bone bio lecture Flashcards

1
Q

what are the stages of intramembranous ossification

A
  1. mesenchymal cells aggregate without a cartilage intermediate.controlled by patterning signals from polypeptides like Wnt and transforming growth factor beta (TGFbeta)
  2. mesenchymal cells differentiate into osteoblasts. A BONE BLASTEMA is formed. osteocytes within the core of the blastema are interconnected by cell processes - forming a functional SYNCTIUM. osteoblasts line the surface of the bone blastema.
  3. bone matrix is deposited by osteoblasts (osteoid). Later, calcium transported from blood is used to mineralize – and primary bone tissue is formed. osteoclasts initiate the remodeling of the bone
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2
Q

what kind of bone growth is intramembranous ossification?

A

It starts as interstitial, however it becomes appositional quickly. at the surface of the osteoid, osteoblasts continue appositional deposit (type I collagen mostly)

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3
Q

what is a functional synctium

A

interconnected osteocytes in the bone blastema during intramembranous ossification

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4
Q

what are the stages of endochondral ossification?

A
  1. cartilage model is made
    (((2. mesenchyme cells in periochondrium become osteoblasts and make bone (matrix, osteoid?) on the outside of the cartilage )))- bone collar is formed around the shaft
  2. cartilage hypertrophies and the matrix begins to calcify in the center
  3. a nutrient artery invades and brings in osteo-precursors (osteoblasts) towards the center and forms a primary ossification center
  4. calcified cartilage is replaced by bone

— bone development extends towards epiphysis from primary ossification center and this same process of primary ossification occurs in epiphysis- as secondary ossification centers (not complete till puberty)

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5
Q

descripe the zones of bone growth

A
  • resting zone: reserve of chondrocytes
  • proliferating zone: chondrocytes proliferate and orient into columns
  • maturation zone: chondrocytes enlarge and calcify the matrix
  • hypertrophic zone: chondrocytes complete mineralization of matrix and undergo apoptosis
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6
Q

what is a basic multicellular unit

A

team of cells that resorb and recreate bone

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7
Q

describe a Basic multicellular unit (BMU)

A
  • osteoclasts cut a tunnel in the cutting zone (first part)
  • osteoblasts are introduced in the reversal zone from capillaries next.
  • then the closing cone, successive lamellae reconstruct a new osteon in the closing cone.
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8
Q

what is gigantism in adults called

A

acromegaly

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9
Q

what are stromal marrow cells

A

AKA mesenchyme cells

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10
Q

describe the hormone process by which bone growth is triggered

A

insulin like growth factor (IGF1) is made by the liver in response to growth hormone.
-igf1 binding its receptor facilitates skeletal actions of hormones like parathyroid hormone. Vitamin D is important too, affects osteoblast proliferation and mineralization.

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11
Q

what do osteoblasts release

A

stuff for bone matrix or osteoid , basically uncalcified bone. it also releases alkaline phosphatase which promotes alkalinity environment that helps to build bone

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12
Q

which hormones induce bone growth?

A

growth factor activates insulin like growth factor (IGF1) which activates parathyroid hormone
-vitamin D also affects osteoblast proliferation and mineralization

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13
Q

describe detailed process of osteoclasts resorbing bone and their recruitment

A

-BMU is activated by mechanical forces, hormones (parathyroid hormone) and cytokines like M-CSF.
-osteoclasts are recruited and attach to bone via PODOSOMES which are actin based. structures.
btw bone deposition occurs in conjunction

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14
Q

what is the area of resorbed bone between osteoclasts and bone?

A

howship’s lacuna

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15
Q

descripe process of osteoclastogenesis

A

Osteoclastogenesis- dependent on two cytokines which are produced by osteoblasts : receptor activator of nuclear factor-kB (RANKL) and monocyte colony stimulation factor (M-CSF)

  • M-CSF controls proliferation of osteoclast precursors and RANKL controls osteoclast differentiation by activating RANK on osteoclast precursors.
  • Osteoblast also secretes osteoprotegerin (OPG) which binds RANKL (better than it does RANK)
  • Binding OPG to RANKL prevents osteoclast precursor differentiation into osteoclasts. Thus the osteoblast via OPG , regulates the population of functional osteoclasts. Parathyroid hormone increases RANKL expression on osteoblasts, and blocks the synthesis of OPG.
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16
Q

how do osteoclasts breakdown bone

A

It starts with demineralization. osteoclast does this by acidifying the howship’s lacuna. The osteoclast forms carbonic acid from CO2 and water. Carbonic acid dissociates to bicarbonate and a proton. protons are transported across the cell membrane into the lacuna and loewer the pH to 4-5. Bone apatite is degraded. After digestion f the mineral, the organic matrix is exposed and is degraded by lysoosmal proteases ssuch as cathepsin K and metalloproteinases secreted by the osteoclast.

17
Q

what is estrogens impact on bone

A

it has a bone protective effect by inhibiting osteoblast RANKL production. it also stimulates osteoblasts to produce OPG which bings RANKL and prevents osteoclast differentiation. Estrogen deficiency with menopause is associated with bone loss and increased risk of fracture.

18
Q

what are some drugs used for osteoporosis

A

drugs inlcuding bisphosphonates and monoclonal antibodies that inhibit osteoclasts are used to treat osteoporosis and other things.

  • alendronate (fosamax)
  • risedronate (actonel, atelvia)
  • zoledronic acid (reclast, zometa)
  • denosumab (prolia)
19
Q

what jaw related disorder can biphosphonate therapy cause

A

biphosphonate related osteonecrosis of the jaw. caused by trauma to dentoalveolar structures that have a limited capcity for bone healing due to effects of biphosphonate therapy.