Bone Pathology Flashcards

1
Q

Secondary

Bone Tumors

A
  • Metastatic tumors
    • Most frequent malignant tumors found in bone
    • Predominant occurrence in adults > 40 yrs and children in first decade of life
    • Multifocal
    • Predilection for the marrow in the axial skeleton (vertebrae, pelvis, ribs and cranium) and proximal long bones
  • Tumors resulting from contiguous spread of adjacent soft tissue neoplasms
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2
Q

Metastatic Origins

A

Most common malignancies producing skeletal metastases:

  • Adults:
    • Prostate, breast, kidney, and lung
    • Thyroid and colon cancers
    • Melanoma
  • Children:
    • Neuroblastoma
    • Rhabdomyosarcoma
    • Retinoblastoma
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3
Q

Osteoarticular System

Primary Tumors

A
  • Relatively uncommon ⇒ 2,400 cases of primary bone sarcoma/year in US
  • Benign tumors more common
  • Occur mostly in the first three decades of life
  • Clinical hx including age, location of tumor and radiological data are very important to diagnosis
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4
Q

Most Common

Benign Tumors

A
  1. Osteochondroma
  2. Non-ossifying fibroma
  3. Enchondroma
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5
Q

Most Common

Malignant Tumors

A

Excluding malignant neoplasms of marrow origin:

  1. Osteosarcoma
  2. Chondrosarcoma
  3. Ewings sarcoma
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6
Q

Bone Tumors

Features

A
  • Some able to dedifferentiate
    • eg., enchondroma or a low-grade chondrosarcoma transforming into a high-grade sarcoma
  • Tendency of high-grade sarcomas to arise in damaged bone
    • Sites of bone infarcts
    • Radiation osteitis
    • Paget’s disease
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7
Q

Primary Bone Tumor

Classifications

A
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8
Q

Age of Onset

A

Predominant occurrence in first 3 decades of life

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9
Q

Common Tumors

Ages 0-10

A
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10
Q

Common Tumors

Ages 10-20

A
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11
Q

Common Tumors

Ages 20-40

A
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12
Q

Common Tumors

Ages 40+

A
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13
Q

Bone Tumor

Frequent Locations

A
  • Distal femur and proximal tibia most common
    • Both benign and malignant
    • Bones with highest growth rate
  • Many lesions favor certain bones or sites
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14
Q

Bone Tumors

Location Preference

A
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15
Q

Bone Tumors

Imaging Studies

A
  • Most bone tumors have relatively specific radiographic presentations
  • In some cases, dx can be confidently made based on radiographic features alone
  • Can provide clues about clinical behavior
    • Estimate tumor growth rate
    • Expansive or infiltrative growth patterns characteristic of locally aggressive and malignant tumors
  • Modalities:
    • Plain Radiograph
    • CT
    • MRI ⇒ method of choice for local staging
    • Bone Scintigraphy ⇒ highly sensitive but relatively non-specific
      • Main role in detection of suspected metastases in the whole skeleton
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16
Q

Bone Tumors

Radiologic Features

A

Radiographic examination should answer the following questions:

  • Location
  • Type of bone (flat, tubular)
    • If long bone affected ⇒ where lesion is centered
      • Cortex or medulla
      • Epiphysis, metaphysis or diaphysis
  • Underlying bone abnormality (eg., bone infarct, Paget’s disease)
    • High-grade sarcomas tend to arise in damaged bone
  • Multifocality
    • Malignant > benign
    • Benign lesions tend to show symmetrical distribution
  • Well-defined margin, rim of sclerotic bone?
    • Presence strongly suggests a benign non-growing or slow growing lesion
  • Cortical expansion or destruction?
    • Findings seen with locally aggressive or malignant tumors
  • Periosteal reaction and, if so, of what type
  • Patterns of Mineralization (calcification or ossification)
    • Helpful in identification of bone-producing and cartilage producing tumors
  • Is there a soft tissue mass?
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17
Q

