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QUESTIONS
NORMAL JOINTS discussion is not included in this material
The most common type of joint disease and is one of the 10 most
disabling conditions in developed nations
Osteoarthritis is characterized by
The role of inflammation in osteoarthritis
When an osteoarthritis occurs without apparent initiating cause, as an
aging phenomenon, it is called as ___
When an osteoarthritis occurs with predisposing conditions such as
previous injuries to a joint; congenital developmental deformity of a
joint; underlying systemic disease (DM, ochronosis, hemochromatosis,
marked obesity)
Pathogenesis of Osteoarthritis
A factor that has strong association with the pathogenesis of the OA
Several phases of pathogenesis of OA
OA- Morphology
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ANSWERS
Osteoarthritis
- Aka degenerative joint disease
by the progressive erosion of articular cartilage
Though the dse implies an inflammatory dse, osteoarthritis is considered to be
an intrinsic disease of cartilage in which biochemical and metabolic alterations
in individuals with genetic susceptibility result in its breakdown
idiopathic or primary osteoarthritis
- Usually oligoarticular
secondary osteoarthritis
- Knees and hands are more commonly affected in women and the
hips in men
has both environmental and genetic components including genes
involved in PG metabolism and WNT signaling
AGE
- 80 to 90% of individuals have incidence of the disease by age 65
1. Chondrocyte injury- related to aging and genetic and biochemical factors
2. Early OA- chondrocytes proliferate (cloning) and secrete inflammatory
mediators, collagens, proteoglycans, and proteases, which act together
to remodel the cartilagenous matrix and initiate secondary inflammatory
changes in the synovium and subchondral bone
3. Late OA- repetitive injury and chronic inflammation lead to chondrocyte
drop out, marked loss of cartilage and extensive subchondral bone
changes
OA
Early stages
chondrocytes proliferate clusters
water content increases
concentration of proteoglycans decreases
vertical and horizontal fibrillation and cracking of the matrix occur as
the superficial layers of the cartilage
type 2 collagen molecules are degraded
Grossly
manifests as a granular soft articular surface
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The dislodged pieces of cartilage and subchondral bone tumble into joint mice
the joint, forming loose bodies known as
The process in which the exposed subchondral bone plate becomes bone eburnation
the new articular surface, and friction with the opposing degenerated
articular surface smooths and burnishes the exposed bone, giving it
the appearance of polished ivory
OA

Mushroom-shaped osteophytes that develop at the margins of the bone outgrowths

articular surface and are capped by fibrocartilage and hyaline cartilage
that gradually ossify is also known as

OA- clinical course insidious, asymptomatic until they are in their fifties
Characteristics symptoms: deep, achy pain that worsens with use,
morning stiffness, crepitus and limitation of movement
Impingement on spinal foramina by osteophytes cervical and lumbar
nerve root compression and radicular pain, muscle spasms, muscle
atrophy and neurologic deficits

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Jts. Commonly involved in OA hips, knees, lower lumbar and cervical vertebrae, proximal and distal
interphalangeal joints of fingers, 1st carpometacarpal & tarsometatarsal joints
Prominent osteophytes at the distal interphalangeal joints w/c are Heberden nodes
common in women
Jts usually spared in the devt. of OA Wrist, elbows and shoulders

Tx of OA still no satisfactory means of preventing primary OA, and there are no effective
methods of halting its progression
A chronic systemic inflammatory disorder that may affect many tissues Rheumatoid arthritis
and organs skin, blood vessels, heart, lungs and muscles but
principally attacks the joints, producing a nonsuppurative proliferative
synovitis that often progresses to destruction of the articular cartilage
and ankylosis of the joints
RA is known to be caused by ____ Cause is unknown
- Incidence is M:F = 1:3 to 5, peak incidence 20s and 40s
Initial morphology in RA synovium becomes edematous, thickened and hyperplastic, transforming its
smooth contour to one that is covered by delicate and bulbous fronds
Histologic features of RA 1. dense perivascular infiltrate of mostly CD4 T cells, plasma cells, dendritic
cells and macrophages
2. Increased vascularity due to vasodilation and angiogenesis, with
superficial hemosiderin deposits
3. Aggregation of organizing fibrin covering the synovium and floating in the
joint space as rice bodies
4. Accumulation of neutrophils in the synovial fluid only along the surface
5. Osteoclastic activity in the underlying bone juxta-articular erosions,
subchondral cysts and osteoporosis
6. Pannus formation fibrocellular mass of synovium and synovial stroma
consisting of inflammatory cells, granulation tissue and synovial
fibroblasts which grows over the articular cartilage and causes its
erosion

