bone A&P Flashcards
6 main functions
support mush
protect (organs etc)
assist movement
mineral homeostasis (Ca2+, P)
blood cell create
(Red bone marrow = RBC, WBC, platelet)
store fat
(yellow bone marrow)
anatomy of long bone
Diaphysis (shaft)
Epiphysis (head/end)
(distal/proximal epiphysis)
Metaphysis (neck)
where is yellow bone marrow?
in diaphysis
what is diaphysis made of? (what type of bone?)
compact bone (cortical bone)
compact vs cancellous bone (spongy bone)
Epiphysis primarily
cancellous bone (spongy bone)
where is red bone marrow?
in epiphysis
structural characteristic of epiphysis
projections and fossae
I.e. forming joints
In other words, around joints are red bone marrow (?)
metaphysis
between diaphysis and epiphysis (Zone of transition)
WEAKEST
where is epiphyseal plate
in metaphysis
what is epiphyseal line
epiphyseal plate becomes epiphyseal line at around 20y.o. when growth (height) stops
epiphyseal plate is area of cartilage where bone growth appears
medullary cavity
cavity in diaphysis
contains YBM
contains blood vessels
endosteum
lines the medullary cavity
what is endosteum made of? (tissue type?)
DENSE IRREGULAR CT
periosteum
surrounds bone
two layers of periosteum
fibrous layer (Dense irr CT)
cellular layer
function of periosteum
covers bone
merges with tendons
sensory nerves
blood vessels
cellular layer holds OSTEOPROGENITOR CELLS (precursors to osteoblasts)
articular (hyaline) cartilage
covers epiphysis
reduce friction
reminder: CT is made of
CT is made of…
a) specialized cells
b) ECM (ground substance + fibres)
histology of bone
GS in bone is very hard
4 main types of cells:
osteoprogenitor
osteoblast
osteocyte
osteoclast
ECM of bone (fibres + GS) – Fibres
Collagen fibres (30% bone weight)
= flexibility of bones
ORGANIC COMPONENT OF ECM
ECM of bone (fibres + GS) – GS
crystalized mineral salts
only enamel is harder
CALCIUM PHOSPHATE
55% bone weight
HYDROXYAPATITE salts
Calcium phosphate
+
Calcium HYDROXIDE
Also incorporates other salts (e.g. calcium carbonate)
and ions (Na+, Mg2+, F-)
INORGANIC COMPONENT OF ECM
ground substance in bone
made of HYDROXYAPATITE
extremely hard
4 bone cell types
osteoprogenitor
osteoblast
osteocyte
osteoclast
osteoprogenitor
stem cells derived from mesenchyme
only bone cells that undergo MITOSIS
develop into OSTEOBLASTS
Part of deep (cellular) layer of periosteum AND ENDOSTEUM
osteoblast
bone building
on bone surface
secrete COLLAGEN
form osteoid
TURN OSTEOID into BONE
osteoid
“Osteoid is an unmineralized organic tissue that eventually undergoes calcification and is deposited as lamellae or layers in the bone matrix.”
TURN OSTEOID into BONE
“assist in depositing the mineral salts (initiate calcification) to turn osteoid into bone”
osteocytes
mature bone cells
inside bone tissue
DENDRITIC processes
nutrient/waste exchange
(METABOLIC ACTIVITY OF BONE)
which bone cell type maintains metabolic activity?
osteocyte (mature bone cells)
where are osteocytes contained
in LACUNAE
where are lacunae?
between concentric layers of LAMELLAE
Interconnected via CANALICULI
Osteoclasts
break down (resorb) bonew
what is resorption
taking Ca2+ from bone
put it back in blood
(OPPOSITE TO OSTEOBLASTS)
what are osteoclasts derived from (common origin)
Macrophage (WBC that performs phagocytosis)
which cells are multinucleated?