Periosteal Reactions

A
  • Periosteum responds to traumatic stimuli or pressure from an underlying growing tumor by depositing new bone
  • Radiographic appearance of response reflects the degree of aggressiveness of the tumor
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18
Q

Benign and Non/Slow-Growing

Lesions

A
  • Well-circumscribed and shows a geographic pattern of bone destruction with a sclerotic rim
  • Slow-growing tumors provoke focal cortical thickeningsolid periosteal reaction or “buttress
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19
Q

Rapidly Growing

Lesions

A
  • May still show a well-demarcated zone of bone destruction (geographic pattern) but will lack a sclerotic rim
  • With continued growth, may show cortical expansion
  • Periosteal reactions include:
    • Codman’s triangle ⇒ elevation of periosteum to a significant degree, forming an acute angle
    • Onion-skinning” ⇒ seen in Ewing sarcoma
    • Spiculated “hair-on-end” appearance due to periosteal new bone formation
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20
Q

Osteoid

A

Malignant osteoid can be recognized radiologically as cloud-like or ill-defined amorphous densities with haphazard mineralization

Pattern is seen in osteosarcoma

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21
Q

Chondroid

A

Usually easier to recognize cartilage vs osteoid by the presence of focal stippled or flocculent densities, or in lobulated areas, as rings or arcs of calcifications.

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22
Q

Bone Tumors

Histologic Evaluation

A
  • Most important histologic features to consider:
    • Pattern of growth (eg., sheets of cells vs. lobular architecture)
    • Cytologic characteristics of the cells
    • Presence of necrosis and/or hemorrhage and/or cystic change
    • Matrix production
    • Relationship between the lesional tissue and the surrounding bone (eg., sharp border vs. infiltrative growth)
  • Dx of bone tumor requires clinical, radiological, and histologic appearances
  • Biologically different types of tumors may have overlapping histologic features
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23
Q

Osteoid Osteoma

Overview

A

Benign, bone-producing neoplasm

  • Small size w/ limited growth potential
  • Lesional tissue ⇒ “nidus
    • Small radiolucent focus < 1 cm
    • Either within the cortex or adjacent to it
  • Predominantly in males 10-25 y/o
  • 50% of cases in the femur and tibia
    • Femoral neck is one of the most common anatomic sites
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24
Q

Osteoid Osteoma

Effects

A
  • Causes extensive reactive changes in surrounding tissues
  • Produces prostaglandin/prostocyclin-mediated effects
  • Induces exuberant, reactive, periosteal sclerosis, soft tissue edema and pain
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25
Q

Osteoid Osteoma

Gross Appearance

A
  • If nidus removed intact ⇒ circumscribed portion of red, trabecular bone < 1 cm in size
    • Either within the cortex or adjacent to it
  • XR shows a small, intracortical, radiolucent focus (nidus), surrounded by dense reactive periosteal bone
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26
Q

Osteoid Osteoma

Microscopic Appearance

A

Lesional tissue (“nidus”) well-demarcated from the surrounding sclerotic bone

Composed of thin, often interconnected spicules of osteoid and woven bone rimmed by osteoblasts

Osteoclast-like giant cells can be seen

Intervening fibrous stroma shows prominent vascularity

Both osteoblasts and stromal cells are without significant nuclear atypia

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27
Q

Osteoid Osteoma

Differential Diagnosis

A
  1. Osteoblastoma
  2. Intracortical osteosarcoma ⇒ significant nuclear atypia and invasive growth pattern are indicative of malignancy
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28
Q

Osteoblastoma

Overview

A
  • Larger than 1.5 cm
  • Slowly and progressively growing neoplasms
  • Term “aggressive osteoblastoma” is applied to large, locally destructive lesions that mimic a low-grade osteosarcoma on microscopic examination
  • Peak incidence during 2nd and 3rd decades of life
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29
Q

