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MSK/Derm > Orthopedic Pathology > Flashcards

Orthopedic Pathology Flashcards

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1
Q

What what are the epiphysis and metaphysis called in immature skeletons?

A

epiphyseal growth plate or “physis”

growth plate cartilage is replaced by bone in skeletally mature individuals

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2
Q

periosteum

A

specialized connective fibrous tissue with osteogenic potential

covers bone but is absent in joint spaces at attachment sites of tendons or ligaments

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3
Q

endosteum

A

inner lining of diaphyis and of cancellous bone

also has osteogenic potential

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4
Q

intramembranous bone

A

arises from collagen

forms flat bones of skull and clavicles and responsible for prepubertal bone widening

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5
Q

enchondral bone

A

arises from epiphyseal cartilage (growth plate)

forms appendicular and axial skeleton and responsible for prepubertal bone lengthening

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6
Q

What are the zones of echondral bone formation, starting from the tip?

A

resting zone

zone of proliferation

zone of hypertrophy

zone of provisional calcification

primary trabeculae

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7
Q

resting zone

A

inactive chondrocytes

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8
Q

zone of proliferation

A

chondrocytes proliferate and begin to secrete cartilaginous matrix

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9
Q

zone of hypertrophy

A

chondrocytes enlarge, form columns, and secrete cartilaginous matrix

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10
Q

zone of provisional calcification

A

vitamin D causes matrix calcification and entrapped chondrocytes undergo apoptosis

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11
Q

primary trabeculae

A

scaffolds of dead cartilage form the framework on which osteoprogenitor cells (transported through newly formed vessels in the growth plate) deposit bone matrix

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12
Q

What diseases arise from defects in the zone of proliferation?

A

thanataphoric/achondroplastic dwarfism

mucopolysaccharidosis

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13
Q

What diseases arise from defects in the zone of provisional calcification?

A

Ricets/Osteomalacia

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14
Q

What diseases arise from defects in the primary trabeculae?

A

osteogenesis imperfecta/scurvy/osteopetrosis

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15
Q

What are the types of bone?

A

immature - osteoid and woven bone

mature - lamellar bone

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16
Q

osteoid bone

A

unmineralized, poorly organized immature bone matrix (Type I collagen) formed rapidly (long arrow)

ex. new bone covering lamellar/woven bone (10% of normal bone is covered by osteoid), tumor bone, rickets (osteomalacic) bone

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17
Q

woven bone

A

mineralized immature bone formed rapidly (short arrow)

high number of active osteoblasts

ex. fracture callus, sites of bone repair, periosteal reaction to infection or neoplasia

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18
Q

lamellar bone

A

mineralized mature bone formed slowly

parallel collagen type I fiber sheets/bundles (lamellae), evenly distributed osteocytes

two types - cortical (compact) bone and cancellous (spongy) bone

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19
Q

cortical (compact) bone

A

85% of lamellar bone

collagen type I first deposited in the circumferential lamellae

concentric lamellae later develop osteons that dissipate mechanical stress

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20
Q

cancellous (spongy) bone

A

15% of lamellar bone

lamella collagen type I aligned longitudinally in response to mechanical stress

formed by enchondral ossification and constantly remodeled to dissipate stress

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21
Q

osteoblasts

A

derived from mesenchymal stem cells and line surface of bone

cell surface receptors include PTH, vitamin D, estrogen, insulin-like growth factor-1 (somatomedin), and others

produce matrix proteins and type I collagen, and initiate mineralization

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22
Q

osteocytes

A

osteoblasts that are incorporated into mature bone (most common cells within bone)

cell processes communicate through canaliculi within osteon unit

important in regulating calcium and phosphate

mechanical forces cause transcriptional activation of cAMP pathways within osteocytes resulting in remodeling of bone (mechanotransduction)

produce sclerostin - protein that inhibits bone formation

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23
Q

osteoclasts

A

multinucleated cells formed from monocytic progenitor cells in response to RANK-ligand secreted from osteoblasts and bone stromal cells

responsible for bone resorption

located in “resorption pits” or Howship’s lacunae

24
Q

What are the functions of osteoclasts that bind in the Howship lacunae?

A

acidify etracellular space resulting in release of minerals into serum and secrete digestive enzymes (cathepsisns) that dissolve organic matrix resulting in bone resorption

release growth factors and cytokines incorporated in bone that stimulate proliferation of osteoblasts

this interaction between osteoclasts and osteoblasts insures normal physiologic bone remodeling throughout life in response to mechanical stress

25
Q

osteoclast “resorption pit”

A

forms a sealed acidified microenvironment in “resorption pits” on the surface of the bone

“ruffled” membrane contains H+ ATPase

HCl mobilizes the mineral phase and proteinase cathepsin K degrades the organic matrix

these actions release minerals and growth factors from bone

26
Q

What is the process of bone remodeling in cancellous bone?

