The guiding principle is to treat the symptoms and disability, not the radiological appearances; depression and poor quadriceps strength are better predictors of pain than is radiological severity in OA of the knee. Education of the individual about the disease and its effects reduces pain, distress and disability and increases compliance with treatment. Psychological or social factors alter the impact of the disease.

Physical measures

Weight loss and exercises for strength and stability are useful. Hydrotherapy helps, especially in lower-limb OA. Local heat, ice packs, massage and rubifacients or local NSAID gels are all used, although the value of NSAID gels is probably marginal.
Complementary medicine is commonly used and, despite lack of scientific evidence, little is lost in trying it since a number of patients do seem to be helped.

Medication

Balance the potential benefit against potential side-effects. Drugs usually should be used only in severe disease. Patients should be prescribed short courses of simple analgesics before NSAIDs (see Box 10.4). NSAIDs should be used intermittently. It has been suggested that some NSAIDs may increase the cartilage damage, while others are ‘chondroprotective’, but these claims remain unproven.

Intra-articular corticosteroid injections produce short-term improvement when there is a painful joint effusion. Frequent injections into the same joint should be avoided.

The role of chondroitin sulphate and glycosaminoglycan (sold as food supplements) is still under investigation and unproven. They appear to do no harm and some patients benefit.

Surgery

Total replacement arthroplasty has transformed the management of severe OA. The safety of hip and knee replacements is now equal, with a complication rate of about 1%; loosening, and late blood-borne infection are the most serious. Unicompartmental knee replacement is a less major procedure and appropriate for some patients. These slight but definite risks make it essential that the patient is certain that surgery is wanted, when all else has been tried. For the vast majority, a total hip or knee replacement reduces pain and stiffness and greatly increases function.

Other surgical procedures include realignment osteotomy of the knee or hip, excision arthroplasty of the first MTP and base of the thumb, and fusion of a first MTP joint.

Primary generalized OA

This is less common than nodal OA of the hands but is usually seen in combination. It is also called ‘nodal generalized OA’ (NGOA). The other joints affected are the knees, first MTP, hip, and intervertebral (spondylosis). There is a female preponderance and a strong familial tendency. NGOA is associated with immune complex deposition and may have an autoimmune cause. Its onset is often sudden and severe.

Erosive OA

This is rare. The DIPs and PIPs are inflamed and equally affected. In contrast to nodal OA, the functional outcome is poor. Radiologically, there are marked subchondral cysts. Erosive OA may develop into RA and may not be a true subset of OA.

Crystal-associated OA

This is most commonly seen with calcium pyrophosphate deposition in the cartilage (chondrocalcinosis). Chondrocalcinosis increases in frequency with age, but is usually asymptomatic. The joints most commonly affected are the knees (hyaline cartilage and fibrocartilage) and wrists (triangular fibrocartilage). There is patchy linear calcification on X-ray.

A chronic arthropathy (pseudo-OA) occurs, predominantly in elderly women with severe chondrocalcinosis. There is a florid inflammatory component and marked osteophyte and cyst formation visible on X-rays. The joints affected differ from NGOA – being predominantly the knees, then wrists and shoulders, but also elbows, ankles and hips. Chondrocalcinosis is associated with pseudogout, an acute crystal-induced arthritis.

A rare, rapidly destructive arthritis in elderly women, affecting shoulders, hips and knees, is associated with finding crystals of calcium apatite in a bloody joint effusion. The outlook is poor and joints require early surgical replacement.

Investigations in OA

• Blood tests. There is no specific test; the ESR and CRP are normal. Rheumatoid factor and antinuclear antibodies are negative.
• X-rays are abnormal only when the damage is advanced.
• MRI demonstrates early cartilage and subchondral bone changes.
• Arthroscopy reveals early fissuring and surface erosion of the cartilage.

Hip OA

Hip OA affects 7-25% of white adult Caucasians but is significantly less common in black African populations. There are two major subgroups defined by the radiological appearance. The most common is superior-pole hip OA, where joint space narrowing and sclerosis predominantly affect the weight-bearing upper surface of the femoral head and adjacent acetabulum. This is most common in men and unilateral at presentation, although both hips may become involved because the disease is progressive. Early onset of hip OA is associated with acetabular dysplasia. Less commonly, medial cartilage loss occurs. This is most common in women and associated with hand involvement (nodal generalized OA – NGOA), and is usually bilateral. It is more rapidly disabling.

Knee OA

The prevalence of knee OA is 40% in individuals aged over 75 years. It is commoner in women than in men. There is a strong relationship with obesity. The disease is generally bilateral and strongly associated with polyarticular OA of the hand in elderly women. The medial compartment is most commonly affected and leads to a varus (bow-legged) deformity. There is often also retropatellar OA. Previous trauma, meniscal and cruciate ligament tears are risk factors for developing knee OA.