Osteoblastoma

Clinical Behavior

A
  • Tend to arise in the axial skeleton
    • Involves spine and sacrum in ~ 40% of cases
    • 2nd most frequent site is the mandible, followed by other craniofacial bones
  • Do not produce prostaglandin/prostocyclin-mediated tissue reaction
  • May grow to a considerable size ⇒ bone expansion and cortical destruction
  • Recurrences in ~ 20% of cases
  • No metastases
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30
Q

Osteoblastoma

Appearance

A

Radiology:

  • XR ⇒ well-circumscribed, low metaphyseal, radiolucent lesion containing matrix-type radiodensities
    • No sclerotic rim
  • Affects long bones and vertebrae

Histology:

  • Resembles osteoid osteoma
  • Osteoblasts and osteoclast-like giant cells surround interconnected spicules of osteoid and woven bone
  • Intervening fibrous stroma shows prominent vascularity
  • No significant cellular atypia
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31
Q

Osteosarcoma

Overview

A

Malignant tumor composed of neoplastic mesenchymal cells synthesizing osteoid or immature bone.

  • Presence of malignant osteoid distinguishes an osteosarcoma from other sarcomas
  • Preferentially affects rapidly growing parts of the skeleton
    • Distal femur and proximal tibia (50% of cases)
    • Proximal humerus
    • Elderly ⇒ tends to involve axial skeleton and flat bones
  • Metaphysis is the most common site in long bones
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32
Q

Osteosarcoma

Epidemiology

A
  • Most common primary sarcoma of bone
  • Bimodal age distribution:
    • Peak incidence in 2nd decade of lifemost active skeletal growth
      • < 5% of cases occur in children younger than 10 years
    • In the elderly ⇒ usu. seen in association with a pre-existing bone disease
      • Paget’s, radiation osteitis, or bone infarct
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33
Q

Osteosarcoma

Classification

A
  • Subdivided into:
    • Intramedullary (largest group)
    • Intracortical
    • Surface osteosarcomas
  • Subclassified into high-grade and low-grade
    • Based on the degree of differentiation
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34
Q

Osteosarcoma

Appearance

A

Histologic findings can be extremely variable

  • Composed of highly pleomorphic cells and haphazard deposits of osteoid
  • Anaplastic cellular features and mitotic activity
  • Malignant osteoid:
    • Lace-like pattern
    • Haphazardly arranged trabeculae of woven bone
  • ± Foci of neoplastic cartilage

May appear identical to MFH ⇒ minimal osteoid production

May contain masses of malignant cartilage or numerous giant cells

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35
Q

Osteosarcoma

Histologic Variants

A
  • Osteoblastic (≈ 50%)
  • Chondroblastic
  • Fibroblastic
  • Telangietatic
  • Small cell
  • Giant cell
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36
Q

Osteosarcoma

Disease Course and Treatment

A
  • One of the most aggressive and highly lethal tumors
  • Most powerful predictor of outcome is the histologic response of the tumor to pre-operative chemotherapy
    • Tumor necrosis following tx graded according to the following system:
      • Grade 1 - 0-50% necrosis
      • Grade 2 - 51-90%
      • Grade 3 - 91-99%
      • Grade 4 - 100% necrosis
    • ≥ 90% tumor necrosis ⇒ nearly 90% 5-year disease-free survival
    • < 90% tumor necrosis ⇒ 14% 5-year disease-free survival in pts with
  • Metastases extremely common
    • Usu. to lungs, bones, and liver
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37
Q

Osteochondroma

Overview

A

Cartilage-capped outgrowth attached to the underlying bone by a bony stalk.

  • Can be solitary or multiple
    • Multiple Hereditary Exostosis ⇒ multiple osteochondromas
      • AD hereditary disease
      • More likely to undergo malignant transformation (<1%)
  • Most common skeletal sites are the metaphyses of long bones
    • It does not occur in bones with membranous type of ossification
  • M:F = 3:1
  • When skeletal maturity is reached, osteochondromas usually stop growing
    • Continued growth may signify malignant transformation
  • Clonal origin of sporadic & hereditary forms supported by clonal cytogenetic abnormalities
    • Deletions of regions q24 of chromosome 8 (EXT1 locus) and p11-12 of chromosome 11 (EXT2 locus) ⇒ inactivation of EXT1 and EXT2 genes
38
Q

