OSTEOARTHRITIS (Degenerative arthritis; arthrosis; osteoarthrosis; hypertrophic arthritis; post-traumatic arthritis)

Osteoarthritis is a degenerative wear-and-tear process occurring in joints that are impaired by congenital defect, vascular insufficiency, or previous disease or injury. It is by far the commonest variety of arthritis.

Cause. It is caused by wear and tear. If a joint were never put under stress it would never become osteoarthritic. Hence the relatively lightly stressed joints of the upper limb are, in general, less prone to osteoarthritis than the heavily stressed joints of the lower limb. Nearly always, however, there is a predisposing cause that accelerates the wear-and-tear process.

Almost any abnormality of a joint may be responsible, indirectly, for the development of osteoarthritis often many years later. The main predisposing factors are:

• congenital ill-development; • irregularity of joint surfaces from previous fracture;• internal derangements, such as a loose body or a torn

meniscus; • previous disease, leaving a damaged articular

cartilage (for example, rheumatoid arthritis or haemophilia);

• mal-alignment of a joint from any cause (for example, bow leg);

• obesity and overweight. Age alone is not a cause of osteoarthritis, though it may be associated with an impaired capacity for tissue repair after injury, and this may be an indirect causative factor

Pathology. Any joint may be affected, the lower limb

joints more often than the upper. The articular cartilage is slowly worn away until eventuallythe underlying bone is exposed . This subchondral bone becomes hard and glossy ('eburnation'). Meanwhile the bone at the margins of the joint hypertrophies to form a rim of projecting spurs known as osteophytes.There is no primary change in the capsule or synovial membrane, but the recurrent strains to which an osteoarthritic joint is subject often lead to slight thickening and fibrosis.

Clinical features. Most patients with osteoarthritis are past

middle- age. When it occurs in younger patients there is usually a clear predisposing cause such as previous injury or disease of the joint. The onset is very gradual, with pain that increases almost imperceptibly over months and years. Movements slowly become more and more restricted. In some joints (notably the hip) deformity is a common feature in the later stages. This means that the joint cannot be placed in the neutral (anatomical) position.

On examination Slight thickening is often found on palpation;

it is mainly a bony thickening caused by the marginal osteophytes. There is no increased warmth. Movements are impaired slightly or markedly according to the degree of arthritis; in most joints movement is accompanied by palpable or audible crepitation of a rather coarse type. Fixed deformity (that is, inability of the joint to assume the neutral anatomical position) is often found in the hip, and sometimes in other joints.

Radiographic features: The characteristic features of osteoarthritis are:

1)diminution of cartilage space; 2)subchondral sclerosis; and 3) spurring or 'lipping' of the joint margins from the

formation of osteophytes . Diagnosis. This is usually made clear by the history,

clinical findings, "and radiographic features. Osteoarthritis is not" easily confused with inflammatory forms of arthritis, because there is no synovial thickening no increased local warmth, and no muscle spasm; radiographs show sclerosisrather than rarefaction, and the erythrocyte sedimentation rate is notincreased.

Course Osteoarthritis usually increases slowly year by year.

In many cases the disability never reaches the stage at which treatment is required. In others increasing pain, stiffness, or deformity drives the" patient to demand measures for its belief.

Treatment. The management of osteoarthritis exemplifies well the three categories of treatment that should be considered in every orthopedic problem namely:

1) no treatment, but advice and reassurance only;• conservative treatment; and • operative treatment . In many cases treatment is not required. The patient may

have sought advice only because of anxiety lest some grave disease be present. Reassurance, with advice to restrict the wear and tear on the affected joint, is all that is required.

When more active treatment is called for, conservative measures should usually be tried first. The methods available include physiotherapy (often by local heat and muscle-strengthening exercises), analgesic drugs, local injections of hydrocortisone, and supportive bandages or appliances. In addition, the stress that is put upon the affected joint should be reduced— for instance, in the case of the joints of the lower limb by restricting the amount of walking or by the use of a stick.

