1. Unit XII SKELETAL SYSTEM
Biology Anatomy & Physiology I
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Unit XII SKELETAL SYSTEM
Chapter 6 pp
E. Gorski/E. Lathrop-Davis/S. Kabrhel

2. Gross Anatomy - Membranes
Periosteum (peri = around, osteo = bone)
double-layered membrane:
fibrous - outer layer (dense irregular connective)
osteogenic - abuts the bone; contains osteoblasts (“bone germinators”) and osteoclasts (“bone breakers”)
nerve fibers, lymphatic and blood vessels
provides insertion for tendons and ligaments
Endosteum (endo = within)
delicate connective tissue layer
covers trabeculae of spongy bone in marrow cavities; lines medullary cavity; lines the central (Haversian) canal
contains osteoblasts and osteoclasts

3. Chemical Composition of Bone
Proper combination of organic and inorganic matrix elements gives strength and durability
1. Organic components (~ 35%):
cells: osteblasts, osteoclasts, osteocytes
osteoid (organic component of matrix): consists of proteoglycans, glycoproteins, collagen fibers (all secreted by osteoblasts)
2. Inorganic components (~65%):
hydroxyapatites (mineral salts), largely calcium phosphates
proteoglycans, glycoproteins are modified proteins other than collagen fibers
osteblasts - secrete new bone matrix; result in calcium storage
osteoclasts - dissolve bone matrix; release calcium into blood
osteocytes - mature bone cells

4. Bone Development (Osteogenesis or Ossification)
The skeleton initially made up of :
hyaline cartilage
elastic cartilage
fibrocartilage
Ossification begins in the second month of gestation
Intramembranous:
within fibrous CT (mesenchyme -->bone)
forms flat bones (most cranial bones and clavicles)
Endochondral:
within hyaline cartilage
mesenchyme --> cartilage --> bone
forms most bones

5. Intramembranous Ossification
Steps:
1. Mesenchymal cells at centers of ossification differentiate into osteoblasts
2. Osteoblasts secrete organic bone matrix within membrane:
followed by calcification
trapped osteoblasts mature into osteocytes
calcification (a.k.a. mineralization) = addition of calcium salts to organic framework
Fig. 6.7, p. 181

6. Intramembranous Ossification
3. Blood vessels enter ossified area resulting in formation of spongy bone (red bone marrow inside)
4. Outer layer of bone reorganized into compact bone
remaining fibrous tissue outside ossified tissue becomes periosteum
Fig. 6.7, p. 181

7. Intramembranous Ossification

8. Endochondral Bone Formation
Ossification begins at primary ossification center (in cartilage at middle of shaft for long bone); continues at secondary ossification centers
in short bones - only have primary ossification centers
in irregular bones - have several ossification centers
perichondrium (dense CT membrane around cartilage)
entrance of blood vessels perichondrium at middle of shaft changes nutritional status of cells leading to formation of osteoblasts from osteoprogenetor cells
hypertrophy = get bigger
chondrocytes burst due to lack of nutrients

9. Endochondral Bone Formation
Ossification begins at primary ossification center (in cartilage at middle of shaft for long bone)
Steps (long bone):
1. Formation of bone collar:
blood vessels enter perichondrium at middle of shaft
selected mesenchymal cells (called osteoprogenetor cells) become osteoblasts
osteoblasts secrete bone matrix creating a bone collar
perichondrium (dense CT membrane around cartilage)
entrance of blood vessels perichondrium at middle of shaft changes nutritional status of cells leading to formation of osteoblasts from osteoprogenetor cells
hypertrophy = get bigger
chondrocytes burst due to lack of nutrients

10. Endochondral Bone Formation
2. Secretion of organic matrix causes chondrocytes in shaft to hypertrophy (signals calcification) and these cells eventually burst resulting in cavity
3. Formation of periosteal bud blood vessels, nerve fibers, osteoblasts, osteoclasts enter shaft --> form spongy bone
perichondrium (dense CT membrane around cartilage)
entrance of blood vessels perichondrium at middle of shaft changes nutritional status of cells leading to formation of osteoblasts from osteoprogenetor cells
hypertrophy = get bigger
chondrocytes burst due to lack of nutrients

11. Endochondral Bone Formation
4. Diaphysis elongates as primary ossification center spreads proximally and distally; medullary cavity forms
5. Formation of secondary center(s) of ossification in one (or both) epiphysis around time of birth (like primary but spongy bone remains)
When secondary ossification completed hyaline cartilage remains as:
articular cartilage
epiphyseal plate
Fig. 6.8, p. 182

