INFLAMMATORY

RHEUMATIC DISORDERS
Christopher Edwards, Louis Solomon

Presented by:
Hary Wahyu Agustono
 INFLAMMATORY
RHEUMATIC DISORDERS

2. SERONEGATIVE 3. JUVENILE 4. CONNECTIVE

1. RHEUMATOID
IDIOPATHIC TISSUE
ARTHRITIS SPONDYLOARTHROPATHIES ARTHRITIS DISEASES

REITER’S SYNDROME
ANKYLOSING AND REACTIVE ENTEROPATHIC
PSORIATIC ARTHRITIS
SPONDYLITIS ARTHRITIS
ARTHRITIS
 1. RHEUMATOID ARTHRITIS

Rheumatoid arthritis (RA) is the most common cause of

chronic inflammatory joint disease.

PREVALENCE:
RA in most populations is 1–3 per cent, with a peak
incidence in the fourth or fifth decades. Women are
more commonly than men affected about 3 or 4 times.
CAUSE:
(1) genetic susceptibility; (2) an immunological reaction; (3) an
inflammatory reaction in joints and tendon sheaths; (4) the appearance
of rheumatoid factors (RF); (5) perpetuation of the inflammatory
process; (6) articular cartilage destruction.

PATHOLOGY:

1. Rheumatoid Arthritis Pathology

(a) Stage 1: pre-clinical. (b) Stage 2: synovitis and joint swelling. (c) Stage 3: early joint
destruction with peri-articular erosions. (d) Stage 4: advanced joint destruction and
deformity.
CLINICAL FEATURES

2. Rheumatoid Arthritis Clinical Features

(a) Early features of swelling and stiffness of the proximal finger joints and the wrists. (b)
The late hand deformities are so characteristic as to be almost pathognomonic. (c)
Occasionally rheumatoid disease starts with synovitis of a single large joint (in this case the
right knee). Extra-articular features include subcutaneous nodules (d,e) and tendon
ruptures (f).
 Imaging, Blood Investigations, and Synovial Biopsy

3. Rheumatoid Arthritis – X-ray Changes

First, there was only soft-tissue swelling and peri-articular osteoporosis; later juxta-articular
erosions appeared (arrow); ultimately, the joints became unstable and deformed

4. Rheumatoid synovitis
(a) The macroscopic appearance of rheumatoid synovitis with fibrinoid material oozing
through a rent in the capsule. (b) Histology shows proliferating synovium with round-
cell infiltration and fibrinoid particles in the joint cavity (x120).
TREATMENT COMPLICATION
Fixed deformities
Muscle weakness
Joint rupture
Infection
Spinal cord compression
Systemic vasculitis
Amyloidosis

PROGNOSIS
Without treatment about
10% improve steadily;
60% remission. Reduction
in life 5–10 yr due to
PHYSIOTHERAPY AND OCCUPATIONAL
premature ischaemic
THERAPY
heart disease.
SURGICAL MANAGEMENT
At first is soft-tissue procedures
Early aggressive medical
(synovectomy, tendon repair or replacement
treatment appears to
and joint stabilization). In late rheumatoid
reduce the morbidity and
disease, severe joint destruction, fixed
mortality.
deformity and loss of function are clear
indications for reconstructive surgery.
 2. SERONEGATIVE
SPONDYLOARTHROPATHIES
2.1) ANKYLOSING SPONDYLITIS
Generalized chronic inflammatory
CLINICAL FEATURES
disease, but its effects are seen mainly
in the spine and sacroiliac joints

CAUSE:
Genetically determined
immunopathological disorder.

PATHOLOGY:
(1) Inflammatory reaction
(2) Replacement of the granulation by
fibrous tissue
(3) Ossification of the fibrous tissue,
leading to ankylosis of the joint.
 IMAGING COMPLICATION
Spinal fracture
Hyperkyphosis
Spinal cord compression
Lumbosacral nerve root
compression

TREATMENT
(1) General measures to maintain satisfactory
posture and preserve movement;
(2) Anti-inflammatory drugs to counteract pain
and stiffness;
(3) TNF inhibitors for severe disease;
(4) Operations to correct deformity or restore
mobility.
2.2) EITER’S SYNDROME AND REACTIVE ARTHRITIS

CAUSE
Familial aggregation, pathogens
include Shigella flexneri,
Salmonella. Lymphogranuloma
venereum and Chlamydia
trachomatis (sexually transmitted
infections).

PATHOLOGY
The pathological changes are same
as ankylosing spondylitis
CLINICAL FEATURE
The acute phase: asymmetrical
inflammatory arthritis of the lower
limb. The chronic phase: polyarthritis
(including upper limb joints).

IMAGING
X-ray examination show severe
destruction of the interphalangeal
joints of the hands and feet.

TREATMENT
Treatment of Chlamydia with tetracycline up to 3 months. If the
inflammatory response is aggressive then local injection of corticosteroids or
even intramuscular methylprednisolone. If symptoms and signs do not
resolve then DMARDs.
2.3) PSORIASIS VULGARIS

CAUSE
Genetic, no specific trigger agent has
identified.