When severe disability is unrelieved by conservative treatment operation may be justified. Chief among the operations available are osteotomy to realign a joint; arthroplasty (the construction of a new joint) ; and arthrodesis (elimination of the joint by fusion

Osteotomy is useful mainly at the knee, to correct varus or valgus deformity, and at the hip.

Arthroplasty is applicable particularly to the hip, knee, shoulder, elbow, certain joints of the hand, and the metatarso-phalangeal joints.

For a few joints arthrodesis may be the operation of choice.

GOUTY ARTHRITIS(Podagra; urate crystal synovitis)

Gout is the clinical manifestation of a disturbed purine metabolism. It is characterized by deposition of uric-acid salts—especially sodium biurate—in connective tissues such as cartilage (of joints, or of the ear), the walls ofbursae, and ligaments.

Cause. The precise cause of the disturbance of metabolism is unknown. There is an inherited predisposition to the disease. In susceptible persons an attack may be induced by excessive consumption of purine-rich foods such as liver, kidneys, sweetbreads, shellfish, beer or Heavy wines, or by recent injury or operation.

Pathology. The primary fault is an impaired excretion of

uric acid by the kidneys. In consequence the level of urate in the plasma is increased, sometimes to 0.5 mmoL per litre or more (normal = 0.1-0.4 mmol per litre (2.0-7.0 mg per 100 ml)). In the blood the uric acid is in solution in a loose combination with proteins; it comes readily out of solution as a sodium salt (sodium biurate) to be deposited in the form of crystals in certain connective tissues, especially those that have been injured or those that have a" sluggish blood "supply, such as the articular cartilage of the joints of the foot. The deposited crystals set up an inflammatory reaction.

In acute gout The deposit is microscopic in "amount and is

soon reabsorbed, with restoration of the tissue to normal.

In chronic gout, however, widespread deposits of sodium biurate in joint cartilages, ligaments and the articular ends of bones lead to considerable disorganization of affected joints. Gouty deposits, known as tophi, are also common at other sites, notably in the olecranon bursa and in the cartilage of the ear, where they may form rounded nodules.

Clinical features. The patient is nearly always over 40, and is more likely to be a man than a woman, in the ratio of 10:1. The chief clinical manifestations are arthritis and bursitis.

Arthritis. Gout affects principally the peripheral joints such as the joints of the toes, tarsus, and ankle, and the small joints of the hands. It occurs in recurrent attacks. The first attack is usually in the great toe; later attacks may affect other joints. In an acute attack the onset is sudden—often during the night. The affected joint is swollen, red and glossy. Pain is very severe. Movements are greatly restricted because of the pain. The attack subsides after a few days and the joint is normal between attacks.

In chronic gout several joints are affected together. They are thickened and nodular, and painful on movement.

Bursitis. The bursa most commonly affected by gout is the olecranon bursa. It becomes distended with fluid, and there may be palpable deposits of uric acid salts.

Other manifestations. Deposits of uric acid salts (tophi) are common in the ear cartilages, where they form palpable nodules. They may also occur at other sites.

Radiographic features. In acute attacks of articular gout the joints do not show any radiographic change. In chronic gout the deposits of uric acid salts in the bone ends show as clear-cut erosions adjacent to the articular surfaces, for the deposits are transradiant.

Investigations. There is sometimes a mild leucocytosis and the erythrocyte sedimentation rate may be increased. The plasma uric acid content is raised. Aspiration of swollen joints may yield a small quantity of turbid fluid, but never organisms.

Diagnosis. Acute gout has to be distinguished from other forms of arthritis of acute onset, especially from acute pyogenic arthritis, acute'pseudogout‘ , haemophilic arthritis, and rheumatic fever.

Features suggestive of gout are: a history of previous attacks, with symptom

free intervals, a raised plasma urate content; the presence of tophi in the earsor elsewhere; detection of crystals in synovial fluid;"and favorable response to treatment. Chronic gout involving several joints may simulate rheumatoid arthritis.

