Osteoarthritis (OA) is the commonest type of arthritis, occurring in about 20% of the population as a whole and in 50% of those aged over 60 years. It is a disease of cartilage, which becomes eroded and progressively thinned as the disease proceeds.
The pattern of development of joint disease in osteoarthritis is additive. The disease moves slowly from joint to joint and also progresses very slowly (in most cases) within individual joints. Its greatest impact is on weightbearing joints such as the hips and knees, and involvement of these joints is the commonest cause of disability in an elderly population.
OA occurs throughout the world and has occurred throughout the history of humanity. It is twice as common in women as in men. It is particularly common in British populations but this has nothing to do with climate, latitude or longitude and is therefore presumably genetic. OA is uncommon in black populations; when it does occur it usually affects the knees and hand involvement is rare.
OA is a disease of cartilage. Normal cartilage is composed of a matrix of collagen fibres stuffed with proteoglycan molecules that attract water and thereby maintain a positive pressure within the structure. There are just a few chondrocytes scattered within normal cartilage. It is likely that different stimuli can initiate the degenerative process but the two most obvious are:
1 Mechanical insults
2 Biochemical abnormalities of cartilage
The chondrocyte is believed to start the deterioration, releasing enzymes that degrade collagen and proteoglycans. Breaks in the collagen fibres allow the uptake of water; cartilage swells and splits. Crystals are released into the joint and are one of the mechanisms of the synovial inflammation that follows and which may perpetuate the destruction of cartilage. Attempts at repair include remodelling of bone, which produces the characteristic osteophytes.
Identifiable aetiological factors in primary OA include:
AGE. The disease tends to start at the age of 50 years. GENETICS. There is a strong familial tendency. Specific abnormalities of collagen caused by a single amino acid defect have recently been identified in a few families with an OA-like disease.
OBESITY AND OTHER SYSTEMIC FACTORS. Obesity is associated with OA of the knees. Chondrocytes may be influenced by sex hormones, growth hormone and other systemic factors. It is probably a mistake to think of primary 0A as a single disease. It is probably a common response to a variety of insults and has identifiable pathophysiological features which vary according to the joint site as well as the cause. Current concepts of the aetiology of primary OA are summarized. The relative importance of different factors varies at different sites. With OA of the small joints of the hand, genetic factors are particularly important, while in the hip abnormal biomechanics may be more relevant.
Most OA is primary but in a small proportion of patients there is an obvious cause. The causes of secondary are listed
There is fibrillation of the superficial layer of cartilage with fissures (splits) developing and extending into the deeper layers. The bases of these fissures contain clusters of chondrocytes, which are increased in number. As the disease advances there is progressive cartilage loss until hard eburnated bone is all that remains. The synovial membrane is heavily infiltrated with mononuclear cells. There is thickening of subchondral bone with cyst formation.
PAIN, typically in the knees, hips or hands, worst in the evenings and aggravated by use and relieved by rest. Sometimes intermittent at first but later chronic with inflammatory exacerbations in particular joints.
MORNING STIFFNESS, usually lasting up to half an hour and stiffness after sitting.
DISABILITY depends upon the joints affected.
SWELLING: characteristically hard and bony, sometimes with associated effusion. CREPITUS on movement.
SIGNS OF INFLAMMATION: warmth in the knees and erythema in the small joints of the hands, particularly in the early stages and during exacerbations.
LIMITATION OF MOVEMENT follows with wasting of muscles around the affected joint.
JOINT DEFORMITIES are particularly important in the knee. Valgus, varus or flexion deformities are seen with instability in the later stages of the disease.
Pattern of disease
Occasionally monoarticular; usually one, two, three or four sites including knees (commonest), hands, hips, feet, ankles and lumbar spine; bilateral and symmetrical. HANDS. Bony swellings occur at the distal interphalangeal joints of the fingers (Heberden’s nodes) and also at the proximal interphalangeal joints (Bouchard’s nodes).
