- Mesenchyme condenses into a membrane permeated with blood vessels, which gives rise to bone
- Bones of skull, and clavicles form this way
intramembranous ossification
- Mesenchyme gives rise to cartilage, which is replaced by bone
- Most bones form this way - limb bones, hip bones, vertebrae, sternum, and scapulae
endochondral ossification
Describe the steps involved in intramembranous ossification
- Begins between week 8 and 12 of development
- Mesenchymal cells surround the blood vessels and differentiate into osteoblasts
- Osteoblasts begin secreting a precursor to bone matrix called osteoid (contains collagen but no calcium phosphate)
- Osteoid begins calcifying and the osteoblasts become trapped, differentiating into osteocytes
- Mesenchyme forms periosteum around bone tissue
- Spongy bone forms in the middle
- Osteoblasts of periosteum lay down compact bone
- Process continues until a typical flat bone structure is obtained. Spongy bone sandwiched between compact. Red marrow present.
Describe the steps involved in endochondral ossification
- Process starts around week 6 of development
Initial skeleton is hyaline cartilage, and is formed during embryonic development - Cartilage then ossifies, completed at around age 20 for some bones
- Cartilaginous skeleton develops from mesenchyme
- Mesenchymal cells differentiate into chondroblasts which make cartilage to be used as a model for bone formation. Covered with perichondrium
- Cartilage begins to calcify. Chondrocytes at center of cartilage enlarge and begin to die. Matrix becomes porous and begins to ossify. Perichondrium becomes periosteum.
- Osteoblasts in newly formed periosteum form “bone collar” around cartilage model
- Epiphyses fill in with spongy bone during infancy and childhood
- Only remaining cartilage in bones are epiphyseal plates and articular cartilages
- Plates continue to grow new cartilage, which continues to ossify
- Damage to epiphyseal plate can stunt growth in that limb
- Sex hormone decline shuts off cartilage growth. At around age 20, growth plates completely ossified. Dense form of spongy bone (called epiphyseal lines) remains.
Blood and lymphatic vessels, nerves, along with blood and bone cells invade the center of calcified cartilage. Bone cells come in from the blood and infiltrate area
periosteal bud
The point where we start the ossification from the inside out. Osteoclasts eventually hollow out the shaft to form the medullary cavity.
primary ossification center
Form in the epiphyses of long bones. Calcified cartilage begins closer to diaphysis.
secondary ossification center
Define interstitial growth. What age does interstitial growth typically occur until?
Growth in the length of a bone (bone elongation). Early in life, rate of cartilage growth and ossification are equal. When sex hormones decline, cartilage growth slows and ossification speeds up. Up to the point where the epiphyseal plates seal up, ossify, and become epiphyseal lines.
5 zones of epiphyseal plate
- Zone of resting cartilage
- Zone of proliferation
- Zone of hypertrophy
- Zone of calcification
- Zone of ossification
cartilage cells aren’t doing anything, maintaining cartilage matrix but are not replicating
zone of resting cartilage
Chondrocytes divide to produce new cells, active mitosis. Pushes resting zone cartilage away from diaphysis.
zone of proliferation
cells enlarge and die, which leave it susceptible to calcification.
zone of hypertrophy
cartilage matrix on diaphysis side calcifies first, and then ossifies
zone of calcification
closest to diaphysis, marrow cavity is distal to this
zone of ossification
Thickening and widening of bones, changing the girth of bones. Technically a type of intramembranous ossification. Will continue to occur throughout adulthood.
appositional growth
Describe the process of appositional growth
Osteogenic cells of periosteum differentiate into osteoblasts, osteoblasts get trapped in lacunae and mature into osteocytes, osteoclasts of endosteum widen medullary cavity so that bone remains lightweight but still strong
-The architecture of bone is directly related to the stresses(or there lack of) bone is exposed to.
-Stress such as exercise releases small electrical pulses that attract osteoblasts.
-Lack of stress reduces osteoblast activity and increases activity of osteoclasts. (midshaft of the femur/diaphysis would be thickest)
Wolff’s Law
Why is it that the bones of infants are relatively smooth and free of bone markings?
They have yet to put their bones under a lot of stress. As they progress, develop, and locomotion increases, those bone markings would develop more over time.
3 calcium regulating hormones
- Parathyroid hormone
- Calcitonin
- Calcitriol
parathyroid hormone
- increase calcium levels in your extracellular fluid.
- parathyroid glands release PTH, causing osteoclasts to become more active.
- PTH binds to osteoblasts, which release a signaling molecule RANKLigand, thereby increasing numbers of osteoclasts.
- Inhibits collagen synthesis by osteoblasts, not putting as much calcium into the bone.
- Has an effect on absorption/reabsorption of calcium. Promotes the final step in calcitriol synthesis so intestines can absorb more dietary calcium. Causes kidneys to reabsorb more/excrete less calcium.
calcitonin
- “calciton it down” will tone down/decrease the amount of calcium in your extracellular fluids
- When calcium levels are high, and/or bones are put under excess stress, clear (C, parafollicular) cells of thyroid secrete calcitonin
- Causes osteoclasts to become less active
- Osteoblast numbers and activity increases
- Intestines absorb less calcium
- Causes kidneys excrete more calcium
- Blood calcium levels decrease and more calcium deposited in bone
- More pronounced effect in children, but not in adults. Children are building a lot of bone matrix, and need that support more so than adults.
calcitriol
- increase calcium levels in your extracellular fluid
- Calcitriol increases the amount of calcium absorption across the small intestine, dependent on PTH release. Increases number of calcium channels and binding proteins
- Binds to osteoblasts, which release RANKL, which increases number of osteoclasts and release of salts from bone
- Weaker reabsorption of calcium by kidneys than in response to PTH
What cause for concern, regarding their skeletal system, might an astronaut or bed-ridden medical patient have?
Loss of bone density due to lack of stress/mobility. Astronauts may come back half an inch shorter.
- Without changes to cartilage
- Genetic mutation that causes chondrocytes in the zone of proliferation to not respond to particular signals, so you don’t get growth in the growth plate. Won’t take that long for complete ossification of the growth plate.
- Long bones are affected
- Axial skeleton is average sized, but limbs are shorter.
achondroplastic dwarfism
