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>> This video is on bone
and the tissues of the skeleton.
The learning objectives
that we'll cover are here.
We'll cover a little bit
about what bone's made of --
cells and matrix.
We'll talk about bone growth
and remodeling.
And quite bit
about calcium homeostasis
which involves our bones.
The functions of bones --
support and protection are
probably pretty obvious
and moving our muscles around.
But also, don't forget
that new blood cells are formed
in our bone marrow.
Also, the bones are going
to play an important role
in calcium homeostasis
in maintaining our extracellular
calcium -- serving
as a calcium reservoir.
In the first learning objective,
we'll cover here is
to describe the cells, matrix,
and organization of bone
and associated tissues.
So we'll mention a little bit
here about cartilage
and ligaments.
But mainly we'll focus on bone
and bone marrow.
So if we look at bone --
so we've learned so far
as the osteocyte.
The extracellular matrix
around those cells is mainly
collagen protein as well
as the minerals calcium
and phosphate.
And so that's what gives bone
its sort of hardened
extracellular matrix is the
calcium phosphate and mineral.
If we look at tendons
and ligaments,
the cell we're interested
in is the fibroblast
which makes this dense
connective tissue of collagen
and elastin.
These proteins make
up these fibers, collagen
and elastic fibers.
A cell I don't think we've
learned yet is the chondrocyte.
Chondrocytes help maintain a
special connective tissue
called cartilage.
Cartilage is mainly collagen
and elastin proteins as well.
So cartilage is kind of famous
for making up things
like your ears and nose
and being on the ends of bones
such as our ribs.
So if you look at each of these,
the sort of thing they share is
that they're made
of extracellular matrix
of collagen built
by certain cells.
Okay, I just wanted
to mention ligaments.
Ligaments attach bone to bone.
And they stabilize our skeleton.
Tendons attach muscles to bone,
and they allow movement
of our bones.
Okay, ligaments
and tendons are basically just
dense connective tissue.
Cartilage, cartilage is
well-known for being at the ends
of our bones.
So wherever we form a joint
so that those bones don't clash
against each other,
it's protected by cartilage
and also our ears and nose
and things like that.
So to summarize, keep in mind
that when we talk
about the skeleton,
we're talking
about the different types
of cells that make
up the different type
of skeletal tissues.
And each of them shares collagen
as an important protein
and then slightly
different cells.
If we look at this picture
of bone here, and it's cut open
to show you
that inside the core,
deep inside bone,
are these marrow spaces
and it includes red bone marrow
and yellow bone marrow.
There's usually an outer sort
of shell of compact bone
and then an inner core
of trabecular bone
for these marrow spaces.
And what's interesting
about bone marrow is
in adults we have yellow bone
marrow in certain places filling
our bones with adipocytes --
kind of space filler,
packaging so energy.
The interesting stuff though is
the red marrow found
in certain parts of our skeleton
which gives rise
to all our new blood cells
whether they're leucocytes
for defense
or erythrocytes carry oxygen
around the body attached
to hemoglobin the protein inside
those erythrocytes.
And also, the bone marrow also
makes those little platelets
which help in blood clotting.
So red bone marrow gives rise
using these hematopoietic stem
cells to all the cells
of our blood.
If we look at real bone,
what we see is this outer shell
of compact dense bone covered
by a fleshy periosteum
which is sort
of like a connective tissue
cover of our bones.
And then deep
to the compact bone is this
trabecular bone.
Trabecular bone has these spaces
or sort of grooves
and little nooks and crannies
where we have our bone marrow.
And there's lots and lots
of living cells in our bone,
and so we need a rich blood
supply that feeds our bone
and helps keep it nourished.
We also have a nervous supply
as well so that's why
if you've ever broken a bone you
know it hurts so badly.
So sometimes your blood supply
can be interrupted to your bone.
And in that case,
we get a condition called
osteonecrosis
or avascular osteonecrosis
which can cause death
to your bone.
Again, we have this fleshy outer
cover of bone called
the periosteum.
