DEPARTMENT OF ANATOMIC PATHOLOGY,

FACULTY OF MEDICINE, GADJAH MADA

UNIVERSITY
 JOINT TRAUMA
 Variable in its severity and effects
 Minor soft tissue damage
 Sprain/strain
 Rapid and complete healing
 Serious damage (and possible sequels)
 Fractures into joint space – articular surface is permanently damage
 Fragment loose in joints – damage to synovium of cartilage
 Capsular and ligamentous tears – ligaments may not heal or are united
by poor scar tissue
 Haemorrhange into joint, may not be resorbed – adhesion form
within joint
JOINT TRAUMA

 In lesser degree of trauma:

 Non reactives changes of synovial membrane
 Hyperemia
 Mild chronic inflammation

 Joint effusion often be found

 Most important sequel

 DEGENERATIVE JOINT DISEASE
 OSTEOATHRITIS

 Commonest disorders of joints

 Causing pain and stiffness
MIDDLE AGE
 Commonest cause of chronic
disabilities after middle age

PATHOLOGY DEGENERATIVE PROCESS

Lesser degree of simple ageing

OSTEOATHRITIS
Classification
1. Secondary osteoarthritis – predisposing factors:
1. Alteration to joint mechanic (e.g. abnormal alignment and
angulation – Charcot’s joint)
2. Abnormality of the articular surfaces (e.g. following injury)
3. Abnormal stresses on the joint (obesity, sports)
4. Previous inflammation e.g. sepsis, rheumatoid arthritis
2. Primary osteoarthritis – no predisposing factors
• Abnormality of chondrocyte metabolism ?
• Some cases : familial pattern
mutation of type II collagen gene
OSTEOATHRITIS

Pathogenesis:
The integrity of the articular cartilagenous
surface represent a fine balance between wear
and tear
Both types have the same process
Early change  chemical composition change of
the matrix – becomes softer
Followed by progressive characteristic
morphological changes
OSTEOATHRITIS

Morphological changes
1. At site of pressure
1. Flaking and fibrilation of surface
2. Loss of cartilage, exposure of bone which become hard
and polished (eburnated)
2. At edge of joint
1. Bone forming from cartilage
2. Outgrowth of irregular bone (osteophyte) forming a lip
round the joint margin
3. Extensive loss of cartilage with exposed eburnated bone
3. The synovial membrane may show mild non specific
inflammation and effusion (but secondary)
 INFLAMMATION
INFECTION ARTHRITIS
Tuberculosis arthritis
 Specific chronic granulomatous inflammation, due to
the extension of lung tb (miliar)
 Clinically: arise after joint destruction
 Histology:
 Granulomatous inflammation, epiteloid tubercle, Langhans
giant cells, caseous necrosis
 Joints and bones erosion  ankilosis
Tuberculous Arthritis
Histologis artritis bakterial dijumpai gambaran peradangan purulen yang ditandai dengan
sebukan sel radang terutama lekosit polimorfonuklear
INFLAMMATION

RHEUMATOID ARTHITIS
 4% of population (in US)
 Female 3X male
 Etiology: autoimmun disease
 Signs and symptoms:
 Local: bilateral, simetry – interphalangeal joints, metacarpo-
phalangeal  morning stiffness, swollen, tenderness,
warm, hyperaemia  angkilosis  deformity
 Systemic: mesodermal involved  pericarditis, pleuritis,
amiloydosis (15% cases)
 Patology:
 Inflammation  diffuse thickening of synovia ,
hyperplasia  pannus  dystruction of joint surface and
bone  hemorrhage and granulation tissue  fibrosis
 Rhematoid nodul: subcutan
Macroscopic picture of rheumatoid
arthritis, rheumatoid nodul and histologic
picture of rheumatoid synovitis
Perbandingan gambaran morfologis antara rhematoid artritis dengan osteoartritis
 DEGENERATIVE AND
METABOLIC DISEASES
Gout
 heterogenous group of diseases
1. increased serum uric acid level
2. deposition of urate crystal in the joints and kidneys

1. all patient with gout display hyperuricaemia, but

2. fewer than 15% of all person with
hyperuricaemia have gout.
DEGENERATIVE AND METABOLIC DISEASES

Gout (2)
 heterogenous group of diseases
1. increased serum uric acid level
2. deposition of urate crystal in the joints and
kidneys

1. all patient with gout display

hyperuricaemia, but
2. fewer than 15% of all person with
hyperuricemia have gout.
DEGENERATIVE AND METABOLIC DISEASES

Gout (3)
Pathogenesis PURINES
-Diet
-De novo synthesize

Catabolism

URIC ACID
Relative insoluble

URATE OXIDASE

ALLANTOIN •URIC ACID LEVEL

Highly soluble •TISSUE DEPOSITION

URINE / RENAL EXCRETION

DEGENERATIVE AND METABOLIC DISEASES

Gout (4)
Pathogenesis
Thus the level of uric acid in the blood reflects the
difference between the amount of purines ingested and
synthesized and the extent of renal excretion.