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After the cartilage has been destroyed, the pannus bridges the fibrous ankyloses ossifies resulting to bony akylosis
apposing bones forming

RA- Morphology (Skin) Rheumatoid nodules are the most common cutaneous lesion
- Arise from skins subjected to pressure: ulnar aspect of the forearm,
elbows, occiput and lumbosacral area
- Firm, nontender, round to oval subcutaneous nodules
- Central zone of fibrinoid necrosis surrounded by a prominent rim of
epithelioid histiocytes and numerous lymphocytes and plasma cells

The rheumatoid
nodule shows
palisading
macrophages

RA- Morphology (Blood Vessels) risk of developing vasculitic syndromes/ rheumatoid arthritis
involvement of medium- to small-sized arteries which is similar to PAN
except that in RA the kidneys are not involved
segments of small arteries such as vasa nervorum and digital arteries are
obstructed peripheral neuropathy, ulcers and gangrene
Leukocytoclastic venulitis produces purpura, cutaneous ulcers and nail
bed infarction

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HANDSWRISTELBOWS

RA- Pathogenesis triggered by exposure of a genetically susceptible host to an

Genetic susceptibility associated with RA
An environmental arthritogen formed in the body (especially in the
lungs of smokers) that have been implicated in the pathogenesis of RA
Responsible for the chronic destructive nature of RA
These are important in the inflammatory reaction because they recruit
neutrophils and monocytes
Antibodies present in RA to form immune complexes in the sera is
identified as
Roles of cytokines secreted by T cells, such as IFN- and IL-17
RA- Clinical course
X- ray hallmarks of RA
arthritogenic antigen breakdown of immunological self-tolerance and a
chronic inflammatory reaction
autoimmune reaction, activation of CD4 helper T cells and the local
release of inflammatory mediators and cytokines that ultimately destroys
the joints
Specific HLA-DRB1 all
- These alleles share a common sequence of amino acids in the 3rd
hypervariable region of the chain, which is designated the shared
epitope
PTPN22
- encodes a protein tyrosine phosphatase, which participates in
activation and control of inflammatory cells, including T cells
citrullinated proteins
autoimmune reaction
- activated CD4+ effector and memory T cells
TH17 cells
o IFN--producing TH1 cells may also contribute to the inflammatory
reaction
IgM
act upon and stimulate synoviocytes and macrophages, which produce pro-
inflammatory molecules such as IL-1, IL-6, IL-23, TNF, PGE2 , NO, and the
growth factors GM-CSF and TGF-
- In the end, the pannus produces sustained, irrervesible cartilage
destruction and erosion of subchondral bone
Begins slowly and insidiously
malaise, fatigue and generalized musculoskeletal pain and after several
weeks to months joints become involved
symmetrical and the small joints are affected before the larger ones
Involved joints are swollen, warm, painful and particularly stiff on rising or
following inactivity
Large synovial cysts, like the Baker cyst in the posterior knee may
develop
presence of RF and CCP antibody are laboratory indicators
joint effusion and juxta-articular osteopenia with erosions and narrowing
of the joint space with loss of articular cartilage

The diagnosis is based primarily on the clinical features and includes 1. Morning stiffness
the presence of 4 of the following criteria 2. Arthritis in 3 or more joint areas
3. Arthritis of hand joints
4. Symmetric arthritis