It's mainly dense connective
tissue of collagen built
by fibroblast.
But there's a couple of layers
of fibroblast
and osteogenic stem cells
in there which will become
important when we talk
about fracture repair
in that periosteum.
Then there's compact bone just
deep to that.
The compact bone has mostly bone
matrix with some osteocytes
in there that maintain the
bone matrix.
And so again,
that bone matrix is collagen
protein with some calcium
phosphate mineral.
Then deeper
to that is the trabecular bone.
The trabecular bone you can see
has little spaces
that are filled
with bone marrow,
either red bone marrow
or yellow bone marrow filling
the trabecular bone.
Trabecular bone is hardened.
Some textbooks call it spongy
bone, which I don't really
like because that makes me think
of it as soft.
But it's really all hard.
I think the reason they
like spongy was
because there were spaces in it.
So we'll call it compact bone
and trabecular bone.
If we zoom in on compact bone,
what we see is very little
space, open space.
It's instead these compact
columns of bone matrix called
an osteon.
And you can see several osteons
in this little picture here.
The osteons have these little
rings of osteocytes which help
to build the osteon.
And then they help maintain it.
Each osteon has a little central
canal, a little tunnel,
that allows things --
soft things like blood vessels
and nerves to run
through the hardened bone.
So again, the bone matrix is
collagen and mineral.
And so we see several osteons
making up this compact
bone section.
If you look at trabecular bone,
you don't see any osteons.
Instead, you see marrow spaces.
And then in the hardened bone
matrix it's a little more
irregularly shaped.
It's still pretty much the same
stuff, osteocytes embedded
in a bone matrix of collagen
and mineral.
And then the other thing you'll
notice is that you see these
lining cells that cling
to the edge of the bone
in the marrow spaces.
This is called endosteum.
So endosteum is the cellular
lining in the interior spaces
of bone.
It includes cells
like the osteoclast,
the osteoblast
and osteogenic cells,
which we'll learn more about.
Again, if you look
at the marrow spaces
of trabecular bone,
you see all these little cells
clinging to the edge
of the bone.
And so we call those cells
endosteum as a group.
Okay, the fleshy outer cover
of bone we call periosteum.
And that's connective tissue,
dense connective tissue somewhat
similar to maybe the dermis
of the skin.
And it has cells
in there as well.
If we zoom in again
to that same picture,
you can pause it
and check this out,
but we can see the osteon.
Compare that to trabecular bone
where we see sort
of this irregularly shaped
bridges of hardened bone.
What I wanted you
to notice were the cells
in there.
You can see the osteoblast
clinging to the edges
of the bone.
But the bones embedded
in the matrix of the osteocytes.
You even see some osteogenic
stem cells clinging
in there near the osteoblast
and some really large osteoclast
that eat away the bone.
Stem cells called the osteogenic
stem cells,
create new osteoblasts
in our bone.
Those osteoblast build bone
around themselves.
And once they're surrounded,
then they mature
to become an osteocyte.
Osteocytes maintain bone.
And they sense any stress that's
in the bone matrix.
So they're going to be important
for maintaining our healthy
bones by sensing the stress.
And they're sort
of all big one family
because each one gives rise
to the other.
Bone marrow stem cells,
hematopoietic stem cells,
give rise to these precursor
cells that then fuse together
to create this big giant large
cell called an osteoclast.
These large osteoclasts are
multinucleated cells
because they're created
by the fusion
of several precursor cells.
The job of the osteoclast is
to chew up bone.
We call that bone reabsorption
or bone break down.
They're not related
to the osteoblast
and the osteocytes.
They're derived
from blood cells.
They are related
to these immune cells that eat
up bacteria called macrophages.
So I like to remember
that they both
like to eat stuff.
The osteoclast eat the bone.
And the macrophages eat bacteria
and bad things in the body
so maybe they're cousins.
If we look at a skeleton,
if we look at a child's
skeleton, most
of the bone is filled
with red marrow
because they're growing lots
and need lots and lots
of new blood cells.
