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.