Osteoarthritis (OA) or degenerative joint disease is a chronic disorder characterized by softening and disintegration of articular cartilage with secondary changes in underlying bone, new growth of cartilage and bone (osteophytes) at the joint margins, and capsular fibrosis.1 It is by far the most common form of chronic arthritis among the elderly. Its prevalence increases with age, occurring in greater than 50% of individuals older than 60.2 OA is particularly common in elderly people, affecting more than 80% of those older than 75 years.1 Susceptibility to OA involves systemic factors affecting joint vulnerability including age, gender and genetic susceptibility, nutritional factors, intrinsic joint vulnerabilities including previous damage, muscle weakness and malalignment, and extrinsic factors including obesity and physical activity.1, 3 The most common joints involved are those of weight-bearing including the knees, hips, cervical and lumbosacral spine, proximal (PIP) and distal (DIP) interphalangeal joints of the hands, first carpometacarpal joints (CMC), and metatarsophalangeal joints (MTP).1 Involvement is typically symmetric, although it can be unilateral at first depending on previous trauma or unusual stress. The pain may be insidious and relieved by rest initially, but as the disease progresses it becomes persistent and more severe with activity. Stiffness following periods of inactivity may also become common. The patient may complain of problems such as knee locking, unsteadiness, or giving away. Some patients, especially women, experience inflammatory OA or erosive OA, which involves particularly the PIPs and DIPs of the hands. These may exhibit inflammatory manifestations such as redness, tenderness and local heat. Knees are often swollen with synovial fluid produced. Cervical and lumbosacral pain is a result of arthritis of hypophyseal joints, bony spur formation, pressure on ligaments or other surrounding tissues, or reactive muscle spasm. Impingement on nerve roots by osteophytes can cause radicular symptoms. Cord compression may result in spinal stenosis. In the cervical area, it causes localized pain and gait unsteadiness. In lumbar areas, it may result in spinal claudication, consisting of pain in the buttocks or legs while walking that is relieved after 10–15 mins of rest. Lumbar flexion and sitting usually relieve these symptoms, as opposed to aggravation of radicular disc symptoms by these positions.4

Examination of the joints may detect crepitus, deformities, subluxation, swelling, bony overgrowths such as Heberden’s nodes of the DIPs, Bouchard’s nodes of the PIPs, or CMC joints, and limitation of motion. Neurological evaluations may detect a radicular pattern of motor or sensory abnormalities, lower motor neuron or upper motor neuron signs in spinal stenosis, and sphincter abnormalities.5

Rheumatoid arthritis (RA) is a chronic inflammatory symmetrical disease of joints of unknown aetiology, affecting about 1% of the general population worldwide and about 2% of persons 60 years of age and older in the United States.6, 7 Extra-articular manifestations may also contribute to disease symptomatology.8 Most elderly patients with RA have the disease onset before age 60 and commonly present with additional therapeutic problems when older because of the long duration of the disease and other illnesses. Older persons are more likely to develop joint deformities. Involvement of the cervical spine may result in pain, decreased range of motion and neurological deficits. Extra-articular manifestations, such as rheumatoid nodules, secondary Sjögren’s syndrome (SS), and vasculitis are more frequent in this group of patients.8

Patients with elderly onset RA (EORA) are those in whom RA develops after age 60. Most patients present with a gradual onset of pain, swelling and stiffness in symmetrical joints, while in others the onset may be more acute. Fatigue, malaise and weight loss may be present. Joint symptoms are characteristically symmetric, although asymmetric presentation may occur. In the aged, asymmetric involvement may be seen in hemiplegic patients with sparing of the paralysed side. All peripheral joints may be involved, but the most common are the PIPs and metacarpophalangeal (MCPs) of the hands involved in 90% as are the wrists, MTPs and ankles. Knees, hips, elbows and shoulders are present to a lesser extent. DIPs of the hands are usually spared. Large joints are commonly involved in EORA, the shoulders more often than in younger patients.8, 9

Gout is an inflammatory arthropathy caused by deposition of sodium monourate crystals in the joint and occurs in an overall prevalence from less than 1–15%.10 Its prevalence increases with age.10 The typical presentation is that of an acute monoarthritis in 85–90% of first attacks, most commonly occurring in the first MTP joint. The joint is usually extremely tender because it is associated with swelling and overlying erythema that sometimes mimics cellulitis or septic arthritis. Patients may be febrile and attacks can be precipitated by alcohol intake, use of diuretics and stress, such as that occurring with surgical procedures or acute medical illness. Gout occurs more readily in joints damaged by other conditions such as OA. Polyarticular involvement of gout is not uncommon in older persons. It sometimes resembles RA. Such attacks tend to have smouldering onset and longer course with a duration as long as three weeks. Chronic tophaceous gout is characterized by episodes of acute arthritis, chronic polyarthritis, joint deformities and tophi. Radiographic findings are non-specific in early stages. Punched out lesions or periarticular bone with overhanging borders are typically seen in chronic gout.5, 10