Nodal OA

Joints of the hand are usually affected one at a time over several years, with the distal interphalangeal joints (DIPs) being more often involved than the proximal interphalangeal joints (PIPs). The onset may be painful and associated with tenderness, swelling and inflammation and impairment of hand function. The inflammation often occurs around the female menopause. PIP-predominant nodal OA has a superficial similarity to early rheumatoid arthritis. Even if a weakly positive rheumatoid factor is found, it is of no significance. The inflammatory phase settles after some months or years, leaving painless bony swellings posterolaterally – Heberden’s nodes (DIPs) and Bouchard’s nodes (PIPs), along with stiffness and deformity. Functional impairment is slight for most, although PIP osteoarthritis restricts gripping more than DIP involvement. On X-ray, the nodes are marginal osteophytes and there is joint space loss.

Carpometacarpal and metacarpophalangeal OA of the thumb coexist with nodal OA and cause pain, which decreases as the joint stiffens. The ’squared’ hand in OA is caused by bony swelling of the carpometacarpal joint and fixed adduction of the thumb. Function is rarely severely compromised.

Polyarticular hand OA is associated with a slightly increased frequency of OA at other sites.

Osteoarthritis affects many joints, with diverse clinical patterns. Hip and knee OA is the major cause of disability. Early OA is rarely symptomatic unless accompanied by a joint effusion, whilst advanced radiological and pathological OA is not always symptomatic.

Box 10.5 Factors predisposing to osteoarthritis

Obesity – Predicts later risk of radiological and symptomatic OA in population studies. Heredity – Familial tendency to develop nodal and generalized OA. Gender – Polyarticular OA is more common in women; a higher prevalence after the menopause suggests a role for sex hormones. Hypermobility – Increased range of joint motion and reduced stability lead to OA. Osteoporosis – There is reduced risk of OA. Other diseases – See Table 10.11. Trauma – A fracture through any joint. Meniscal and cruciate ligament tears cause OA of the knee. Congenital joint dysplasia – Alters joint biomechanics and leads to OA. Mild acetabular dysplasia is common and leads to earlier onset of hip OA. Joint congruity – Congenital dislocation of the hip or a slipped femoral epiphysis or Perthes’ disease; osteonecrosis of the femoral head in children and adolescents causes early-onset OA. Occupation – Miners develop OA of the hip, knee and shoulder, cotton workers OA of the hand, and farmers OA of the hip. Sport – Repetitive use and injury in some sports causes a high incidence of lower-limb OA.

Table 10-11. Causes of osteoarthritis

Primary OA	No known cause
Secondary OA	Pre-existing joint damage:
	Rheumatoid arthritis
	Gout
	Seronegative spondyloarthropathy
	Septic arthritis
	Paget’s disease
	Avascular necrosis, e.g. corticosteroid therapy
	Metabolic disease:
	Chondrocalcinosis
	Hereditary haemochromatosis
	Acromegaly
	Systemic diseases:
	Haemophilia – recurrent haemarthrosis
	Haemoglobinopathies, e.g. sickle cell disease
	Neuropathies

Some flare-ups are due to inflammation but are not associated with an increased ESR or CRP. Focal synovitis is caused by fragments of shed bone or cartilage. Radiological OA is usually, but not inevitably, progressive. This progression may be stepwise or continual. Radiological improvement is uncommon but has been observed, suggesting that repair is possible. This may be the basis for effective drug treatments in the future.

Symptoms

• Joint pain
• Joint gelling (stiffening and pain after immobility)
• Joint instability
• Loss of function.

Table 10-12. Features of nodal OA

Familial

Has a higher incidence in women

Typical pattern of polyarticular involvement of the hand joints

Develops in late middle age

Has a generally good long-term functional outcome

Associated with OA of the knee, hip and spine

Signs

• Joint tenderness
• Crepitus on movement
• Limitation of range of movement
• Joint instability
• Joint effusion and variable levels of inflammation
• Bony swelling
• Wasting of muscles.

