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 fingers-
prominent 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