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5. Rheumatoid nodules
6. Serum RF
7. Typical radiographic changes
This condition encompasses all forms of arthritis that develop before Juvenile Idiopathic Arthirtis (JIA)
16 years of age and that persist for a minimum of 6 weeks - Formerly known as juvenile RA
- Etiology: UNKNOWN
7 discrete clinical subsets of JIA 1. Systemic arthritis
2. Oligoarthritis
3. RF-positive polyarthritis
4. RF-negative polyarthritis
5. Enthesitis (inflammation of a point of attachment of skeletal muscle to
bone)-associated arthritis
6. Psoriatic arthritis
7. Undifferrentiated arthritis
How does JIA differs from RA? Oligoarthritis is more common
Systemic disease is more frequent
Large joints are affected more often than smaller joints
Rheumatoid nodules and RF are usually absent
ANA seropositivity is common
Characteristics systemic arthritis in JIA abrupt onset, is associated with remitting, high spiking fevers, migratory
and transient skin rash, hepatosplenomegaly, and serositis
Arthritis affecting 4 or fewer joints during the first 6 months of disease oligoarthritis variant
in the absence of psoriasis and an HLA-B27 genotype defines the - asymmetric, develops at an early age (younger than 6 years), and
is commonly associated with iridocyclitis and a positive ANA
Involves more than 5 joints within the first 6 months and consists of RF-negative polyarthritis
several subtypes that have features that overlap with oligoarthritis and
RF-negative arthritis in adults, and a subset that shows stiffness and
contractions, but little swelling
Similar to the adult form of the disease and is mainly seen in teenage RF-positive polyarthritis
girls
This mainly affects male children younger than 6 years, and most Enthesitis-related arthritis
affected individuals are HLA-B27 positive - affects tendoligamentous insertion sites and joints of the lower
extremities
What is undifferentiated arthritis? It encompasses patients who do not fulfill inclusion criteria of the other groups
or have overlapping features
SERONEGATIVE SPONDYLOARTHROPATHIES ANKYLOSING SPONDYLOARTHRITIS
REACTIVE ARTHRITIS
REITER SYNDROME
ENTERITIS-ASSOCIATED ARTHRITIS
PSORIATIC ARTHRITIS
ARTHRITIS ASSOCIATED WITH INFLAMMATORY BOWEL DISEASE
Group of diseases that develop in genetically predisposed individuals Seronegative spondyloarthropathies
and are initiated by ubiquitous environmental factors, especially - manifestations are immune mediated and are triggered against an
infectious agents undefined antigen
- disease produce inflammatory peripheral or axial oligoarthritis and
enthesopathies
Genetic susceptibility involved in seronegative spondyloarthropathie HLA-B27 allele and a triggering infection but without specific autoantibodies
(hence the term seronegative)
Chronic synovitis that causes destruction of articular cartilage and Ankylosing spondyloarthritis
resultant ankylosis, especially of the sacroiliac and apophyseal joints - Also known as rheumatoid spondylitis and Marie-Strumpell disease
(between tuberosities and processes)
Ankylosing spondyloarthritis- clinical features becomes symptomatic in the 2nd and 3rd decades of life
men 2-3 times > than women
affected individuals present with low back pain, which frequently follows a
chronic progressive course
1/3 of the affected individuals have involvement of peripheral joints, such
as the hips, knees and shoulders
Fracture of the spine, uveitis, aortitis, and amyloidosis are other
recognized complications

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Genetic alleles associated with the development of ankylosing ARTS1
spondyloarthritis IL23R

A form of reactive arthritis and is defined by a triad of arthritis,
nongonococcal urethritis or cervicitis, & conjunctivitis
Reiter syndrome is caused
Early sxs of Reiter syndrome
Jts more commonly afftected by Reiter syndrome
Reiter syndrome
- Most are men and >80% are positive for HLA-B27
- Also affects individuals infected with HIV
by an autoimmune reaction initiated by prior infection of the GIT (Shigella,
Salmonella, Yersinia, Campylobacter) and the GUT (Chlamydia)
joint stiffness & low back pain
ankles, knees and feet in asymmetric patterns
Synovitis of digital tendon sheath produces the sausage finger and toe and
ossification of tendoligamentous insertion sites leads to calcaneal spurs and
bony outgrowths from tendons

Extraskeletal manifestations of Reiter syndrome inflammatory balanitis, conjunctivitis, cardiac conduction abnormalities, aortic
regurgitation
Other clinical manifestations of Reiter syndrome 50% have recurrent arthritis, tendinitis, fasciitis, lumbosacral back pain that
can cause significant functional disability

Enteritis- associated arthritis Caused by GIT infection by Yersinia, Salmonella, Shigella, Campylobacter
lipopolysaccharides as a major component of these organisms, and they
stimulate a host of immunological responses
Arthritis appears abruptly and tends to involve the knees and ankles
Arthritis lasts for about a year then generally clears
A chronic inflammatory arthropathy that affects peripheral and axial Psoriatic arthritis
joints and entheses and is associated with psoriasis
Susceptibility to psoriatic arthritis is genetically determined and related HLA-B27 and HLA-Cw6 alleles
to
Joints first affected by psoriatic arthritis distal interphalangeal joints of the hands and feet and >50% of patients and
may be associated with a sausage-like finger
Extra-articular manifestations common in psoriatic arthritis conjunctivitis and iritis
INFECTIOUS ARTHRITIS BACTERIAL ARTHRITIS
TUBERCULOUS ARTHRITIS
LYME ARTHRITIS
VIRAL ARTHRITIS
Mode of transmission for infectious arthritis hematogenous dissemination
direct inoculation
from contiguous spread from a soft-tissue abscess or focus of
osteomyelitis