Osteochondroma

Appearance

A
  • XR ⇒ pedunculated bony outgrowth @ proximal tibial metaphysis
  • Histology:
    • Cortex and medulla are continuous with those of the lesion
    • Mature trabecular and cortical bone
    • Uniform, cartilaginous cap with stippled calcifications
      • Mature, focally calcified hyaline cartilage
      • < 1 cm thick
39
Q

Chondroma

Overview

A

Common, benign, intramedullary bone tumor composed of mature hyaline cartilage.

  • Wide age distribution
  • Peak incidence during 3rd and 4th decades of life
  • Limited growth potential
  • Many lesions remain small and asymptomatic
40
Q

Chondroma

Appearance

A
  • Three characteristic features:
    • Vague lobularity (“soap bubbles”)
    • Abundant cartilaginous matrix
      • Can be focally calcified
    • Low cellularity
  • Clustered and scattered chondrocytes with small, uniform, darkly-stained nuclei
  • Occasional bi-nucleated chondrocytes present
  • No mitotic figures
41
Q

Ollier’s Disease

A
  • Rare, non-hereditary disorder
  • Characterized by multifocal proliferation of dysplastic cartilage (enchondromatosis)
  • Usually dx in children and adolescents between 10 and 20 years of age
  • Very high risk of malignant transformation (20% - 30%)
    • Usually to chondrosarcoma
42
Q

Marfucci’s Syndrome

A

Multiple cartilaginous tumors associated with hemangiomas

Similar to Ollier’s

43
Q

Enchondromas

A
  • Associated with pain and fracture or thinning of the overlying cortex
  • Long bones ⇒ suspicious for malignancy
  • Small bones ⇒ no dx of chondrosarcoma unless a tumor permeates into soft tissue
44
Q

Chondroblastoma

Overview

A
  • Rare, benign neoplasm
  • Occurs in the 2nd decade of life (75%) ⇒ growth plates are still open
  • One of two neoplasms of incompletely differentiated cartilage
    • The other neoplasm is chondromyxoid fibroma
  • 70% arise in the proximal humerus and at the knee
    • Long bones ⇒ almost always occurs in the epiphysis
  • Recurrence rate ~ 10% within the bone or in the adjacent soft tissue
  • It can occasionally produce “benign”, clinically non-progressive lung implants
45
Q

Chondroblastoma

Appearance

A
  • Irregular but circumscribed, radiolucent epiphyseal lesion surrounded by reactive bone sclerosis
  • Highly cellular tumor consisting of sheets of round to polygonal chondroblasts
    • Folded or clefted nuclei
    • Fine chromatin pattern
    • Occasional inconspicuous nucleoli
    • Stains ⊕ for S-100
  • Mitotic activity is low
  • Multiple small foci of immature bluish-pink chondroid ⇒ vaguely lobular appearance
  • Multinucleated giant cells scattered throughout lesion
    • Are of different cell line and stain ⊕ for histiocytic markers (CD68)
  • “Chicken-wire” calcification is virtually pathognomonic of chondroblastoma
46
Q

Chondroblastoma

Differential Diagnosis

A
  • Giant Cell Tumor (GCT):
    • Also occurs @ epiphysis but in skeletally mature individuals
    • Lacks chondroid matrix
    • ⊖ staining with S-100
  • Chondromyxoid fibroma:
    • Centered in the metaphysis and lacks calcification
  • Clear cell chondrosarcoma:
    • Epiphyseal tumor of pts > 40 y/o
    • Malignant chondrocytes and characteristic large cells with clear cytoplasm
47
Q

Chondromyxoid Fibroma

Overview

A
  • Benign tumor
  • Occurs in pts < 40 y/o
  • Peak incidence is between ages 10 and 20
  • 30% occur at the knee area
  • Long bones ⇒ involves the metaphysis or meta-diaphysis and is often eccentric
  • ± Secondary aneurysmal bone cyst formation
48
Q

