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MSS > Bones > Flashcards

Bones Flashcards

1
Q

4 functions of bone

A
  1. Provides infrastructure for the body
  2. Contains bone marrow components: erythroid, myeloid, and stem cells
  3. A specialized mineralized ECM connective tissue
  4. Storage of Calcium and Phosphate.
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2
Q

Which cell type is responsible for bone resorption?

A

Osteoclasts

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3
Q

Which hormone induce osteoclast action and which hormone antagonizes osteoclast action?

A

PTH induces osteoclasts for bone resorption;

Calcitonin inhibits osteoclasts for bone resportion

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4
Q

What is two major components of bone?

A

cells and matrix

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5
Q

what are the major cell types within bone?

Where are they located?

A

Osteoclasts; (endosteum)
Osteocytes (within lacunae inside lamellae) in the main bone portion incased in periosteum and endosteum
Osteoblasts; mostly in periosteum; some in endostum

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6
Q

Two components of bone matrix?
What percentage are they?
Specific composition of each of the 2 major components?

A 
Inorganic component (70%): hydroxyapetite (calcium and phosphate) (99%) of body's calcium. 
Organic component/ Osteoid (30%): type 1 collagen (acidophilia), proteoglycans (not a lot), glycoproteins (mostly protein; some surgars)--> promote calcification
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7
Q 
Comparing bone vs Hyaline Cartilage on the following dimensions: 
Mineral
Water
Collagen
Neurovascular structures
A

Hyaline cartilage: no mineral, 75% water, type II collagen, no neurovascular structures

Bone:70% minerals (cal and phosph), 25% water, Type I collagen, has neurovascular structures

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8
Q

Glycoproteins within bone matrix promote what?

What are the major proteins?

A

Glycoproteins promote calcification of bone.

Major proteins are Osteocalcin (ONLY FOUND IN BONE), sialoprotein, osteopontin

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9
Q

What makes bones hard?

A

Hydroxyapetite and Type I collagen.

(for hydroxyapetite presence… need osteocalcin.

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10
Q

Osteoblasts

  • What type of cells are they?
  • What’s their major function?
  • They’re under control of which factors?
  • Which two gene products are specific to osteoblasts?
A

Osteoblasts are fibroblasts.
Their major function is to SYNTHESIZE the bone ECM
They’re under control of BMPs.
Two gene products: Cbfa-1 which is the “master gene” for bone development in embryos (knockouts have cartilaginous bones).
Osteocalcin is the other osteoblast specific product

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11
Q

What is Osteoid?
What is it synthesized by?
Where does it deposit?

A

The organic component of bone matrix (type I collagen, proteolycans; glycoproteins)
Synthesized by osteoblasts; deposited where hydroxyapetite is.

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12
Q

Clinical Significance of Tetracycline in bones?

A

Tetracycline intercalates into ECM of bones–> autofluorescence–> can monitor apposition growth.

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13
Q

Osteomalacia

What’s the defect?

A

Calcification is impaired

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14
Q

Osteitis Fibrosa Cystica

What’s the defect?

A

rapid osteoclast destruction of bone matrix as it is made.

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15
Q 
Osteocytes
Main function
Half life
Structure in bone
What is different about osteocytes vs chondrocytes in terms of structure
A

Main function is to MAINTAIN the bone ECM

  • T1/2=25 years
  • Single osteocytes occupy single lacunae, which are embedded in lamellae, Cytoplasmic processes protrude from the lacunae via “canaliculi” to allow osteocytes to touch and form gap junctions for neurishment.
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16
Q 
Osteoclasts
Main function
Cell origin/cell morphology
where do they reside?
What activates it? What inhibits it?
A

to breakdown and remodel bone ECM

  • they are fused macrophages
  • They are polarized cells with with one ruffled border that attaches to and degrades bone minerals.
  • They reside in “Howship’s lacunae”
  • Activated by PTH; inactivated by calcitonin
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17
Q

Type I collagen

Acidophilic or basophilic?

A

Acidophilic

18
Q

Bone formation process is completed by

A

after osteoblasts make osteoid (type I collagen, proteoglycans, glycoproteins)… Osteocalcin mediates calcium deposition into osteoid… allowing for weight bearing.

19
Q

How does PTH affect bone?

What’s the mechanism? Specific

A

PTH activates osteoclasts to release LYSOSOMES–>Cathepsin-K–> release in to the microenvironment…
Acid–> released into microenvironment

20
Q

Paget’s Disease

  • patient population
  • mechanism
  • what cell type is affected? what’s the morphology of the cells?
A

affects adults over 40
abnl osteoclasts –> high remodeling rate… leading to an over abundance of weak immature bone “Primary/woven bone”;
largely increased number of nuclei (normally 7 nuclei per osteoclast)

21
Q

Osteoporosis (general)

  • patient population
  • How to prevent
  • How to screen
  • Therapeutic targets (theoretical)
A

Overactive osteoclasts

  • ->hollow fragile bones
  • post menopausal women (via 2% bone loss per year)
  • prevention with Calcium and Vitamin D supplement +weight bearing exercises
  • Screening of (bone mineral density) BMD (g/cm^2)
    • compare BMD to young subjects every 2-5 years
  • therapeutic targets: iincrease osteoblasts and decrease osteoclasts
22
Q

Two general parts of a piece of bone? upon cross section

Upon microscopic analysis what is different?