In the adult, we don't need
as much red marrow
so it's concentrated usually
in our pelvis and in our skull.
And some of the epiphysis,
the proximal epiphysis
of our long bones will have red
bone marrow.
So like at the near end
of your femur
or your humerus will have some
of that red marrow.
That red marrow is famous
for bone marrow transplants.
So you can take some
of that bone marrow out
and transplant it
to another person.
Why would you want to do that?
Well, if you remember what's
in the red bone marrow,
it's those hematopoietic
stem cells.
Hematopoietic stem cells
from the donor can then help a
patient who receives them grow
new erythrocytes and leucocytes.
Obviously erythrocytes carry
oxygen, and leucocytes will
defend you.
Okay, so that's the good reason
for bone marrow transplants.
What is bone made of?
Again, the extracellular matrix
we said hopefully is collagen
and mineral.
And so let's make sure we're
clear on that.
So the extracellular matrix is
the material found outside the
cells that the cells have built
or that they maintain.
Collagen is just a big,
giant rope of protein,
and specifically type one
collagen is found in our bones.
The calcium phosphate mineral is
called hydroxyapatite.
Hydroxyapatite is the
mineralized form
of calcium phosphate
that makes our bones very,
very hard.
So I like to think
of hydroxyapatite like rocks.
So if we look at bone,
it's about 30% protein,
including collagen,
and about 70% mineral
which includes
that hydroxyapatite
calcium phosphate.
A couple of the genes
for collagen are collagen 1a1
and 1a2.
And so if you have any problems
in your collagen genes,
then that can affect your bones.
So again, the collagen makes
your bones flexible
and very strong.
The calcium phosphate mineral
hydroxyapatite makes your bones
hard and resist compression.
If you don't have collagen,
your bones are brittle,
and they break really easily.
If you don't have calcium
phosphate, the mineral,
then you'll have bendy bones.
Examples of diseases we'll talk
about later.
Osteogenesis imperfecta
and rickets can affect
your bones.
Next, we're going
to describe the mechanisms
of bone growth both before
you're born,
when you're a child or teen.
And then also
when you're an adult.
A vocabulary word we need
to take note of is ossification.
Ossification basically is
bone formation.
And it usually involves
transformation
of one tissue type into bone.
And so we'll talk a little bit
about different ways we can
get ossification.
If you look at a little embryo
and early fetus,
you can see
that your bones will form
very early.
So I want to talk a little bit
about how your bones form
and development.
One way is to use this collagen
connective tissue made
by mesenchymal stem cells
or connective tissue stem cells.
And they come in these sheets.
And these sheets
of connective tissue are then
turned into bone by osteoblast.
And remember turning something
into bone we call
that ossification.
So this form of ossification
because it involved sheets
of connective tissue is called
intramembranous ossification.
So intramembranous ossification
is how our skeleton forms
when we have flat bones
like your skull.
And I believe, I'm not sure,
part of the pelvis.
So for sure the skull.
How do we form the other bones
in our skeleton?
Well, in these cases,
we start off with sort
of a cartilage framework.
Remember cartilage is just
collagen and connective
tissue too.
In this case,
we had chondroblast
which might build some
of that cartilage.
And then we have osteoblast
that are going to turn
that collagen cartilage
into bone.
And again, if we turn another
tissue into bone we just call
that ossification.
In this case, to remind us
that it's coming from cartilage,
we call it
endochondral ossification.
So endochondral ossification
and intramembranous ossification
is how we get our
early skeleton.
So again, if we look at a fetus,
we'll see that some
of the bones formed
by intramembranous ossification,
while others
like the long bones will form
from endochondral ossification.
So much of our skeleton forms
from this cartilage model
which is then turned into bone.
And then other bones
like in our skull start
from this sheet
of connective tissue.
And I believe some
of the pelvis too.
All right, so that's how we get
our skeleton.
We start with one tissue.
And then it's ossified,
ossification, into actual bone.
Most of this involves collagen
connective tissue being turned
into bone.
