions varies.

There are two types of joints – synovial and fibrocartilaginous.

Synovial joint

These include the ball-and-socket joints (e.g. hip) and the hinge joints (e.g. interphalangeal).

They possess a cavity and permit the opposed cartilaginous articular surfaces to move painlessly over each other. Movement is restricted to a required range, and stability is maintained during use. The load is distributed across the surface, thus preventing damage by overloading or disuse.

Synovium and synovial fluid

Normal synovium is a few cells thick and vascular. Its surface is smooth and non-adherent and is permeable to proteins and crystalloids. As there are no macroscopic gaps, it is able to retain normal joint fluid even under pressure. The surface layer comprises macrophages and fibroblast-like cells. The fibroblasts release hyaluronan into the joint space, which helps to retain fluid in the joint. Synovial fluid is a highly viscous fluid secreted by the synovial cells and has a similar consistency to plasma. Glycoproteins ensure a low coefficient of friction between the cartilaginous surfaces. Tendon sheaths and bursa are also lined by synovium.

Fibrocartilaginous joints

These include the intervertebral discs, the sacroiliac joints, the pubic symphysis and the costochondral joints.

Juxta-articular bone

The bone which abuts a joint (epiphyseal bone) differs structurally from the shaft (metaphysis). It is highly vascular and comprises a light framework of mineralized collagen enclosed in a thin coating of tougher, cortical bone. The ability of this structure to withstand pressure is low and it collapses and fractures when the normal intra-articular covering of hyaline cartilage is worn away – as, for example, in osteoarthritis (OA). Loss of surface cartilage also leads to the abnormalities of bone growth and remodelling typical of OA

Hyaline cartilage

This forms the articular surface and is avascular. It relies on diffusion from synovial fluid for its nutrition. It is rich in type II collagen that forms a meshwork enclosing giant macromolecular aggregates of proteoglycan. These heterogeneous macromolecules comprise protein chains (aggrecans) to which are attached side-chains of the carbohydrates keratan and chondroitin sulphate. These molecules retain water in the structure by producing a dynamic tension between the retaining force of the collagen matrix and the expansive effect of osmotic pressure. Intermittent pressure from ‘loading’ of the joint is essential to normal cartilage function and encourages movement of water, minerals and nutrients between cartilage and synovial fluid. Chondrocytes secrete collagen and proteoglycans and are embedded in the cartilage. They migrate towards the joint surface along with the matrix they produce.

Ligaments and tendons

These structures stabilize joints. Ligaments are variably elastic and this contributes to the degree of stiffness or laxity of joints. Tendons are inelastic and transmit muscle power to bones. The joint capsule is formed by intermeshing tendons and ligaments. The point where a tendon or ligament joins a bone is called an enthesis and may be the site of inflammation.

All connective tissues contain an extracellular matrix of macromolecules – collagens, elastins, non-collagenous glycoproteins and proteoglycans – in addition to cells, e.g. fibroblasts. There are several different types of cell surface receptors that bind extracellular matrix proteins including the integrins, CD44 and the proeoglycan-family of receptors e.g. syndecans.

Collagens

Collagens consist of three polypeptide chains (alpha chains) wound into a triple helix These alpha chains contain repeating sequences of Gly-x-y triplets, where x and y are often prolyl and hydroxyprolyl residues. Collagen fibres show considerable genetic heterogeneity, with genes on at least 12 chromosomes. The majority of collagen in the body is type I – the major component of bone, tendon, ligament, skin, sclera, cornea, blood vessels and the hollow organs. Types III, V and VI are also present in most tissues although little collagen type III is found in bone or cartilage. Other types of collagen are tissue specific, i.e. types II, IX, X and XI are found in hyaline cartilage, type IV in basement membrane and type VII in anchoring structures at junctions between epithelium and mesenchyme. There are several classes of collagen genes, based on their protein structures, and abnormalities of these may lead to specific diseases.

