JOINT PATHOLOGY

CONTENTS

ARTHRITIS
OSTEOARTHRITIS
GOUT AND PSEUDOGOUT
INFECTIOUS ARTHRITIS
LYMES ARTHRITIS

TUMORS
CANGLION AND SYNOVIAL CYSTS
PVNS AND GCT OF TENDON SHEATH

Osteoarthritis

Primary degenerative disorder

of articular cartilage
Age
65

or more

Types
Primary

Oligoarticular and in older people

 Secondary

Youth
Traumatic, developmental deformity,
underlying systemic disease like
diabetes, ochronosis,
hemochromatosis, obesity
May be poly articular and has gender
differences

Knees

and hands- women

Hips- men

Morphology
Enlargement, proliferation and
disorganization of chondrocytes in
superficial part of articular cartilage
Vertical and horizontal fibrillatioon and
cracking of matrix
Degradation of superficial layers
Soft granular articular cartilage surface
Sub chondral bone plates are exposed
and appearance of polished ivory (bone
eburnation) Underlying cancellous bone
becomes sclerotic and thickened
Small fractures dislodge pieces of
cartilage and subchondral bone- joint
mice

Synovial fluid forced to subchondral

region- fibrous walled cysts
Mushroom shaped osteophytes at
margins of articular surface
Fibrous synovial pannus covers
peripheral portions
Cartilage has more water and less
proteoglycan
Collagen network also decreased
Increased chondrocyte apoptosis
Deeper layers proliferate to compensate
and repair the damage

Pathology
The elastic and tensile strengthh
provided by proteoglycans and type 2
collagen produced
Imbalance in the matrix degradation and
replacement by chondrocytes
Causes

Mechanical stress
Genetic factors
Increasing bone density
High estrogen level

Clinical course
Insidious

onset
Deep aching pain increasing with
use, morning stiffness, crepitus
Osteophyte impingement in spinal
foramina can cause neurologic
symptoms like muscle spasms,
muscle atrophy and neurologic
deficits

 Hips,

knees, lower lumbar and

cervical vertebrae, proximal and
distal interphalangeal joints, 1st
carpometacarpal and
tarsometatarsal
Heberden nodes in fingersprominent osteophytes
Slowly progressive
Fusion dosent take place like
rheumetoid arthritis

Gout

Disorder caused by tissue

accumilation of excessive
amounts of uric acid
Types
Primary

Basic cause is unknown

Secondary-

Those due to leukemia and CRD

Inborn errors of metabolism(HGPRT)

Morphology
acute arthritis
Dense

neutrophilic infiltrate
permeating synovium and fluid
Needle shaped monosodium urate
crystals in the cytoplasm of
neutrophils and synovium
Synovium is edematous and
congested
Scattered mononuclear infiltrates

Chronic tophaceous arthritis

Evolves

from repetitive
precipitation of urate crystals
during acute attacks
Urates heavily encrust the
articular surface and form visible
deposits in synovium
Synovium- hyperplastic, fibrotic by
the inflammatory cells
Pannus destroys underlying
cartilage
Fibrous or bony ankylosis

Tophi in various sites

Large

aggregates of urate crystals

surrounded by intense
inflammatory reaction of
lymphocyes, macrophages and
foreign body giant cells in attempt
to engulf the masses of crystals
They appear in articular cartilage of
jointsand periarticular ligaments,
tendons and soft tissues including
ear lobes, nasal cartilages and skin
of fingertips
Superficial tophi can lead to large
ulcers

Gouty nephropathy
Multiple

renal complications
associated with urate deposition
Medullary tophi
Intratubular precipitations
Free uric acid crystals
Renal calculi
pyelonephritis

Pathology
Primary

Overproduction
Decreased renal excretion
Overproducion of uric acid due to
enzyme deficit in denovo or salvage
pathway- PRPP synthetase, amido
PRT, HGPRT
HGPRT deficit- Lesch Nyhan
syndrome

Secondary

Increased urate production due to

chemotherapy for lymphoma or leukemia
Decreased excretion- CRD or azide diuretics

Mechanism
Increased levels of uric acid
Ppt of monosodium urate

Chemotaxis
Activation of
Complement
Local accumilation of neutrophils and
macrophages in joint

Chemokines, toxic free radicals and LTs(LT4).

