Everything Flashcards
Longitudinal Growth Compact Bone
occurs @ epihyseal plate,
as chondrocytes lay the new cartilage at the plate, the cells begin to go through 4 stages to further expand the bone lenght wise.
stage 1 chondrocytes lay the new cartilage
- zone of resting cartilage
stage 2 - chondrocytes begin to divide and proliferate
- proliferating zone
stage 3 - hypertrophic zone
- chondrocytes get bigger
stage 4 - calcification
- osteoclasts eat chondrocytes and signal osteoblasts to lay bone (collagen 1 & 5 )
As this occurs the epihpseal plate gets further away from the chondrocytes and bone
endochondral ossification
when type 1 and 5 collagen creplace cartilage and push away the growth plate (last stage- calcification)
cartilage is made from what collagen fibres
heterofibrils - Collagen Type 2 & 9 to 11
diameter growth of bone
osteons contain osteocytes and lamella. outside of osteons we have osteoblasts adn a couple osteoclasts.
for diameter growth. the osteoblasts begin to fold around the perosteum of the bone, circling the blood vessels, creating more concentrics of the osteons
osteocytes get stuck in here and we get a new osteon for diameter growth.
male vs female diameter growth
pre puberty - both same growth
puberty - chicks get thicker
- males grow bigger circumference wise
aging - chicks get a little circumference bigger, but the thickness goes down
guys continue to grow circumference big and a bit thicker
circumferecnce never regressses
hormones bone growth
PTH, IGF-1 , Estrogen, TEST , Insulin, TH, progesterone
bone growth is…
depositing more than you degrade
remodeling does not equal
growth
what cells remodel bone
osteoblasts, osteoclasts, osteocytes
tension in bone…..
both osteoblasts and osteo cytes can sense tension in bone.
when tension arrives, cytes signal blasts VIA GAP JUNCTIONS and tell them to begin secreting collagen and bone apatite
how does resoprtion of bone work
osteoclasts secrete H+ions (acid to break down bone)
osteoclasts secrete MMP to break down bone
osteoclasts eat away the bone and resorb it
REGULATED by - hormones and signals to the cytes and blasts
what do steriods do to tendons
fibroblasts are senstiive to steroids.
wehn fibroblasts get steroids they secrete lots of collagen . unfortunately this is unnorganizied collagen annd calcium spots in between fibrils and cannot transmit force very well.
the tendon growns thicker but it doesnt produce the most efficent force.
wehn we take steroids we increase force produciton by the muscle. adn evene though our tendon is getting thicker to withstand more force, the muscles are also getting bigger adn produceing too much force.
this is why there is more risk of rupture.
exercise on tendon
exercises increases tension
tension increases fibroblast activity adn number.
more activity adn fibroblasts = more collagen,
tension + collagen = organization
organized fibres equal better at transmitting force.
more collagen = thicler tendon = more force transmission
bone marrow
yellow marrow in medullary cavity post puberty
red marrow in epihysis all the time and in cavity pre puberty
osteons made of
Extracellular matrix
osteons have blank and blank and trap blank inside
nerves and blood vessels
adn trap osteocytes inside inbetwen lamella
chondrocytes
initial cartliage layers at growth plate
osteocytes
- inbetween lamella in osteons - signal osteoblasts to lay bone
- maintain bone via - waste, nutrients, metabolism
osteoblasts
outside of osteons - secrete collagen and apatite
osteoclasts
HSC Monocytes fused together
- found in bone compact and spongy
- secrete H+ and MMP to eat away bone mineral, for resorption
most in endosteum
bone apatite
bone mineral - secreted by chondrocytes and osteoblasts within vesicles that layer into type 1 collagen fibrils to give rigidty
mechanical stims simple
any mechanical stim to bone or CT causes adaptiations that make them become more resistant and stronger
(3) possibel causes for CT adaptation
- increase fibro activity/ number of fibroblasts
- increased collagen density
- type of collagen
how do me measure collagen turnover
terminal pro-peptides (snippets off of tropocollagen)
- taken from ECM
72 hours post exercise
collagen synthesis increases heavy
4 weeks (1 months)
msot collagen synthesis
11 weeks (3 months)
still lots of synthesis but not as much as 1 month. ( comes back down a bit)
acute exercise causes collagen sytheiss
acute exercise causes collagen synthesis to stop during the workout and then turn on afterwards (72hours)
why is a biggger tendon good?