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Most common organisms causing bacterial arthritis
Predisposing conditions of bacterial arthritis
Classic presentation of bacterial arthritis
Systemic findings of bacterial arthritis
Usually develops as a complication of adjoining osteomyelitis or after
hematogeneous dissemination from a visceral (pulmonary) site of
infection
Tuberculous arthritis- morphology
LYME ARTHRITIS
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Gonococcus, Staphylococcus, Streptococcus, Haemophilus influenzae, gram-
negative bacilli (E. coli, Salmonella, Pseudomonas)
H. influenzae arthritis predominates in children under 2 years of age
S. aureus is the main causative agent in older children and adults,
gonococcus is prevalent during late adolescence and young
adulthood
Individuals with sickle cell disease are prone to infection with
Salmonella at any age
immune deficiencies (congenital/acquired), debilitating illness, joint
trauma, chronic arthritis of any cause, intravenous drug abuse
sudden development of an acutely painful and swollen infected joint that has
restricted range of motion
fever, leukocytosis, increased ESR are common
Tuberculous arthritis
formation of confluent granulomas with central caseation necrosis
affected synovium may grow as a pannus over the articular cartilage and
erode into bone along the joint margins
Chronic disease results in severe destruction with fibrous ankylosis and
obliteration of the joint space
The weight-bearing joints are usually affected
Caused by Borrelia burgdorferi (spirochete), which is transmitted by the
ticks of the Ixodes ricinus complex
Initial infection of the skin is followed within several days to week by
dissemination of the organism to other sites, especially the joints
arthritis tends to be remitting and migratory and primarily involves the
large joints, knees, followed in descending order by shoulders, elbows
and ankles
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Infected synovium takes the form of a chronic papillary synovitis with
synoviocyte hyperplasia, fibrin deposition, mononuclear cell infiltrates
(especially CD4+ T cells), and onion-skin thickening of arterial walls
hypothesized that specific HLA-DR molecules bind an epitope of B.
burgdorferi outer surface protein A, which initiates a T-cell reaction to this
epitope
joints in these patients have synovial pannus, which cause articular
cartilage destruction and permanent deformities

The morphology in severe cases can resemble that of RA

VIRAL ARTHRITIS Viral infections include alphavirus, parvovirus B19, rubella, EBV and
hepatitis B and C
variety of different rheumatic conditions including reactive arthritis,
psoriatic arthritis, and septic arthritis, have developed in individuals
infected with HIV
Endogenous pathogenic crystals causing arthritis Endogenous:
monosodium urate (gout)
calcium pyrophosphate dehydrate
basic calcium phosphate (hydroxyapatite)
Exogenous:
corticosteroid ester crystals and talcum
the biomaterials polyethylene
methyl methacrylate
How do endogenous and exogenous crystals produce disease? triggering the cascade that results in cytokine-mediated cartilage destruction
Enzyme responsible for the degradation of uric acid in other mammals Uricase
but is absent in man thats why hyperuricemia and gout develop
Gout is caused by hyperuricemia, marked by transient attacks of acute arthritis initiated by
crystallization within and about joints leading eventually to chronic gouty
arthritis and the appearance of tophi
Tophi represent large aggregates of urate crystals and the
surrounding inflammatory reaction
Plasma urate level necessary for the development of gout above 6.8 mg/dL
Conditions producing hyperuricemia and gout 1. Primary basic metabolic defect is unknown or gout is the main
manifestation of a known defect
2. Secondary the cause of hyperuricemia is known or gout is not the main
clinical dysfunction
Calssifications of gout PRIMARY (90% of cases)
A. Overproduction of uric acid
1. Diet
2. Unknown enzyme defects (80 to 90%)
3. Known enzyme defects (e.g. partial HGPRT deficiency, rare)
B. Reduced excretion of uric acid with normal production
SECONDARY (10% of cases)
A. Overproduction of uric acid with increased urinary excretion
1. Increased nucleic acid turnover (e.g., leukemias and other
aggressive neoplasms)