12. Endochondral Bone Formation

13. Postnatal Bone Growth: 1. Interstitial Growth (length)
cartilage cells in epiphysial plate form tall columns:
zone 1 - growth zone (dividing chondrocytes) (zone of proliferation)
zone 2 - transformation zone (zone of hypertrophy and calcification), closer to shaft, chondrocytes enlarge then die, matrix calcifies

14. Postnatal Bone Growth: 1. Interstitial Growth (length)
zone 3 - osteogenic zone (zone of retrogression and ossification), long spicules of calcified cartilage form at the epiphysis-diaphysis junction and become covered with bone matrix of spongy bone (tips later digested by osteoclasts to enlarge medullary cavity)
at adolescence, chondrocytes divide less often  epiphysial plate becomes thinner -> entirely replaced by bone between age years.

15. 2. Appositional Growth (thickness)
osteoblasts in periosteum secrete bone matrix on external surface of bone
osteoclasts on endosteal surface (diaphysis) remove bone
more built than broken matrix -> bone gets thicker
Fig. 6.10, p. 184

16. Hormonal Regulation of Bone Growth
1. Growth hormone (GH)
active from infancy through childhood
acts on epiphyseal plate to stimulate division of chondrocytes
disorders
gigantism - hypersecretion of GH
dwarfism - hyposecretion of GH or T3/T4
2. Calcitonin - inhibits osteoclast activity
3. Parathyroid hormone - stimulates osteoclast activity
Masculanization - e.g., increase in bone mass
Feminization - e.g., widening of hips

17. Hormonal Regulation of Bone Growth
4. Thyroid hormones (T3 and T4) modulate activity of cells in response to GH to ensure proper proportions of the skeleton
5. Sex hormones (testosterone and estrogens)
active at puberty
initial growth spurt (hormones stimulate osteoblasts)
masculinization or feminization (affects shape of bone)
later, cause epiphyseal plate to close
Masculanization - e.g., increase in bone mass
Feminization - e.g., widening of hips

18. Bone Remodeling
5-7% of bone mass recycled every week (distal femur fully replaced every 5-6 month)
spongy bone replaced every 3-4 years,
compact bone replaced every 10 years
Remodeling occurs at periosteal and endosteal surfaces
Bone deposit - formation of osteoid followed by later mineralization
Bone resorption - osteoclasts secrete lysosomal enzymes that digest the organic matrix and metabolic acids that digest calcium salts (release calcium)
Osteoclasts arise from same hematopoietic stem cells that form macrophages

19. Control of Bone Remodeling
Blood calcium requirement
mg/day (child)
mg/day (young adult)
1. Hormonal control
PTH released when blood calcium level declines
increases osteoclast activity
calcitonin released when blood calcium level rises
inhibits osteoclast activity
promotes osteoblast activity
2. Mechanical stress
heavy usage leads to heavy bones
disuse leads to wasting
Fig. 6.11, p.186

20. Bone Repair Steps (simple fracture):
1. Formation of hematoma - mass of clotted blood forms at the fracture site
2. Formation of fibrocartilaginous callus (soft callus = granulation tissue)
capillaries and phagocytic cells invade hematoma
fibroblasts secrete collagen fibers
osteoblasts begin formation of spongy bone

21. Bone Repair 3. Formation of bony callus (hard callus)
new bone trabeculae appear in fibrocartilaginous callus and gradually convert into hard bone (callus)
4. Remodeling - excess material in bone shaft exterior and within the medullary cavity is removed and hard wall are remade
*Healing time of simple fracture: 6-8 weeks (sometimes as few as 3 weeks)
Fig. 6.13, p. 189

22. Examples of Common Types of Fractures
closed (simple) - completely internal
open (compound) - bone ends penetrate the skin
linear - break parallels the long axis of the bone
transverse - break across the bone long axis
complete - bone is broken through
incomplete (greenstick) - on side of the shaft breaks, the other side bends

23. Bone - Homeostatic Imbalances
1. Dietary Causes: Insufficient calcium, vitamin D, vitamin C:
Osteomalacia - soft bone, inadequate mineralization, pain when weight is applied
Rickets - soft bones in children, bowed legs, deformities of pelvis, skull, and rib cage
Osteoporosis - normal composition; mass decreases

24. Bone - Homeostatic Imbalances
2. Other Known Causes: Estrogen deficiency, insufficient calcium, protein deficiency, abnormal vitamin D receptors, immobility, hyperthyroidism, diabetes:
Osteoporosis - bone resorption outpaces bone deposit
3. Unknown Cause (probably initiated by virus):
Paget’s disease - excessive bone formation and break down leading to weakened bones, irregular thickening, and/or filling of marrow cavities
Osteoporosis - normal composition; mass decreases