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D1 BS1 + II/ FSI + II > bs2 mod 3 > Flashcards

bs2 mod 3 Flashcards

1
Q

What forms appendicular skeleton

A

Lateral plate mesoderm

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2
Q

Describe osteogenesis

A

Making of bone. Start out with BMP stim of Runx (then TRAF6) leading to progenitor to diff into osteoprotenitor. Then osterix leads it to differentiate into osteoblast. The ones that get trapped become osteocytes. The ones that don’t differentiation become periosteum and endosteum

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3
Q

periosteum layers

A

Fibrogenic outer layer with BP and sharpens fibres (extension of tissue into bone)
Osteogenic inner

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4
Q

bone formation

A

collagen deposition (steel bars) then ground substance made then seeding where ground substance saturated with Ca and P and precipitate out then mineralization when crystals are tethered to collagen by proteoglycans that give bone strength

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5
Q

Describe osteoclastogenesis

A

MCSF binds to monocyte to make macrophage.
Start out with MCSF stim on osteoblast?? RANKL made by osteoblast, t cells and MSCm chondrocytes too. Binds to RANK on monocyte to turn it into osteoclast

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6
Q

type 11 collagen

A

Type 11 is minor that attaches to type 2

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7
Q

Describe chondrogenesis

A

mesenchyme prolif and condense to prechondrocyte (signal by TGFb and WNT) then mature and hypertrophy to make room for vascular invasion

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8
Q

where do you find hyaline cart

A

respiratory passage, larynx, nose, articular surface of bones, ventral ends of ribs
Transient: skeleton model, epiphyseal growth plate

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9
Q

Sox9 mutation:

A

campomelic dysplasia

controls type 2 coll and aggrecan so autosomal dominant and bad. Bowing and angulation of long bones (sock shape) and Craniofacial abnormality

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10
Q

when does posterior fontanelle close

A

3 mos

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11
Q

intramem ossification

A

Mac to prolif and condense then diff to osteoblast via BMA stim of RUNx2. Vascular invasion via VEGF then form ossification centre
*priosteum is fiber layer where vascular MSC condense
starts in suture lines and periosteum from progenitor cells

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12
Q

endochondral ossification

A

Msc prolif then chondrocytes make type 2 collagen, then FGF and RUNX2 make hypertrophy then VEGF
- MSC to prechondrocyte is TGFb and want
- Prechondrocyte to chondrocyte is sox9 (disorder is campomelic dysplasia)
- Starts from growth plates and end plates from chondrocytes

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13
Q

Vascular growth plate makes what

A

type 1 coll

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14
Q

process of bone width growth

A

Width bone growth: periostea ridge pinches off to form endosteum that grows out by secreting matrix and forming lamella by making type 1 fibres
appositional is where bone resorbed in thick area to add to thin area

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15
Q

What does thyroid hormone do to bone growth

A

DELAYED

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16
Q

activation of bone remodelling

A

activation (recruit osteoclast) to resorption then reversal (osteoclasts die and osteoblast recruited) then formation/mineralization

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17
Q

osteocyte control

A

Cites make OPG and NO to stop osteoclast. Stim osteoclast by making MCSF and RANKL

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18
Q

runx mutation

A

Cleidocranial dystosis
- messed up collarbone, open fontanelle
- teeth

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19
Q

osterix mutation

A

osteogenesis imperfecta

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20
Q

b catenin does what

A

Regulates osteoclastogenesis since controls osteoprotegin and RANKL on osteoblast

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21
Q

TGFb signal

A

tgfb is stored in ECM. Binding turns on canonical and non canonical. Stops osteoblast progenitor and makes osteocyte instead

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22
Q

how does indian hedgehog work

A

Allows osteoblast prolif by increasing Runx2 and sox. Inhibited by PTCH

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23
Q

what does FGF do

A

regulate both endochondral and intramem ossification by control osteoblast prof, diff and APOPTOSIS
turns on Runx

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24
Q

What happens in RANKL mutation?