PATHOLOGY
The joint changes are similar to those
in rheumatoid arthritis. Chronic
synovitis with cell infiltration and
exudate, going on to fibrosis. Cartilage
and bone destruction may be unusually
severe (‘arthritis mutilans’).

CLINICAL FEATURE & IMAGING

CLINICAL FEATURE & IMAGING

DIAGNOSIS
(1) asymmetrical joint distribution;
(2) involvement of distal finger joints;
(3) the presence of sacroiliitis or
spondylitis;
(4) the absence of rheumatoid
nodules.

TREATMENT
Topical preparations to control the skin disease and NSAIDs for the
arthritis. In resistant forms of arthritis, immunosuppressive agents
(methotrexate) and TNF inhibitors. Surgery may be needed for unstable
joints. Arthrodesis of the distal interphalangeal joints may greatly improve
function.
 2.4) ENTEROPATHIC ARTHRITIS
Both Crohn’s disease and ulcerative colitis may be associated with
either peripheral arthritis or sacroiliitis and spondylitis.

PERIPHERAL ARTHRITIS SACROILIITIS AND SPONDYLITIS

Larger joints are involved. Pain Clinical picture closely of
and swelling. Synovitis is usually ankylosing spondylitis. Unaffected
the only feature but joint erosion by treatment of the bowel disease.
can occur.
TREATMENT
TREATMENT Same as ankylosing spondylitis
Anti-inflammatory, local
corticosteroid injection and
methotrexate. In severe cases TNF
inhibitors may be needed.

COMPLICATION ENTEROPATHIC ARTHRITIS

Septic arthritis of the hip, Psoas abscess, and Osteopaenia.
 3. JUVENILE IDIOPATHIC
ARTHRITIS
DEFINITION:
Juvenile idiopathic arthritis (JIA) is disorders in all of which
pain, swelling and stiffness of the joints. The prevalence is
about 1 per 1000 children under 16 years of age, and boys and
girls are affected with equal frequency.

CAUSE & PATHOLOGY

Similar to that of rheumatoid arthritis, however rheumatoid
factor is usually absent.
 CLINICAL FEATURE, IMAGING, & INVESTIGATION
The white cell count and ESR are raised in JIA. Rheumatoid factor tests
are positive. Joint aspiration and synovial fluid examination may be
essential to exclude infection or haemarthrosis.
 DIAGNOSIS
In the early stages, diagnosis may be difficult. problem is resolved with
blood investigations, joint aspiration and synovial biopsy.

TREATMENT
General treatment Systemic treatment is similar to that of rheumatoid
arthritis. Local treatment to prevent stiffness and deformity. Night splints
may be useful for the wrists, hands, knees and ankles; prone lying for some
period of each day may prevent flexion contracture of the hips. Between
periods of splinting, active exercises are encouraged.

COMPLICATION
Ankylosis, Growth defects, Fractures, Iridocyclitis, Amyloidosis.

PROGNOSIS
5–10% are severely crippled and require treatment throughout life. 3%
still die as a result of renal failure due to amyloidosis.
 4. CONNECTIVE TISSUE DISEASES
Like RA, these are ‘autoimmune disorders’, probably triggered by
environmental exposures, such as viral infections, in genetically
predisposed individuals. They include systemic lupus erythematosus,
scleroderma, etc.

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

Systemic lupus occurs mainly in young females. Characteristic clinical
features are ‘butterfly rash’ of the face, Raynaud’s, peripheral vasculitis,
splenomegaly, and disorders of the kidney, heart, lung, eye and central
nervous system. Anaemia, leucopaenia and elevation of the ESR.

TESTS FOR ANA ARE USUALLY POSITIVE.

TREATMENT : Corticosteroids
COMPLICATIONS
Avascular necrosis (usually of the femoral head), Bone ischaemia,
Antiphospholipid (Hughes) syndrome
 REFERENCES AND FURTHER READING
Deighton CM, George E, Kiely PDW,
Ledingham, J et al. Updating the
British Society for Rheumatology
guidelines for anti-tumour necrosis
factor therapy in adult rheumatoid
arthritis (again). Rheumatology
2006; 45: 649–52.
Kennedy T, McCabe C, Struthers G,
et al. BSR guidelines on standards of
care for persons with rheumatoid
arthritis. Rheumatology 2005; 44:
553–6 Manadan AM, James N, Block
JA. New therapeutic approaches for
spondyloarthritis. Curr Opin
Rheumatol 2007; 19: 259–64.
Scott DL, Kingsley GH. Tumor
necrosis factor inhibitors for
rheumatoid arthritis. N Engl J Med
2006; 355: 704– 12.
Sidiropoulos PI, Hatemi G, Song M, et
al. Evidencebased recommendations
for the management of ankylosing
spondylitis: systematic literature
search of the 3E Initiative in
Rheumatology involving a broad
panel of experts and practising
rheumatologists. Rheumatology
2008; 47: 355–61.
Thank You