Osteoporosis
inadequate inorganic matrix in the ECM results in brittle bone.
Risk Factors: dietary factors, female sex, advanced age, lack of exercise, hormonal factors, genetic factors, & diseases of the skin, digestive system, & urinary system
Hormonal factors: lack of protective estrogen in post-menopausal women; (older women w/ loss of estrogen)
Nutritional factor: deficient in calcium ion & Vitamin D
The process of fracture repair:
4 Step:
- Blood clot formation–>hematoma (inflammation increases healing)
- Fibrous network forms a soft callus
- Osteoblasts enter the callus & begin cancellous bone formation
- The bone callus is remodeled & primary bone is replaced with secondary bone
Bone Repair
replacement of primary bone with secondary bone
o Causes: damage
Bone Remodeling
the continual process of bone growth & bone loss that takes place within healthy bone. Gives you mature bone.
Causes: Stress (amount of compression), Tension (stretching force), Pressure (continuous downward force)
Factors: stress, damage, nutrition (Vitamin D, C, K & protein), hormones (PHT & Calcitonin), age
Vitamin D
a steroid synthesized by the body in response to exposure of the skin to UV light; absorbed from the intestines
Calcitonin
produced by the cells of the thyroid gland, located in the anterior neck. Decrease blood calcium ion concentration by stimulating osteoblasts to build bone.
Triggers negative feedback loop when there is an increase in the number of calcium ions. Reduces osteoclast activity and increases osteoblasts activity which means that calcium ions are stored in bone.
High blood calcium–>calcitonin released from thyroid; calcium ions stored in bone
Parathyroid Hormone (PTH)
increases calcium ion level in blood; causes bone resorption
- Increases osteoclasts activity; calcium ions released from bone
- Retained in kidney’s (not “peeped” out)
- Absorbed from gut because helps activate vitamin D
Low blood calcium–>Parathyroid Hormone (PTH) released from parathyroid; calcium ions released from bone
Calcium Homeostasis
important for cardiac muscle & neurons; negative feedback loops maintain homeostasis.
Estrogen
female sex hormone
- Increases rate of longitudinal bone growth
- Inhibits osteoclasts”growth spurt”
- Increase mitosis of cartilage & osteogenesis
- Accelerates closure of epiphyseal plates, more potent effect women are shorter (closes 3-4yrs)
Testosterone
male sex hormone
- Increase appositional growth (thinker bones in males)
- Increase rate of mitosis chondrocytes at the epiphyseal plate–> “growth spurts”
- Accelerates the closure of the epiphyseal plate b/c bone grows slightly faster than cartilage (closes 5-7 yrs)
Thyroid hormone
increases the metabolism of most cells & is important for the effect of GH on the skeleton. Regulates activity of growth hormone
Growth Hormone (GH)
produced by the anterior pituitary, an endocrine gland below the brain. Enhances protein synthesis and cell division. Infancy & childhood
- Increase rate of mitosis, promoting longitudinal growth; make more cartilage
- Increases activity of osteogenic cells including their activity in the zone of ossification; more osteoblasts mean more matrix
- Direct stimulation of osteoblasts in periosteum, triggering appositional growth
When growth is finished, what does the epiphyseal plate become?
The epiphyseal plate becomes an epiphyseal line which is osseous tissue & can no longer grow in length. Adults have “closed” epiphyseal lines so there is NO potential for growth in adults.
Why is a break at the epiphyseal plate of bone is potentially a problem?
Affect how the bone will grow, resulting in crooked or shorter than its opposite limb
Epiphyseal plate growth
Epiphyseal plate growth:
- Chondrocytes replicate & enlarge (more cells make more matrix)
- Cartilage plate grows, increasing bone length
- Cartilage dies & is replaced by bone
- Epiphyseal plate remains same size, while bone grows
* **completed becomes–>Epiphyseal line
* **Cartilage plate doesn’t get bigger during growth b/c rate of which cartilage is made (zone of proliferation) is equal to the rate at which cartilage is replaced by bone (Zone of ossification)
What role do osteoclasts have in endochondral ossification? When the bone is formed, where might cartilage still be found and why it is important?
- Osteoclasts role in endochondral ossification is breaking down the newly formed bone to open the medullary cavity. osteoclasts enlarge medullary cavity.
- Hyaline cartilage would be found at the end of long bones creating a smooth surface in body joints; its important b/c it reduces friction at the joints
- Cartilage would be found between epiphysis and diaphysis called the epiphyseal plate (growth plate)
Differences in Endochondral & Intramembranous Ossification
Intramembranous: forms skull & clavicle (mostly flat bones). Membrane model
Endochondral: from bone below the head; except the clavicles (mostly long bone). Cartilage model