Course. Gout usually occurs in recurrent attacks. Early attacks subside in a few days, leaving the joint clinically normal. In chronic gout the affected joints are gradually disorganized, and permanent disability is inevitable.

Treatment. For acute attacks reliance is usually placed upon a non steroidal anti-inflammatory drug such as indomethacin or naproxen. Colchicine is also effective.The affected joint should be rested until the attack has subsided. A large effusion in a major joint such as the knee should be aspirated and replaced by an instillation of hydrocortisone.

For patients with frequent attacks or with chronic gout, especially if the plasma urate level is persistently raised, long-term drug therapy to reduce the plasma urate level may be required.

The two types of drug available are represented by:1) probenemid, which paralyses renal tubular

reabsorption of urates and thus increases their excretion in the urine; and

2) allopurinol, which reduces the formation of uric acid by inhibiting the enzyme xanthine oxydase. Provided its long-term use is not associated with toxic reactions, allopurinol is probably to be preferred because it does not increase the load of urate in the urine, with its hazard of stone formation.

HAEMOPHILIC ARTHRITISJoint manifestations are common in

haemophilia,'but examples are seen only infrequently because haemophilia is itself an uncommon disease.

Pathology. The term-'haemophilia' is used loosely to

embrace a group of different defects in the process of coagulation of the blood. Classical haemophilia, the commonest of the group, occurs in males but is transmitted by females. There is an inherited deficiency of a specific clotting factor known as antihaemophilic factor (factor VIII).

In consequence the clotting time of the blood is prolonged and there is a tendency to undue bleeding when even quite small vessels are cut or torn. Joint manifestations are caused by haemorrhage into a joint, occurring after a minor strain or even without any known injury. The joints most commonly affected are those most vulnerable to strain—especially the knee, elbow, and ankle. The joint cavity is distended with blood (haemarthrosis), which is later slowly reabsorbed if the joint is rested. Recurrent haemarthroses lead eventually to degenerative changes in the articular cartilage and to fibrosis of the synovial membrane.

Clinical features. The boy is often a known sufferer from haemophilia or can recall previous episodes of bleeding. He suddenly finds that a joint has become painful and swollen.

On examination the findings vary according to the phase and duration of the arthritis. In the absence of specific treatment the joint remains swollen for several weeks after the acute onset partly from effused blood and partly from the synovial thickening that results from interstitial extravasations. The overlying skin is abnormally warm. Joint movements are restricted and very painful.

In the quiescent phase between attacks of haemarthrosis there is moderate thickening of the joint from synovial fibrosis, movements are slightly impaired, and often there is some degree of fixed deformity for instance, inability to straighten the knee fully.

Diagnosis.

Because of the synovial thickening, increased warmth of the skin, and restriction of joint movements, haemophilic arthritis is easily mistaken for acute or chronic inflammatory arthritis. The history of previous episodes of bleeding, the sudden onset, and the recurrent nature of the attacks are important diagnostic features; and the prolonged clotting time of the blood is confirmatory evidence.

Treatment. When the necessary facilities are available,

the correct treatment for a recent acute incident is to promote coagulability of the blood by the administration of antihaemo-philic factor in the form of factor VIII concentrate or of cryoprecipitate, and then to treat the joint as for ordinary traumatic haemarthrosis by aspiration and temporary support in a plaster splint. Early treatment on these lines should reduce the incidence of irreversible fibrosis of the synovial membrane.

Failing adequate supplies of antihaemophilic factor, resort must be had to prolonged splintage.

In the chronic degenerative phase that follows repeated haemarthroses it is often necessary to give permanent support to the joint by means, of a moulded plastic splint or other appliance. Operation must be avoided whenever possible, though it may if necessary be undertaken safely as long as adequate cover by antihaemophilic factor can be provided.

NEUROPATHIC ARTHRITIS(Charcot's osteoarthropathy)

In neuropathic arthritis a joint is disorganized by repeated minor injuries because it is insensitive to pain.

