histology of developing bone, Part II

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Author:
ghrelin23187
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227422
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histology of developing bone, Part II
Updated:
2013-07-17 15:38:42
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system4
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hormone
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  1. GH function in bone development
    drives chondrocyte proliferation in the epiphyseal plate

    –Stimulates osteoprogenitor cells in the periosteum to proliferate and differentiate into osteoblasts.
  2. Lanron syndrone
    –a rare condition where a genetic abnormality prevents GH from binding to GH receptors. 

    -Lack of cartilage bone from defective liver not producing insulin-like growth factor. Chondrocytes can't proliferate and produce cartilage --> bone can't growth. 

    - Causes dwarfism.
  3. Growth of tumor and heart disease  relies on
    GH
  4. Acromegaly
    GH overproduction post epiphyseal plate closure.  Increase in bone size and/or thickness.
  5. Acromegaly's clinical complain
    hat and ring can't fit on head and finger

    Vision problem
  6. Gigantism
    GH overproduction pre-epiphyseal plate closure.  Increases in bone length, and bone size and/or thickness.
  7. Adenocarcinoma could cause what in skeletal system
    acromegaly and gigantism
  8. Achondroplasia
    • –A point mutation in the FGFR-3 receptor, causes the receptor to be constitutively
    • activated.  This results in a dramatic decrease in chondrocyte proliferation at the epiphyseal
    • plate.

    most common form of dwarfism
  9. most common form of dwarfism
    Achondroplasia
  10. Fibroblast Growth Factor (FGF)
    –Found in a range of tissues across the body ranging from brain to connective tissue.

    • –Used as a signaling molecule to affect wound healing, proliferation of connective
    • tissue and other functions. 

    –Effects of FGF depend on the receptors being expressed.

    • –Chondrocytes in
    • the epiphyseal
    • plate express a particular receptor, known as FGFR-3. 

    –Inhibitor of proliferation and migration.
  11. Fracture healing - step 1
    1st week

    hematoma formation 

    The hematoma will become a blood clot and will be filled with granulation tissue and fibroblasts.

    immune cells is delivered
  12. fracture healing - step 2
    osteoprogenitor --> chondroblast make cartilage 

    and fibroblast make type I collagen 

    together with fibrocartilage forming soft callus
  13. fracture healing - step 3
    turn cartilage matrix into bone matrix 

    removal of hard callus --> complete healing of bone
  14. During the first week post-fracture
    At the site of fracture, ruptured blood vessels will bleed into any gap produced by the fracture and form a hematoma. 

    • The damaged blood vessels will recede from
    • the immediate site of the fracture, and as a result any osteocytes contained in
    • the fractured bone that are now deprived from their vascular supply will
    • die. 

    • The hematoma will become a fibrin
    • clot that allows for the formation of granulation tissue.
  15. Around the beginning of the second week
    post-fracture
    Periosteal osteoprogenitor cells and mesenchymal stem cells will proliferate in the area of the fracture. 

    At the ends of the fracture where the blood vessels have receded, oxygen supply will be at its greatest, and in these areas osteoprogenitor cells will differentiate into osteoblasts, and begin producing new bone (a process resembling intramembranous ossification). 

    • Meanwhile, in the areas where blood supply is low or absent (in the center of the blood clot, for instance) mesenchymal stem cells will differentiate into chondroblasts and begin producing a rudimentary fibrocartilage
    • in roughly the middle of the fracture site. 

    • Osteoclastic activity will begin
    • breaking down the fractured and damaged bone.

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