You are on page 1of 5

RHEUMATOID ARTHRITIS

Rheumatoid arthritis is one type of inflammatory polyarthritis, characterized by a


variable but usually prolonged clinical course with exacerbations and remissions of joint
pains and swelling that frequently lead to progressive deformities and permanent
disability.
Rheumatoid arthritis of the hip joint is not primarily a disease of articular
cartilage, but systemic disease (rheumatoid arthritis ) involving mesenchymal tissue of
the body as a whole with most pronounced affect a synovium ( hip joint ).

Incidence
Rheumatoid arthritis is relatively common. Women are afflicted three times more
than men, may begin at almost any age with peak period of onset is between the ages of
20 and 40 years. The peripheral joints, especially those of the hands, are the most
frequent sites of initial involvement, and the distribution in paired limbs tends to be
symmetrical.

Etiology
This is a relatively new disease has sparked the speculation that the causative
agent may be an occult mycobacterium or a relatively new microorganism, such as the
ubiquitous Epstein-Barr retrovirus or some other virus.
Some of the features of rheumatoid arthritis suggest an exaggeration of normal
immune mechanisms, or hypersensitivity_a continuous immunological response of an
immunogenetically susceptible host. Affected individuals exhibit disease susceptibility
markers on the major histocompatibility complex (MHC) on chromosome 6 to a
persistent antigen. Many of the patients who test positive for the rheumatoid factor
possess the human leukocyte antigen (HLA-DR4 haplotype).
In the past, it was thought that psychological factors may predispose an individual
to this disease. The anxiety-ridden and depressed person who tends to suppress feelings
of hostility and aggression seemed more prone to acquire rheumatoid arthritis than the
average whereas the psychotic individual seemed less prone.

Pathogenesis and Pathology


The primary “target” of the disease is the synovial membrane of joints and tendon
sheaths. This membrane reacts to the inflammation by congestion, edema, fibrin
exudation, proliferation, and villous formation. The characteristic inflammatory cells in
the synovial membrane are monocytes (T and B lymphocytes, plasma cells, and
macrophages).
The resultant immune process within the diseased synovium produces immune
complexes that in turn, activate a multitude of chemical mediators of inflammation. In the
acute inflammatory exudates in the synovial fluid, polymorphonuclear leukocytes engulf
immune complexes, and they extrude hydrolytic enzymes (neutral proteases such as
cathepsin G, elastase, and collagenase) that are capable of degrading the proteoglycans
and collagen of cartilage matrix and thereby inducing an autoimmune response that can
lead to destruction of the joint.
Inflammatory granulation tissue infiltrates the subsynovial connective tissue,
causing it to become swollen and boggy. The fibrous capsule and joint ligaments may be
involved , they become sufficiently softened and stretched and joint may become
subluxated or even dislocated. Furthermore granulation tissue is eventually replaced by
reparative fibrosis or scar formation, with resultant joint contracture and deformity.
The inflammatory granulation tissue also creeps across the joint surface to form a
pannus (from the Latin word meaning “a rug”), which interferes with the normal nutrition
of articular cartilage from synovial fluid and causes cartilage necrosis. Furthermore, the
same tissue erodes subchondral bone at the margins of the joint and burrows beneath the
cartilage to produce local areas of osteolysis (erosions) in the bone. If the process
continues over a period of months or years, fibrous adhesions eventually form between
opposing joint surfaces with a resultant fibrous ankylosis and fibrous ankylosis may
eventually ossify to become a bony ankylosis.
Approximately 30% of patients exhibit subcutaneous rheumatoid nodules over
areas subjected to pressure, particularly in the upper limbs. These extra-articular lesions,
which seem to begin as an area of rheumatoid vasculitis with subsequent necrosis, are
composed of a central zone of fibrinoid material and cellular debris surrounded by a
middle zone of mononuclear cells and an outer zone of granulation tissue.

Clinical Features and Diagnosis


The clinical manifestations of rheumatoid arthritis are so variable in their mode of
onset, distribution, degree of severity, and rate of progression. The disease usually begins
in several joints (rheumatoid polyarthritis) and the most common joints involved are
those of the hands, wrists, knees, elbows, feet, shoulders, hips and tends to be bilaterally
symmetrical.
In the early phases, systemic manifestations such as malaise, fatigability, and
weight loss are common, particularly among young and middle-aged patients. Initially,
the most frequent local symptoms are vague pain and stiffness of involved joints; most
noticeable in the morning and when begins to move inflamed joints that tend to “stiffen
up” during sleep ( “morning stiffness”).
In each involved active joint, four manifestations of inflammation (swelling, heat,
pain, and loss of function) become progressively more marked. The joints, which have a
characteristic boggy feel, are tender to pressure and painful on movement, both active
and passive. Protective muscle spasm is apparent in the muscles that control the inflamed
joints that soon become stiff if immobilized.
Deformities develop fairly rapidly with rheumatoid arthritis because of a
combination of the following factors:
1) muscle spasm, which maintains the joint in the least painful position, usually flexion;
2) muscle atrophy, with decreasing strength to move the joint;
3) muscle contracture resulting from fibrosis in the inflamed muscles;
4) subluxation and dislocation caused by a stretched joint capsule and ligaments;
5) late capsular and ligamentous contracture resulting from fibrosis; and
6) rupture of tendons, particularly in the hands, resulting from rheumatoid involvement
plus friction against bony spurs.
Radiographic examination reveals : periarticular soft tissue swelling, joint effusion,
regional osteoporosis, osteolytic erosion in subchondral bone, narrowing of the cartilage
space, subluxation, dislocation and bony ankylosis ( related to the history ). In the hip
radiographic appearance can be classified and related to the natural history :
1. Loss of joint space : this is appearance of loss of articular cartilage.
2. Protusio acetabuli
3. Collapse of femoral head : occur when uniform lost of the articular cartilage has
occurred
4. Ankylosis and arthrodesis
5. Charcot type joint