Elastin

Elastin is an insoluble protein polymer and is the main component of elastic fibres. Tropoelastin, its precursor, is synthesized by vascular smooth muscle cells and skin fibroblasts. Cross-linkages with desmosine and isodesmosine are specific to elastin fibres.

Glycoproteins

Fibronectin is the major non-collagenous glycoprotein in the extracellular matrix. Its molecule contains a number of functional domains, or cell recognition sites that bind ligands and are involved in cellular adhesion. A peptide sequence (Arg-Gly-Asp), which mimics some of the functions of fibronectin, is also found in other adhesion proteins (e.g. vitronectin, laminin and collagen type VI). Fibronectin plays a major role in tissue remodelling. Its production is stimulated by interferon-gamma and by transforming growth factor-beta and inhibited by tumour necrosis factor and interleukin-1.

Proteoglycans

These proteins contain glycosaminoglycan (GAG) side-chains and are of variable form and size. Many have been identified at different sites in connective tissue, e.g. aggrecan, biglycan, fibromodulin, decorin (in extracellular matrix), syndecan, CD44, fibroglycan (on cell surfaces), cerebroglycan (in brain), serglycan (in intracellular tissues) and perglycan (in basement membranes). Their function is to bind extracellular matrix together, retain soluble molecules in the matrix and assist with cell binding. Abnormalities of any of these structures may lead to periarticular or articular symptoms and/or predispose to the development of arthritis.

Joint sensation

The ligaments, periosteum, synovial tissue and capsule of the joint are richly supplied by blood vessels and nerves. Pain usually derives from inflammation of these sites because the synovial membrane is relatively insensitive.

Taking a musculoskeletal history

The following questions are helpful in assessing the problem and making a diagnosis. A history, taken carefully, can often lead to a diagnosis. Pattern recognition is the key to accurate diagnosis in rheumatic diseases.

Pain

• Where is it? Is it localized or generalized? The pattern of joint involvement is a useful clue to the diagnosis (e.g. distal interphalangeal joints in osteoarthritis).
• Is it arising from joints, the spine, muscles or bone? Soft tissue lesions and inflamed joints are locally tender.
• Could it be referred from another site? Joint pain is localized but may radiate distally – shoulder to upper arm; hip to thigh and knee.
• Is it constant, intermittent or episodic? How severe is it – aching or agonizing? For example, the pain of gout, or of septic arthritis in a previously fit, non-immunocompromised patient is agonizing. Joint pain lasting a day or so may indicate palindromic rheumatism, whilst longer bouts of a few days are typical of untreated gout or pseudogout. Constant pain, especially pain at night, may be due to an underlying malignancy.
• Are there aggravating or precipitating factors? For example:
• Mechanical problems are made worse by activity and eased by rest.
• Inflammatory joint and spine pain are worse after rest and improve with activity.
• Trauma is a common cause of musculoskeletal pain.
• Are there any associated neurological features? Numbness, pins and needles and/or loss of power suggest ‘nerve’ pain. Consider carpal tunnel syndrome, a spinal problem such as disc prolapse or spondylosis , or neurological disease. Nerve root pain, such as that due to a disc prolapse, reflects the anatomical distribution of the affected root.

Stiffness

• Is it generalized or localized? Spine or joint stiffness is common after injury.
• Does it affect the limb girdles or periphery?
• Is it worse in the morning and relieved by activity? Joints that are stiff for more than 15 minutes each morning are usually inflamed – think of rheumatoid arthritis (RA) or another cause of inflammatory arthritis. Spinal stiffness and pain which is much worse in the morning may indicate ankylosing spondylitis , especially in patients in their twenties or thirties. Shoulder and pelvic girdle stiffness and pain, which are worse in the morning in a patient over 55 years, may be polymyalgia rheumatica.