Osteoclasts
where are osteoclasts?
also found on surface of bone
grooves called HOWSHIP’S LACUNAE
two types of bone tissue
compact
spongy (cancellous/trabecular)
why compact
“structure comprising mostly of calcium, phosphate, collagen, and other minerals “
No SPACE between cells
where compact?
diaphysis
external layer of all bones
3 types of LAMELLAE in bone matrix
concentric lamellae
interstitial lamellae
circumferential lamellae
Osteon
individual structural units of bone
made via concentric lamellae
haversian/central canal
at centre of concentric lamellae
note lacunae and canaliculi
note osteocytes via lacunocanalicular network
interstitial lamellae
between osteons
circumferential lamellae
next to medullary cavity
next to periosteum
not part of osteon
haversian canals
longitudinally along shaft of bone
blood vessels
lymph vessels
nerves
Volkmann’s canal (PERFORATING canals)
perforating canals
perpendicular
interconnect haversian/central canals
(bv/lymph/nerve
superficial to deep
note about canaliculi
filipodia of osteocytes
FILIPODIA
Spongy bone (trabecular/cancellous)
no osteon units – no haversian system
which bone GREATER BLOOD SUPPLY
spongy
Red bone marrow
= RBC, WBC, platelets
trabeculae
contain lamellae of spongy bone
less organized
weaker
where spongy? …
epiphyses of long bones
flat bones – periosteum and thin layer of compact bone – but primarily spongy at centre/core
ossification/osteogenesis
“bone formation”
begins during 6th week of embryo development
2 types of bone formation
endochondral ossification (replacement of cartilage w/ bone)
intramembranous ossification
(replacement of connective tissue membranes with bone tissue)
ENDOCHONDRAL ossification
initial skeleton of embryo = hyaline cartilage
cartilage replaced via endochondral ossification
cartilage is “small model”
occurs in LONG BONES
where endochondral ossification?
long bones
6 Steps in endochondral ossification
1 – development of cartilage model
chemical messages cause MESENCHYME cells to gather in shape of future bone —> develop into chondroblasts
chondroblasts secrete ECM of cartilage –> create hyaline cartilage
perichondrium wraps cartilage model
Steps in endochondral ossification
2 – growth of cartilage model
chondroblasts –> chondrocytes
then…
INTERSTITIAL GROWTH
(replication of chondrocytes = LENGTHENING OF CARTILAGE MODEL)
and…
APPOSITIONAL GROWTH
(ECM on cartilage surface & periphery = THICKENING OF MODEL)
Steps in endochondral ossification
3 – development of primary ossification centre
nutrient artery penetrate to centre
then OSTEOPROGENITOR cells @ perichondrium —-> OSTEOBLASTS
PERICHONDRIUM becomes PERIOSTEUM
cartilage calcifies into bone (spreads towards ends)
Steps in endochondral ossification
4 – development of marrow cavity
osteoclasts create marrow cavity (diaphysis shaft)
wall of diaphysis replaced with compact bone
Steps in endochondral ossification
5 – development of secondary ossification centres
epiphyseal plate via epiphyseal arteries
growth outward from epiphysis
cartilage continuously converted to bone
6 Steps in endochondral ossification
6 – formation of articular cartilage and epiphyseal plate
final stage
hyaline cartilage –> articular cartilage
hyaline cartilage also remains @ epiphyseal (growth) plate until adulthood (around 20) – when plate closes and becomes epiphyseal line
primary / secondary ossification centres – when?
primary = prenatal
secondary = after birth
intramembranous ossification
bone formation without cartilage model
mesenchyme (Stem) cells differentiate into osteoblasts
occurs in deep layers of dermis
bones called DERMAL BONES / membrane bones
E.g.