 Gout can result from:

1. overproduction of purine
2. augmented catabolism of nucleic acid as a result of
increased cell turnover
3. decreased salvage of free purine bases
4. decreased urinary excretion of uric acid.
PENYAKIT DEGENERATIF DAN METABOLIK
Gout (5) - Classification
Clinical Category
Primary Gout (90% of cases)
Enzyme defect unknown (85% to 90% of
primary gout
Known enzyme defects (eg. Partial
HGPRT deficiency (rare))
Secondary Gout (10% of cases)
Associated with increased nucleic acid
turnover (e.g., leukemia
Chronic renal disease
Inborn error of metabolism (e.g., complete Overproduction of uric acid with increased
HGPRT deficiency (Lesch-Nyhan syndr)
Metabolic Detect
Overproduction of uric acid: normal
(majority)/increased (minority) excretion
Under excretion of uric acid + normal prod
Overproduction of uric acid
Overproduction of uric acid with increased
urinary excretion
Reduced excretion of uric acid with normal
production
urinary excretion
Patogenesis artritis akut gout
Makroskopic and radiology
picture of base of foot
thumb joint menderita
artritis gout.
 Histology of tophus. The tophus
(urate crystals) consist of
eosinophilic amorphous mass,
surrounded by reactive fibroblast,
inflammatory mononuclear cells,
and giant cells

Microscopic
appearance of
monosodium
urate crystals
PENYAKIT DEGENERATIF DAN METABOLIK
CALCIUM PYROPHOSPHATE DIHYDRATE
(CPPD)-DEPOSITION DISEASE (CHONDRO
CALCINOSIS AND PSEUDOGOUT)

• Accumulation of CPPD compound in synovial membrane

(pseudogout), joint cartilage (chondrocalcinosis),
ligament, and tendons.
• It can be idiopathic, associated with trauma, linked to a
number metabolic disorders, or rare cases, hereditary.
• Principally a condition of old age – ½ > 85 y
• Most cases in elderly are asymptomatic
• 2/3 manifest in preexisting joint damage – trauma and
aging process in cartilago promote nucleation of CPPD
crystals
PENYAKIT DEGENERATIF DAN METABOLIK
CALCIUM PYROPHOSPHATE DIHYDRATE (CPPD)-
DEPOSITION DISEASE (CHONDRO CALCINOSIS AND
PSEUDOGOUT) (2)

Pathogenesis
• Excessive levels of inorganic pyrophosphates (IP) in the
synovial fluid
• IP derives from the hydrolysis of nucleoside tri
phosphates in the chondrocytes of the joint
• Increased IP levels can result from: increased
production or decreased catabolism
PENYAKIT DEGENERATIF DAN METABOLIK
CALCIUM PYROPHOSPHATE DIHYDRATE (CPPD)-
DEPOSITION DISEASE (CHONDRO CALCINOSIS AND
PSEUDOGOUT) (3)

Pathology and clinical features – classification

• Pseudogout: self limited, acute, lasting 1-4 weeks, one
or two joints.
25% have an acute onset of gout like sympt. – inflamm
and swelling of knees, ankles, elbows, hips or shoulders.
• Pseudorheumatoid arthritis: multiple joints are
chronically involved – mild and resemble RA
• Pseudoosteoarthritis: symptompa are similar to OA
• Pseudoneurotrophic disease: characterized by joint
destruction severe enough to resemble a neurotrophic
joint
 TUMOR AND TUMOR LIKE
LESIONS
Ganglion
 Is a thin walled, simple cyst containing clear mucinous
fluid
 Occurs most commonly in the extensor surfaces of the
hands and feed, especially the wrist
 Origin: from small outpouching of the synovium or
areas of myxoid change in the connective tissue
(tendon), possibly after trauma

Baker’s cyst
 Herniation of synovium of the knee joint into the
plopiteal space – associated with various form of
arthritis  intraarticular pressure increased
Pigmented villonodular synovitis
 Tumors arise on the synovium or tendon
sheaths, bursae, and diarthrodial joints.
 Characterized by an exuberant proliferation of
synovial lining cells with extension into the
subsynovial tissue
 Single joint, young adult, male = female
 80% knee, other  hip, ankle, calcaneocuboid
joint, elbow, tendon sheaths of the fingers and
toes
Pigmented villonodular synovitis (2)

Microscopic:
 Tumor is composed of bland mononuclear cells
with scattered multinucleated giant cells in which
the nuclei are arrayed peripherally. Hemorrhagic
laden macrophages reflect previous hemorrhage
 MALIGNANT TUMORS
SYNOVIAL SARCOMA
 More frequent in large joint: knee, ankle, toes.
 Histology:
 Usually biphasic: groups of pseudo glandular cells and
spindle cells sarcoma like.
 Rarely monophasic: only consist of groups of pseudo
glandular cells or spindle cells

EPITHELOID SARCOMA
 Predominantly occur: area of hand, upper arm
 Often missdiagnosed as granulomatous inflammation
 Biphasic synoviosarcoma

Monophasic synoviosarcma
Epitheloid sarcoma
 REFERENSI
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Philadelphia.
 Kumar V, Abbas AK, Fausto N (eds.). 2004. Robbins and Cotran
Pathology Basis of Disease. 7th ed. Elsevier Saunders.
Philadelphia.
 Rosai J. 2004. Rosai and Ackerman’s Surgical Pathology. 9th ed.
Mosby. Philadelphia.
 Underwood JCE (ed.). 2004. General and Systemic Pathology.4th
ed. Edinburgh: Churchill Livingstone.
 Kumar V, Cotran RS, Robbins SL (eds.). 2003. Robbins Basic
Pathology. 7th ed. Saunders. Philadelphia.