bigger tendon is good because -
increase the amount of load/ stress via increasing CSA
decrease the amount of deformation per load.
stress = force/area
can we increase performance with a bigger tendon?
yes V02 seems to decrease as the tendon increases due to expenditure of energy becomes more economical.
trained mice
- more fibroblasts
- bigger tendons
- stress fibres of costameres had more contractile phenotype
- this means that he myosin and actin were mroe dense - genereating more contractile force intracellularly
- more type 1 collagen
run training did what
increased torque and force
decreased deformation
increased tendon stifness
Research Article (RA) - how many people
15
RA explain control and experimental
control group adn experimental group were both volunteers with tendonosis 2-6cm above achilles insertion.
control group - did surgery adn regualar
protiens
amino acid + amino acid + amino acid…. bonds between AA are covalenet
how are proteins folded
folds occur between R groups on the amino acids that are attracted to eachother based on how electronegative a molecule is. they attract and fold
DNA down the line
DNA - mRNA - ribosomes - proteins -
dna makes instructions
mRNA copies instructions
Ribosomes read instructions
and make proteins to then be added to the AA chain
functions of proteins
structure
motors - produce force
enzymes
hormones/recpetors/signals
pH and Temp
proteins work at optimal ranges - pH and Temp denature proteins
post transcriptional modification
after proteins are in their chain and DNA has formed a protein with an original function, a modification occurs to the protein changing its finction ( phosphorylation) - turning it on or off
sk. muscle layers
epimysium - protector and force transducer
perimysium - fascicle man
endomysium -between myofibres
BM -
(reticular lamina)
(basal lamina)
plasmolemma (sarcolemma + BM)
myofibre
myofibril
sarcomere
myofilament
what makes up CT
collagen 1-6 and elastin
how are endomysium and BM bound together
dense collagen fibres of endomysium and loose collagen fibres of BM (reticular lamina), velcro together.
BM proteins
collagen
acetylecholine esterase - cancels contraction
laminan and fibrrenectin- connect fibre to BM
BM membrane is lined with what types of proteins
Glycoproteins
Basement membrane functions
connect endo to fibre
cancel contractions
attract motor neurons - muscle repair
Plasmalemma Proteins
Integrins / Dystroglycan Complex - transmit force and anchor between fibre and contractile proteins
Kinases - for integrin and target protein phosphorylation
Signals
Channels
Receptors
stress equation
stress=force/area
- more area = less stresss
- less force = less stress
highest point of tension
highest point of tension on a muscle is where the area is the lowest - therfore the myotendinous junction (tendon) - high force created in middle of tendon, passed down to little area of MTJ
tendon composition
60% water
39% protein (80% of that is collagen)
1% groundsubstance - glycans
tendon layers like muscle layers are..
collagen fibril
collagen fibre
1st collagen bundle
endotenon - perimysium and BM (tougnness)
2nd collagen bundle
endotenon - BV and Nerves
3rd collagen bundle
endotenon
epitenon
paratenon - synovial
where are fibroblasts in tendons
- fibroblasts in tendons can be found in between the primary collagen bundles
where are fibroblasts found in muscle
fibroblasts in muscle can be found in between myofibres
which tenon (epi, endo, para) transmits force and what do the others do
endotenon doesnt transmit force - it just divides collagen bundles
epitenon transmit force as it is the most superficial portion of tendon
paratenon - decrease friction agianst other tissues
what is a fibroblast
- a mesenchymal cell
- large fairly
- 1 nucleus
- stress fibres are connected to the connective tissue that surrounds them by FAKs - Focal Adhesion Kinases
- contains a cytoskelton - called stress fibres ) makes its own tension
- responds to tension to secrete collagen
where do we find stress fibres -
cytoskelton of fibroblasts
tension organizes what
tennsion organizes tropocollagen to fibrils
tension organizes fibrisl to fibres
how many myofibres
up to 1000
do myofibres have nuclei
yes and satellite cells
myonuclei vs satellite cells
satellite cells used for tissue repair
satellite cells are found under the basement membrane but above the plasma lemma - and they have their own membrane
myonuclei under both
mitchondria are where in muscle
mitochonrdria squish beteween myofibrils
two types of mitochondria
mitochondria have two differeetn pools
subsarcolemma poools -
intramyofibrular- (IMF) - IMF are the highly aerobic pools
IMF and Subsarcolemma Pools of Mitochondria
mitochondria pools
IMF and subsarcolemma decrease with age
mitochondria are highly branched
branching fibres? fibrils?