some bones of skull
lower jaw (mandible)
clavicle
sesamoid bones (patella)
steps of intramembranous ossification
1 – development of ossification centres
chemical messages cause mesenchymal cells to cluster –> become osteoprogenitors
osteoprogenitors –> osteoblasts
osteoblasts secrete bone ECM
Steps in intramembranous ossification
2 – calcification
ECM secretion stops
osteoblasts become osteocytes
within lacunae
extend processes into canaliculi
calcium and other minerals are deposited and ECM hardens (calcifies)
Steps in intramembranous ossification
3 – formation of trabeculae
matrix continues to harden
forms trabeculae
RBM forms within spongy bone trabeculae
Steps in intramembranous ossification
4 – development of periosteum
outer layer of mesenchyme becomes PERIOSTEUM
compact bone replaces spongy bone @ OUTER layer
spongy @ inner
remodeling continues until adult size/shape
bone growth types
length (interstitial)
thickness (appositional)
interstitial (length)
via epiphyseal plate
= hyaline layer of cartilage in metaphysis
plate becomes line after skeletal maturity (around 20)
4 zones of epiphyseal plate
1) resting cartilage zone
2) proliferating cartilage zone
3) hypertrophic cartilage zone
4) calcified cartilage zone
1) resting cartilage zone
nearest to epiphysis
small chondrocytes
connect epiphyseal plate to epiphysis
“RESTING” b/c not involved in bone growth
2) proliferating cartilage zone
large chondroblasts
replicate and divide
replace old chondrocytes
“Stack of coins” apperance
3) hypertrophic cartilage zone
large mature chondrocytes
columns
4) calcified cartilage zone
dead chondrocytes
area is calcified
osteoblasts take over
create ECM
convert from calcified cartilage to NEW DIAPHYSIS
about interstitial bone growth and puberty
@ puberty, hormones stimulate increased bone growth
epiphyseal cartilage is replaced
osteoblast activity OUTPACES chondroblast/chondrocyte activity
Thus, Epiphyseal plate/cartilage closes
= “Epiphyseal closure”
leaves epiphyseal line
note about anatomical neck of the humerus and the residual epiphyseal plate/line
APPOSITIONAL GROWTH (growth in thickness of bone)
bone diameter increase
osteogenic cells differentiate osteoblasts
–> add bone matrix (ECM) under periosteum
adds layers of CIRCUMFERENTIAL lamellae
Trapped osteoblasts become osteocytes
osteoclasts adjust size of MEDULLARY cavity
bone blood supply
rich supply
why?
constant remodeling
Blood cell production
major arteries/veins supporting bone tissue
Periosteal arteries/veins
Nutrient artery/vein
metaphyseal arteries/veins
epiphyseal artery/vein
(?)
periosteal blood vessels
via Volkmann’s Canals (PERFORATING CANALS)
transport blood
@ PERIOSTEUM
@ outer portion of compact bone
nutrient artery/vein
enter via NUTRIENT FORAMEN of Diaphysis
= nutrient foramen location depends on bone
supply blood @
@ inner portion of compact bone
@ proximal portion of spongy bone (?)
metaphyseal arteries/veins
enter @ metaphysis
blood supply to…
= metaphysis
= to RED BONE MARROW
Epiphyseal artery/vein
enter @ epiphysis
blood supply to…
= epiphysis
= to RED BONE MARROW
bone remodeling
mature bone tissue removed
replaced by new bone tissue
why Remodeling?
structural integrity
strengthen bone areas specifically (where stress)
fracture
repair micro-stress
blood calcium homeostasis
2 processes of remodeling
1) resorption
2) deposition
1) resorption
osteoclasts break down bone ECM
remove COLLAGEN & minerals
I.e.