Neutrophils release lysosomal enzymes
and macrophages ILs(IL1,IL6,TNF)
Activate synovial cells and cartilage cells
Release protease(collagenase)
Acute arthritis

Pseudogout

Chondrocalcinosis
Age
>50yrs. 50-60% in >80
No gender predesposition
Pathology
Enzyme that produce or
degrade pyrophosphate

In hereditary varient, there is

mutation of the transmembrane
pyrophosphate transport channel
Recruitment and activation of
inflammatory cells like in gout
Mono or poly articular
Supportive therapy. But not to
prevent or retard crystal formation
50% has significant joint damage

INFECTIOUS ARTHRITIS
Suppurative

Cause
Children

under 2- H influenzae
Older children and adults- S
aureus
Late adolescence and young
adults- gonococcus
SCC- Salmonella
Deficiency in certain complement
(C5,C6,C7)- disseminated
gonococcal infection

Clinical features
Sudden

onset pain redness and

swelling of joint
Restricted motion
Fever leukocytosis
ESR
90% nongonococcal inf in single
joint, usually knee, hip, shoulder,
elbow, wrist, sternoclavicular joints
Aspiration is purulent and used for
diagnosis

Lyme Arthritis

Borrelia burgdorferi
Four stages for disease
Stage 1
Sprirochetes

multiply at site of bite

Expanding area of redness with
indurated pale center- erythema
chronicum migrans
Fever, LNE
Disappears in few wks time

Stage 2 (Early disseminated stg)

Spread

hematogenously
Secondary annular lesioins
LNE, migratory joint and muscle
pain, cardiac arrythmias,
meningitis with CN involvement
Abs develop in theis stage and
useful for serodiagnosis
Some spirochetes escape host
response by sequestering in CNS
and IC forms in endothel cells

Stage 3 (late disseminated st)

2-3 yrs after initial bite
Chronic arthritis
Severe damage to large joints
Encephalitis
Pathology

Due to immune response, borrelia Ags cross

reacting with proteins in joints
Remitting and migratory
Involve large joints- knees, shoulder, elbow,
ankle

 Histology

Chronic papillary synovitis with

synoviocyte hyperplasia
Fibrin deposition
Mononuclear infiltration
Onion skin thickening of arterial walls

Diagnosis

Serology and history

TUMORS
Ganglion

Small (<1.5 cm) cyst

Often seen near joint capsule or tendon
sheath of wrist
Firm nodules
Lack true cell lining as they arise by cystic
degeneration of connective tissue
Can be multilocular by coaleasion of of
adjacent areas of myxoid change
Cyst fluid similar to synovial fluid
No communication with joint space
Often asymptomatic
Bible therapy as treatment

Synovial cyst

Herniation of synovium through a join

capsule
Massive enlargement of bursa
Eg:- Baker cyst seen in popletial fossa

Villonodular Tenosynovitis

Several closely related neoplastic clonal

proliferations
PVNT

Joint synovium is affected

Morphology

Red brown to orange yellow

Contorted mass of red brown folds, finger like
projections and nodules
Cells resemble synovicytes
It spread along surface andinfiltrate the
subsynovial compartment
Hemosiderin deposits
Foamy macrophages, multinucleate giant cells
scarring

 Clinical

features

Monoarticular arthritis affecting

knee(80%), hip, ankle
Pain, locking and recurrent swelling
Aggressive lesion erode to adjacent
bones and soft tissue

Giant Cell tumor

Tendon

sheath commonly involved

(single tendon nodule)
Age 20-40

Morphology

Red brown to orange yellow

Well circumscribed and contained
Cells grow in solid nodular aggregate
Cells resemble synovicytes
Hemosiderin deposits
Foamy macrophages, multinucleate giant
cells
Scarring

Clinical features
Solitary, slowl growing, painless mass

Affect wrist and finger tendon sheaths

Treatment

Surgical resection, recur locally