Chondromyxoid Fibroma

Clinical Behavior

A

Recurrence rate averages 15%-20%

Large or recurrent lesions may be locally aggressive

49
Q

Chondromyxoid Fibroma

Appearance

A
  • Well-defined, expansile lytic lesion
  • Centered at the metaphysis
  • Bordered by a sclerotic rim
  • Moderately cellular chondromyxoid tissue with two characteristic features:
    • Vague lobularity caused by alternating highly cellular and less cellular areas
      • ↑ Cellularity @ periphery of lobules
    • Mildly pleomorphic, angular and stellate cells set in bluish-pink chondromyxoid stroma
50
Q

Chondromyxoid Fibroma

Differential Diagnosis

A
  • Chondroblastoma
  • Chondrosarcoma
51
Q

Chondrosarcoma

Overview

A

Malignant, cartilage-producing tumor

  • Patient age is typically 30-50 years
  • Extremely rare in children ⇒ almost always high grade
    • Most chondroid tumors in children and adolescents are chondroblastic osteosarcomas
  • Common sites:
    • Bones of the trunk including the pelvis
    • Long bones such as the femur and humerus
  • Osteochondroma, enchondroma and fibrous dysplasia may undergo malignant transformation into a chondrosarcoma
52
Q

Chondrosarcoma

Appearance

A
  • Large, lobulated, ill-defined lesion
  • Centered in the distal femoral metaphysis
  • Moderately cellular, lobulated cartilaginous tumor
53
Q

Chondrosarcoma

Clinical Behavior

A

Aggressiveness predicted by histologic grade.

Based on three parameters:

  1. Cellularity
  2. Degree of nuclear atypia
  3. Mitotic activity
54
Q

Chondrosarcoma

Grade 1

A
  • Very similar to enchondroma with higher cellularity and mild cellular pleomorphism
  • Small nuclei show open chromatin pattern and small nucleoli
  • Frequent binucleated cells
  • Mitoses are very rare
  • Locally aggressive and prone to recurrences but usually do not metastasize
55
Q

Chondrosarcoma

Grade 2

A
  • Cellularity higher than Grade 1 tumors
  • Moderate cellular pleomorphism
    • Plump nuclei
    • Frequent bi-nucleated cells
    • Occasional bizarre cells
  • Mitoses are rare
  • ± Foci of myxoid change
  • ~ 10% to 15% of Grade 2 chondrosarcomas produce metastases
56
Q

Chondrosarcoma

Grade 3

A
  • High cellularity
  • Marked pleomorphism
  • ↑ N/C ratio
  • Many bizarre cells
  • Frequent mitoses (more than 1 per hpf)
  • These are high grade tumors with significant metastatic potential
57
Q

Non-Ossifying Fibroma (NOF)

Overview

A

Common, non-neoplastic, self-healing fibrous tissue forming tumor

  • Occurs in skeletally immature individuals
    • Usu. between 5-20 y/o
  • Small lesions usu. incidental radiological findings
  • Larger lesions occupying > ½ of bone diameter ⇒ ± pathologic fracture
  • Usu. a solitary lesion in the metaphysis or meta-diaphysis of the long bone at the knee, distal tibia or proximal humerus
  • Can resemble GCT
    • Epiphyseal location and occurrence in adults
58
Q

Non-Ossifying Fibroma (NOF)

Radiologic Findings

A

Sharply demarcated, lucent, loculated, meta-diaphyseal lesion surrounded by a rim of sclerotic bone.