Laboratory findings include hyperuricaemia in most cases.10 Most individuals with hyperuricaemia never experience acute or chronic gout. About 10% have normal serum levels during the attack. Therefore, the diagnosis should be established by the identification of typical sodium monourate crystals in synovial fluid, preferably with the use of a polarized microscope. This is accompanied by evaluating serum uric acid level and also performing a 24-hour urine for total serum urate spillage to define if the patient is an over-producer or under-secreter of uric acid.

Calcium pyrophosphate deposition disease (CPDD) is also a crystalline deposition arthropathy.11 Women may be more commonly affected by CPPD crystal deposition than men.12 Its prevalence increases with age, being 10% in age 60–75 years and 30% in those 80 years of age or older.13 Most cases are primary, but in some people it is associated with certain conditions such as hypothyroidism, hyperparathyroidism and haemochromatosis. Many patients merely have asymptomatic chondrocalcinosis, commonly noted by X-rays in the knees and wrists where linear punctate radiodensities are found within the cartilage.11

Typical presentation is usually of two types, chronic arthropathy, which is sometimes polyarticular and presents with or without acute attacks with the knees most predominantly affected. Clinically, it may resemble OA or RA. Radiography may show features of both OA and CPDD, so it is not clear whether CPDD is primary or secondary. The second presentation is pseudogout, which is an acute monoarthritis, affecting mainly the knees and other large joints primarily and these resolve spontaneously within three weeks. It may infrequently affect a few articulations. Attack of pseudogout can be precipitated by stress or local trauma and fever is common.12

Connective tissue disease, primary SS and systemic lupus erythematosus (SLE), may present in the older population. Fifteen percent of cases of SLE may begin after age 55.14 It may present with arthralgias or symmetric polyarthritis involving primarily finger joints, best resembling RA at this stage. Previous studies indicated older onset SLE tended to be milder than the disease in younger patients with a lower incidence of nephropathy, neuropsychiatric manifestations, fever and Raynaud’s symptoms.15 However, a recent study suggested that older age-onset SLE is not benign.16 There is an increased frequency of serositis, interstitial lung disease, myalgias and sicca symptoms.14 Primary SS also often presents in the aged.17 Patients complain of dryness of their eyes and also dryness in their mouth with swallowing difficulty. Nasal dryness, hoarseness, bronchitis, and skin and vaginal dryness may occur. The parotid glands may be swollen. Sicca symptoms (dry eyes and dry mouth) may be subtle and not obvious to the patients. Individual patients commonly have polyarthritis or arthralgias. Other features of the disease are myalgias, low-grade fever and fatigue. Most have hypergammaglobulinemia and the frequency of developing lymphoproliferative disease is increased.17

Antinuclear antibodies are present in most SS and SLE patients, with antibodies to SS-A (Ro) and SS-B (La) occurring in the SS patients and SLE patients; and SLE patients having antibodies alone to double-stranded DNA, Sm and RNP.18 Other laboratory studies for evaluation include complement levels, antiphospholipid antibody studies, and other specific tests that may be helpful in diagnosing a particular connective tissue disease that is involved in the elderly patient.19, 20

Drug-induced lupus (DIL) is also a disease of older patients because inciting drugs are prescribed more frequently in the elderly. Symptoms are mild in most patients and resemble those of older onset SLE. The diagnosis is suggested by a history of administration of drugs like procainamide, hydralazine, alpha-methyldopa, propylthiouracil, or minocycline.21 Most of these patients have positive ANA tests and antibodies to histones or chromatin in 70–95% of the cases and occasionally antibodies to myeloperoxidase. Other antibodies occur infrequently.22

Infectious arthritis typically presents as an acute monoarthritis of a large joint in more than 80% of cases with the knee involved in more than 50% of cases.23 It is associated with systemic signs of infection such as high fever, chills and leukocytosis. Several factors predispose to an infected joint, including pre-existing joint disease, a prosthetic joint, an infectious process elsewhere, or an immunocompromised state, such as diabetes mellitus or treatment with corticosteroids or immunosuppressives.24