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GOUT PATHOGENESIS
2 pathways involved in purine metabolism
Deficiency of this enzyme leads to increased synthesis of purine
nucleotides through the de novo pathway and increased uric acid
production
An uncommon x-linked disorder seen only in males with complete lack
of HGPRT.
Factors that contribute to the conversion of hyperuricemia into primary
gout
Central to the pathogenesis of arthritis is precipitation of ____
The solubility of MSU in a joint is modulated by
Crystallization in the pathogenesis of gout is dependent on
Gout- pathogenesis
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2. Inborn error of metabolism (e.g., complete HGPRT deficiency)
B. Reduced excretion of uric acid with normal production
1. Chronic renal disease
Uric acid is the end product of purine metabolism
hyperuricemia develops from overproduction of urate in approximately
10% of cases and reduced excretion in the remainder
Approximately 90% of the filtered urate is reabsorbed, and the urate
transporter 1 gene (URAT1) has an important role in the reabsorption
process
Decreased filtration and underexcretion of uric acid underlies most cases
of primary gout
1. De novo pathway purines are synthesized from nonpurine precursor
2. Salvage pathway free purine bases derived from the breakdown of
nucleic acids of endogenous or exogenous origin are recaptured
(salvaged)
Hypoxanthine guanine phosphoribosyl transferase (HGPRT)
- involved in the salvage pathway
Lesch-Nyhan syndrome
- characterized by hyperuricemia, severe neurologic deficits with
mental retardation, self-mutilation and in some, gouty arthritis
1. Age and duration of hyperuricemia gout rarely appears before 20 to
30 years of hyperuricemia
2. Genetic predisposition primary gout follows multifactorial inheritance
and runs in families
3. Heavy alcohol consumption predisposes to attacks of gouty arthritis
4. Obesity increases the risk of asymptomatic gout
5. Drugs (thiazides) reduce excretion of urate and predispose to the
development of gout
6. Lead toxicity increases the tendency to develop saturnine gout
monosodium urate (MSU) crystals into the joints
temperature (the lower the less soluble)
by the intra-articular concentration of urate and cation
presence of nucleating agents such as insoluble collagen fibers, chondroitin
sulfate, proteoglycans, cartilage fragments and other crystals
urates in the joint fluid become supersaturated more easily, particularly in
the peripheral joints (ankles and toes), where temperatures are as low as
20oC
prolonged hyperuricemia, crystals and microtophi of urates develop in
the synovial lining cells and in the joint cartilage
trauma causes the release of crystals into the synovial fluid, which
begins a cascade of events that initiates, intensifies, and sustains a
powerful inflammatory response that is the hallmark of the acute attack
MSU crystals are phagocytosed by macrophages and this activate the
NALP3 inflammasome, a multiprotein complex that induces the protease
caspase 1 cleaves and activates several cytokines, most notably IL-
1 and IL-18 IL-1 induces the expression of adhesion molecules
and the synthesis of neutrophil chemokine CXCL8
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GOUT MORPHOLOGY Changes include:

1. Acute arthritis
- Characterized by dense neutrophilic infiltrate that permeates the
synovium and synovial fluid
- edematous and congested, and also contains scattered
lymphocytes, and macrophages
2. Chronic tophaceous arthritis
- from repetitive precipitation of urate crystals during acute attacks
- urates may heavily encrust the articular surfaces and form visible
deposits in the synovium
- Synovium becomes hyperplastic, fibrotic and thickened by
inflammatory cells and forms a pannus
3. Tophi in various sites
- Formed by large aggregations of urate crystals surrounded by an
intense inflammatory reaction by macrophages, lymphocytes and
large foreign body giant cells, which may have completely or
partially engulfed masses of crystals
4. Gouty nephropathy
Acute arthritis in gout