A

Mutation causes pages disease: bone bending, tooth loss. Too much osteoclast
OPG mutation is juvenile pages where suture problem effects osteoblast diff (OBGYN = baby)

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25
Q

What are proinflammatory factors vs inflammatory and what do they do

A

ROS in age, proinflam induce OC Diff (TNFa, Il1 and Il6) and antiinflam does inhibit of OC (il 4, 10, IFN a and IFN b).

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26
Q

ca release from ER

A

IP3 then ca out then protein kinase c then calmodulin

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27
Q

Which organs/cells have PTH receptors

A

Receptor is PTH1R is mostly on kidney and bone!! Also in growth plate chondrocytes!

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28
Q

which organs have serum ca sensing receptor

A

Serum Ca sensing receptor is GPCR. ON parathyroid and c cells of thyroid. Also in kidney, chondrocytes and osteoblasts

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29
Q

catabolic and anabolic functions of PTH

A

catabolic PTH: high PTH means promote osteolysis using higher RANKL
Anabolic: low PTH is 4 stage: promotes RUNX2 and osx to diff to osteoblast. Sclerotin is the wet inhibitor so decrease it to promote bone formation

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30
Q

Describe calcitonin structure

A

32 AA peptide. No diff if its taken out on ca homeostasis!

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31
Q

Describe the PO4 levels in the body

A

Po4 normal level is 3.0 to 4.5 mg/dl. 87% is diffusible with 35% completed to diff ions and 52% ionized.
13% is non diffusible protein bound. 85-90% is in bone.

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32
Q

progenitor, unipotent, differentiation and specialized cells

A

Progenitor is terminally diff
Unipotent is self renewal Postnatal or adult
Differentiation is specific function
Specialized cells are DIFF NOT DIVIDING

33
Q

DPSC< SHED< SCAP< PDLSC< HODSC

A

DPSC make dentin
SHED is prolif
SCAP is apical. NEURAL
PLSC is PDL and cementum
HODSC is human odontoma. Does dentin and pulp

34
Q

chondrocyte diff factors

A

TGFb, BMP and WaNt control chondrocyte diff

35
Q

which bmp factors are osteoinductive

A

2,4, and 7

36
Q

sphenoid bone origin

A

Wings of sphenoid are neurocranium, while body is mesodermal sclerotome! (Back of head)

37
Q

how does palate form

A

cortical drift? deposition of bone on oral side, resorption on nasal side. Creates the maxillary tuberosity and alveolar process

38
Q

middle mechels cart becomes

A

middle is sphenmand ligament

39
Q

mand vs max growth

A
  • first grows width, length then height through bone remodelling
    max: Down and out sutural growth
40
Q

Median palatine suture

A

is important for transverse growth of maxilla —> expander thing

40
Q

Median palatine suture

A

is important for transverse growth of maxilla —> expander thing

41
Q

p and vit d levels in renal osteodystrophy and osteomalacia

A

Describe renal osteodystrophy
increase serum phosphate, no vit D
Describe tumor induced osteomalacia
phosphate wasting, abnormal vit D meta

42
Q

3 stim of bone formation

A

PTH 1-34 (teriparatide), strontium ranelate: dual action on osteoblast and class, anti-sclerostin (evenity): stim wnt
All are osteoblast stim

43
Q

What are the 5 bone resorption inhibitors

A

Cold BEER
Cathepsin inhibitor, bisphosphonate (ends in -onate), estrogen and estrogen mimic, RANKL antibody (most effective, only 2 injection per year)

44
Q

denosumab

A

limits rank interaction and decrease osteoclast formation

45
Q

Odanacatib

A

cathepsin inhibitor): stop bone matrix degradation
Most strong since stop bone loss and also increase bone formation!

