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MSK > Bone Physiology > Flashcards

Bone Physiology Flashcards

1
Q
A
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2
Q

[…] bone gives supporting strength to the ends of weight-bearing bones

A

Trabecular

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3
Q
A
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4
Q

Bone mass is influenced by peak applied […] in response to […]

A

Strain

Load

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5
Q

What are the implications for exercise as it relates to bone health?

A

People who exercise are perfectly modeling their bones to resist the compressive and tensile forces of the exercises that they are performing

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6
Q

What is the mechanical sensing cell of bone?

A

Osteocyte

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7
Q
A

Sesamoid fibrocartilage has high level of proteoglycans that hold onto water to be stronger in compression

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8
Q

What are the 4 major categories of bone (hint: NOT talking about cortical, trabecular, woven)?

A

Long bones (femur, humerus, etc.)

Short bones (wrist and ankle)

Flat bones (ribs, cranial bones, etc)

Irregular bones (vertebrae)

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9
Q

Osteocytes arise from osteoblasts and osteoblasts arise from mesenchymal stem cells in the bone marrow. These stem cells can differentiate into other types of cells also. What are these other types?

A

Adipocytes

Fibroblasts

Chondrocytes

Muscle cells

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10
Q

Intramembranous bone formation results when mesenchymal stem cells differentiate […] into […] and secrete […] resulting in intramembranous ossification.

A

Directly

Osteoblasts

Type 1 collagen

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11
Q

Endochondral bone formation results when mesenchymal stem cells differentiate into […] and secrete […]. These cells then undergo […] and are replaced with […] which secrete […] and result in endochondral ossification.

A

Chondrocytes

Type 2 collagen

Apoptosis

Osteoblasts

Type 1 collagen

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12
Q

What bones in the body are formed by intramembranous ossification?

A
  • Calvaria of skull
  • Mandible
  • Maxilla
  • Lateral end of clavicle
  • Sub-periosteal bone layer of long bones
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13
Q

Do compact and trabecular bone structures form in the same manner as intramembranous or endochondral ossification?

A

Intramembranous

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14
Q

What effect does Wnt signaling have on bone formation?

A

When Wnt binds to its receptor (frizzled), it prevents the degradation of Beta catenin by trapping APC and kinases that trigger degradation at the receptor. Beta catenin then travels into nucleus and activates transcription of Runx2 gene, which promotes differentiation of mesenchymal stem cells into osteoblasts.

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15
Q

What effect does the absence of Wnt signaling have on bone formation?

A

When Wnt is not present, there is no binding to frizzled, APC is able to bind to beta catenin and complex with kinases which phosphorylated beta catenin and lead to its degrdation. This prevents transcription of the Runx2 gene and instead allows transcription of the SOX-9 gene, which promotes differentiation of mesenchymal stem cells into chondrocytes.

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16
Q

The figure below shows the process of endochondral bone formation. Describe this process and fill in the missing information.

A
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17
Q

What is VEGF and MMP?

A

Collagenases

18
Q

Would levels of Wnt/Beta Catenin be low or high during intramembranous ossification?

A

High

19
Q

What is cleidocranial dysplasia?

A

An genetic disease caused by autosomal dominant loss of function mutation in Runx2. Results in decreased bone formation, specifically affecting bones that form via intramembranous ossification (clavicles, cranial bones).

20
Q
A
21
Q

[…] is the major mitogen that stimulates chondrocyte proliferation.

A

IGF-1

22
Q

The figure shows what is occurring at the growth plate, which is the means by which bones grow in length. What changes are occurring in each of the zones of the growth plate?

A
23
Q

[…] stimulates growth plate closure at the end of long bone growth.

A

Estrogen

24
Q

Testosterone is converted to estrogen by what enzyme?

A

Aromatase (CYP 19 A1)

25
Q

What phenotype would you predict with a loss of function mutation of CYP 19 A1 on the growth plate and long bone growth?

A

Short stature - premature closure of GP

26
Q

Rickets is a disease of the […]

A

Growth plate

27
Q

What is rickets?

A

A softening and widening of the growth plate due to insufficient vitamin D. This is ONLY a disease in children, b/c adults don’t have growth plates anymore. Insufficient vitamin D leads to insufficient calcium, so the body is unable to calcify the skeleton properly. This results in expansion of late hypertrophic chondrocytes because they are unable to undergo apoptosis due to lack of mineral present (involved in signaling that leads to apoptosis).

28
Q

What prediction would you make regarding the growth plate phenotype with rickets?

A

The bones would be shorter b/c there is an accumulation of hypertrophic chondrocytes that won’t undergo apoptosis. GP chondrocytes MUST undergo apoptosis for mineralization to occur.

29
Q

Phosphate stimulates the expression of […], which is an important molecule in the apoptosis of hypertrophic chondrocytes.

A

Caspase 3

30
Q

What causes osteomalacia?

A

Either insufficient calcium or insufficient phosphate

31
Q

FGF23 inhibits the […] of growth plate chondrocytes. As such, it is a physiological antagonist of […]

A

Proliferation

IGF-1

32
Q
A
33
Q

Individuals with achondroplasia have an […] mutation of […]

A

Activating

FGF23

34
Q

What does the term bone remodeling mean?

A

The coupled process whereby bone is replaced by the sequential action of osteoclasts and osteoblasts to maintain the mechanical strength of bone.

35
Q

What cell makes PTHrP?

A

Osteoblast

36
Q

What is this figure showing?

A

An osteoclast.

The osteoclast recognizes the surface via integrin receptors. It then secretes chloride ion into the bone below. Binding also promotes trafficking of lysosomes with collagenases and cathepsins to secrete their contents into the bone below. The osteoclast also generates acid via carbonic anhydrase to degrade the mineral and proteins in bone. These are all the components of the “resorption pit” that osteoclasts make to resorb bone.

37
Q

What is the function of osteocyte’s cannaliculi?

A

To communicate with eachother and the surface of the bone

38
Q

Osteocytes respond to mechanical stimuli through […] to send signals for […] and […].

A

Gap junctions

Formation

Resorption

39
Q

How are mechanical signals sensed by osteocytes translated into changes in bone remodeling?

A

By altering levels sclerostin, which is exclusively expressed by the osteocyte

40
Q

What is the function of sclerostin?

A

Sclerositin inhibits Wnt signaling when present, thus inhibiting bone formation

41
Q

Loss of function mutations in the SOST gene results in […] bone mass

A

Increased

42
Q

What is Van Buchem disease?

A

A loss of function mutation in the SOST gene that results in loss of sclerostin and increased bone mass. Patients are tall, show facial asymmetry and have syndactyly

MSK (38 decks)

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