At first the joints are often red, warm, swollen and very tender (‘hot Heberden’s nodes’). Later the inflammation disappears, leaving knobbly but often painless swellings. The pattern of hand involvement is shown; the distal interphalangeal and first carpometacarpal joints are most often affected.
FEET. The metatarsophalangeal joint of the big toe is often affected, sometimes called ‘poor man’s gout’. Problems may arise from valgus deformity (hallux valgus) or progressive restriction of movement (hallux rigidus). OA is characterized by inflammation of joints but, unlike rheumatoid arthritis, there is no systemic involvement. Thus there are no non-articular features and there is no systemic illness.
The pattern of hand involvement should be contrasted with that of rheumatoid arthritis (see later), in which metacarpophalangeal and proximal interphalangeal joint involvement is usual and the distal interphalangeal joints are characteristically spared. The pattern of involvement of other joints in OA is contrasted with that in rheumatoid arthritis. The number of joints affected in OA is much less than in rheumatoid arthritis. Apophyseal joints in the cervical and lumbar spine are not uncommonly involved but it is difficult to distinguish OA at this site from chronic disc disease.
The X-ray changes in OA are shown . Narrowing of the joint space is due to loss of cartilage and is the most important change. It is accompanied by the formation of osteophytes at the margins of the joint, sclerosis of the underlying bone and cyst formation. There is often calcification, which takes one of two forms:
1 Linear calcification, which is characteristic of pyrophosphate deposition
2 Spotty calcification, which is characteristic of hydroxyapatite
There are no diagnostic markers for OA. The ESR is normal and there are no biochemical abnormalities. Rheumatoid factor and antinuclear antibodies are negative but remember that positive low titre tests can occur in the elderly.
The nature of the condition, treatment and prognosis should be discussed with the patient. There are three main types of treatment: drugs, physical measures and surgery. Obese patients should be encouraged to lose weight but, apart from this, it is seldom possible to alter the aetiological factors of the disease.
There is no specific therapy to control the disease process. Simple analgesics and non-steroidal anti-inflammatory drugs (NSAIDs) are used to control symptoms. The latter are more effective because of the part played by inflammation in OA. Systemic corticosteroid therapy is not used. Drugs such as gold and pencillamine that are used for rheumatoid arthritis are not effective in OA. Intra-articular corticosteroids can be used for inflammatory exacerbations. Injection should be preceded by aspiration of any fluid in the joint.
The application of heat to an osteoarthritic joint may provide pain relief. Exercises are useful to maintain muscle power and are especially required for the quadriceps muscle in patients with knee involvement. Hydrotherapy is particularly useful for the hip joint, sometimes enabling a stiff joint to be mobilized and providing symptomatic relief A walking stick may be useful for a patient with involvement of one hip or knee and should be held in the opposite hand.
The greatest advance in the management of OA has been joint replacement. Many joints can be successfully replaced. For example, a total hip replacement offers a 99% chance of almost complete pain relief and increased mobility. Knee replacements are now as successful. For disease of the first carpometacarpal joint, the trapezium can be removed or replaced with a plastic prosthesis. The
first metatarsophalangeal joint can also be replaced. Replacements of knees and hips have a limited lifespan. Hip replacements fail at the rate of 1% per year, the cement fixation becoming loose and the joint becoming painful. X-rays often fail to show this loosening but a
bone scan becomes ‘hot’ and is a useful way of confirming the diagnosis. Treatment is surgical revision but the success rate falls with each procedure. A much less common but much more serious problem with replacements is infection. Antibiotics seldom solve the problem of infection around a metal prosthesis, which acts as a foreign body; it is often necessary to remove the prosthesis, drain the site and replace the prosthesis at a later date using cement containing antibiotics. An un cemented hip prosthesis is sometimes used in young people needing total hip replacement when it is anticipated that revision will be required. It is easy to remove such a prosthesis and replace it with the cemented variety.