The primary problem is seen as a change in structure of cartilage and BONE, rather than an in?ammatory SYNOVITIS. Osteoarthritis usually implies a loss of the central load-bearing area of articular hyaline cartilage, with outgrowth of cartilage at the articular margin and subsequent ossi?cation to form bony outgrowths known as OSTEOPHYTES. Osteophytes form with increasing age, whether or not there is signi?cant cartilage loss, and in the elderly may lead to local frictional symptoms, and in the spine, to nerve compression.
The condition has a wide range of causes, of which some, like dysplasia and trauma, are known and others have yet to be identi?ed. The main clinical problems occur in the hip and knee. The cartilage loss in the hip usually occurs in the sixth or seventh decade. It may affect both hips in fairly rapid succession, or only one hip; such patients often have no problems in other joints. Cartilage loss in the knee occurs from the ?fth decade onwards and is often associated with cartilage loss in small joints in the hand and elsewhere. Cartilage loss in the distal interphalangeal joints of the hand is associated with the formation of bony swellings known as Heberden’s nodes.
Treatment Management is largely directed at maintaining activity, with physical and social support as necessary. ANALGESICS may be of some value, particularly in the management of night pain. NON-STEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDS) may help patients with early-morning sti?ness and may also reduce pain on movement and night pain. Their bene?t, however, tends to be less marked than in RHEUMATOID ARTHRITIS and their long-term usage has considerable toxicity problems. Advanced cartilage loss is best treated by joint replacement. Hip- and knee-joint replacements – with a wide variety of arti?cial joints – are now common surgical procedures which greatly improve the mobility of affected individuals. (See ARTHROPLASTY.)
People with arthritis and their relatives can obtain help and advice from Arthritis Care.... osteoarthritis
BURSITIS, TENDINITIS and non-speci?c back pain (see BACKACHE).
Osteoarthritis (OA) rarely starts before 40, but by the age of 80 affects 80 per cent of the population. There are structural and functional changes in the articular cartilage, as well as changes in the collagenous matrix of tendons and ligaments. OA is not purely ‘wear and tear’; various sub-groups have a genetic component. Early OA may be precipitated by localised alteration in anatomy, such as a fracture or infection of a joint. Reactive new bone growth typically occurs, causing sclerosis (hardening) beneath the joint, and osteophytes – outgrowths of bone – are characteristic at the margins of the joint. The most common sites are the ?rst metatarsal (great toe), spinal facet joints, the knee, the base of the thumb and the terminal ?nger joints (Heberden’s nodes).
OA has a slow but variable course, with periods of pain and low-grade in?ammation. Acute in?ammation, common in the knee, may result from release of pyrophosphate crystals, causing pseudo-gout.
Urate gout results from crystallisation of URIC ACID in joints, against a background of hyperuricaemia. This high concentration of uric acid in the blood may result from genetic and environmental factors, such as excess dietary purines, alcohol or diuretic drugs.
In?ammatory arthritis is less common than OA, but potentially much more serious. Several types exist, including: SPONDYLARTHRITIS This affects younger men, chie?y involving spinal and leg joints. This may lead to in?ammation and eventual ossi?cation of the enthesis – that is, where the ligaments and tendons are inserted into the bone around joints. This may be associated with disorders in other parts of the body: skin in?ammation (PSORIASIS), bowel and genito-urinary in?ammation, sometimes resulting in infection of the organs (such as dysentery). The syndromes most clearly delineated are ankylosing spondylitis (see SPINE AND SPINAL CORD, DISEASES AND INJURIES OF), psoriatic or colitic spondylitis, and REITER’S SYNDROME. The diagnosis is made clinically and radiologically; no association has been found with autoantibodies (see AUTOANTIBODY). A particularly clear gene locus, HLA B27, has been identi?ed in ankylosing spondylitis. Psoriasis can be associated with a characteristic peripheral arthritis.
Systemic autoimmune rheumatic diseases (see AUTOIMMUNE DISORDERS). RHEUMATOID ARTHRITIS (RA) – see also main entry. The most common of these diseases. Acute in?ammation causes lymphoid synovitis, leading to erosion of the cartilage, associated joints and soft tissues. Fibrosis follows, causing deformity. Autoantibodies are common, particularly Rheumatoid Factor. A common complication of RA is Sjögren’s syndrome, when in?ammation of the mucosal glands may result in a dry mouth and eyes. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) and various overlap syndromes occur, such as systemic sclerosis and dermatomyositis. Autoantibodies against nuclear proteins such as DNA lead to deposits of immune complexes and VASCULITIS in various tissues, such as kidney, brain, skin and lungs. This may lead to various symptoms, and sometimes even to organ failure.
Infective arthritis includes: SEPTIC ARTHRITIS An uncommon but potentially fatal disease if not diagnosed and treated early with approriate antibiotics. Common causes are TUBERCLE bacilli and staphylococci (see STAPHYLOCOCCUS). Particularly at risk are the elderly and the immunologically vulnerable, such as those under treatment for cancer, or on CORTICOSTEROIDS or IMMUNOSUPPRESSANT drugs. RHEUMATIC FEVER Now rare in western countries. Resulting from an immunological reaction to a streptococcal infection, it is characterised by migratory arthritis, rash and cardiac involvement.
Other infections which may be associated with arthritis include rubella (German measles), parvovirus and LYME DISEASE.
Treatment Septic arthritis is the only type that can be cured using antibiotics, while the principles of treatment for the others are similar: to reduce risk factors (such as hyperuricaemia); to suppress in?ammation; to improve function with physiotherapy; and, in the event of joint failure, to perform surgical arthroplasty. NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS) include aspirin, paracetamol and many recently developed ones, such as the proprionic acid derivatives IBUPROFEN and naproxen, along with other drugs that have similar properties such as PIROXICAM. They all carry a risk of toxicity, such as renal dysfunction, or gastrointestinal irritation with haemorrhage. Stronger suppression of in?ammation requires corticosteroids and CYTOTOXIC drugs such as azathioprine or cyclophosphamide. Recent research promises more speci?c and less toxic anti-in?ammatory drugs, such as the monoclonal antibodies like in?iximab. An important treatment for some osteoarthritic joints is surgical replacement of the joints.... joints, diseases of