Physiology of Bone - Brownell Flashcards

1
Q

What are some of the functions of bone?

A
  • Protection
  • shape–>social identification
  • movement
  • sensory processing (ear)
  • hemopoesis (blood cell and platelet production)
  • mineral storage
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2
Q

What is the difference in density and turnover in compact vs. trabecular bone?

A

compact: high density, low turnover
trabecular: low density, high turnover

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3
Q

What are osteoblasts derived from and what is their function?

A

derived from stromal (bone marrow) stem cells

  • secrete osteoid (collagen fibers + glycoproteins + hydroxyapotite)–> build new bone
  • control osteoclastogenesis through releasing RANK-L and OPG upon sensation of mechanical stress of bone–> stimulate osteocytes to make new bone (can be affected by emotion and SNS
  • OPG blocks osteoclast differentiation

(only 15% differentiate into osteocytes and the rest undergo apoptosis)

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4
Q

What are osteocytes derived from and what is their function?

A

mature osteoblasts, make up > 90% of bone cells

  • Embedded in mineralized bone matrix
  • Intracellular communication via canaliculi
  • Load sensing, molecular mechanism unknown
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5
Q

What are osteoclasts derived from and what is their function?

A
  • Derived from hemopoietic stem cells in the bone marrow (not osteoblasts!)
  • Resorb bone
  • Multinucleate
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6
Q

What are the important regulators of osteoblast/osteoclast interactions? (3)

A
  • RANKL: receptor activator from osteoblasts acting to excite osteoclast activity
  • OPG: inhibits RANKL actions
  • DKK: a WNT antagonist that blocks osteoblast proliferation
  • feedback interaction*

RANKL and OPG are secreted by osteoblasts and develop the relationship between osteoblasts and osteoclasts

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7
Q

How is prostate cancer related to osteoblast cells?

A

+ feedback loop between prostate cancer and osteoblasts

Cancerous cells release factors that destabilize (commonly promote) osteoblast proliferation and activity

osteoblast growth factors can also stimulate prostate cell proliferation

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8
Q

What do osteoclast growth factors cause during bone remodeling?

A

osteoblast differentiation

osteoclast apoptosis

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9
Q

What are the functions of PTH and Calcitonin? What is the [Ca2+] in the extracellular fluid?

A

PTH: mobilization of Ca2+ from the bone into circulation

Calcitonin: moves Ca2+ from circulation into the formation of new bone

2.5 mmol Ca2+ in the ECF

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10
Q

What do PTH and Vitamin D doto plasma [Ca2+]?

A

increase it!

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11
Q

What 2 things are essential for the formation of Vitamin D?

A

kidney and PTH

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12
Q

How do FSH and Estrogen regulate osteoclast activity?

A

FSH stimulates osteoclast resorption activity

Estrogen blocks pre-osteoclast formation (by blocking FSH)–> when estrogen levels are low, preosteoclasts can become osteoclasts and break down bone.

estrogen also induces OPG which causes osteoclast apoptosis and promotes one formation

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13
Q

What effects does PTH have on bone remodeling? (3)

A

Increases extracellular [Ca2+] by…

  • Increasing Ca2+ reabsorption in kidneys
  • Activation of vitamin D3 in kidneys
  • Promoting activation of osteoclasts
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14
Q

What effects does Vitamin D3 have on bone remodeling?

A
  • Increases dietary Ca2+ absorption

- Requires PTH, UV light for biosynthesis

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15
Q

What is Achondroplasia?

A

Dwarfism

FGF R3 is hyperactive –> inhibit chondrocytes and elongates endochondral bone but NOT membranous bone (skull, face-> normal size head)

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16
Q

What is osteoporosis? What are the 2 types? What causes it?

A

Normal ossification/mineralization but less dense bone => compression fracture of weight-bearing bone, acute pain, loss of height, kyphosis (back curvature).

Type 1: postmenopausal women (decrease in estrogen leads to increase FSH levels–> stimulate osteoclasts)
Type 2: senile men/women.

Decreased estrogen => increased RANK ligand from osteoblasts=> +RANK receptors on osteoclasts=> bone desorption.

Treatments (e.g., bisphosphonates => inhibit osteoclasts)

17
Q

What is osteopetrosis?

A

thick, dense bone from bone building but not breaking down –> can cut off circulation and make bone easier to break

18
Q

What is Osteomalacia?

A

Rickets

normal bone mass but defective bone mineralization due to
vitamin D deficiency.

bone fragility, chronic pain, mm weakness

increase PTH and decreased serum phosphate

19
Q

What is Paget’s Disease?

A

accelerated bone formation & degradation due to high alkaline phosphatase

20
Q

What will the Ca2+, phosphate, alkaline phosphatase and PTH levels look like in Osteomalacia (rickets)?

A

Ca2+=decreased
phosphate=decreased
PTH =elevated

alkaline phosphatase=variable

soft bones

21
Q

What will the Ca2+, phosphate, alkaline phosphatase and PTH levels look like in Osteopetrosis?

A

phosphatase=elevated

Ca2+=unaffected
phosphate=unaffected
alkaline
PTH =unaffected

thick dense bone

22
Q

What will the Ca2+, phosphate, alkaline phosphatase and PTH levels look like in Osteoporosis?

A

Ca2+=unaffected
phosphate=unaffected
alkaline phosphatase=variable
PTH =unaffected

decreased bone mass

23
Q

What will the Ca2+, phosphate, alkaline phosphatase and PTH levels look like in Pager’s disease?

A

Ca2+=unaffected
phosphate=unaffected
alkaline phosphatase=variable
PTH =unaffected