Swelling

• Is it of one joint, or of several? Look for symmetry or asymmetry, and/or a peripheral or proximal pattern; these are important clues to the type of arthritis. Rheumatoid arthritis is typically polyarticular. An acute monarthritis may be due to trauma, gout (in a middle-aged male) or sepsis (fever or immunosuppression).
• Is it constant or episodic?
• Are episodes of swelling short-lived, or longer?
• Is there associated inflammation (redness and warmth)?

Gender

Gout, reactive arthritis and ankylosing spondylitis are more common in men. Rheumatoid arthritis and other autoimmune connective tissue diseases are more common in women.

Age

• Is the person young, middle-aged or older? Injury is common in young people but can occur at any age.
• How old was the patient when the problem first started? Osteoarthritis and polymyalgia rheumatica rarely affect the under-fifties. Rheumatoid arthritis starts most commonly in women aged 20-50 years.

General health

• Is there any associated ill-health or other worrying feature, such as weight loss or fever? Systemic illness is a common feature of many rheumatic diseases. If there is weight loss and/or fever, think of autoimmune rheumatic disease, sepsis (joint infection may be due to septicaemia and is a medical emergency) or malignancy.
• Are there other associated medical conditions that may be relevant? Psoriasis or inflammatory bowel disease is associated with asymmetrical arthritis. Charcot’s joints are seen in diabetics.

Medication

Could a drug be a cause? Diuretics may precipitate gout in men and older women. Hormone replacement therapy or the oral contraceptive pill may precipitate systemic lupus erythematosus (SLE). Steroids can cause avascular necrosis. Some drugs cause a lupus-like syndrome.

Race

Is this relevant? Sickle cell disease causes joint pain in young black Africans, but osteoporosis is uncommon in older black Africans.

Past history

Have there been any similar episodes or is this the first? Are there any clues from previous medical conditions? Gout is recurrent; the episodes settle without treatment in about 10 days. Acute episodes of palindromic rheumatism may predate the onset of rheumatoid arthritis.

Family history

Does anyone in the family have a similar problem or another related disorder? Osteoarthritis may be familial. Sero-negative spondyloarthropathies is seen in families with a history of arthritis, psoriasis, ankylosing spondylitis, iritis or inflammatory bowel disease. Autoimmunity has a familial tendency.

Occupational history

What job does the patient do? This can be a factor in soft tissue problems and osteoarthritis (e.g. in heavy labourers and dancers). Work-related problems are becoming more common and are complained of more.

Psychosocial history

• Has there been an injury for which a legal case for compensation is pending?
• Has there been any recent major stress in family or working life? Could this be relevant? Stress rarely causes rheumatic disease but may precipitate a flare-up of inflammatory arthritis. Stress also tends to reduce a person’s ability to cope with pain or disability. Remember that the diagnosis of a chronic arthritis has a major influence on the lifestyle of patients and their families. The extent of disability should be noted.

The World Health Organization describes the impact of disease on an individual in terms of:

• Impairment: any loss or abnormality of psychological or anatomical structure or function
• Disability (activity limitation): any restriction or lack of ability to perform an activity in the manner or within the range considered normal for a human being
• Handicap (participation restriction): a disadvantage for an individual resulting from an impairment or disability that limits or prevents the fulfilment of a role that is normal for that individual.

The patient’s own perception of limitation must be taken into account during assessment, as well as the impact of physical causes due to disease. Subjective and objective assessments must be made. Quality of life (QoL) involves physical and psychosocial factors. The aim of treatment is to reduce or cure physical and/or psychological disease and to reduce the impact of any impairment or disability on the individual. A variety of different standard questionnaires can be used to assess pain, disease impact and outcome (e.g. Health Assessment Questionnaire (HAQ), Arthritis Impact Measurement Scale (AIMS)).

Always observe a patient, looking for disabilities, as he or she walks into the room and sits down. General and neurological examinations are often necessary. Guidelines for rapid examinations of the limbs and spine are shown in Practical box 10.1.