So we'll summarize a little bit
here and make sure those steps
are clear for you.
So in endochondral ossification,
we're starting
with our product is cartilage
which is mainly collagen.
And then osteoblast turn that,
which we call ossification,
into bone.
And we'll start
with trabecular bone.
And we could always remodel
that into compact bone or back
and forth, all right?
So intrachondral ossification is
one way if we start
with cartilage
that we can make bone.
The other way we can make bone
is if we start
with connective tissue
and stem cells.
And if we take some connective
tissue stem cells
that make collagen
and connective tissue
and then sheets
of that connective tissue are
ossified into bone
through osteoblast,
we call that
intramembranous ossification.
Again, we can create trabecular
bone or layers outside
of our compact bone.
All right, so two different ways
that we make bone
from other tissues.
What about when you're a child
or a teenager?
How do you grow taller
and how does your skeleton
grow bigger?
Well, it's similar methods
that we just said.
In the case of your long bones,
it's endochondral ossification.
You have have these little
islands of cartilage
that cause your bones
to grow taller and taller
or longer and longer.
And this involves bones famous
in the arms and legs
and things like that.
As far as the pelvis or skull,
that's going
to involve continuing
that intramembranous
ossification
where those bones really become
longer -- or excuse me --
larger rather than longer.
So if we look
at how do long bones grow,
there's something called the
epiphyseal growth plates
which simply means these growth
plates at the end of our bones.
And so if we look at long bones
in our fingers and hands
and arms and legs,
we see this little island
of cartilage
which continues to grow.
And then osteoblast turn part
of that island of cartilage
into new bone.
And your bones continue
to grow and go.
And hormones will regulate a lot
of that.
In the adult,
your growth plates are no
longer active.
And so you don't keep
growing taller.
So if you look at an x-ray
of a child or a teen,
you'll actually see this
epiphyseal growth plate.
It looks almost like a fracture,
but it's really just a cartilage
not showing up on the x-ray
because of these growth plates
the cartilage looks similar
and dark.
It doesn't look actually
like bone.
And when you're actually an
adolescent or child,
you can actually sometimes get
fractures if too much force is
placed on these growth plates.
And that's called an
epiphyseal fracture.
So some of the hormones
that signal to your bones
to grow taller or longer
or bigger are growth hormone
testosterone and estrogen.
In all of these, you'd expect
to go up during your various
growth spurts.
Until you get to an adult,
then those little growth plates
are turned into bone.
And you're no longer
growing taller.
But your bones are
still remodeling.
The bones repair if they break.
They can weaken
if you don't exercise
or you just get older.
And so it's important
to remember
that bones are dynamic
and always remodeling throughout
our life.
The next thing we're going
to do is talk a little bit
about bone repair looking
at remodeling after a fracture
and also when you exercise.
So obviously,
you know bones can repair
after you break a bone.
And they can actually change
when you stress them.
They can get stronger
or weaker depending
on what you're doing.
So bones are
in a continual state of change.
So let's look at the steps
in fracture repair
or actually just as a summary.
In an adults,
we can either increase the
diameter of our bones.
That seems to be intramembranous
ossification
that happens right underneath
that little periosteum
where our bones slowly grow
in diameter,
and they can grow stronger.
Again, it involves stem cells
and connective tissue
and so we call
that
intramembranous ossification.
If you ever fracture a bone,
that seems to be collagen --
cartilage excuse me --
cartilage collagen
and connective tissue being
turned into bone
which seems a lot
like endochondral ossification.
And so we'll go
through the specific steps
of that next of fracture repair.
So again, fractures heal
on their own, hopefully,
most of the time.
This was a really bad break.
That probably needs some help
to fix that fracture.
But what are the steps needed
for the body
to repair that bone.
And again, we said it's very
similar to
endochondral ossification.
So the first thing
that happens is you break your
bone which rips
through the periosteum
and crushes and destroys some
of that compact
and trabecular bone.
And there's lots and lots
of bleeding
because we have the bone marrow
spaces, and all the blood
vessels get torn
through our bone
and so we have lots of bleeding.
