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Module 7 > Bone Pathology > Flashcards

Bone Pathology Flashcards

1
Q

how do osteocytes and osteoblasts interact

A

connected by long cytoplasmic processes

changes in bone tissue fluid (BTF) when changes in stress/strain on bone or microcracks

osteocytes detect changes in BTW flow –> signal to osteoblasts –> bone formation or resorption

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2
Q

what can osteoclasts not bind to

A

unminderalized bone

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3
Q

what role does parathyroid hormone play (4)

A
  1. osteoblasts retract and secrete collagenases –> osteoclasts have access to bone
  2. osteblasts secrete RANKL –> activates resorption process
  3. osteoblasts also produce osteoprotegrin –> inhibition of formation of osteoclasts
  4. osteoblasts can both upregulate and downregulate osteoclastic bone resorption
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4
Q

what is the organic matrix made up of

A

type I collagen arranged in parallel

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5
Q

what is the ground susbtance of bone matrix made up of

A

non-collagenous proteins, proteoglycans, lipids

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6
Q

what is the mineral of bone matrix

A

hydroxyapatite

contains minderals (Ca and P) –> hardness

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7
Q

how do flat bones develop

A

intramembranous ossification

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8
Q

how do long bones develop

A

endochondral ossification

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9
Q

how do bones grow in length

A

metaphyseal growth plates via endochonral ossification

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10
Q

how do bones grow in width

A

osteogenic layer of periosteum

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11
Q

what is the cortex and subchondral bone made of

A

osteons –> concentric layers of lamellae

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12
Q

what is the bone in the medullary cavity made of

A

trabecular bone –> lamellae arranged in parallel to sruface of trabecules

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13
Q

what is bone remodelling

A

change of shape or contour of bone in response to normal growth, changed mechanical use or disease

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14
Q

what is the reaction to a bone injury

A
  1. change of size and shape
  2. change of density
  3. disruption of endochondral ossification –> change to metaphyseal trabeculae
  4. rapidly deposited bone is woven (not lamellar)
  5. injured periosteum often also forms bone
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15
Q

what is a traumatic bone fracture

A

force exceeding design

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16
Q

what is a pathological bone injury

A

force below design

abnormal bone (osteomyelitis, neoplasm, metabolic bone disease) is broken by minimal trauma or normal weight bearing

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17
Q

what is a stable fracture

A

fracture ends have been immobilized (clinical stability) –> callus formation

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18
Q

what is a unstable fracture

A

callus formation

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19
Q

what is a rigid fracture

A

usually surgical intervention

bone ends in close contact or close proximitity

ideally contact feeding

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20
Q

what is an external callus

A

formed by the periosteum

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21
Q

what is an internal callus

A

between ends of fragments and in medullary cavity

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22
Q

what is the function of a callus

A

bridge the gap

encircle the fracture site

stabilize the area

23
Q

what does a callus contain

A

hyaline cartilage if the blood supply is less than optimal –> not as strong but eventually undergoes endochondral ossification

24
Q

what are the steps in callus formation

A
  1. hematoma –> immediate
  2. invasion of mesenchymal cells and neovascularization –> 24-48h
  3. earliest woven bone: 36h –> primary callus 4-6 wks
  4. months to years for secondary cells (trabecular bone) and restoration of normal bone
25
Q

what is the histological difference between woven and lamellar bone

A

collagen not in parallel

irregularly arranged

26
Q

what are the advantages of healing by callus

A
  1. natural process
  2. minimal intervention - minimal risk
  3. minimal intervention - lowest cost option
27
Q

what are the disadvantages of healing by callus

A
  1. callus may not be able to stabilize fracture
  2. callus takes time to stabilize fracture
  3. large callus may interfere with function of joints or tendons
28
Q

what is healing with fixation or by 1st intention

A

direct osteonal bridging of fracture site, no callus formation

29
Q

what occurs if the gap is less than 1mm in healing by fixation

A

osteoblasts form lamellar bone at right angle to fracture line –> become osteons parallel to long axis

30
Q

what occurs if the gap is greater than 1mm in healing by fixation

A

first formation of woven bone –> remodelled into osteons

31
Q

what are the complications of fracture healing (8)