The pathognomonic hallmark of gout Tophi

Tophi

Tophi

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Gouty nephropathy

GOUT CLINICAL FEATURES (4 stages) a. Asymptomatic hyperuricemia

- Appears in puberty in males and after menopause in females
b. Acute gouty arthritis
- Appears after several years in the form of the sudden onset of
excruciating joint pain associated with localized hyperemia, warmth,
exquisite tenderness
- Majority of 1st attack is monoarticular, in descending order: insteps,
ankles, knees, wrists, fingers, elbow
c. Intercritical period
- A period when patients never have another attack
d. Chronic tophaceous gout
- about 12 years between the initial acute attack and the
development of chronic tophaceous arthritis
- shows juxta-articular bone erosion caused by osteoclastic bone
resorption and loss of the joint space
Other clinical features of gout CVS: atherosclerosis and hypertension
Renal: renal colic with passage of gravel and stones
Calcium pyrophosphate crystal deposition disease occurring in >50 Pseudo- gout
years of age - Aka chondrocalcinosis
Pseudo- gout is divided into: 1. sporadic (idiopathic)
2. hereditary- deposition occurs early in life and associated with OA and is
caused by germline mutations in the ANKH gene
3. secondary types- associated with previous joint damage,
hyperparathyroidism, hemochromatosis, hypomagnesemia,
hypothyroidism, ochronosis, and DM
Pathogenesis of pseudo gout Basis of crystal deposition is unknown, but altered activity of the matrix
enzymes that produce and degrade pyrophosphate is suspected
PSEUDOGOUT MORPHOLOGY 1st develop in the articular matrix, menisci and intervertebral discs, and
as deposits enlarge they rupture and seed the joint

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PSEUDOGOUT CLINICAL FEATURE
TUMORS AND TUMOR-LIKE LESIONS OF JOINTS
A small (1 to 1.5 cm) cyst that is almost always located near a joint
capsule or tendon sheath
Ganglion usually is a result of ___
Herniation of synovium through a joint capsule or massive
enlargement of a bursa may produce a
The term for several closely related benign neoplasms that develop in
the synovial lining of joints, tendon sheaths, and bursae
Chromosomal translocation in tenosynovial GCT
Variants of the tenosynovial GCT include
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deposits are phagocytosed by macrophages activate the NALP3
inflammasome pro-inflammatory events similar
crystals form chalky white friable deposits, seen histologically as oval
blue-purple aggregates
Frequently asymptomatic
produces acute, subacute, or chronic arthritis that can be confused with
OA or RA
commonly affected: knees, followed by the wrists, elbows, shoulders and
ankles
50% of patients experience significant joint damage
no known treatment that prevents or retards crystal formation
GANGLION AND SYNOVIAL CYSTS
TENOSYNOVIAL GIANT CELL TUMOR (LOCALIZED AND DIFFUSE)
commonly involve joints and tendon sheaths
usually result from trauma or degenerative processes and are much more
common than neoplasms
Benign tumors are much more frequent than their malignant counterparts
Ganglion
- Commonly location is wrist
- Appears as a firm fluctuant pea-sized translucent nodule
result of cystic or myxoid degeneration of connective tissue, cysts lack a true
cell lining
Synovial cyst
- Example is Baker cyst
- Synovial lining may be hyperplastic and contain inflammatory cells
and fibrin but is otherwise unremarkable
Ganglion
Tenosynovial GCT
t(1;2)(p13;q37), which fuses CSF1 coding sequences to the promoter of the
collagen type VI alpha-3 gene tumor cells overexpress CSF1
diffuse type (previously known as pigmented villonodular synovitis), and
localized type (also known as GCT of tendon sheath)
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TENOSYNOVIAL GCT MORPHOLOGY GROSS
both are red-brown to mottled orange-yellow
both are heavily infiltrated by macrophages which contain hemosiderin
and lipid filled vacuoles, or coalesce into multinucleated giant cells
In diffuse:
smooth joint synovium is converted into a tangled mat by red brown
folds, finger-like projections and nodules
spread along the surface and infiltrate the subsynovial compartment
localized tumors: well-circumscribed and resembles a small wallnut
cells grow in a solid nodular aggregate that may be attached to the
synovium by a pedicle

PVNS/GCT

TENOSYNOVIAL GCT CLINICAL: DIFFUSE TYPE
TENOSYNOVIAL GCT CLINICAL: LOCALIZED VARIANT
Recommended tx for both variants
Usually presents in the knee in 80% of cases
Patients typically complain of pain, locking, recurrent swelling
Tumor progression limits the range of motion and joints become stiff and
firm
significant recurrence rate because it is difficult to excis
Manifests as a solitary slow-growing painless mass that frequently
involves the tendon sheaths along the wrists and fingers
most common mesenchymal tumor of the hand
Surgery

The author of this document wishes you a successful examination. Dont forget to check your notes and books if anything seems
confusing. This is not intended to replace your review materials, instead this is primarily designed to assist you in your study regimen.
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