Cause. The underlying cause is a neurological disorder interfering with deep pain sensibility. In patients with involvement of joints, of the lower-limbthe commonest cause in the past was tabes dorsalis, a manifestation of syphilis; but tabes is now uncommon; and there has been a correspondingdecline in the incidence of neuropathic arthritis in the lower limb. Other causes are diabetic neuropathy, cauda equina lesion . In those with upper limb involvement the usual cause, apart fromleprosy, is syringomyelia.

Pathology. Any of the large joints may be affected,

including the joints of the spine. The knee, ankle and subtalar joint are most commonly affected in the lower limb, and the elbow in the upper limb. In a normal joint harmful strains are prevented by a protective reflex whereby muscle contraction is evoked by incipient pain. When joint sensibility is destroyed the protective function of pain is lost. Strains are unrecognized and, cumulatively, they lead to severe degeneration of the joint. The changes may be regarded as a much exaggerated form of osteoarthritis. The articular cartilage and subchondral bone are worn away, but at the same time there is sometimes massive hypertrophy of bone at the joint margins. The ligaments become lax and the joint is unstable. Indeed it is often subluxated or even dislocated

Clinical and radiographic features. The patient is usually in adult life. The main

symptoms are swelling and instability of the affected joint. Since the joint is insensitive pain is slight or, sometimes, absent.

On examination the joint is thickened, mostly from irregular hypertrophy of the bone ends. The range of movement is moderately restricted, and there is marked lateral laxity leading to instability. In extreme cases the joint may be dislocated. Further examination will reveal evidence of the underlying neurological disorder.

Radiographs show severe disorganization of the joint. The changes are basically those of osteoarthritis, but enormously exaggerated. There are loss of cartilage space and some absorption of the bone ends, often with considerable hypertrophy of bone at the joint margins.

Treatment. In most instances the best treatment is

simply to provide support for the joint by a suitable appliance. Sometimes operation may be undertaken to fuse the joint, but fusion may be difficult to achieve. The primary neurological disorder will usually demand appropriate treatment.

ARTHRITIS OF RHEUMATIC FEVERIn adolescent children and young adults

arthritic manifestations are a prominent feature of rheumatic fever. This has now become an uncommon disease in Western countries; so joint manifestations from this cause are hardly ever seen except in under developed parts of the world.

Cause. Rheumatic fever is ascribed to a sensitivity reaction associated with infection by a haemolytic streptococcus. There may be an inherited predisposition to the disease.

Pathology. Any joint may be affected. The synovial membrane is acutely inflamed, but there is no suppuration. Clear fluid is effused into the joint.

Clinical features. The patient is usually a child over 10, or a young

adult. There is constitutional illness, with malaise and pyrexia. A joint becomes painful and svyollen, and soon afterwards other joints are likewise affected.

On examination an affected joint is swollen, partly from contained fluid and partly from synovial thickening. The overlying skin is warmer than normal. Movements are markedly restricted, and painful if forced. Other features of rheumatic fever, such as carditis and chorea, should be looked for.

Radiographs of affected joints do not show any alteration from the normal.

Investigations: There is a mild leucocytosis. The erythrocyte sedimentation rate is increased.

Diagnosis. Arthritis of rheumatic fever has to be distinguished from other forms of arthritis—especially from acute pyogenic arthritis, rheumatoid arthritis, gout and haemophilic arthritis and from acute osteomyelitis. Features suggestive of rheumatic fever are: onset in adolescence; affection of several joints together or in succession.; severe pain with' signs of acute inflammation, but without suppuration; a mild rather than a marked leucocytosis; a concomitant cardiac lesion; and a rapid favorable response to salicylates.

Treatment. For joint involvement alone salicylates are

adequate, but prednisone or a related steroid may be required if the heart is affected. A therapeutic comes of penicillin-should also be given to eliminate streptococci, and thereafter twice-daily oral penicillin should be continued well into adult life to reduce the risk of recurrent attacks.