Several mechanisms have been suggested for the pathogenesis:

• Matrix loss is caused by the action of matrix metalloproteinases such as collagenase (MMP-1), gelatinase (MMP-2) and stromelysin (MMP-3). These are secreted by chrondrocytes in an inactive form. Extracellular activation then leads to the degradation of collagen and proteoglycans.
• Tissue inhibitors of metalloproteinases (TIMPs) regulate the MMPs. Disturbance of this regulation may lead to increased cartilage degradation and contribute to the development of OA.
• There is synovial inflammation in OA, producing interleukin-1 (IL-1) and tumour necrosis factor (TNF-α). These cytokines stimulate metalloproteinase production and IL-1 inhibits type II collagen production.
• Growth factors, including insulin-like growth factor (IGF-1) and transforming growth factor (TGF-β), are involved in collagen synthesis, and their deficiency may play a role in impairing matrix repair.
• Vascular endothelial growth factor from macrophages is a potent stimulator of angiogenesis and may contribute to inflammation and neovascularization in OA.
• Mutations in the gene for type II collagen (COL2A1) have been associated with early polyarticular OA.
• Twin studies suggest a strong hereditary element underlying OA, and further studies may reveal genetic markers for the disease. The influence of genetic factors is estimated at 35-65%.
• In the Caucasian population there is an inverse relationship between the risk of developing OA and osteoporosis.
• A large population study has suggested that a high intake of vitamin C and other antioxidants may reduce the risk of OA. The lack of antioxidants is thought to contribute to many ageing processes.
• In women, weight-bearing sports produce a two- to threefold increase in risk of OA of the hip and knee.
• In men, there is an association between hip OA and certain occupations – farming and labouring.
• Obesity is a risk factor for developing OA in later life.

The term primary OA is sometimes used when there is no obvious known predisposing factor.

Box 10.5 shows some of the predisposing factors for the development of OA, whilst Table 10.11 shows other conditions that sometimes cause secondary arthritis.

In the UK, 60% of HIV-infected patients have characteristic oral lesions. Lesions strongly associated with HIV infection include candidiasis (with erythema and/or white exudates), erythematous candidiasis, oral hairy leucoplakia, Kaposi’s sarcoma, non-Hodgkin’s lymphoma, necrotizing ulcerative gingivitis, and necrotizing ulcerative periodontitis.

Oral hairy leucoplakia is almost pathognomonic of HIV infection and may be an early sign. It is more common in HIV-infected homosexual men than in any other high-risk group. It is characterized by white vertical corrugations on the lateral borders of the tongue, and immunostaining shows Epstein-Barr virus.

Kaposi’s sarcoma presents as a red, purple or blue macule or nodule, most commonly on the palate. It is diagnostic of AIDS. The lesion is associated with herpesvirus 8.

All lesions are much less common since the introduction of HAART.

Streptococcus mutans is the main bacterial cause of dental caries in man. These bacteria are cariogenic only in the presence of dietary sugar. Dental caries can progress to pulpitis and pulp necrosis, and spreading infection can cause dentoalveolar abscesses. If there is soft tissue swelling, antibiotics (e.g. amoxicillin or metronidazole) should be prescribed prior to dental intervention. Erosion of the teeth can also result from exposure to acid or, very occasionally, in patients with gastro-oesophageal reflux disease.

The gingivae consist of the mucous membranes covering the alveolar process of the mandible and the maxilla.

Chronic gingivitis is the most common cause of bleeding gums and is an inflammation following the accumulation of bacterial plaque. It resolves when the plaque is removed.

Acute (necrotizing) ulcerative gingivitis (Vincent’s gingivitis) is characterized by the proliferation of spirochaete and fusiform bacteria. Young male smokers with poor oral hygiene are predominantly affected. It responds to oral metronidazole 200 mg three times daily for 3 days, used with chlorhexidine gluconate mouthwash.

Desquamatous gingivitis is a clinical description of smooth, red atrophic gingivae caused by lichen planus or mucous membrane pemphigoid. The diagnosis is confirmed by biopsy.

Gingival swelling is due to fibrous hyperplasia or is a result of inflammatory changes. Fibrous gingival hyperplasia is a result of hereditary gingival fibromatosis or associated with drugs (e.g. phenytoin, ciclosporin, nifedipine). Inflammatory swellings are seen in pregnancy, gingivitis and scurvy. Swelling due to infiltration is seen in acute leukaemia and Wegener’s granulomatosis.

White lesions may be transient or persistent. Transient white patches are either due to Candida infection or are very occasionally seen in systemic lupus erythematosus. Oral candidiasis in adults is seen in seriously ill or immunocompromised patients, or following therapy with broad-spectrum antibiotics or inhaled steroids.

Local causes include mechanical, irritative or chemical trauma from drugs (e.g. aspirin).

Leucoplakia describes white patches for which no local cause can be found. It is associated with alcohol and (particularly) smoking, and is regarded as a premalignant condition. A biopsy should always be undertaken; histology shows alteration in the keratinization and dysplasia of the epithelium; aneuploidy is associated with a very high risk of cancer. Treatment is unsatisfactory. Isotretinoin possibly reduces disease progression. Oral lichen planus presents as white striae.

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