RHEUMATOID ARTHRITIS

Sukirman
Nenda Mayang Azti
Ferry
Erick
Davien
DEFINITION

Rheumatoid Arthritis is a chronic inflammatory

disease of unknown origin marked by a symmetric,
peripheral poly arthritis. It's most common form
chronic inflammatory arthritis and often make a
joint damage and physical disability
 Morphological evidence for
immunological activity
– Joint change in RA can produce by dysregulated and invasive growth of the
synovial cells developing (called it pannus) overlays and destroy cartilage and
bone.
– Synovial membrane surrounds and maintains joint space becomes intensely
cellular as result immunological hyperreactivity.
– Immunological reactivity provides an intense stimulus to the synovial lining cells
that transform into invasive pannus thereby bringing about join erosion through
the release of destructive mediators
– Granulomatous rheumatoid nodules may be develop

Roitt. 2011. Roitt’s Essential Immunology: Rheumatoid arthritis. Wiley-Blackwell: UK (pg. 496)
ETIOLOGI
1. GENETIC SUSCEPTIBILITY
2.THE INFLAMMATORY REACTION
3.RHEUMATOID FACTOR
4.CHRONIC SYNOVITIS AND JOINT DESTRUCTION
Solomon. 2010. Apley’s System of Orthopedics and Fractures: Inflammatory Rheumatic Disorders. London: Hodder Arnold
(pg: 2)
 1. Genetic Susceptibility
 Association genetic suggested by the fact RA is more common in first
degree relatives of patients than in the population at large.
 Human Leucocyte Antigen (HLA) DRA occur in about 70% with RA patient.
 HLA-DR4 is encoded in the major histocompatibility complex (MHC) region
on chromosome 6. Strong associations between HLA-DR4 and RA.
 HLA class II molecules appear as surface antigens on cells of the immune
system (B lymphocytes, macrophages, dendritic cells), can act as antigen
presenting cells (APCs).
 T-cell immune reactions initiated only when the antigen peptide is
presented in association with a specific HLA allele.

Solomon. 2010. Apley’s System of Orthopedics and Fractures: Inflammatory Rheumatic Disorders.
London: Hodder Arnold (pg: 2)
 2. The Inflammatory Reaction
 APC/T-cell interaction is initiated, various local factors come into play and
lead to a progressive enhancement of the immune response
 Marked proliferation of cell in the synovium, with the appearance of new
blood vessel formation
 Immune cells coordinate their action by the use of ‘short-range hormones’
(cytokines), which can active inflammatory cells such as macrophages and
B cells.
 Important role of RA is Tumour Necrosis Factor (TNF), interleukin-1 (IL-1) and
interleukin-6 (IL-6)
 Resulting synovitis, both in joints and in tendon sheath, is the hallmark of
early RA

Solomon. 2010. Apley’s System of Orthopedics and Fractures: Inflammatory Rheumatic Disorders.
London: Hodder Arnold (pg: 2)
 3. Rheumatoid Factor

 B-cell activation in RA leads to the production of anti-IgG autoantibodies,

which are detected in the blood as ‘rheumatoid factor (RF)’.
 Other autoimmune conditions such as systemic lupus erythematous (SLE)
and Sjorgen’s syndrome are also associated with the presence of RF,

Solomon. 2010. Apley’s System of Orthopedics and Fractures: Inflammatory Rheumatic Disorders.
London: Hodder Arnold (pg: 2)
 4. Chronic Synovitis and Joint Destruction

 Chronic rheumatoid synovitis is associated with the production of

proteolytic enzymes, prostaglandins and the cytokines TNF and IL-1
 Immune complexes are deposited in the synovium and on the articular
cartilage, where there appear to augment the inflammatory process.
 Combination factor leads to depletion of the cartilage matrix and,
eventually, damage to cartilage and underlying bone.
 Vascular proliferation and osteoclastic activity, most marked at the edges
of the articular surface, may contribute to cartilage destruction and peri-
articular bone erosion

Solomon. 2010. Apley’s System of Orthopedics and Fractures: Inflammatory Rheumatic Disorders.
London: Hodder Arnold (pg: 2)
Clinical Features

– Increase between 25 and 55 years, plateaus until 75 years.

– Presenting symptoms of RA: joint inflammation, tendon, and bursae.
– Early morning stiffness lasting more than 1 hour with physical activity.
– Pattern joint involvement may be monoarticular, oligoarticular (≤4 joints), or
polyarticular (>5 joints), usually in a symmetric distribution.