A

activation of osteoclasts

resorption of bone in Howship’s lacuna

“reversal” of cell type with osteoblasts

bone formation

27
Q

What is the process of osteon formation in cortical bone?

A

osteons form in response to stress

first osteoclastic resorption (“cutting cones”)

osteon then filled with bone produced by osteoblasts in a concentric fashion

osteocytes (most common cellular element) within rings of the osteon communicate through dendritic processes and regulate bone remodeling and mineral stores

28
Q

What are the primary causes of acute osteomyelitis?

A

primarily caused by bacterial infection resulting from:

1) hematogenous spread
2) contiguous spread from adjacent extra-osseous site
3) direct inoculation of organism into bone
4) ischemia (vascular insufficiency)

**Staphyloccocus aureus is the most common

infection localizes in the vascularized regions of bone, can seed periosteal tissue through the Volkman canals

29
Q

What are the histological features of acute osteomyelitis?

A

microscopically, acute inflammatory cells are ultimately associated with non-viable bone (sequestrum)

periosteum/endosteum responds by forming new bone (involucrum) around the dead, infected bone

managed by surgery and a long course of antibiotics

30
Q

categories of bone diseases

A

abnormal matrix

too little matrix

too little mineralization

too much bone resorption

too little bone resorption

31
Q

What are the types of osteogenesis imperfecta? What is the cause?

A

four distinct phenotypic and genetic groups

autosomal recessive form is most severe and lethal in perinatal period

caused by defect in syhtnesis of Type I collagen - abnormal type I collagen results in more serious disease than decreased synthesis of collagen

32
Q

What are the physical outcomes of osteogenesis imperfect?

A

affects bone (fractures that resolve with excess callus formation)

dentin of teeth (dentinogenesis imperfecta)

eyes (thin sclera allow visualization of choroidal vasculature resulting in blue sclera)

ligaments (joint laxity and early osteoarthritis)

and ossicles of the ear (hearing defects).

33
Q

What are the histological features of osteogenesis imperfecta?

A

cartilaginous columns are not converted to bone

medullary cavity containing thin trabecular bone and marrow fibrosis

34
Q

osteoporosis

A

Definition: Bone that is histologically normal but decreased in quantity. Clinically defined as ≥ 1 atraumatic fractures or low bone mineral density on bone density scan (dual-energy x-ray absorptiometry). Process can be-

  1. ) Localized-immobility (Sudeck’s atrophy), inflammation
  2. ) Generalized -Senile & postmenopausal osteoporosis are the two most common forms of the disorder. Osteoporosis also occurs with endocrinopathies, type 1 diabetes mellitus, scurvy, OI, drugs (corticosteroids), ¯Vitamin D, and space travel.
35
Q

pathogenesis of senile and postmenapausal osteoporosis

A

Depends upon initial bone density and subsequent loss of bone that occurs with age

Bone mass peaks in early adulthood (75% dependent on genetics & 25% function of environment)

With aging, osteoblasts lose their ability to form new bone and growth factors lose potency

Bone loss is further accentuated by activation of osteoclasts

36
Q

postmenopausal osteoporosis

A

after menopause, estrogen deficiency up-regulates osteoclastogenic factors IL-1, IL-6, & TNF-a and decreases OPG resulting in osteoclastogenesis

up to 2% cortical and 9% cancellous bone lost per year

affects bones with large surface area (ie., vertebral body) (right). Fractures of vertebra and wrist

high-turnover osteoporosis-activity of osteoclasts>osteoblasts

37
Q

senile osteoporosis

A

men and women > 80 years of age

caused by:

1) osteoblasts have decreased reproductive and biosynthetic potential with age
2) growth factors in matrix less potent

thin cortex leads to fractures involve hip and vertebra

low-turnover osteoporosis (decreased activity of osteoblasts, normally active osteoclasts)

38
Q

vitamin D deficiency (RIckets/Osteomalacia)

A

Increased PTH (due to decreased serum calcium) and decreased serum phosphate stimulate Vitamin D synthesis by 1-hydroxylation of 25-hydroxycholecalciferol in kidney

Vitamin D, in turn, suppresses PTH gene expression and PTH secretion from parathyroid gland

Hypovitaminosis D is presently considered a pandemic problem. 25% of elderly individuals suffer mild osteomalacia due to lack of sun exposure and ↓ calcium and magnesium intake.

39
Q

What are the results of vitamin D deficiency?

A

inability to calcify the zone of hypertrophy in developing growth plate (so chondrocytes do not die and are not replaced by bone)

inability to calcify osteoid formed throughout life during remodeling process

40
Q

What is the role of vitamin D?

