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Osteoarthritis is a disease that primarily affects the cartilage lining of the joints and the bones associated with the joints, called the subchondral bones.
However, all the tissues surrounding the affected joint eventually become abnormal. The cartilage lining the joint frays and outgrowths of bone form around the joint in an attempt at healing. Fragments of this bone break off and irritate the joints, which then lose their natural lubrication and become stiff and noisy.
Osteoarthritis used to be seen as a result of wear and tear of the joints. In fact, the disease is now thought to have several subtypes, of which some are more aggressive and related to immune mechanisms, resulting in inflammation against self and an erosion of the cartilage and adjacent bone, called erosive osteoarthritis.
The mechanism is a complex system of interacting mechanical, biological, biochemical and enzymatic feedback loops. When one or more of these fail, osteoarthritis occurs. Anything that changes the microenvironment of the bone cell may initiate the chain of events, which lead to osteoarthritis – congenital joint abnormalities, genetic defects, infectious processes, metabolic processes and neurological disease. Trauma to a joint may initiate osteoarthritis, including prolonged overuse of a joint or group of joints.
Osteoarthritis has a large tendency to be a genetically primed disease, especially in the end joints of the fingers and the spine.
Osteoarthritis is the most common of all disorders of the joints. The first symptoms appear usually in the 4th decade and 60-70% of people are affected by the 7th decade.
Early on, more women than men are affected, but this discrepancy is less marked in the elderly. There is a strong hereditary tendency, especially when hand joints are involved in women. There is evidence that gene coding for collagen components within cartilage may be abnormal, explaining the family clustering of this condition.
The earlier the onset and the greater the genetic factors, the greater the risks of developing OA are. Patients who have both parents affected will almost certainly develop osteoarthritis.
Obesity is an independent risk factor for osteoarthritis of the knee, and may predict development of the condition 30 years later. Although mechanical loading is the obvious explanation for this link, other metabolic abnormalities associated with obesity may be at play.
Joint hypermobility is also an independent risk for the development of OA. Some patients may have extreme hypermobility, leading to recurrent stress injuries and early OA of weight-bearing joints.
However, all the tissues surrounding the affected joint eventually become abnormal. The cartilage lining the joint frays and outgrowths of bone form around the joint in an attempt at healing. Fragments of this bone break off and irritate the joints, which then lose their natural lubrication and become stiff and noisy.
Osteoarthritis used to be seen as a result of wear and tear of the joints. In fact, the disease is now thought to have several subtypes, of which some are more aggressive and related to immune mechanisms, resulting in inflammation against self and an erosion of the cartilage and adjacent bone, called erosive osteoarthritis.
The mechanism is a complex system of interacting mechanical, biological, biochemical and enzymatic feedback loops. When one or more of these fail, osteoarthritis occurs. Anything that changes the microenvironment of the bone cell may initiate the chain of events, which lead to osteoarthritis – congenital joint abnormalities, genetic defects, infectious processes, metabolic processes and neurological disease. Trauma to a joint may initiate osteoarthritis, including prolonged overuse of a joint or group of joints.
Osteoarthritis has a large tendency to be a genetically primed disease, especially in the end joints of the fingers and the spine.
Osteoarthritis is the most common of all disorders of the joints. The first symptoms appear usually in the 4th decade and 60-70% of people are affected by the 7th decade.
Early on, more women than men are affected, but this discrepancy is less marked in the elderly. There is a strong hereditary tendency, especially when hand joints are involved in women. There is evidence that gene coding for collagen components within cartilage may be abnormal, explaining the family clustering of this condition.
The earlier the onset and the greater the genetic factors, the greater the risks of developing OA are. Patients who have both parents affected will almost certainly develop osteoarthritis.
Obesity is an independent risk factor for osteoarthritis of the knee, and may predict development of the condition 30 years later. Although mechanical loading is the obvious explanation for this link, other metabolic abnormalities associated with obesity may be at play.
Joint hypermobility is also an independent risk for the development of OA. Some patients may have extreme hypermobility, leading to recurrent stress injuries and early OA of weight-bearing joints.
