INFLAMMATORY APLEY CHAPTER III
RHEUMATIC DISORDER
DEPARTEMEN ORTHOPAEDI
RHEUMATOID ARTHRITIS RSUD DR. SOETOMO
SURABAYA
Is the most common cause of chronic
inflammatory joint disease
Is a systemic disease and changes can be
widespread in a number of tissues of the
body
INTRODUCTION
The reported prevalence of RA in most
populations is 1–3 per cent
Women are affected 3 or 4 times more
commonly than men
CAUSE GENETIC AN
IMMUNOLOGICAL
SUSCEPTIBILITY REACTION
Still incompletely worked out
Important factors in the AN INFLAMMATORY THE APPEARANCE
evolution of RA REACTION IN OF RHEUMATOID
JOINTS AND FACTORS (RF) IN THE
TENDON SHEATHS BLOOD & SYNOVIAL
PREPETUATION OF ARTICULAR
THE INFLAMMATORY CARTILAGE
PROCESS DESTRUCTION
GENETIC SUSCEPTIBILITY
The human leucocyte antigen (HLA) DR4 occurs in about 70% of
people with RA
HLA Class II molecules appear as surface antigens on cells of the
immune system
which can act as antigen-presenting cells (APCs)
In some T-cell immune reactions, the process is initiated only when
the antigenic peptide is presented in association with a specific
HLA allele
THE INFLAMMATORY REACTION
Once the APC/T-cell interaction is initiated, various local factors
come into play and lead to a progressive enhancement of the
immune response
Immune cells coordinate their action by the use of cytokines
Some cytokines called chemokines attract other inflammatory cells
to the area
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 autoantibodies associated with RA have been identified.
The most important are anti-cyclic citrullinated peptide antibodies
(anti-CCP)
Anti-CCP is very specific for RA
Patients with a positive RF test tend to be more severely affected
than those with a negative test
CHRONIC SYNOVITIS AND JOINT DESTRUCTION
Associated with the production of pro- teolytic enzymes,
prostaglandins and the cytokines TNF and IL-1
Immune complexes are deposited in the synovium and on the
articular cartilage
Leads to depletion of the cartilage matrix and, eventually,
damage to cartilage and underlying bone
PATHOLOGY
JOINTS & TENDON
EXTRA-ARTICULAR TISSUES
Rheumatoid nodules
Nodules occur under the skin (especially over bony prominences), in the
synovium, on tendons, in the sclera and in many of the viscera
Lymphadenopathy
The nodes draining inflamed joints
Also those at a distance such as the mediastinal nodes, can be affected
Mild splenomegaly, is due to hyperactivity of the reticuloendothelial system
EXTRA-ARTICULAR TISSUES
Vasculitis
Muscle weakness
It may be due to a generalized myopathy or neuropathy
but it is important to exclude spinal cord disease or cord compression
Visceral disease
Ischaemic heart disease and osteoporosis are common complications
CLINICAL FEATURES (EARLY STAGE)
The picture is mainly that of polysynovitis, with soft-tissue swelling and
stiffness.
Generalized stiffness after periods of inactivity, and especially after
rising from bed in the early morning.
Early morning stiffness typically lasts longer than 30 minutes
Usually there is symmetrically distributed swelling and tenderness of the
metacarpophalangeal joints, the proximal interphalangeal joints and the
wrists
Movements are often limited but the joints are still stable and deformity is
unusual.
CLINICAL FEATURES (LATER STAGE)
More constant ache of progressive joint destruction
The combination of joint instability and tendon rupture
produces the typical ‘rheumatoid’ deformities
1. Ulnar deviation of the fingers
2. Radial and volar displacement of the wrists
3. Valgus knees
4. Valgus feet
5. Clawed toes
BLOOD INVESTIGATIONS
Normocytic, hypochromic anaemia is common and is a reflection
of abnormal erythropoiesis
In active phases the ESR and CRP concentration are usually raised
Rheumatoid factor are positive in about 80 per cent of patients
and antinuclear factors are present in 30 per cent
Anti-ccp antibodies have added much greater specificity
DIAGNOSIS
SYMMETRICAL
POLYARTHRITIS PERSISTING FOR AT
BILATERAL INVOLVING THE LEAST 6 WEEKS
PROXIMAL JOINTS OF
THE HANDS OR FEET
SUBCUTANEOUS X-RAY SIGNS OF POSITIVE TEST FOR
NODULES PERIARTICULAR RHEUMATOID FACTOR
EROSIONS
TREATMENT
There is no cure for rheumatoid arthritis
Treatment should be aimed at controlling inflammation as rapidly as possible
Likely to require the use of corticosteroids for their rapid onset
Disease-modifying antirheumatic drugs (dmards)
Control of pain and stiffness with nsaids
Maintaining muscle tone and joint mobility by a balanced programme of exercise
Additional measures include the injection of long- acting corticosteroid preparations
into inflamed joints and tendon sheaths
Surgical management
COMPLICATIONS
Fixed deformities
Muscle weakness
Joint rupture
Infection
Spinal cord compression
Systemic vasculitis
Amyloidosis
PROGNOSIS
Bad Prognostic Sign :
• High titres of rheumatoid
factor
• Periarticular erosion
• Rheumatoid nodules
• Severe muscle wasting
• Joint contracture
• Evidence of vasculitis
DEPARTEMEN ORTHOPAEDI
AKYLOSING SPONDYLITIS RSUD DR. SOETOMO
SURABAYA
INTRODUCTION
Generalized chronic inflammatory disease, its effects are seen
mainly in the spine and sacroiliac joints
It is characterized by pain and stiffness of the back, with
variable involvement of the hips and shoulders and (more rarely)
the peripheral joints
There is a strong tendency to familial aggregation and
association with the genetic marker HLA-B27
The usual age at onset is between 15 and 25 years
CAUSE
Genetically determined immunopathological disorder
Much more common in family members of patients than in the
general population
HLA-B27 is present in over 95 per cent of Caucasian patients
May be a bacterial antigen, which closely resembles HLA-B27
that induces an antibody response
PATHOLOGY
Basic lesions
Synovitis of diarthrodial joints
Inflammation at the fibro-osseous junctions of syndesmotic joints and tendons
Synovitis of the sacroiliac and vertebral facet joints causes destruction of articular
cartilage and peri-articular bone
Pathological stages:
1. An inflammatory reaction with cell infiltration, granulation tissue formation and erosion
of adjacent bone
2. Replacement of the granulation tissue by fibrous tissue
3. Ossification of the fibrous tissue, leading to ankylosis of the joint
CLINICAL FEATURES
A teenager or young adult complains of backache and stiffness recurring at
intervals over a number of years Simple Mechanical Back Pain
The symptoms are worse in the early morning and after inactivity
Referred pain in the buttocks and thighs may appear as ‘sciatica’
Other symptoms begin to appear: general fatigue, pain and swelling of
joints, tenderness at the insertion of the Achilles tendon, ‘foot strain’, or
intercostal pain and tenderness.
In established cases the posture is typical: loss of the normal lumbar lordosis,
increased thoracic kyphosis and a forward thrust of the neck
‘WALL TEST’: the patient is asked
to stand with his back to the wall;
heels, buttocks, scapulae and
occiput should all be able to touch
the wall simultaneously. If
extension is seriously diminished,
the patient will find this impossible
loss of the normal lumbar lordosis
increased thoracic kyphosis and a forward thrust of the neck;
upright posture and balance are maintained by standing with the hips and knees
slightly flexed
in late cases these may become fixed deformities.
Spinal movements are diminished in all directions, but loss of extension is always
the earliest and the most severe disability.