Maybe even some internal
bleeding and swelling.
One of the first things
to happen is a blood clot forms.
And the clot formation is
important because part
of that blood clot will involve
the protein called fibrin.
So we create this little fibrin
protein meshwork which is going
to help create a scaffold
for healing.
We're also going to have a lot
of hematopoietic stem cells --
blood stem cells
from both the blood
and also the bone marrow
and also osteogenic stem cells
as well.
And so that fibrin clot will be
important to help those little
stem cells grab on
and start getting activated.
The next step is going to be
when those little stem cells
help create a callus formation
which is mainly cartilage.
So it's probably going
to involve chondroblast
and fibroblast
which start making a lot of,
a lot of collagen.
And some of this collagen is
going to be in the form
of cartilage.
And so you make this big,
giant knot of cartilage.
We call that a callus.
That collagen now is going
to be our scaffold
for bone formation.
And so you remember
when we turn one tissue
into bone it's
called ossification.
Since we're turning mostly
cartilage, connective tissue,
into bone we call it
endochondral ossification.
So slowly over time now our
osteoblast turn
that cartilage into bone.
And so now we have a
bony callus.
Eventually,
we'll start remodeling
that bony callus with things
like osteoblast and osteoclast.
And hopefully get
that periosteum back covering
the bone.
And get the bone remodeled more
like the bone
that we had before the break.
So now again,
through ossification we have
this bone remodeling
that now the bone is repaired.
And so again, I'm just drawing
in some compact bone.
That compact bone will be
remodeled eventually
to trabecular bone creating any
marrow spaces
that are needed that'll involve
coordination of osteoblast
and osteoclast.
And you might be saying, hey,
it looks good
as new except it's a
little crooked.
Well, that's why often we need
things like plates and screws
and things like that
to help it remodel perfectly.
The other thing I wanted
to remind you is
that there's quite a rich blood
supply to our bones
that comes kind
of through the periosteum
through the compact bone.
There's little tunnels,
and there's also lots of nerves.
So that's why there's
so much bleeding and pain
when you break a bone.
There can even be bone death
if the blood vessels are
interrupted
that supply your bones.
And, of course,
sometimes we need help
in repairing our bones
like hardware and casts.
Bones remodel in response
to forces like gravity
and muscles pulling on them.
So examples are sports
which stress our bones
or being lazy
which causes your bones
to not be stressed.
And our bones are actually
modeled to meet those demands.
If you've had braces,
your teeth had to move around.
Inside, your bones were modeled
around those little teeth
so that they could move.
So a classic study is
to study unilateral athletes.
So unilateral athletes use one
arm versus the other.
And so we can actually see does
that arm --
does the bone
in that exercised arm
when it's stressed,
does it actually change
and does the bone adjust.
So remember the dominant arm is
the one stressed by throwing
or pitching or tennis.
And then the nondominant arm is
not stressed as much.
And the results
of these studies seem
to show mostly
that the dominant arm will have
a greater diameter,
bone diameter.
And a greater bone density,
meaning it's more dense
and more strong.
So the bone is actually bigger
than the nondominant arm
in these pictures.
And then, of course,
in sedentary or normal students,
there's no difference
in the dominant
versus nondominant arm.
How does this take place?
Well, stress
on the bone is sensed
by osteocytes which live
in the bone matrix.
The osteocytes then turn
on osteoblast
and turn off osteoclast
so that the bones seems
to grow thicker in diameter
and higher in density.
And that then makes the strength
of the bone increased.
So the osteocyte seems
to be the main sensor
of stress activating the other
cells to either build bone
or remove bone.
In the case of exercise
in the dominant arm,
it'll actually slow
down the osteoclast and turn
on the osteoblast
so your bones become bigger
and stronger.
We can actually see that.
So again, the dominant arm
increases in density,
increases in strength
to meet the demands
of the stress.
An interesting thing is
if you look
at the nondominant leg
and the dominant leg,
so comparing the leg,
people push off their opposite
leg which is called the
nondominant leg.