Practical Box 10.1 Rapid examinations of the limb and spine

Rapid examination of the upper limbs Raise arms sideways to the ears (abduction). Reach behind neck and back. Difficulties with these movements indicate a shoulder or rotator cuff problem. Hold the arms forward, with elbows straight and fingers apart, palm up and palm down. Fixed flexion at the elbow indicates an elbow problem. Examine the hands for swelling, wasting and deformity. Place the hands in the ‘prayer’ position with the elbows apart. Flexion deformities of the fingers may be due to arthritis, flexor tenosynovitis or skin disease. Painful restriction of the wrist limits the person’s ability to move the elbows out with the hands held together. Make a tight fist. Difficulty with this indicates a loss of flexion or grip. Grip strength can be measured. Rapid examination of the lower limbs Ask the patient to walk a short distance away from and towards you, and to stand still. Look for abnormal posture or stance. Ask the patient to stand on each leg. Severe hip disease causes the pelvis on the non-weight-bearing side to sag (positive Trendelenburg test). Watch the patient stand and sit, looking for hip and/or knee problems. Ask the patient to straighten and flex each knee. Ask the patient to place each foot in turn on the opposite knee with the hip externally rotated. This tests for painful restriction of hip or knee. Abnormal hips or knees must be examined lying. Move each ankle up and down. Examine the ankle joint and tendons, medial arch and toes whilst standing.

Rapid examination of the spine

Stand behind the patient. Ask the patient to (a) bend forwards to touch the toes with straight knees, (b) extend backwards, (c) flex sideways, and (d) look over each shoulder, flexing and extending and side-flexing the neck. Observe abnormal spinal curves – scoliosis (lateral curve), kyphosis (forward bending) or lordosis (backward bending). A cervical and lumbar lordosis and a thoracic kyphosis are normal. Muscle spasm is worse whilst standing and bending. Leg length inequality leads to a scoliosis which decreases on sitting or lying (the lengths are measured lying). Ask the patient to lie supine. Examine any restriction of straight-leg raising. Ask the patient to lie prone. Examine for anterior thigh pain during a femoral stretch test (flexing knee whilst prone), which indicates a high lumbar disc problem. Palpate the spine and buttocks for tender areas.

Examining an individual joint involves three stages – looking, feeling and moving:

• Appearance. Look at it for swelling, rash or erythema, muscle wasting, deformity such as a distal bone displaced laterally as in knock knees (genu valgus) or bowed legs (genu varus), fixed flexion or hyperextension, loss of normal range and lack of fluidity of movement, and any pain caused by movement.
• Feel it for tenderness, warmth (indicates inflammation) and swelling which may be due to fluid, soft tissue or
  bone. Common descriptors are ‘fluctuant’ (fluid), ‘firm’ or ‘boggy’ (swelling of the synovium), and ‘hard’ (bony).
• Movement. Move it to assess the passive range of movement (e.g. flexion, extension, abduction, adduction and rotation), any instability, or the production of pain and crepitus (grating) seen with cartilage damage. The normal range varies between individuals. Comparing right with left and asking the patient about any change in range help to assess whether the endpoints are normal or not. A screening examination of the locomotor system, known by the acronym GALS (global assessment of the locomotor system) has been devised.

X-ray of the joint often forms an integral part of the examination.

Investigations are unnecessary in many of the common regional musculoskeletal problems and osteoarthritis (OA); the diagnosis is clear from the history and examination findings. Tests help to exclude another condition and to reassure the patient or their primary care physician.

