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Lecture 6

Physiology 4530A/B Lecture 6: Lecture 6

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Western University
Physiology 4530A/B
Frank Beier

Lecture 6: Bones and Endocrinology - Bone as a tissue: when talking about cortical or cancellous bone o Cortical = compact o Cancellous = trabecular/spongy o Composition  Cells: osteocytes, osteoblasts, osteoclasts  ECM: collagen I (organic), hydroxyapatite crystals (inorganic; Ca, PO4), proteoglycans - Bone as an organ: the whole structure of a bone (multiple types of tissue that come together to perform a function) o Tissues in a bone: bone tissue, cartilage tissue, bone marrow, periosteum, fat, endosteum, vasculature, innervation, lymphatics  Periosteum: soft, connective, fibrous tissue lining inside surface of bone  Endosteum: soft, connective tissue lining inside of bone o Function of bone:  1. Mechanical function: support and allow movement (both cortical, cancellous)  2. Ca and PO4 homeostasis: cancellous because it has spaces which increases SAof bone so more of the bone is exposed to nutrients  3. Protection of internal organs: cortical because it’s strong, rigid, continuous Structural Organization ofAdult/Lamellar Bone - Immature bone is called woven bone, which gets replaced/remodeled by lamellar - Haversian canals run longitudinally w blood vessels and nerves inside o Concentric lamellae surround canals o Canal + concentric lamellae = osteon - Circumferential lamellae run all the way around outside of bone - Outside of bone is formed by intramembranous ossification - Inside of bone is formed by endochondral ossification - In 1 sheet of bone, collagen fibres + hydroxyapatite crystals all going in 1 direction, and in adjacent sheet, opposite direction  great resistance/strength Origin, Function, Fate of Bone Cells - Bone marrow is at the top of this diagram - MSCs give rise to osteoblasts (and also adipocytes which end up in marrow) o 3 fates of osteoblasts:  Trapped in matrix and becomes osteocyte  Becomes lining cells (quiescent and flatten out to cover bone surface)  Apoptosis - Osteoid: unmineralized bone matrix that osteoblasts produce and secrete (gets mineralized over time) - Osteocytes communicate w e/o through canaliculi with their long cell processes that meet at gap junctions o They sense mechanical stimulus and communicate it to bone surface  E.g. astronauts lose bone b/c no stimulus  E.g. orthodontics: force pulling tooth forward so on one side osteoclasts resorb bone and other side osteoblasts forming o Fate of osteocyte: bone remodels and osteocytes are replaced - Osteoclasts: precursor is macrophages that fuse together to form multinucleated osteoclasts o Can come from blood vessels or marrow o Resorb bone by secreting acid/proteases  Inorganic CaPO4 component (hydroxyapatite) dissolved by acid  Organic proteins digested by proteases o Fate of osteoclast: apoptose in 2 weeks Growth - We don’t continue to get taller as we age b/c the bone plates fuse so there’s no possibility for longitudinal bone growth - Main factors in driving growth: hormones (esp GH), environmental factors (nutrients, disease), genetics Major Hormones Influencing Skeletal Growth (0-20 years) - GH: stimulates growth plate, increase chondrocyte proliferation and matrix synthesis in long bones o Many indirect effects: stimulates tissue to produce IGF1 which then stimulates cell division/protein synthesis o If too much GH: gigantism; if too little: dwarfism  If too much after age of 20: acromegaly (not taller b/c growth plates fused, but thicker bones, swollen tongue, nose, etc.)  Dwarfism is less common now b/c we can just inject GH -
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