Hand osteoarthritis: Risk factors

Heredity seems to play a part in osteoarthritis. Numerous epidemiological studies have established that there is a family character for osteoarthritis of the fingers and hip. Hence, a woman risks having osteoarthritis of the fingers when her mother or maternal or paternal aunt suffers from it.

Studies of homo- and heterozygous twins evaluated the genetic contribution at around 39 to 45% with the remainder related to environmental factors.

It is known that women, especially after the menopause are more prone to osteoarthritis than men. This is particularly true for osteoarthritis of the fingers, knees and osteoarthritis affecting several joints.

Osteoarthritis of the hip, if not more frequent, is more painful in women.

Lastly, the number of joint prostheses (especially of the hip) is greater in women.

It is thought that sex hormones may be involved, but currently no hormonal treatment administered after the menopause has shown a protective effect against osteoarthritis.

We are now certain that obesity is a situation that promotes the development of osteoarthritis.

Thus, for the knee joint, being overweight exposes you in the future to a greater risk of knee osteoarthritis.

Similarly, in cases of already confirmed osteoarthritis of the knee, weight gain leads to increased cartilage damage and symptoms.

The Framingham study specifies that a loss of 5 kg in the previous 10 years, can reduce the risk of knee osteoarthritis in women by 50%.

The risk of osteoarthritis is not only due to mechanical reasons (caused by being overweight), but also endocrine and metabolic factors. Studies have demonstrated a connection between osteoarthritis and high blood sugar.

If we can more easily understand the role of weight in the occurrence of osteoarthritis of the knee and hip, its role in osteoarthritis of the hands is more surprising. Researchers are currently looking for factors in the blood of obese people that could explain the deterioration of the cartilage.

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Abnormalities of certain metabolisms can lead to a deposit of microscopic crystals in the joints. This is the case in the disease that everyone knows: gout where the crystals are composed of uric acid.

Hence, other crystals may occur such as those of calcium phosphate compounds that are deposited on the surface of joints in chondrocalcinosis, or hydroxyapatite crystals that tend to be deposited in the tendons.

It is in fact the repetition of inflammatory flare-ups triggered by these deposits that promotes the development of osteoarthritis in the joint in question.

For a better understanding of the phenomena that occur in the joint in osteoarthritis take a look at:

Understanding

Hence, these diseases may be responsible for diffuse osteoarthritis involving joints spared by primitive osteoarthritis (wrists, elbows, shoulders, ankles). The same is true for other diseases due to excess weight: hemochromatosis, Wilson's disease,

Paget's disease and chondrodysplasia. 

Often a fracture, dislocation or tendon injury can lead to osteoarthritis.

Microscopic lesions caused by too much stress can traumatize some joints and lead under certain conditions to the onset of osteoarthritis.

This is the case not only in certain occupations in which subjects are subjected to mechanical vibration and repeated shocks (users of pneumatic drills, drivers of construction equipment), but also when it is necessary to make repetitive movements such as data entry operators or pianists.

Whether congenital or acquired structural abnormalities will alter mechanical stress and promote the development of secondary osteoarthritis.

This may include dysplasia, protrusions, subluxations or acquired anomalies (fractures) or osteonecrosis of the wrist.

Destructive inflammatory diseases may also alter some joint mechanisms.