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Rheumatoid arthritis and psoriatic arthritis

Autoimmune conditions in which immune cells begin to attack the synovial membrane lining the joints, leading to unwanted inflammation and damage.

The inflammation associated with rheumatoid arthritis primarily attacks the lining of the joints (the synovium). If it persists, cartilage and bone erosion can occur and the joint becomes deformed and immobile. The muscles, tendons and ligaments surrounding affected joints can also weaken, which worsens the overall effects. The reason for the immune system reacting in this way is not yet fully understood. As is the case with other autoimmune diseases it’s very likely due a combination of genetic and environmental factors.

Inflammation is normally a sign that the body’s protective mechanisms are at work in response to infection: nearby blood capillaries swell, and fluid and immune cells move into damaged tissue to contain any infection present. However, in autoimmune conditions like rheumatoid arthritis, immune cells begin to attack the synovial membrane lining the joints; leading to unwanted inflammation and damage. The onset of rheumatoid arthritis is usually in middle life (between ages 25 and 45), although it can also affect young children – this is called juvenile idiopathic rheumatoid arthritis. 

Most people with rheumatoid arthritis have the potential to continue leading active lives, provided they receive appropriate treatment. There is currently no cure for rheumatoid arthritis, although symptoms can be readily treated and disease progression significantly slowed in most cases. Early diagnosis and management are vital in order to preserve joint movement and minimise pain and long-term disability.

About rheumatoid arthritis

  • Factors that increase your likelihood of developing rheumatoid arthritis include:

    • age (it's most likely to develop between the ages of 25 and 45)
    • gender (three quarters of those affected are female)
    • family history of rheumatoid arthritis or other autoimmune diseases like lupus and Sjögren’s syndrome
    • obesity.

    Complications associated with inadequately treated rheumatoid arthritis (in addition to joint damage) include lung fibrosis, anaemia, eye disorders and inflammation around the heart, as well as a general increased risk of cardiovascular problems.

  • Symptoms vary from person to person and can include:

    • swelling, pain and heat in the joints (most commonly, in the wrist and hands)
    • joint stiffness (particularly in the morning or after rest)
    • sleeping difficulties because of pain
    • muscle weakness.
    • persistent fatigue
    • unexplained weight loss
    • dry eyes and mouth due to associated Sjögren’s syndrome
    • intermittent fever and rash particularly in patients with the juvenile form of the disease.

    In general, both sides of the body are affected similarly, in contrast to osteoarthritis and gout. The adult form of rheumatoid arthritis tends to be chronic, whereas over 50% of children with the juvenile form ‘grow out of it’.

  • Rheumatoid arthritis usually manifests over a period of several months. However for some people it can appear much more rapidly. A thorough examination by an experienced doctor is the first step to diagnosis. They may ask if there’s a family history of the disease.

    Blood tests can reveal signs of inflammation and the presence of ‘rheumatoid factor’ (an antibody present in about 80% of people with rheumatoid arthritis), although this antibody can also be found in other inflammatory autoimmune diseases. A different autoantibody directed against so called citrullinated peptides is specific for rheumatoid arthritis – it too occurs in around 80% of cases.

    An x-ray may also be taken to determine if any damage to cartilage or bones has occurred, although this is usually only seen in later stages of the  disease.

    Supportive treatments include:

    • Physiotherapy – heat, cold and exercises to relieve pain and stiffness, improve joint movement and strengthen the muscles
    • Rest – when there is a worsening of joint inflammation
    • Occupational therapy – including training, advice, counselling, splinting, as well as walking aids and specialised utensils to help with daily activities.

    Drugs (often taken in combination) play an important role in dampening the underlying inflammatory and autoimmune process, but must be taken under the supervision of a rheumatologist to minimise the risk of side effects. They include:

    • Non-steroidal anti-inflammatory drugs (NSAIDs) – these lessen inflammation
    • Corticosteroids – used sparingly in more severe cases. These work by suppressing the immune response
    • Disease-modifying anti-rheumatic drugs (DMARDs) – these can slow the progress of disease. They now include antibodies directed either against inflammatory substances known as ‘cytokines’, in particular one called TNF which work against the immune cells responsible for joint inflammation. These antibodies represent the most significant advance in treating rheumatoid arthritis in the past 40 years.

    Diet is a factor that may influence the severity of symptoms. Fish oils that contain omega-3 fatty acids have been found to help reduce inflammation associated with arthritis. In some cases, surgery (for example, a knee replacement) is an option, especially if a joint has been badly damaged.

