Rheumatoid arthritis in the human body

Rheumatoid arthritis is one of the inflammatory rheumatic diseases and often affects the synovial tissue of the joints. Synovial tissue forms the inner layer of the joint capsule and plays an essential role in joint lubrication and nutrition.

In RA, the synovial membrane is attacked by immune cells. This causes inflammation and leads to the formation of so-called pannus tissue. Pannus tissue is an abnormal, highly inflammatory layer of tissue that destroys the joints.

As the disease progresses, the synovial membrane becomes increasingly inflamed, which leads to damage to the cartilage and the underlying bone structure. If left untreated, RA can lead to a significant restriction of mobility as the joint structures are destroyed. In addition to the joints, organs such as the lungs, heart and eyes can also be affected, making the disease systemic.

RA is a chronic disease. As such, it cannot currently be cured, but it can be treated. Treatment aims to reduce inflammation, relieve pain, maintain mobility and slow the progression of the disease.

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In Germany, around 800,000 people are affected, with women suffering from the disease three times more frequently than men. Rheumatoid arthritis often occurs in middle age, but can also affect younger and older people.

Rheumatoid arthritis is classified as a chronic, systemic autoimmune disease and belongs to the group of inflammatory rheumatic diseases. As such, it is usually diagnosed and treated by rheumatologists.

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Pathomechanisms & progression

The central pathological feature of rheumatoid arthritis is inflammation of the synovial membrane. This process is triggered by a misdirected immune response in which immune cells such as T and B lymphocytes and macrophages are activated and release inflammatory messengers [3]. These intensify the inflammatory reaction and cause tissue damage.

There are two main disease mechanisms in RA:

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1. Inflammation of the synovial membrane: Inflammation leads to thickening of the synovial membrane and formation of pannus tissue. This pannus attacks the cartilage and bone structure and causes progressive joint damage [4-8].
2. Cartilage and bone destruction: The ongoing inflammation destroys cartilage cells (chondrocytes) and bone cells (osteocytes). This leads to deformation and ultimately to immobility of the affected joint [4,5].

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Rheumatoid arthritis often progresses in episodes. Acute inflammatory reactions such as pain and restricted joint mobility occur during flare-ups. During periods of rest, the symptoms recede almost completely so that the disease is barely noticeable.

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Causes

The exact causes of rheumatoid arthritis are not yet fully understood and are therefore still the subject of intensive research. Several key factors have been identified that can contribute to the development of RA:

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Genetic predispositions

There is evidence that RA tends to run in families. In this context, genes have been identified that are associated with a higher susceptibility to RA. Heritability is estimated at 40-65% for seropositive RA and 20% for seronegative RA [9-11]. However, RA is not a purely genetic disease, as environmental factors also play a role.

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Environmental factors

Studies show that certain environmental factors can increase the risk of developing RA:

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• Smoking: Smoking has been strongly associated with the risk of developing RA through several complex mechanisms. It also influences the course of the disease. This is because, among other things, smoking can disrupt the healthy function of the immune system and increase the production of autoantibodies associated with RA [12,13].
• Infections: Certain viral and bacterial infections are also suspected to be able to trigger RA in people with genetic predispositions. Bacteria such as Aggregatibacter actinomycetemcomitans, which cause gum disease, can contribute to the development of RA [13]. Viral diseases such as Epstein-Barr virus [14], cytomegalovirus [15] and parvovirus B19 [16] have also been linked to RA. Most RA patients have antibodies against the Epstein-Barr virus.

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