Useful blood screening tests

• Full blood count
• Haemoglobin. Normochromic, normocytic anaemia occurs in chronic inflammatory and autoimmune diseases. Hypochromic, microcytic anaemia indicates iron deficiency, often due to non-steroidal anti-inflammatory drug (NSAID) induced gastrointestinal bleeding.
• White cell count. Neutrophilia is seen in bacterial infection (e.g. septic arthritis). It also occurs with corticosteroid treatment. Lymphopenia occurs with viral illnesses or active systemic lupus erythematosus (SLE). Neutropenia may reflect drug-induced bone marrow suppression. Eosinophilia is seen in the Churg-Strauss syndrome.
• Platelets. Thrombocythaemia occurs with chronic inflammation. Thrombocytopenia is seen in drug-induced bone marrow suppression.
• Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). An increase reflects inflammation. Plasma viscosity is also raised in inflammatory disease and measured in some laboratories in place of the sedimentation rate.
• Bone and liver biochemistry. A raised serum alkaline phosphatase may indicate liver or bone disease. A rise in liver enzymes is seen with drug-induced toxicity. For other investigations of bone, .

Other blood and urine tests:

• Protein electrophoretic strip and urinary Bence Jones protein – to exclude myeloma as a cause of a raised ESR.
• Serum uric acid – for gout.
• Antistreptolysin-O titre – in rheumatic fever.

These are detected on fixed human neutrophils. Two major ANCA patterns are recognized:

• proteinase 3 (PR3-ANCA), formerly called cytoplasmic or cANCA
• myeloperoxidase (MPO-ANCA), formerly called perinuclear or pANCA.

PR3-ANCA is present in up to 90% of serum from patients with Wegener’s granulomatosis. MPO-ANCA is found in up to 60% of other vasculitides, such as microscopic polyarteritis (polyangiitis) and Churg-Strauss syndrome. An MPO-ANCA is found in inflammatory bowel disease and rheumatic disease, which is not associated with vasculitis.

Antiphospholipid antibodies

These are detected in the antiphospholipid syndrome and SLE.
The principal autoantigen is β2-glycoprotein 1 (apolipoprotein H), which binds to cardiolipin and other anionic phospholipids. Anticardiolipin antibody and β2-glycoprotein are measured by ELISA. The lupus anticoagulants are antibodies against β2-glycoprotein 1 as well as prothrombin and annexin. They are detected by coagulation tests, such as prolongation of the activated partial thromboplastin time (APTT), as some of these antibodies interfere with phospholipid-dependent clotting systems in vitro.

Anti-RNA polymerase antibodies I, II and III

I and III are present in systemic sclerosis.

Immune complexes

Immune complexes are infrequently measured, largely because of variability between assays and difficulty in interpreting their meaning. Assays based on the polyethylene glycol precipitation method (PEG) or C1q binding are available commercially.

Complement

Low complement levels indicate consumption and suggest an active disease process in SLE.

Practical Box 10.2 Joint aspiration

This is a sterile procedure which should be carried out in a clean environment

Explain the procedure to the patient; obtain consent 1 Decide on the site to insert the needle and mark it. 2 Clean the skin and your hands scrupulously; remove rings and wristwatch. Gloves are not obligatory, but many prefer to use them. 3 Draw up local anaesthetic (and corticosteroid if it is being used) and then use a new needle. 4 Warn the patient, insert the needle, injecting local anaesthetic as it advances and, if a joint effusion is suspected, attempt to aspirate as you advance it. 5 If fluid is obtained, change syringes and aspirate fully. 6 Examine the fluid in the syringe and decide whether or not to proceed with a corticosteroid injection. 7 Cover the injection site and advise the patient to rest the affected area for a few days. Warn the patient that the pain may increase initially but to report urgently if this persists beyond a few days, if the swelling worsens, or if they become febrile, since this might indicate an infected joint.

Examination of joint (or bursa) fluid is used mainly to diagnose septic, reactive or crystal arthritis. The nature of the fluid is an indicator of the level of inflammation. Clear fluid indicates little inflammation in the joint, whereas translucent or opaque fluid indicates increasing cellularity and underlying inflammation. Purulent fluid is seen in septic arthritis, but crystal arthritis and reactive arthritis may also produce a highly cellular effusion. The procedure is often undertaken in combination with injection of a corticosteroid. Aspiration alone is therapeutic in crystal arthritis.

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