Laboratory examinations
They are useful in the diagnosis and differential diagnosis of rheumatoid disease
even though there is as yet no specific laboratory test. Anemia, an elevated white blood
cell count and an elevated erythrocyte sedimentation rate (ESR) are characteristic
findings, and the elevated erythrocyte sedimentation rate usually correlates with acute-
phase reactants such as fibrinogen and C-reactive protein. Rheumatoid factor, which is an
autoantibody to gamma globulin, is detectable because of its ability to agglutinate
particles of latex coated with the human immunoglobulin IgG.

Treatment
The initial complete assessment of a patient and the initiation of treatment for the
early phase as well as for exacerbations are most effectively carried out in hospital.
Aggressive medical treatment of rheumatoid arthritis early in the course of the disease is
more effective than treatment later in the disease.
Aims of Treatment
1)to help the patient understand the nature of the disease, 2)to provide psychological
support, 3)to alleviate pain, 4)to suppress the inflammatory reaction, 5)to encourage the
patient to remain as physically active as possible in order to maintain joint motion and
prevent deformity, 6)to correct existing deformity, 7)to improve function, 8)to strengthen
weak muscles, and 9)to rehabilitate the individual patient.
Methods of Treatment
- Psychological Considerations
- Therapeutic Drugs
The multiplicity of drugs prescribed for patients with rheumatoid arthritis can be
categorized in the order of frequency of their administration: short-or fast-acting
nonsteroidal anti-inflammatory drugs (NSAIDs), slow-acting antirheumatic drugs
(SAARDs), corticosteroids, and immunosuppressive agents.
Corticosteroids are usually reserved for extremely severe forms of rheumatoid
arthritis and for serious complications of the disease. For patients whose disease has been
refractory to the preceding forms of medication and continues to progress, there is a place
for immunosuppressive drugs and cytotoxic agents, preferably under the direction of a
rheumatologist. Suppressive measures for local disease include the intra-articular
injection of corticosteroids, which should not be repeated frequently with short intervals
in a given joint because of the harmful effects on articular cartilage and “radiation
synovectomy” by means of the intra-articular injection of radioactive material such as
yttrium90.
The therapeutic hope for the future is the discovery of biological agents that
block the pivotal steps in the pathogenesis of rheumatoid arthritis. Such “biologics” could
be targeted to the specific cells that create the arthritis. Gene therapy of rheumatoid
arthritis also has the potential for eradicating the disease process.

- Orthopaedic Appliances
In addition to adequate general rest (bed rest), local rest of painfully inflamed
joints by removable splints ( traction ) is of great value, not only in relieving pain but also
in the prevention of deformity.
Physical Therapy
Active movements of involved joints within the limits of pain are important in the
attempt to preserve joint motion and maintain muscle strength.
Orthopaedic Surgical Operations
For many years it was thought that surgical operations for rheumatoid arthritis
should not be performed during the active stage of the disease for fear of producing an
exacerbation of both the local and systemic inflammatory process. Consequently, in the
past, operations were performed only as a last resort and in the very late, “burned out”
stage of the disease, by which time the joints had suffered irreparable damage. Such
operations included fusion of joints (arthrodesis) and reconstruction of joints by various
means (arthroplasty).
It is now known, however, that surgical operations can be performed with relative
safety, even during the active stages of rheumatoid arthritis to prevent some of the joint
and tendon damage as well as the associated deformities. Severe chronic pain is the
primary indication for surgical operations. General indication : 1. persistent pain which
fail to settle with conservative treatment, 2. restriction of movement in the hip
A. Synovectomy : Excision of synovial tissue may have 3 benefits : 1. removal the
target tissue, 2. reduction of intraarticular swelling which may be responsible for
joint laxity, 3. reduction of pannus formation in the preservation of articular
cartilage.
B. Arthrodesis and Arthroplasty

Prognosis
As might be expected, is least favorable in patient whom the process remains
active over several years or longer. Approximately 50% of treated patient be able to
return their previous occupations.
DAFTAR PUSTAKA

1. Krishnan Unni K. Dahlin’s Bone Tumors, 5th ed. Philadelphia-New York, Lippincott
- Raven, 1996, p : 333-53.
2. Toolan BC, Steiner GC, Kenan S, Miscellaneous Tumors in Orthopedics A Study
Guide, International edition, 1999, p : 289-1

You might also like