  • Predominantly involves the lateral portion of the bone ⇒ eccentric location
  • Produces mild cortical expansion
  • Large lesions can involve the entire diameter of the bone expanding the cortex
  • Dx by XR alone if located in the typical skeletal site and in appropriate age group
59
Q

Non-Ossifying Fibroma (NOF)

HIstology

A
  • Moderately cellular
  • Uniform spindle cells in a storiform pattern w/ bland appearance
  • Scattered giant cells
  • Multiple collections of foamy histiocytes (xanthoma cells)
  • ± Hemosiderin-laden MΦ
  • Mitotic figures are easily found averaging 4 per 10 hpf
    • No atypical mitoses
60
Q

Jaffe-Campanacci

Syndrome

A

Multiple non-ossifying fibromas & cutaneous cafe au lait spots

61
Q

Benign Fibrous Histiocytoma

A
  • Lesions w/ histologic features of NOF but occur in unusual locations
    • Pelvis, ribs or vertebrae
  • Designation controversial and is not generally accepted
62
Q

Fibrous Dysplasia

Overview

A

Benign fibro-osseous lesion

  • Considered a hamartoma
  • Occurs sporadically during the period of skeletal growth (10-25 y/o)
  • Intramedullary location
  • Most common locations include the long bones (ribs, femur, tibia, jaw and humerus) in the metaphysis or diaphysis
  • Hallmark of FD is inability of tissue @ affected site to produce mature lamellar bone
    • Arrested @ level of woven bone
63
Q

Fibrous Dysplasia

Types

A

Two forms:

  • Monostotic (70% of cases)
  • Polyostotic
    • McCune-Albright syndrome
      • FD, cutaneous café au lait pigmentations, and precocious puberty
    • Mazabraud’s syndrome
      • FD in close proximity to soft tissue myxomas
64
Q

Fibrous Dysplasia

Overview

A
  • Three characteristic histologic features:
    • Thin wavy spicules of woven bone (“Chinese characters”)
    • Lack of osteoblastic rimming or osteoclastic activity
    • Moderately cellular, bland fibrous background
  • In children ⇒ stromal mitoses may be frequent (1 to 5 per hpf)
  • In adults ⇒ mitotic figures are very rare to absent
65
Q

Giant Cell Tumor

Overview

A

Relatively uncommon, locally aggressive neoplasm

  • 4% of all primary bone tumors
  • Affects skeletally mature individuals, 20-50 y/o
    • Extremely rare in children and patients older than 60 years
  • Centered in the epiphysis
  • 65% in the distal femur, proximal tibia and distal radius
    • May affect any long bone, pelvis, sacrum, and spine (3%)
66
Q

Giant Cell Tumor

Clinical Behavior

A
  • ± Bone destruction and soft tissue invasion
  • Intravascular invasion in 30% of cases
    • Not correlated with local aggressiveness or development of pulmonary implants
  • Common secondary changes:
    • Hemorrhage and necrosis
    • Fibrohistiocytic (xanthomatous) change
    • Aneurysmal bone cyst formation
  • Complications:
    • Pathologic fractures
    • Malignant transformation (dedifferentiation)
  • Local recurrences common if not completely excised (40% - 60%)
    • May involve bone and/or soft tissue
67
Q

Giant Cell Tumor

Appearance

A
  • Radiologic appearance:
    • Well-defined, lytic lesion
    • Eccentrically located in the distal epiphysis
    • Subchondral and metaphyseal extension
  • Histology:
    • Multinucleated giant cells
    • Small, ovoid, mononuclear stromal cells
      • Monocyte/MΦ derived
      • Poorly defined cytoplasmic borders and bland nuclei
    • Mitoses average 4 per 10 hpf
      • No atypical mitoses
    • ± Areas of prominent fibrohistiocytic changes
      • Storiform arrangement of stromal cells
      • Clusters of foamy histiocytes (xanthoma cells)
68
Q

Ewing’s Sarcoma (ES)

Overview

A
  • 80% of cases occur in pts 5-20 y/o
  • Most common sites:
    • Diaphysis of femur, tibia and humerus
    • Pelvis and ribs
      • Askin tumor of the chest if in ribs
  • Arises in the medullary cavity
    • Invades cortex and periosteum
    • Fequently produces a soft tissue mass
  • Positive for CD99/O13
  • Chromosomal translocation ⇒ EWS-FLI-1 fusion gene
69
Q

Ewing’s Sarcoma (ES)

vs.

