Osteoarthritis (OA) is a disease of synovial joints (Fig. 7.1) and is the most common form of arthritis.
Epidemiology
The prevalence of OA increases with age, and most people over 60 years will have some radiological evidence of it although only a proportion of these have symptoms. OA occurs world-wide, it is more common in women and there is a familial tendency to develop nodal and generalized OA. Other risk factors are obesity, a fracture through a joint, congenital joint dysplasias, pre-existing joint damage of any cause, occupation (e.g. OA of the hip in farmers and labourers) and repetitive use and injury associated with some sports.
Pathology and pathogenesis
OA is the result of active, sometimes inflammatory but potentially reparative processes, rather than the inevitable result of trauma and ageing. It charac-terized by progressive destruction and loss of articular cartilage with an accompanying periarticular bone response. The exposed subchondral bone becomes sclerotic, with increased vascularity and cyst formation. Attempts at repair produce cartilaginous growths at the margins of the joint which later become calcified (osteophytes).
Several mechanisms have been suggested for the pathogenesis:
■ Metalloproteinases, e.g. stromelysin and collagenase, secreted by chondrocytes degrade collagen and proteoglycans.
■ Interleukin (IL)-1 and tumour necrosis factor (TNF)-a stimulate metallo-proteinase production and inhibit collagen production.
■ Deficiency of growth factors such as insulin-like growth factor and trans-forming growth factor impairs matrix repair.
■ Genetic susceptibility (35-65% influence) from multiple genes rather than a single gene defect. Mutations in the gene for type II collagen have been associated with early polyarticular OA.
Most OA is primary with no obvious predisposing factor. Secondary OA occurs in joints that have been damaged in some way or are congenitally abnormal.
Clinical features
Joint pain is the main symptom, made worse by movement and relieved by rest. Stiffness occurs after rest (‘gelling') and in contrast to inflammatory arthritis there is only transient (<30 minutes) morning stiffness. The joints most commonly involved are the distal interphalangeal joints (DIPJs) and first carpometacarpal joint of the hands, first metatarsophalangeal joint of the foot and the weight-bearing joints - vertebrae, hips and knees. Elbows, wrists and ankles are rarely affected. On examination there is deformity and bony enlargement of the joints, limited joint movement and muscle wasting of surrounding muscle groups. Crepitus (grating) is a common finding and is probably due to the disruption of the normally smooth articulating surfaces of the joints. There may be a joint effusion. Heberden's nodes are bony swellings at the DIPJs. Bouchard's nodes are similar but occur at the proximal IPJs (Fig. 7.2).
Differential diagnosis
OA is differentiated from RA by the pattern of joint involvement and the absence of the systemic features and marked early morning stiffness that occur in RA. A chronic arthropathy (pseudo-OA) occurs, predominantly in
Fig. 7.2 Severe nodal osteoarthritis (OA). The distal interphalangeal (DIP) joints demonstrate Heberden’s nodes (arrows). The middle finger DIP joint is deformed and unstable. The thumb is adducted and the bony swelling of the first carpometacarpal joint is clearly shown - ‘the squared hand of nodal OA’.
elderly women with severe chondrocalcinosis (p. 296) but the wrists and shoulder are usually involved and the hands rarely involved. Chronic tophaceous gout (p. 293) and psoriatic arthritis affecting the DIPJs (p. 292) may mimic OA.
Investigations
■ Full blood count and ESR are normal. Rheumatoid factor is negative, but positive low-titre tests may occur incidentally in elderly people.
■ X-rays are only abnormal in advanced disease and show narrowing of the joint space (resulting from loss of cartilage), osteophytes, subchondral sclerosis and cyst formation.
■ MRI demonstrates early cartilage changes. It is not necessary for most patients with suggestive symptoms and typical plain X-ray features.
Management
Treatment should focus on the symptoms and disability, not the radiological appearances. Patient education about the disease, non-pharmacological measures, drugs and surgery all have a role. Obese patients should be encouraged to lose weight, particularly if weight-bearing joints are affected.
■ Physical measures are the keystone of OA treatment. Local strengthening and aerobic exercises improve local muscle strength, improve the mobil-ity of weight-bearing joints and improve general aerobic fitness. Local heat or ice packs applied to an affected joint may also help. Bracing devices, joint supports, insoles for joint instability and footwear with shock-absorbing properties for lower limb OA are also used. A walking stick held on the contralateral side to the affected lower limb joint is useful. Acupuncture helps knee OA.
■ Medication. Paracetamol (p. 317) is the initial drug of choice for pain relief, with the addition of a weak opioid, e.g. dihydrocodeine (p. 317), if neces-sary. NSAIDs (p. 317), e.g. ibuprofen or coxibs are used in patients who do not respond to simple analgesia and should be used in short courses rather than a continuous basis. NSAIDs can also be given topically. Intra-articular corticosteroid injections produce short-term improvement when there is a painful joint effusion; systemic corticosteroids are not used.
■ Surgery. Total hip and knee replacement has transformed the manage-ment of severe symptomatic OA. There is reduced pain and stiffness and an associated increase in function and mobility. Complication rates are low with loosening and late bone infection being the most serious.
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