A Definition Of Terms
The terms ‘arthritis’ and ‘rheumatism’ encompass a range of painful musculoskeletal conditions. This article provides a brief overview of the definitions of arthritis and rheumatism.
What is Arthritis?
The term arthritis describes a range of readily diagnosable inflammatory conditions of the joints. The classification, diagnostic criteria and treatment approaches to these conditions have all been established to a greater or lesser extent in the international literature. The term arthritis therefore includes rheumatoid arthritis, osteoarthritis, infective arthritis, psoriatic arthritis, arthritis associated with inflammatory bowel disease, Reiter’s syndrome, ankylosing spondylitis, gout and pseudogout.
What is Rheumatism?
Pain at or around a joint which is not due to joint disease is rheumatism. Unlike arthritis, the concept of rheumatism is less clearly defined. In fact, ‘rheumatism’ is often used as a ‘catch-all’ term for the musculoskeletal aches and pains we nearly all suffer from at some time. These aches and pains often have no clearly defined underlying pathology. Rheumatism may therefore include neck pain, tennis elbow, lumbago and fibromyalgia. These musculoskeletal disorders are recognised by health practitioners around the world as a common source of pain and distress. They are also generally responsive to treatment with analgesics, anti-inflammatory medications and physical therapy.
Is That All There Is To It?
Well, actually no. Many patients with an inflammatory arthritis will also have symptoms of rheumatism, such as fibromyalgia. Other patients may have severe symptoms of muscular pains with inflammation, but no arthritis, as in polymyalgia rheumatica. Yet others will have arthritis as part of a more diverse inflammatory disorder (e.g. systemic lupus erythematosus) or as a presenting feature of another disease (e.g. haemochromatosis).
The Aetiology of Arthritis and Rheumatism
The arthritic and rheumatic diseases represent a spectrum of musculoskeletal disorders, among the most common of which are rheumatoid arthritis (RA) and osteoarthritis (OA). Although much is known about the pathophysiology of these conditions at a cellular level, there is considerably less information about the aetiology of RA and OA in terms of causative factors.
RA is an autoimmune disease in which an as yet unknown trigger results in a chronic inflammatory process affecting the synovial membrane of the joints. While T cells are the dominant cell type in the involved synovial tissues, B cells also play a role.
The onset of RA can be sudden (in about I 0% of cases), but in most patients the course of the disease is slow and insidious. This fact makes the identification of the trigger even more difficult to pinpoint. Current understanding of the aetiology of RA suggests that this condition is caused by a complex interaction between genetic, environmental and physiological factors.
Some of the aetiological factors implicated in the development of RA are shown below:
Aetiological factors implicated in the development of RA
• Exposure to certain pets/animal products
• Dietary allergies (e.g. dairy products).
There is now emerging evidence of a relationship between diseases of the immune system and genes that map the major histocompatibility complex (MHC). The genetic basis of RA is complex, but the presence of HLA-DRB1 alleles of the MHC appears to increase an individual’s susceptibility to developing RA.
Endocrine factors are closely associated with immune function, and RA patients often show hormonal abnormalities that indicate changes in pituitary function. Some of the hormonal changes may however be a consequence of the systemic inflammatory condition rather than a cause. Hormone changes implicated in the development of RA include:
Oestrogen level dysregulation – this may explain why women are 2 to 3 times more likely to develop RA than men are, and why the peak incidence of RA in women coincides with menopause. in addition, both pregnancy and oral contraceptives appear to mitigate or postpone the onset of RA in susceptible women
Low androgen levels – androgen levels are low in patients with RA and are decreased further during RA flares
Altered bioactivity of prolactin – prolactin levels are high during the postpartum period, which is also a time when women are at high risk of developing RA. In addition, prolactin has been implicated as a causal factor in the high rate of RA among infertile women.
Because of the inflammatory nature of RA, infectious agents have long been considered potential triggers. Bacteria and viruses are most commonly cited as likely triggers.
Bacteria – the pathogens implicated in the development of RA include Mycobacterium, Proteus, Yersinio, Salmonella, Shigello, Eubocterium, Chiamydio, Borrelia and Bifidobacterium species.
Viruses – retroviruses and parvovirus have been suggested as possible triggers for RA. In addition, synovial lymphocytes from RA patients have been found to react to rubella virus, adenovirus, cytomegalovirus, mumps virus, and paramyxovirus antigen.
Exposure to Animals
A case-control study suggested that a close association with a cat during childhood (pre-puberty) is strongly associated with the development of RA, and the risk increases with increasing duration of exposure to cats.’ A weaker association was found between childhood exposure to birds (budgerigars, in particular). These data suggest that certain household pets may act as a reservoir for environmental agents that, after a latency period, may trigger RA.
Sensitivity to particular foods has been implicated in the development of RA in some patients, but the evidence is scant. A small proportion of RA patients (<5%) can be described as having RA as a result of a food ‘allergy’. A handful of RA patients are hypersensitive to milk and dairy products, and benefit from a dairy-free diet.
Because so many patients with OA are elderly, this condition is often thought to be a result of natural ‘wear and tear’ on joint surfaces. However, OA is not an inevitable consequence of aging, and a number of aetiological factors have now been implicated in the development of this condition.
Aetiological factors implicated in the development of OA
• Mechanical stress on joints
Mechanical stress on joints has been strongly implicated in the development of hip and knee OA in men and women, especially stress associated with physically demanding occupational activities such as heavy lifting, frequent knee bending or stair climbing. Wearing high heeled shoes has also been suggested as a cause of altered mechanical stress on the knee that may predispose to OA. Moreover, the changes in subchondral regions of bones that occur during the pathogenesis of OA can alter the mechanical forces on bones. These changes in turn exacerbate the chondropathic processes in the joint by changing joint morphology.
Obesity is associated with an increased risk of both hip and knee OA. Obesity also increases the risk of OA associated with injury. Obesity may therefore be one of the few risk factors for OA that is amenable to treatment.
Injury to the hips and knees is associated with the development of OA in these joints later in life.
It has been estimated that genetic factors account for 50 to 65% of the risk of OA. Allelic variation in the vitamin D receptor is also implicated as a possible determinant of spinal disease severity.
A study has shown that smoking increases the prevalence, and severity, of degenerative spinal disease in elderly people.’ In addition, smoking increases the risk of hip OA.
The role of oestrogen in the development of OA is not clear. One study has shown that use of contraceptive pills was associated with an increased risk for total hip replacement later in life,’ but oestrogen replacement therapy appears to lower the risk of developing OA.
The aetiology of both RA and OA is not yet clearly defined, although a number of potential causative factors have been implicated. It seems that these conditions result from a complex interaction of genetic, environmental, hormonal and lifestyle factors, only a few of which can be altered or influenced at present.
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2. ]ones G, White C, Sambrook P Eisman J. Allelic variation in the vitamin D receptor, lifestyle factors and lumbar spinal degenerative disease. Ann Rheum Dis 1998, S7 (2): 94-9
3. Vingard E, Alfredsson L, Malchou H. Lifestyle factors and hip arthrosis. A case referent study of body moss index, smoking and hormone therapy in 503 Swedish women. Acta Orthop Scand 1997,- 68 (3): 2 7 6-20