And in baseball pictures that's
actually stronger
with a higher bone density
and bone diameter.
So the remodeling is
very specific.
Probably more appropriate
for all of us is whether you're
exercising or not.
So for example,
if you're injured
and in a hospital,
your bone density will decrease
because your bones aren't being
stressed and same
if you don't exercise.
Your bone aren't stressed
so the bones will actually sort
of have less density,
and they'll slowly break down.
The reason is the osteocytes
don't feel any stress.
They signal to the osteoblast
to turn off.
And they turn on the osteoclast.
So when you turn
on the osteoclast,
they start chewing up the bone.
And the osteoblast stop building
the bone.
And so you start releasing the
bone matrix of collagen
and calcium and phosphate
into the extracellular fluids.
So basically,
your bones start breaking
down if they're not stressed.
Explain the mechanism
of calcium homeostasis.
So hopefully you remember
that homeostasis is stability
in the body.
In the case of calcium,
we're talking
about keeping calcium levels
stable in the body's fluid
or very bad things can happen
like your brain and your heart
and your skeletal muscles
and other organs can
stop working.
So we want to keep our
extracellular calcium stable.
And you've probably seen ads
before talking
about how good milk is for you
and for your bones.
And so, of course,
calcium's good for our bones.
But we're going to talk more
about calcium being good
for the rest of our body.
So calcium is for your cells.
I want you to remember that.
So since our cells live
in extracellular fluid,
that extracellular fluid has
things like sodium and chloride
and potassium,
but also now calcium.
Calcium floats around in
that extracellular fluid.
And calcium's going
to be critical,
important for all of our cells
in our body, especially cells
like our heart cells,
our cardiac muscle cells,
our skeletal muscle cells,
and smooth muscle cells.
So all the cells
of the body actually need
calcium in order to function.
The most famous ones will be
ones like our heart
and muscles --
smooth muscle in your stomach
and your intestines,
neurons in your brain
and in your spinal cord --
all of those.
Every time they're active,
they need calcium to rush
in in a little burst.
And so calcium's going
to be important
for all these cells to function.
If you don't have the right
levels of calcium, too high
or too low,
you can start messing
with the function of your brain
and messing with the function
of your heart,
which is never good.
All right, so when we talk
about homeostasis, we're talking
about the extracellular fluid.
And extracellular fluid calcium
level's about the same
as the plasma fluid
calcium levels.
So when doctors talk
about plasma calcium,
they're really just talking
about the calcium levels
in your extracellular fluid.
Or if we just say blood calcium,
again we're talking
about extracellular fluid.
Calcium levels inside your cells
is usually pretty low.
Of course, it's important,
but what we can measure easily
is the extracellular
or plasma calcium levels.
So what about calcium
in our bones?
Well, of course,
calcium's important
for our bones --
for our bones to be strong
with the mineral being partially
calcium and then the other
part phosphate.
So if you have enough calcium
in your body, of course,
you can store it in your bones
which will give you strong
healthy bones.
But that calcium's also
important to keep your
cells alive.
So if you ever don't have enough
calcium floating around
and your cells need more,
you'll take that calcium
from your bones to give it
to the cells.
So now I like to think
of calcium's more important not
for your bones
but for your body's cells.
So again, head and the heart,
the brain, the heart require
that calcium
and will literally take it
and steal it from your bones
in order to give these cells
enough calcium
to keep you alive.
In order to understand how the
body regulates calcium levels
in the fluid, we need to think
about the endocrine system a
little bit and hormones.
Hopefully, you remember
that hormones are chemical
signals carried around the body
in the bloodstream.
So if you make a hormone,
it'll circulate
around your entire body
in your blood vessels.
And so the endocrine system's
all about hormones and signaling
to the body.
We're going to just look
at two hormones
that are critical
for extracellular
calcium regulation.
The first hormone is called
parathyroid hormone,
or PTH for short.
It's made by these little teeny,
tiny glands in your neck,
right by your thyroid gland.