A

Vitamin D increases calcium and phosphate absorption from the intestine

During enchondral bone formation, it is required for the calcification of cartilaginous matrix that surrounds chondrocytes in the Zone of Provisional Calcification of the growth plate (rickets)

In adults, required for calcification of osteoid (osteomalacia)

41
Q

pathological findings in Rickets (osteomalacia)

A

In children (Vitamin D deficiency), growth plate becomes widened with cartilage (“metaphyseal flare”)

Cartilage matrix (star) and newly formed osteoid (right lower) do not calcify. (normal growth plate on left)

42
Q

What are the important features of osteomalacia?

A

osteomalacia in adults is usually due to chronic renal failure (renal osteodystrophy) caused by-

1) Decreased serum calcium, phosphate retention and decreased synthesis of Vitamin D (due to loss of kidney mass).
2) Decreased serum calcium leads to increased PTH (“secondary” hyperparathyroidism)

Osteomalacia results in long bone ”insufficiency” fractures on Xray and bone pain.

43
Q

What are the histological features of osteomalacia?

A

Osteomalacia in adults is usually due to chronic renal failure (renal osteodystrophy)

osteomalacic bone shows excess osteoid (LEFT, calcium stains black; RIGHT, trichrome stain with red osteoid).

44
Q

What are the clinical findings of hyperparathyroidism?

A

(GI tract) moans, bones,(renal) stones, and psychiatric overtones

45
Q

What is the pathogenesis of hyperparathyroidism?

A

primary (most commonly, adenoma and less often, primary chief cell hyperplasia) and secondary causes (most often in response to chronic renal failure)

increased PTH results in osteoclastogenesis

affects cortical > cancellous bone (bone loss in fingers & clavicles by Xray)

46
Q

What are the histological findings of hyperparathyroidism

A

microscopically, aggregates of activated osteoclasts form “cutting cones” that resorb bone

“dissecting osteitis” - railroad track appearance of bony trabeculi due to central resorption by osteoclasts (leads to loss of bone-osteoporosis)

subperiosteal cortical bone resorption by osteoclasts

severe disease (most often occurring in secondary hyperparathyroidism) causes fractures that result in hemorrhage, cyst formation,& fibrosis (“osteitis fibrosa cystica” or “brown tumor of bone”)

enlarged Haversian canals

47
Q

dissecting osteitis

A

result of hyperparathyroidism

aggregates of activated osteoclasts form a “cutting cone” along the longitudinal axis of a trabecula

48
Q

brown tumor of bone “osteitis fibrosa cystica”

A

spindled stromal cells, osteoclasts, foci of hemorrhage, and hemosiderin deposits (arrow)

49
Q

What is the definition of Paget’s disease of bone

A

“Collage of matrix madness” due to dyssynchrony of osteoclastic/osteoblastic activity Older population; European Caucasians

50
Q

What are the types of Paget’s disease of bone, and what are the phenotypic manifestations?

A

Polyostotic (85%) > monostotic (15%)

femur or axial skeleton involved in 80% of cases

Results in “chalk stick” fractures, cranial/spinal nerve deficits, high-output cardiac failure (↑ marrow vascularity), & rarely, sarcomatous transformation (mostly, craniofacial and axial bones)

51
Q

What are the three phases of Paget’s disease of bone?

A

Marked bone resorption followed by rapid new bone formation:

1) osteolytic - numerous, enlarged osteoclasts >100 nuclei per cell and highly vascular marrow
2) “mixed” osteoblastic/osteolytic
3) sclerotic - thickened bone exhibiting a haphazard arrangement of cement lines

52
Q

What are the histologic findings of Paget’s disease of bone?

A

abnormally large osteoclasts with >100 nuclei per cell, thickened bone with hapazard cement lines

53
Q

What is the pathogenesis of Paget’s disease of bone?

A

Pathogenesis involves viral and genetic interactions: Mutated p62, a key regulator of RANKL/NFKB

mediated osteoclastogenesis, sensitizes osteoclast precursors to RANKL, while paramyxovirus stimulates osteoclastogenesis resulting in an increased number of multinucleated osteoclasts with enhanced resorption capacity

54
Q

What are the radiographic and histologic findings of Paget’s Disease?

A

radiograph shows characteristic tapering lytic process in the distal femur (top,left)

highly vascularized stroma occasionally results in high-output cardiac failure (top, right)

enlarged osteoclasts active during the early osteolytic phase of the disease (bottom, left; arrows)

osteosclerotic phase of disease is characterized by thickened bone with a haphazard (mosaic) pattern of cement lines (bottom, right)

55
Q

What are the characteristics of osteopetrosis?

A

absent or defective osteoclast activity (in most cases, osteoclasts fail to acidify “resorption” pits)

failure of bone remodeling resulting in abnormally thickened bone

56
Q

What are the clinical features of osteopetrosis?

A

fractures (no osteon formation)

anemia/thrombocytopenia/infections

deforming extramedullary hematopoiesis

cranial nerve defects

MSK/Derm (54 decks)

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