Calcium released to blood
2) Deposition
Osteoblasts create new bone ECM
osteoblasts create OSTEOID (osteoid becomes lamellae (ECM))
OSTEOID receives minerals via osteoblasts
(CALCIUM via blood)
resorption and deposition
continuously & simultaneously
Wolff’s law
bone tissue deposition along LINES OF STRESS
bone markings via muscle attachments
Wolff’s law = bone added where demand, lost where no demand (stress)
exercise and bone
strengthens bone
stresses bone = more bone deposition
Wolff’s law = bone added where demand, lost where no demand (stress)
bone growth important factors
minerals
vitamins
hormones
bone growth important factors (Minerals)
Calcium
phosphorus
fluoride
magnesium
manganese
bone growth important factors (vitamins)
Vitamin A (osteoblasts)
Vitamin C (Collagen)
Vitamin D (Calcitriol)
= helps Calcium absorbtion in GI tract
Vitamin K (bone proteins)
Vitamin B12 (“ proteins)
bone growth important factors (hormones)
T3 & T4 (thyroid hormones)
GH (growth hormone)
= stimulate IGFs
= from liver
= bone growth
Sex hormones
= testosterone = bone growth
Calcitonin & PTH (parathyroid hormone)
= Calcium homeostasis
calcium important functions
nerve/muscle cell function
(Ca2+ ion muscle contract)
blood clotting (acts as enzyme –> clotting factors)
other chemical reactions (as “COFACTOR”)
blood calcium homeostasis
8.5 - 10.5 mg/dL
hypercalcemia
hypocalcemia
hypercalcemia (>10.5mg/dL)
cardiac arrest
respiratory arrest
blood homeostasis where? (3 locations
3 locations:
1) Bone
= bone resorption increase blood Ca2+
= bone reposition decrease blood Ca2+
2) Kidney
= increased calcium reabsorption increase blood Ca2+
= decreased calcium reabsorption decrease blood Ca2+
3) GI tract
= increased vs decreased absorption
3 hormones that regulate calcium homeostasis
1) Calcitonin
= decrease blood Ca2+
= puts calcium in bone
2) Parathyroid hormone (PTH)
= increase blood Ca2+
= puts calcium in blood
3) Calcitriol
= activated form of Vitamin D
= INCREASE blood Ca2+
1) Calcitonin
via Parafollicular cells
(C CELLS)
of THYROID GLAND
decrease blood Ca2+
effect antagonistic to PTH and Calcitriol
How does Calcitonin decrease blood Ca2+ (TWO ways)
1) Decreases bone resorption
= inhibit OSTEOCLASTS
= Osteoblasts outpace Osteoclasts
= more deposited than resorbed
2) Decreases Kidney reabsorption of Calcium
= more Calcium stays in Urine
= leaves body
2) PTH (parathyroid hormone)
via Parathyroid glands
= increase blood Ca2+
antagonist to Calcitonin
synergist to Calcitriol
How does PTH increase blood Ca2+? (THREE ways)
1) Increase bone resorption
= osteoclasts activity outpaces Osteoblasts
= more resorbed than deposited
2) Increase kidney reabsorption of Calcium
= less Ca2+ lost in urine
3) Activates Calcitriol/Vitamin D
= in kidney (?)
PTH/Calcitonin and negative feedback system
regulated by negative feedback loop
3) Calcitriol
made in EPIDERMIS
= via Cholesterol precursor
= precursor activated by UV radiation
Increase blood Ca2+ levels
antagonistic to Calcitonin
synergistic to Calcitriol
how does Calcitriol increase blood Ca2+ (one way)
increase GI tract absorption of Ca2+
increase amount of Ca2+ in blood
menopause and osteoporosis
osteoblasts activate osteoclasts
ESTROGEN protection
= blocks activation of osteoclasts
sudden drop in estrogen = active Osteoclasts
Active osteoclasts = more resorption = increased chance of Osteoporosis
Bone pathologies
fractures
osteoporosis
rickets/osteomalacia
fracture
any break in bone
types, severities, locations, causes
open fracture
aka compound fracture
broken ends of bones protrude through skin
complications:
= infection
= non-union (not healing after 3 months – fracture persists for 9 months)
treatment:
= surgery
= antibiotics
via plate/screws
closed fracture
aka simple fracture
broken ends don’t protrude through skin
may or may not require surgery
comminuted fracture
2 or more spots
forms fragments
requires surgery
internal fixation (e.g. plate/screws)
external fixation
= metal frame/scaffolding outside leg
= not quite same as cast (?)