Primitive Neuroectodermal Tumor (PNET)

A
  • Both are “small round blue cell” tumors
  • Similar neural phenotype
    • Positive for CD99/O13
  • Identical chromosomal translocation
    • t(11;22)(q24;q12) → EWS-FLI-1 fusion gene
  • Degree of neural differentiation distinguishes them from one another:
    • EM ⇒ cells are undifferentiated and show prominent glycogen deposits
    • PNETneural differentiation
      • NSE and/or S100 positive
70
Q

Ewing’s Sarcoma (ES)

Clinical Manifestations

A
  • Frequently produces a soft tissue mass
  • Tumor site is often painful, swollen and warm
  • Patients may have fever, elevated ESR and leukocytosis mimicking infection
71
Q

Ewing’s Sarcoma (ES)

Radiologic Appearance

A
  • Large destructive, diaphyseal lesion
  • Permeative periosteal reaction of a “hair-on-end” or “onion-skin” type
  • MRI superior to XR in showing cortical disruption and soft tissue involvement
72
Q

Ewing’s Sarcoma (ES)

Histology

A
  • Sheets of primitive cells with little histologic evidence of differentiation
  • Mitotic rate is relatively low
  • Positive for CD99/O13 immunostain
73
Q

Osteoporosis (OP)

Overview

A
  • A common, severe, and debilitating disease
  • Estimated 15 million symptomatic cases in the U.S. and many more asymptomatic
  • More common in women, esp. post-menopausal women
  • Cause is unknown
74
Q

Osteoporosis (OP)

Pathophysiology

A
  • ↑ Bone resorption
    • Occurs as part of aging
    • Especially ↑ in postmenopausal women
  • ↓ Bone formation
  • Overall organic to mineral matrix balance remains the same
  • Spicules are smaller, thinner and more fragile
    • Bone looks the same histologically
    • Much weaker and thinner structurally
75
Q

Senile Osteoporosis

A

OP seen in older people

Development of the disease is due to hormonal imbalances that occur in the aged, especially post-menopausal women

76
Q

Osteoporosis

Other Etiologies

A
  • Hereditary
  • Osteogenesis imperfecta
  • Exercise ⇒ ↑ bone mass, ↑ bone density, and ↓ incidence of OP
    • Females who exercise to amenorrhea (e.g. long-distance runners) are more susceptible to OP
  • Bone size ⇒ smaller people at ↑ risk for OP
  • Greater incidence in whites than blacks
  • Hormones ⇒ those on steroids lose bone mass and are at risk
  • Long-term heparin therapy ↑ risk of OP
77
Q

Osteoporosis

Clinical Manifestations

A

↓ Structural integrity ⇒ fractures

Most common sites of thinning due to OP:

  • Neck of femur
  • Vertebral column
    • Normal thickness
    • Microfractures d/t thinning of the bone
    • Can result in fracture of the spine & collapse of vertebral column
  • Metacarpals
78
Q

Osteoporosis

Diagnosis

A
  • Best way to dx OP is by dual photon beam densitometry
  • Blood levels of calcium, phosphorus, and alkaline phosphatase will be normal
  • XRs will also be normal
79
Q

Osteoporosis

Treatment

A

Tx with estrogens, ↑ calcium, and calcitonin injections.

  • Estrogens given to ↓ bone loss
    • ↑ Risk of endometrial carcinoma in post-menopausal woman
    • ? ↑ risk of breast cancer
  • Calcitonin shown to be successful in tx of OP
80
Q

Osteomalacia (OM)

Overview

A
  • Most common remedial bone disease of the elderly
  • Due to Vit D deficiency
    • Usu. d/t poor diet in the elderly
    • Also seen in underdeveloped countries d/t poverty and poor diet
  • Inadequate calcium absorption d/t ↓ Vit D
  • Widened organic matrix that is not mineralized
81
Q

Osteomalacia

Clinical Manifestations

A
  • Bending, bowing, and breaking of bones
  • Overabundance of organic matrix
    • Matrix is not mineralized
      • Normal bone takes 6-10 days to mineralize
      • In OM, it takes 2-3 months to mineralize
82
Q

