Bone Physiology Flashcards
organic material
collagen and ground substance that give flexibility and resilience to bone
inorganic material
calcium and phosphate that make bones stiff
functions of the skeletal system
storage: calcium, phosphorus, bone marrow, immune cells (B and T cells), fat, and growth factor
support and protect: the body structures and internal organs
anchorage: muscles and ligaments
hematopoeisis: RBC production in red bone marrow cavity
hormones: osteocalcin from osteoblasts that regulates metabolism and insulin secretion
cortical (compact) bone
outer layer of diaphysis
spongy (cancellous, trabecular) bone
inside of cortical bone
trabeculae: 3D latticework of thin pieces of bone
benefit: make bones much lighter
epiphysis
ends of long bones
diaphysis
shaft of long bones
bones are oriented along lines of stress. can these lines of stress change over time?
yes, repetition of activity, aging, pregnancy, and growth can change lines of stress
ossification begins in what week of gestation?
week 8
endochondral ossification
formed by replacing hyaline cartilage and making it bone
forms all bones except skull and clavicles
beings at primary ossification center in the diaphysis where mesenchymal cells specialize into osteoblasts
requires breakdown of hyaline cartilage first
epiphyseal plate: cartilage separating epiphysis and diaphysis (calcified by about 18-21)
intramembranous ossification
w/in the membrane
formation of osteocytes
replacing fibrous membranes w/bones
forms skull and clavicles
calcification occurs later (allows easier passage through the birth canal)
where is the primary ossification center?
diaphysis (shaft of long bone)
where is the secondary ossification center?
epiphysis (ends of long bone)
interstitial growth
growth lengthwise
requires epiphyseal plate
appositional growth
growth in thickness
bone thickens in response to increases stress (Wolff’s Law)
osteoblasts beneath the periosteum secrete bone matrix
osteoclasts remove bone on the endosteal surface
can occur throughout life
osteoblasts activity>osteoclast activity (bone formation>bone resorption)
epiphyseal plate
growth plate
calcified by 18-21 but can go until 25
maintains constant thickness
- cartilage growth on one side is balanced by bones replacement on the other
epiphyseal plate: 5 zones (from epiphyseal side to diaphysis side)
resting zone: area on epiphyseal side
proliferation zone: growth zone
- starts mitosis
- new cells pushed away from this zone
- young cartilage cells
hypertrophic zone: cells become bigger
calcification zone: chondrocytes dying
- chondrocytes deteriorate to become bones
- cartilage matrix becomes calcified
ossification zone: calcified cartilage replaced by ossified bone tissues
growth hormone during youth
too much=giantism
too little=dwarfism
thyroid hormone during youth
increases metabolic rate, insulin regulation, cortisol, heart function, thermoregulation
testosterone and estrogen during youth
promote growth spurts
end growth by inducing epiphyseal plate closure
age related changes in bone
children and adolescents:
- osteoblasts>osteoclasts (bone formation>bone resorption)
- higher bone mass in boys
young adults:
- balanced bone formation and resorption
adults (over 40 y/o):
- osteoclasts>osteoblasts (bone resorption>bone formation)
- bone mass, mineralization, and healing abilities decrease w/age
- increased bone loss in white females (can reduce the trend w/exercise)
lifelong bone remodeling and repair
5-7% bone mass is recycled each week
spongy bone replaced every 3-4 years
cortical bone replaced every 10 years
occurs at surfaces of both periosteum and endosteum
osteoclasts
bone resorption
osteoblasts
bone formation
hormones
determines whether/when remodeling occurs
parathyroid hormone, calcitonin, estrogen, leptin, and serotonin
parathyroid hormone
responds to low blood calcium and dumps calcium from the bone into the blood.
stimulates osteoclasts to resorb bone
secretion stops when homeostatic calcium levels are reached
calcitonin
in humans, it has negligible activity but can lower blood calcium temporarily
estrogen
regulates osteoclasts’ and blasts’ activities
leptin
released by adipose tissue
regulates appetite
inhibits osteoblasts (less bone formation)
serotonin
same as leptin
more of a neurotransmitter
inhibits osteoblasts (less bone formation)
biomechanical stress
weight, growth, body mechanics, etc.
determines where remodeling occurs
aging
increases osteoclast activity (overall bone loss)
nutrition
little calcium and vitamin D=weaker bones
metabolic and disease processes
substance use can lead to brittle bones
osteomalacia
lines of force in the body
usually no straight lines
compressive force medially, tensive force laterally on the femur
- no force in middle
- thickness greater at mid-shaft where the loads are the greatest
Wolff’s Law
bones thicken in response to increases stresses
larger bony projection are due to the muscles pulling on them
cortical bone is thickest where bending stress is greatest
application of new forces increases osteoblast activity
reduction of usual forces increases osteoclast activity, resulting in decreased bone mass
- decreased WB/muscle activity=weaker bones bc the bone remodels to adapt to decreased stress
right handed-bones thicker in right arm
spurring
muscles pulling on bone causes new tuberosity
common in the heel w/plantar fasciitis
stress strain curve of cortical bone vs spongy bone
cortical bone is stiffer=more vertical curve=less likely to deform upon stress
spongy bone is more compliant=more horizontal curve=more likely to deform upon stress
longitudinal loading
stiffer
transverse loading
bone is weaker and won’t be able to w/stand as much force as longitudinal loading
more compliant
fast loading
bones act stiffer than slow loading
stress and strain with large load over short time
high stress, low strain
stress and strain with low loads over long time
low stress, high strain
stress fx
response to compression
bone withstands greater compression than tension
structure shortens and widens
failure occurs in response to oblique cracking of osteons
osteons
structural and functional unit of bone that looks like concentric rings
response to tension
failure occurs in response to de-bonding at cement lines in b/w osteons and pulling out of osteons
avulsion fx
influence of muscles on stress distribution in bone
muscle contractions alters stress distribution of bone
ski boot injury: overall compressive force from compressive force produced by gastrocs leads to fracture