    This content is provided for informational purposes only. It is not a substitute for professional medical advice, diagnosis or treatment. If you have any concerns or questions about your health, please consult a suitably qualified healthcare professional.

Our research into rheumatoid arthritis & psoriatic arthritis

Rheumatoid arthritis and psoriatic arthritis are chronic, lifelong diseases. Current treatments, which suppress the immune system non-specifically, improve symptoms but have variable success and create long-term side effects. They often fail to prevent unpredictable, debilitating rheumatoid arthritis and psoriatic arthritis disease flares. Every flare causes measurable, irreversible joint damage and increased risk of cardiovascular disease.

Recent technological advances now allow the study of genes and proteins from thousands of individual cells within blood and inflamed joints. These single-cell sequencing technologies, alongside genome sequencing and high-dimension flow cytometry, provide unprecedented resolution to identify ‘rogue’ immune cells causing joint inflammation in arthritis.

You can help us find better treatments for rheumatoid arthritis and psoriatic arthritis by supporting our research.

Key areas of investigation

The below studies of rheumatoid arthritis and psoriatic arthritis are led by Dr Etienne Masle-Farquhar (Garvan), in close collaboration with Dr Mandeep Singh (New York Genome Centre) and rheumatologists including Dr Laila Girgis (Head of Rheumatology, St Vincent’s Hospital Sydney) and Dr Mihir Wechalekar (Head of the Synovial Tissue Biobank, Flinders University).

These studies are supported by the Exceptional Responders in Autoimmune/Inflammatory Diseases (ERAD) Program, the HOPE Research Project, Associate Professor Owen Siggs and Professor Chris Goodnow.

Studying immune cells during rheumatoid arthritis & psoriatic arthritis disease flares

Rheumatoid arthritis and psoriatic arthritis disease flares are unpredictable, debilitating and of unknown causes. To tackle these critical problems, Dr Etienne Masle-Farquhar and Dr Mandeep Singh are using cutting-edge single-cell sequencing methods to study immune dysregulation during flares, in close collaboration with a growing network of NSW rheumatologists, including Dr Laila Girgis, Dr Terry Kwong, Dr Ross Penglase and Dr Ric Day.

During flares, synovial fluid can accumulate excessively around joints. This excess fluid can be aspirated to reduce inflammation and pain, and rather than being discarded is now being used as a precious scientific resource. Within hours of a patient’s visit to hospital, aspirated synovial fluid is processed for experiments at Garvan, by members of the Genomic Medicine and Immunogenomics laboratories.

Studying rogue cells within affected joints

How immune cells cause joint damage in rheumatoid arthritis remains unknown, and choosing optimal preventative treatments is difficult. To address this, Dr Mandeep Singh and Dr Etienne Masle-Farquhar are collaborating with Dr Mihir Wechalekar, to study immune cells within the affected joint tissue of individuals with rheumatoid arthritis, before and over the course of their treatments.

Studying underlying genetic mechanisms of arthritis

There is a striking genetic association between rheumatoid arthritis and the rare cancer of CD8 T cells called T cell large granular lymphocytic leukemia (TLGL). TLGL cells often acquire genetic changes (mutations) in the gene STAT3. Relative to the general population, individuals with TLGL with STAT3 mutations are up to 40 times more likely to develop rheumatoid arthritis. In investigating why, Dr Etienne Masle-Farquhar and Professor Chris Goodnow demonstrated that CD8 T cells with acquired STAT3 mutations proliferate excessively, increase expression of cytotoxic molecules and cause autoimmune pathology.

The team had previously shown that acquired mutations can cause B cell-mediated autoimmune disease in Sjögren’s syndrome. They are now investigating acquired genetic mutations in immune cells, as a possible root cause for rheumatoid and psoriatic arthritis.

National and international collaborations

  • Exceptional Responders Program, Sydney, Australia.
  • St Vincent’s Hospital, Sydney, Australia.
  • Royal Prince Alfred Hospital, Sydney, Australia.
  • Westmead Hospital, Sydney, Australia.
  • Flinders University, Adelaide, Australia.
  • The Bill and Patricia Ritchie Foundation, Sydney, Australia.
  • University of Queensland, Brisbane, Australia.
  • Helsinki University Hospital, Helsinki, Finland.
  • New York Genome Centre, New York, USA.

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