Arthritis is a descriptive term applied to more than 100 rheumatic
diseases, ranging from localized, self-limiting conditions to those that
are systemic autoimmune processes. Arthritis can affect persons of all
age groups and is the second leading cause of disability.
Although the condition cannot be cured completely, much can be done to control its progress.
In
systemic rheumatic diseases—those affecting body systems in addition to
the musculoskeletal system, the inflammation is primary, resulting from
an immune response.
In rheumatic conditions limited to a single or few diarthrodial joints,
the inflammation is secondary, resulting from a degenerative process
and the resulting joint irregularities that occur as the bone attempts
to remodel itself
Rheumatoid arthritis is defined as a chronic systemic inflammatory disease characterized by bilateral involvement of synovial or diarthrodial joints
The initial joint changes involve the synovial cells that line the joint. In the process, the inflammatory cells accumulate and angiogenesis and
pannus formation follow proceeding to cover the articular cartilage and
isolate it from its nutritional synovial fluid take place.
Causes and pathogenesis of rheumatic arthritis
The
exact cause of rheumatoid arthritis is idiopathic meaning it isn't
exactly known. Although there is evidence of a genetic predisposition
and immunologically mediated joint inflammation.
The development of rheumatoid arthritis is initiated in a genetically predisposed person by the activation of a T-cell–mediated response to an immunologic trigger, such as a microbial agent.
It has been shown that certain major histocompatibility complex (MHC) genes are expressed in a nonrandom manner in persons with RA.
An important genetic locus that predisposes to RA is present on the human leukocyte antigen (HLA)
loci on the MHC class II molecules, with a specific set of HLA DR
alleles (DR4, DR1, DR10, DR14) being consistently increased in persons
with RA.
These HLA DR alleles form a shared epitope in the
hypervariable segment of the HLA-DRB1 gene, which forms a rheumatoid
pocket on the HLA molecule.
Pathogenesis of rheumatoid arthritis
The
pathogenesis of RA is an aberrant immune response that leads to
synovial inflammation and destruction of the normal joint architecture.
This process is usually initiated by the activation of helper T cells,
the release of cytokines, and antibody formation. The majority of people
suffering from rheumatoid arthritis have detectable, self-produced
antibodies (IGF) known as the rheumatoid factor (RF). This rheumatoid factor reacts with a fragment of immunoglobulin G (IgG) to form immune complexes.
This
Immune complexes of immunoglobulin G and immunoglobulin F (Ig RF + IgG)
together with complement proteins are found in the synovium, synovial
fluid, and extra-articular lesions.
When lab tests are done in patients suffering from rheumatoid factor, these individuals with RA may be seronegative without any Ig RF present in their serum.
Conversely, the presence of a high RF titer is associated with severe disease and systemic complications.
At
the basic cellular level, neutrophils, macrophages, and lymphocytes are
attracted to the area. These neutrophils and macrophages phagocytize
the immune complexes and, in the process, they release lysosomal enzymes
capable of causing destructive changes in the joint.
The
inflammatory response that follows attracts additional inflammatory
cells, setting into motion a chain of events that perpetuates the
condition. As the inflammatory process progresses, the synovial cells
and subsynovial tissues undergo reactive hyperplasia. Vasodilation and
increased blood flow cause warmth and redness.
The joint swelling that occurs is the result of the increased capillary permeability that accompanies the inflammatory process.
Characteristics of rheumatoid arthritis
The
characteristic of rheumatoid arthritis is the development of an
extensive network of new blood vessels in the synovial membrane that
contributes to the advancement of rheumatoid synovitis.
This destructive vascular granulation tissue, which is called pannus, extends from the synovium to involve the “bare area,” which is a region of unprotected bone at the junction between cartilage and subchondral bone.
Pannus is a feature of RA that differentiates it from other forms of inflammatory arthritis.
The
inflammatory cells found in the pannus have a destructive effect on the
adjacent cartilage and bone. Eventually, pannus develops between the
joint margins, leading to reduced joint motion and the possibility of
eventual ankylosis.
With the progression of the disease,
joint inflammation and the resulting structural changes lead to joint
instability, muscle atrophy from disuse, stretching of the ligaments,
and involvement of the tendons and muscles.
The effect of the
pathologic changes on joint structure and function is related to the
degree of disease activity, which can change at any time. These
destructive changes in the joints are irreversible.
Signs and symptoms of rheumatoid arthritis
Classical features of rheumatoid arthritis are associated with extra-articular as well as articular manifestations.
Its onset is insidious in
nature and is marked with systemic features such as excessive fatigue,
loss of appetite, weight loss, and generalized body malaise and
stiffness.
Rheumatoid arthritis characterized by
exacerbations and remissions may involve only a few joints for brief
durations, or it may become relentlessly progressive and debilitating.
Joint Manifestations.
RA has a characteristic symmetrical and polyarticular Joint involvement consisting of any diarthrodial joint.
Patients may complain of joint pain and stiffness that lasts for 30 minutes and frequently for several hours.
There
is a limited joint motion that occurs early in the disease mainly as a
result of joint pain; later, this limited joint motion results from
fibrosis.
The commonly affected joints initially are the
fingers, hands, wrists, knees, and feet. Later, other diarthrodial
joints may become involved.
Spinal involvement usually is
limited to the cervical region. In the hands, there usually is bilateral
and symmetric involvement of the proximal interphalangeal (PIP) and
metacarpophalangeal (MCP) joints in the early stages of RA; the distal
interphalangeal (DIP) joints rarely are affected.
The fingers often take on a spindle-shaped appearance because of inflammation of the PIP joints.
Progressive joint destruction may lead to subluxation or a dislocation of the joint resulting in misalignment of the bone ends and instability of the joint and limitation of movement.
Swelling and thickening of the
synovium can result in stretching of the joint capsule and ligaments.
When this occurs, muscle and tendon imbalances develop, and mechanical
forces applied to the joints through daily activities produce joint
deformities.
In the metacarpophalangeal joints, the extensor
tendons can slip to the ulnar side of the metacarpal head, causing ulnar
deviation of the fingers.
Subluxation of the MCP joints may develop when this deformity is present.
Hyperextension of the PIP joint and partial flexion of the DIP joint is called a swan neck deformity.