46
Q

where do bisphosphonates inhibit

A

acetyl coa merges with acetyoacetyl coa to make geranyl PP INHIBIT THE FARNESYL DISPHOSPHATE SYNTHASE (SO NO FARNESYL PP)
No cholesterol or isoprenylation (essential to osteoclast)

47
Q

Describe ONJ histologically

A

empty lacunae and ragged border

48
Q

bevacizumab

A

anti VEGF, less blood invasion

49
Q

sunitinib

A

tyros kinase inhibitor

50
Q

radionecrosis pic

A

Cells look less pink, more white

51
Q

Strain

A

deformation and is dimensionless measure of shape change (length and angle)

52
Q

Stiffness

A

measure of how stress and strain. Change in stress required for change in strain
slope of stress strain curve

53
Q

viscoelastic bone property

A

Rate of force applied. Slow rate is more high fracture!!!

54
Q

anisotropic bone quality

A

Direction of load. Cancels is for bending, cortical is for compressive! (Less marrow)
Good for longitudinal force, not transverse

55
Q

aging in bone

A

Increase resistance to torsion but less to compression
Wider marrow hole thing

56
Q

Bone healing

A

need GIRLS CAN PLEASE VERY HORNY GUYS

Growth factors, cytokines, prostaglandins/leukotriens, vascular factors, hormones, GF antagonist

57
Q

fracture steps

A

hematoma, fibrocart callous, bony callous then remodelling

58
Q

Hematoma fracture

A

6-8 hours

59
Q

Fibrocart callous

A

3 wks: hematoma is granulated into pro callous then fibroblast and osteogenic cells invade. Form collagen fibres to connect ends then hondroblast begin to produce fibrocart

60
Q

Bony callous

A

after 3 weeks, lasts 3-4 months. Osteoblasts make woven bone
** callous is internal spongey bone but also external in cart!

61
Q

lamina dura and pdl

A

Lamina dura is opaque and PDL is Lucent

62
Q

odontoma

A

Big radiopacity

63
Q

mucous cyst

A

Easily seen in CT ?? scan due to radiographic contrast

64
Q

Hyperparathyroidism radiograph

A

increased bone resorption
Adenoma tumor can cause primary increase in PTH
Secondary is chronic renal failure so low ca meaning more PTH
More broken bones
Salt and pepper appearance or tumors
Radionuclide diagnosis: #bug

65
Q

Hypothyroidism radiograph

A

missing bones

66
Q

Acromegaly

A

too much growth hormone so big organs/head random parts
gigantism is height overall big

67
Q

pet scan markers

A

Red light thing fluorodeoxyglucose FDG and NAF (bright light) as markers

68
Q

progenitor cell differentiation

A
  • fibrous dysplasia
    gnas, gra, mono or poly,
    MORE in mand and max
  • mas syndrome
  • bendy
    can be cancer
  • lion tarsus ossea
  • bad maturation of bone cells
69
Q

ossification disorder

A

achondroplasia
- bad FGFR disorder
- no cart growth trigent

70
Q

pagets disease

A
  • many factors like runx2 and osx (juvenile)
  • no osteoclast diff, more resorption, weak holy bone
  • higher alp weird pee thick skull
  • whiter jaw bone
71
Q

remodelling bone defect

A

osteopetrosis
- cfos/mos gene
0 brittle bone with less osteoclast
- white skull
- anemia stuff

72
Q

ECM problem

A
  • COL1a gene osteogenesis imperfecta
  • JEEST so joints, eyes, ears, skin, stiff, teeth
  • osterix problem
  • messes up endochondral
  • dentinogenesis imperfecta
  • type 1 collagen
  • 1st is nondeforming and messes up quantity
  • 2-4 is deforming and mess up structure
73
Q

mineralization disorder

A
  • hypophosphatasia
  • less alp so lethal
  • tooth loss, more big pulp chamber
  • no bone mineralization
  • beaten copper frontal bone
74
Q

transverse, linear fracture

A

perp and parallel

75
Q

oblique displaced and non

A

moved by muscle

76
Q

spiral and greenstick

A

spiral is torsion and greenstick is surface

77
Q

comminuted

A

many places fracture

D1 BS1 + II/ FSI + II (12 decks)

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