Obesity – Predicts later risk of radiological and symptomatic OA in population studies
Heredity – Familial tendency to develop nodal and generalized OA.
Sex – 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 to lead to OA.
Osteoporosis – There is reduced risk of OA.
Other diseases
Trauma – A fracture through a joint or 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 Perthe’s disease; osteonecrosis of the femoral head in children and adolescents cause early-onset of 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.
Osteoarthritis is a condition of synovial joints characterized by cartilage loss with an accompanying peri-articular bone response. There is no simple definition of OA as it requires consideration of three overlapping areas – pathological changes, radiological features and clinical consequences. Pathologically there is an alteration in cartilage structure, radiologically there are osteophytes and joint space narrowing, and clinically patients complain of pain and disability.1
EPIDEMIOLOGY
Osteoarthritis is the most common type of arthritis. The prevalence increases with age, and most people over 60 years will have some radiological evidence of it. It occurs worldwide, although OA of the hip is less common in black and Chinese populations, than in Caucasians.1
Women over 55 years are affected more commonly that men of a similar age. There is a familial pattern of inheritance in women with distal interphalangeal joint involvement. OA has a variable distribution. The resulting disabilities have major socio-economic resource implications, particularly in the developed world where individuals have ever increasing expectation of health-care.1
AETIOLOGY
Osteoarthritis is the result of active, sometimes inflammatory but potentially reparative processes rather than the inevitable result of trauma and ageing. It includes a wide spectrum of idiopathic joint disorders with focal destruction of the articular cartilage as the common pathological features. The spectrum ranges from atrophic disease in which the bone destruction occurs without any subchondral bone response, to hypertrophic disease in which there is massive new bone formation at the joint margins.1
Under normal circumstance there is a dynamic balance between cartilage degradation by wear and its production by chondrocytes. Early in the development of OA the surface of cartilage become fibrillated and fissured as the collagen matrix breaks down. These changes lead to focal erosion or cartilage. Chondrocytes die and, although repair is attempted from adjacent cartilage, the process is disordered. Cartilage ulceration exposes underlying bone to increased stress, producing microfractures and cysts. The bone attempts to repair but produces abnormal sclerotic subchondral bone and overgrowths at the joint margins, called osteophytes.1
In osteoarthritis (OA), articular cartilage destruction follows changes in cartilage cell metabolism that alters the functional load bearing properties of the extracellular matrix and culminates in loss of joint function. This extracellular matrix is comprised of water, collagen and proteoglycans (present mainly as large molecular aggrecans which serve to retain and maintain the water content of the cartilage). The slow, progressive changes seen in osteoarthritis is characterized by the progressive deterioration of the articular cartilage, the protective "cushion" at the articulating surfaces of bones. This degenerative process is caused primarily by a defect in the metabolism of the component macromolecules including aggrecans and type II collagen. The gene for human aggrecan has been cloned and polymorphisms of the gene have been correlated with OA of the hand in older men.
Causes of Osteoarthritis
| Primary OA | No known cause | ||||||||||||||||||||||||||||||||||||||
| Secondary OA |
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References:
1. Kumar, P and Clark, M: Clinical Medicine. (4th Edition). London, W.B. Saunders, Harcourt Publishers Ltd, (1998).