greenstick fracture
incomplete/partial fracture
one side broken, other side bent
common in children
b/c bones not fully ossified
(more organic material)
impacted fracture
one end forcefully driven into other (of 2 fractured ends)
transverse fracture
perpendicular to length
oblique fracture
@ an angle
spiral fracture
warps around shaft
like corkscrew shape
via fracture during twisting motion
Pott’s fracture
distal fibula
via ankle sprain
Colle’s fracture
distal radius fracture
distal end moves posteriorly
= dinner fork deformity
avulsion fracture
bone attached to ligament or tendon
pulled away
young athletes
common @
@hip
@foot/ankle
@elbow
Note also…
MALLET finger
= small bone fragment pulled away with extensor digitorum tendon
stress fracture
micro-fracture
repetitive stress
E.g. running, jumping, dancing
can be missed by X-ray
Growth plate fracture
break in growth plate of child/teen
if goes through growth plate, can result in shortened/crooked limbs
vertebral compression fracture (VCF)
vertebral body fracture
can become compressed
via injury/trauma
more common in those w/ osteoporosis
osteoporosis
“porous bone”
loss of bone mass
resorption frequently outpaces deposition
osteoporosis some causes
decreased estrogen in women (post-menopause)
decreased testosterone in males
poor diet/low calcium intake
lack of exercise
drug use
e.g. also steroids
smoking
genetics
osteoporosis more common in
women and elderly
bone pathologies numbers
2.3 million Canadians with osteoporosis
1.3 million fractures per year
1/3 females experience fracture due to osteoporosis
1/5 males experience fracture due to osteoporosis
best prevention
= regular exercise
= healthy diet
osteomalacia and rickets
failure of bones to calcify
in children, called “Rickets”
in adults, called osteomalacia
osteomalacia = “soft bones”
organic matrix present
calcium salts not deposited
lack of vitamin D
lack of sunlight
poor diet
extreme/prolonged calcium or vitamin D deficiency
soft bones = bow legs
pain, tenderness, fractures
osteoporosis vs osteomalacia
in osteoporosis bone mass decreases
bone mineral to matrix is same
in osteomalacia bone volume not necessarily different
bone mineral to matrix ratio is lower
note Vitamin D deficiency
4 steps in fracture repair
1) formation of fracture hematoma (reactive phase)
2) fibrocartilage callus formation
3) bony callus formation
4) bone remodeling
1) formation of fracture hematoma (reactive phase) – (SEVERAL WEEKS)
damaged blood vessels form clot (hematoma)
circulation stops
bone cells in area DIE
inflammation via DEAD cells
Phagocytes/osteoclasts remove DEBRIS (dead cells)
= SEVERAL WEEKS
2) Fibrocartilage callus formation (THREE WEEKS)
fibroblasts create COLLAGEN fibres
CHONDROCYTES (from periosteum)
= CREATE fibrocartilage
FC callus is formed
THREE WEEKS
3) Bony Callus formation (FOUR MONTHS)
osteogenic cells (OSTEOPROGENITOR CELLS)
= become osteoblasts
= convert FC callus into SPONGY BONE trabeculae
= join bone fragments with bone
bony/hard callus = 3-4 (FOUR) MONTHS
4) Bone remodeling
osteoclasts resorb remaining dead portions
COMPACT BONE replaces SPONGY bone
(around periphery)
X-ray (radiography) discovered by…
in 1895 by William Conrad Roentgen in Germany
“He was experimenting with an electron accelerator, called a cathode, and discovered that a nearby barium plate became fluorescent due to the massive exposure of electrons.
Roentgen called these fluorescent beams ‘X’ for their unknown quantity.
X-rayed his wife’s hand soon after and received Nobel prize for physics same year.”
how X-ray (radiography) works
via electron beams
soft tissue & air does not reflect “
hard/dense objects do
E.g.
metal, bone, teeth, etc.
note radiopaque vs radiolucent
“Radiolucent
Refers to structures that are less dense and permit the x-ray beam to pass through them.
Radiolucent structures appear dark in the radiographic image.”
“Radiopaque
Refers to structures that are dense and resist the passage of x-rays.”
DEXA scan
dual energy X-ray absorptiometry scan
measures bone density
tracks bone loss as you age
diagnose osteoporosis
radioactive tracer
chemical substance
injected
“taken up” by bone
scanning device detects area of activity (via tracer)
hot spot = higher metabolism (= potential pathologies)
cold spot = lower metabolism
E.g.
healed fracture
degeneration
arthritis
etc.
most useful bone scan method?
via radioactive tracer
efficiency, accuracy
