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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
What are proinflammatory factors vs inflammatory and what do they do
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).
26
ca release from ER
IP3 then ca out then protein kinase c then calmodulin
27
Which organs/cells have PTH receptors
Receptor is PTH1R is mostly on kidney and bone!! Also in growth plate chondrocytes!
28
which organs have serum ca sensing receptor
Serum Ca sensing receptor is GPCR. ON parathyroid and c cells of thyroid. Also in kidney, chondrocytes and osteoblasts
29
catabolic and anabolic functions of PTH
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
30
Describe calcitonin structure
32 AA peptide. No diff if its taken out on ca homeostasis!
31
Describe the PO4 levels in the body
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.
32
progenitor, unipotent, differentiation and specialized cells
Progenitor is terminally diff Unipotent is self renewal Postnatal or adult Differentiation is specific function Specialized cells are DIFF NOT DIVIDING
33
DPSC< SHED< SCAP< PDLSC< HODSC
DPSC make dentin SHED is prolif SCAP is apical. NEURAL PLSC is PDL and cementum HODSC is human odontoma. Does dentin and pulp
34
chondrocyte diff factors
TGFb, BMP and WaNt control chondrocyte diff
35
which bmp factors are osteoinductive
2,4, and 7
36
sphenoid bone origin
Wings of sphenoid are neurocranium, while body is mesodermal sclerotome! (Back of head)
37
how does palate form
cortical drift? deposition of bone on oral side, resorption on nasal side. Creates the maxillary tuberosity and alveolar process
38
middle mechels cart becomes
middle is sphenmand ligament
39
mand vs max growth
- first grows width, length then height through bone remodelling max: Down and out sutural growth
40
Median palatine suture
is important for transverse growth of maxilla —> expander thing
40
Median palatine suture
is important for transverse growth of maxilla —> expander thing
41
p and vit d levels in renal osteodystrophy and osteomalacia
Describe renal osteodystrophy increase serum phosphate, no vit D Describe tumor induced osteomalacia phosphate wasting, abnormal vit D meta
42
3 stim of bone formation
PTH 1-34 (teriparatide), strontium ranelate: dual action on osteoblast and class, anti-sclerostin (evenity): stim wnt All are osteoblast stim
43
What are the 5 bone resorption inhibitors
Cold BEER Cathepsin inhibitor, bisphosphonate (ends in -onate), estrogen and estrogen mimic, RANKL antibody (most effective, only 2 injection per year)
44
denosumab
limits rank interaction and decrease osteoclast formation
45
Odanacatib
cathepsin inhibitor): stop bone matrix degradation Most strong since stop bone loss and also increase bone formation!
46
where do bisphosphonates inhibit
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
Describe ONJ histologically
empty lacunae and ragged border
48
bevacizumab
anti VEGF, less blood invasion
49
sunitinib
tyros kinase inhibitor
50
radionecrosis pic
Cells look less pink, more white
51
Strain
deformation and is dimensionless measure of shape change (length and angle)
52
Stiffness
measure of how stress and strain. Change in stress required for change in strain slope of stress strain curve
53
viscoelastic bone property
Rate of force applied. Slow rate is more high fracture!!!
54
anisotropic bone quality
Direction of load. Cancels is for bending, cortical is for compressive! (Less marrow) Good for longitudinal force, not transverse
55
aging in bone
Increase resistance to torsion but less to compression Wider marrow hole thing
56
Bone healing
need GIRLS CAN PLEASE VERY HORNY GUYS Growth factors, cytokines, prostaglandins/leukotriens, vascular factors, hormones, GF antagonist
57
fracture steps
hematoma, fibrocart callous, bony callous then remodelling
58
Hematoma fracture
6-8 hours
59
Fibrocart callous
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
Bony callous
after 3 weeks, lasts 3-4 months. Osteoblasts make woven bone ** callous is internal spongey bone but also external in cart!
61
lamina dura and pdl
Lamina dura is opaque and PDL is Lucent
62
odontoma
Big radiopacity
63
mucous cyst
Easily seen in CT ?? scan due to radiographic contrast
64
Hyperparathyroidism radiograph
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
Hypothyroidism radiograph
missing bones
66
Acromegaly
too much growth hormone so big organs/head random parts gigantism is height overall big
67
pet scan markers
Red light thing fluorodeoxyglucose FDG and NAF (bright light) as markers
68
progenitor cell differentiation
- 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
ossification disorder
achondroplasia - bad FGFR disorder - no cart growth trigent
70
pagets disease
- 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
remodelling bone defect
osteopetrosis - cfos/mos gene 0 brittle bone with less osteoclast - white skull - anemia stuff
72
ECM problem
- 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
mineralization disorder
- hypophosphatasia - less alp so lethal - tooth loss, more big pulp chamber - no bone mineralization - beaten copper frontal bone
74
transverse, linear fracture
perp and parallel
75
oblique displaced and non
moved by muscle
76
spiral and greenstick
spiral is torsion and greenstick is surface
77
comminuted
many places fracture

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

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