myofibres arent branched, fibrils are
in the heart myocardial fibres are branched
myofibril (contractile)
sarcomere - myosin actin all that jazz
myosin
2 heavy chains 4 light chains
actin
actin with tropomyosin and troponin
how many thin surround thick filaments
6 thin around 1 thick
what is titin?
titin is a structural/accesory protein that spans the entire lenght of a sarcomere - from z-line to m-line
largest protein in our body
gives resting tension to our muscles
allows myosin and actin to contact eachother
can scaffold for other protiens, like dystopphin or inte
coiled up at z disk
when lengthened muscle (relaxed) titin uncoils and reveals tension sensors and signalling proteins.
thesse proteins phosphorylate down to another target protein, chanign gits turning it on configuration therfore important for muscle hypertrophy and growth
titin uncoiled
titin uncoilded shows its kinase domains as wwell as signalling proteins, thesse proteins phjsophorylate and signal target proteins that can lead to adaptation
z disk proteins
nebulin, desmin and plectin
nebulin
lets actin build off it
intergrins
interns connect the basement mebrane to the fibre
they transmit force alongside dystroglycan complexes - pulling on the contractile fibres of actin via accesory proteins (FAK)
costamere
- at the z disk of sarcomeres - act as the anchors and traducers of tension (integrins adn dystroglycan complexs)
myotendinous junctin (MTJ)
sarcolemma invaginates the tendon at its ECM
high density of costameres, and integrins because lots of tension here
FAK
focal adhesion kinases - act as the costameres in fibroblasts and in sarcomeres, are connected to integrins which phosphorylate subsequent protiens to their target protein in order to change configuration, important for hypertophy of muscl and growht
Muscular Dystophy types
Duchene and Beckers - duchene more common - worse
beckers less common and not as bad
muscular dytrophy what is
something wrong with your dystophin protien whihc connects plasmalemma and contractile proteins - allows us to tranduice force
muscular distrophy rates
1/20000 have a hereditary myopathy
1/3500 boys have dystrophy = common
muscular distrophy cycle
breakdown regeneration cycle
fibres chronically breakdown
imfllamatory cells go to the site adn secrete collagen
satellite cells help to repair - but this happens so much those deplete adn then we lose the regeneeration part
chromosome linked muscular dystophy
x recessive
xx okay xy no good
collagen type 1
all mysiums /tendon
collagen type 2
cartliage
collagen type 3and 5
mysiums and MTJ
collagen type 4
BM non fibrillar
collagen type 6
BM to endo
collagen fibres are non fibrillar are?
collagen 4 and 6 in BM
flexibility depends on…
addition of sarcomeres
ECM pliability
sensory neuromuscular feeback (ROM)
more force = less flixibilty therfore
more flexibility = less force
more fibres, density, type, crimp, glycation, organization, determine
flexibility and stifness
free cells
blood cells
fixed cells
everything else
whats its pair
irregular and loose
dense and regular
endomysium tissue is what type
dense irregular
epi and parimysium CT is waht type
dense regular
25% of protein mass in our bodies is what protein
collagen
acute bone remodeling
lack of Ca+ in blood, osteoclasts send Ca+ to blood - osteoclasts activsated by PTH
what activates osteoclasts to send calcium to blood
Para Thyroid Hormone
osteoclasts purpose adn make up
made up of HSC - monocytes that fuse together with osteoblasts
these resorp bone mineral
osteoclasts secrete
H+ioons and MMP to breakdown bone for resorption
resorption is based on
activity of osteoclasts and number of osteoclasts.
what nhibits resorption
estrogen and testosterone
4 roles of estrogen
tells mature osteoclasts to kill themselves
slows release of PTH from PT
stims IGF production in osteoblasts
stims epiphyseal plate closure in late puberty by inhibitj g IGF
exercise and bone
more exercise = more tension = more osteoblasts/cytes = more collagen/apatite = more BMD
OsteoTEndinous Junction
the oppostie to the MTJ
high degree of osteoblast/cyte acitivty here
more dense none at these insertion points as this is where most force gets exerted too,
4 zones of OTJ
tendon - fibroblasts T1C
fibrocartilage - chondrocytes T2C some T1
mineralized fibro cartilage - more chondrocytes w/ apatite mainly TYPE 2C
bone - sharpeys fibres connect thriug perisosteum into mineralized fibrocartilage as anchors
osteoporosis -
low BMD (more than 2.5vStandard Deviations from average)