A

Cortical/Compact bone (dense; no cavitation)
Spongy/ Trabecular/cancellous bone (has cavitation)
-Nothing is different microscopically.

23
Q

Flat bones

Example; structure

A

calvaria bones; compact bone surrounding a “diploe” of spongy bone

24
Q

Long bone
Example;
Structure

A

femur;

diaphysis, metaphysis, and epiphysis

25
Q

What is an osteon
What is all within an osteon?
What is in the inner most lamella?

A

an osteon is a concentric tube of lamellae
Within an osteon there’s layers of lamellae; 1 osteocyte resides in each lacunae;
In the inner most lamella there’s the haversian canal, which holds blood vessels, nerves, and lymph

26
Q

What are two types of canals within bone? which one is horizontal and which one is vertical?
What is within these?

A

Haversian canal: vertical
Volkmann’s canal: horizontal
contents: artery, vein, lymph vessels, and nerves

27
Q

What is immature bone called? (2 names)
What is mature bone called? (2 names)

What is the distinction?

A
  • primary bone or woven bone
  • lamellar bone or secondary bone

Difference is immature bone do not have lamellae

28
Q

Two ways of bone development

A
  1. Intramembranous: Osteoblasts deoposit osteoid onto mesoderm
  2. endochondral: osteoblasts deposit osteoid onto cartilage (long bones in embryo and s/p fx)
29
Q

Endochondral bone development

-diaphysis and epiphysis what’s different?

A

bone forms on hyaline cartilage

  • at diaphysis: osteoblasts invade calcified catilage and secret osteoid
    - THIS IS CALLED OSSIFICATION
  • at the epiphysis: same process but leaves articular cartilage and epiphyseal growth plate.
30
Q

Hormonal stimulation process for long bone growth

A

Sex steroid hormones–> pituitary stimulation–> release of GH AKA somatotropin–> liver–>somatomedin (IGF1)–> epiphyseal plate stimulated in the “zone of proliferation”

31
Q

4 zones of the epiphyseal growth plate

A

Zone of proliferation: proliferation upon IGF1 (somatomedin) stimulation

Zone of Hypertrophy: 20% of fractures occure here because it’s relatively hollow in nature

Zone of calcification: basophilic–occupied by calcified cartilage with abundant (TYPE X cartillage)

Zone of Ossification: eosinophilic: deposition of type I collage by osteoblasts

32
Q

Process of fracture repair

A
  1. Macrophages remove debris
  2. Chondroblasts secrete callus (hyaline catillage)
  3. Osteoblasts replace hyaline cartillage with “bony callus”…primary bone
  4. primary bone is replaced by secondary bone
33
Q

Methods of Bone Tissue Engineering in cases that need “grafting of bone”

A

GF: such as BMP 2 and BMP 7
Stem cells: mesenchymal stem cells (MSC) will mature in to osteoblasts

one or both of the above are implanted onto biodegradable matrix made from type 1 collagen.

34
Q

Osteopetrosis

A

dense heavy bone; osteoclasts lack ruffled borders…so cannot degrade bones

35
Q

Osteoclast activity regulated by Bone stromal cells

-How does it work?

A

Bone stromal cells produce:
M-CSF, RANKL, and OPG (osteoprotegerin)
which act on macrophages that induce or inhibit action of osteoclasts

36
Q

M-CSF-where is it from, what does it do

A

From stromal cells
macrophage colony stimulating factor
Induces macrophage proliferation

37
Q

RANK L: receptor for activator of nuclear factor kB ligand

where is it from what does it do?

A

from stromal cells

induces macrophage differentiation to osteoclasts

38
Q

OPG/ Osteoprotegerin
where is it from?
what does it do?

A

from stromal cells of bone

antagonizes RANK L receptors, so that macrophages cannot differentiate into osteoclasts.

39
Q

Alpha5beta3
What is it?
What does it do?
what if it’s not present?

A

It attaches osteoclasts to bone

if blocked…then osteoclasts cannot bind and degrade bome.

40
Q

Osteoblasts Vs Osteoclasts

Inducers, inhibitors

A

Osteoblasts:
Induced by BMP
Inhibited by leptin
Spikes in concentration of PTH levels

Osteoclasts:
Induced by RANK L
Inhibited by Calcitonin, and osteoprotegerin
constant PTH levels

41
Q

Osteoporosis

Two therapeutic drug types?

A

Anabolic drugs (proosteoblasts)
-PTH 1-34 “Teriparatide”: to mimic spikes in PTH
When T score is less than -2.5 in BMD antiresorptive drugs will not work… so this is drug of choice…

Antiresorption drugs (antiosteoclasts)

  • SERMs (selective estrogen receptor modulars): raloxifene
  • Bisphosphonates: Iabndronate (boniva)
  • Calcitonin

Other methods:

  • OPG
  • anti alpha5beta3
  • CBFA-1 (anabolic)

MSS (7 decks)

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