Osteomalacia

Diagnosis

A
  • ↓ Phosphorus
  • Calcium is low to low normal
  • ↑ Bone turnover ⇒ ↑ alkaline phosphatase
  • Biopsy: widening of osteoid seams
83
Q

Paget’s Disease

Overview

A

Osteitis Deformans

  • Affects 3% of the population
  • Primarily a disease of the elderly (seen after age 40-50)
    • By age 90, it affects 10% of males and 15% of females
84
Q

Paget’s Disease

Types

A
  • Monostotic (15% of cases)
    • Occurs at a single site
    • Most common site is the tibia
  • Polyostotic (85% of cases)
    • Occurs at multiple sites
    • Most common sites include the spine and pelvis
85
Q

Paget’s Disease

Stages

A
  1. Osteolytic stage
    • Osteoclast ⊕ by virus and resorbs bone
      • Bone digestion ⇒ ↑ fibrous tissue and vascularity between the bony spicules
    • Can cause red hot skin over the bone
    • ↑ Vascularity ⇒ ± high out cardiac failure
  2. Osteolytic / osteoblastic stage
    • Continued bone lysis
    • ↑ osteoblastic activity ⇒ ↑ bone formation
      • Balance b/t lysis & formation abnormal
      • Resulting bone is not in normal Haversian canal structure
      • Abnormal mineral deposition patterns
    • Mosaic pattern is pathognomonic for Paget’s
86
Q

Paget’s Disease

Pathogenesis

A
  • Believed to be caused by an infection of the osteoclast by a Paramyxovirus
  • Thick bone made w/ poor structural integrity ⇒ deformity & fracture
  • ↑ Osteoblastic activity ⇒ osteogenic sarcoma in 1-10% of pts
    • Longer disease duration ⇒ ↑ likelihood of eventually developing osteogenic sarcoma
  • Rapid rate of bone turnover called Matrix Metabolic Madness
87
Q

Paget’s Disease

Clinical Manifestations

A
  • Highest levels of alkaline phosphatase of any bone disease
  • Most pts asymptomatic
    • Incidental findings on XR
  • Some pts present w/ pain or bone deformity
  • Skeletal changes:
    • Thickening of arms, tibia, femur, pelvis, and clavicles
    • Skull is also thickened but d/t loss of integrity and nl structure, if you fill the skull with water it will leak like a sieve
88
Q

Fracture Types

A
  • Closed fracture (simple)
    • Skin intact
    • Complete vs incomplete (greenstick)
    • Stable fracture ⇒ broken ends line up and are barely out of place
  • Comminuted fracture
    • Bone shatters into three or more splintered spicules
  • Compound fracture (open)
    • Penetrates skin
    • Most serious due to potential for infection
89
Q

Fracture Repair

A

Healing occurs in 4 stages:

  1. Hematoma formation
    • Blood clot @ site of fx
  2. Soft callus formation
    • ⊕ collagen production @ ends of the bone ⇒ fibrous procallus (10-14 days)
      • Fracture stable but weak
      • Poor immobilization ⇒ shearing forces ⇒ abnormal collagen formation
      • Comminuted fx ⇒ splinters can stop formation of fibrous and cartilaginous tissue
      • Comminuted and compound fx ⇒ soft tissue invasion can delay collagen deposition and healing
    • Chondrocytes start to form cartilage ⇒ cartilaginous procallus
      • Poor immobilization ⇒ ± pseudoarthrosis
        • Joint space w/o cartilage or bone formation ⇒ insufficient healing
  3. Hard callus formation
    • Immature spongy bone deposited onto cartilage matrix
  4. Bone remodeling
    • Lamellar bone deposition
90
Q

Healing Fracture

Histology

A
91
Q

Fracture

Complications

A
  • Malalignment
  • Comminution w/ bone spicules at fracture site
  • Inadequate immobilization
  • Infection ⇒ prevents healing from taking place