A
  1. inadequate blood supply/O2 –> cartilage formation; if anoxia –> necrosis
  2. instability (movement and high tension) –> development of fibrous tissue –> no bone formation –> non-union, false joint/pseudarthrosis
  3. infection –> osteomyelititis, sequestra
  4. malnutrition, age
  5. tissue between fracutre ends –> delayed or non-union
  6. too large metallic implants –> lack of mechanical force to bone –> atrophy
  7. intramedullary implants may damage blood supply
  8. premature closure of growth plates –> deformed limbs
32
Q

what are the disorders of bones

A
  1. vascular
  2. inflammatory (infectious/immune-mediated)
  3. traumatic
  4. anomaly (congenital)
  5. metabolic/toxic
  6. idiopathic/iatrogen
  7. neoplastic
  8. degenerative

(VITAMIND)

33
Q

what are the terms used to describe bone inflammation

A
  1. osteitis: inflammation of bone
  2. periostitis: inflammation of periosteum
  3. osteomyelitis: involves the medullary cavity
  4. sequestrum: fragment of dead bone isolated from blood supply and surrounded by a pool of exudate
34
Q

what are the portals of entry for bone infection

A
  1. direct
  2. hematogenous
35
Q

what are the causes of direct trauma that cause infectious inflammation

A

trauma (may or may not break bone)

extension from direct inflammation (eg. periodontitis/otitis)

36
Q

how does indirect entry of infectious inflammation of bone occur

A

mostly young animals

usually bacterial (embolic) –> suppurative inflammation

most commonly on metaphyseal side of growth plate at articular-epiphyseal complex

capillaries with sharp bends to join medullary viens (slow flow, turbulence, lower phagocytic capacity, discontinuous endothelial lining, no anastomosis)

37
Q

what are the consequences of infectious inflammation of bone

A
  1. thrombosis, infarction, inflammation –> bone resorption
  2. possible sequela –> extension into joint and periosteum, formation of sequestra, formation of sinus tracts, spread to other bones and soft tissues, pathological fractures
38
Q

what are the types of fractures of cortical bone

A
  1. closed: skin unbroken
  2. open/compound: skin broken
  3. simple: clean break into two parts
  4. comminuted: bone shattered into fragments
  5. greenstick: cortex on one side broken, on other side only bent (no displacement of fracture site)
  6. transverse/spiral: depending on fracture line
39
Q

what occurs when there is a fractrure of growht plates or trabecular bone

A

metaphyseal cortex is very thin (weakest part) –> growth plate fractures in young animals

40
Q

what are the types of growth plate fractures

A

type I and II: few or no complications

type III-V: may have growth abnormalities as growth plate involved

41
Q

what is an infraction

A

fracture of trabeculae without involvment of cortex

42
Q

what are the congential/anomaly abnormalities in growth and development

A
  1. osteopetrosis
  2. osteogenesis imperfecta
  3. chondrodysplasia
43
Q

what is osteopetrosis

A

too much bone

defect in bone resorption by osteoclasts (also infectious)

44
Q

what is osteogenesis imperfecta

A

too little bone

mutations in genes for collagen I

45
Q

what is chondrodysplasia

A

disproportionate dwarfism

mutations in genes which control formation of cartilage, storage dx (MPS)

46
Q

what is metabolic bone disease

A

osteoporosis

rickets/osteomalacia

fibrous osteodystrophy

47
Q

what is osteoporosis

A

less bone (reduction in the amount of normally mineralized bone)

malnutrition, immobilization, low dietary Ca, oestrogen/androgen deficiency

48
Q

what is rickets/osteomalacia

A

soft bones (defect in mineralization of bone)

Vit D/phosphorus deficiency

rubberjaw

49
Q

what is fibrous osteodystrophy

A

replacement of bone by fibro-osseus tissue

hyperparathyroidism

50
Q

what are the types of primary neoplasms of bone (7)

A
  1. fibroma: ex. ossifying fibroma –> maxilla and mandible of horse and cattle
  2. fibrosarcoma: ex. oral masses in dogs
  3. chondroma: often arise from flat bones, very rare
  4. chondrosarcoma: most often flat bones, large breed dogs and sheep, grow slower than osteosarcomas, develop metastases later
  5. osteoma: usually bone of head
  6. osteosarcoma
  7. liposarcoma, hemangiosarcoma
51
Q

what is an osteosarcoma

A

malignant neoplastic cells form osteoid, bone or both

most common tumour of bone in dogs and cats

52
Q

where do osteosarcomas most commonly occur

A

giant breed dogs; metaphyses (distal radius, distal tibia, proximal humerus)

early hematogenous spread to lungs and soft tissues and other bones

53
Q

what is a secondary neoplasm

A

carcinoma is most common

dogs: rib shafts, vertebral bodies, humoral and femoral metaphyses; most common primary site: mammary gland, lung, liver, prostate gland
cats: rare; mets to appendicular skeleton; lung carcinoma to digits

Module 7 (50 decks)

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