The other hormone is called
calcitriol or sometimes we'll
just call it active vitamin D 3.
Vitamin D 3 is made
in places throughout your body,
but mainly activated
in your kidneys.
So your kidneys are going
to be important
for making calcitriol.
So these two hormones are going
to be important
in regulating our body calcium.
Let's start
with parathyroid hormone made
by our parathyroid glands.
You actually have cells
in those parathyroid glands
which literally are
calcium sensors.
Whenever calcium's too low,
those little cells get concerned
-- well, they don't really care
-- but they notice it.
And when calcium's low
in your body or your plasma
or your blood,
those little parathyroid gland
cells will release
and secrete PTH,
parathyroid hormone
into your bloodstream.
It'll circle all
around your body
and target specific organs.
So again, parathyroid hormone is
a hormone released
to target body cells in order
to regulate your calcium levels.
Well, if the problem is reduced
calcium and those little cells
make PTH, we're going to signal
to our bones in order to slow
down our osteoblast and turn
on our osteoclast
so that would chew up the bone
and release that stored calcium.
So PTH signals
to those little cells
to release calcium
into the fluid of the body.
And that's going
to help correct our problem
with low calcium.
It's going to tell the kidneys
and the little cells
in the kidney tubules,
which you remember those little
tubules cells.
It's going to tell those little
tubules cells to keep calcium
in our body.
Don't let the calcium go
out in your pee, in your urine.
And so again,
that's PTH is signaling
to your kidneys
to help keep calcium
in your body
which is helping our problem
which is low blood calcium.
So we're going to reabsorb
that calcium in our kidneys.
The other thing that PTH does,
it tells those little kidney
cells to make the other hormone
we talked about
called calcitriol.
So calcitriol gets activated
in the kidneys there.
And then the target
for calcitriol is mainly
the intestines.
It also targets the bones,
but in the intestines it tells
those little intestinal cells
to pick up the calcium
from your food.
So again, all of these responses
in response to PTH
by our cells is
to help increase our calcium
levels back up to normal.
And so in that way PTH
and calcitriol are regulating
our calcium homeostasis
because in this case we
have hypocalcemia.
We release lots of PTH,
made come extra calcitriol.
Those signaled
to our body's cells
to bring our calcium levels back
up towards normal.
Again, that's an example
of negative feedback regulation
and homeostasis trying
to keep calcium stable
in our body.
Okay, so if you have low blood
calcium, you're going
to make lots of PHT
and more calcitriol.
So summary,
parathyroid glands sense
low calcium.
We increase the amount
of PTH circulating in our body.
Tells your kidneys
to keep the calcium.
Tells your intestines
absorb calcium.
And tells your bones
to release stored
up calcium, okay?
And so when you look
at your urine, if you have lots
of PTH, you'll have very little
calcium in your urine.
Funny, you actually have lots
of phosphate.
That's one of the signals
of PTH is to get rid
of that phosphate
from your bones.
So you want to keep the calcium
and get rid of the phosphate.
If you have too much calcium
in your body,
so if you have too much
from your diet
or maybe your bones are breaking
apart for whatever reason,
in that case your PTH will go
down because your little
parathyroid cells will be like,
well, we have too much calcium.
So we'll have low PTH secretion.
The kidneys
in that case will let the
calcium go out in your pee.
And you'll pee out lots
of calcium.
Your intestines will absorb less
calcium, and it'll just stay
in your food and go
out in your poop.
And, of course,
the bones won't be chewing up
and releasing
as much stored calcium.
Again, that will help reduce our
calcium back down to normal.
All of it involved just changes
in PTH.
All right, so that's how our
body regulates calcium mainly
with PTH.
I just wanted
to mention a little bit
about where does calcitriol
come from.
Again, calcitriol has a couple
of names active vitamin D 3.
If you go to medical school
125 cholecalciferol.
Where does vitamin D
and calcitriol come from?
Well, active vitamin D needs
to be made in your body.
But vitamin D can come
from your milk
and your pop-tarts
and your food.
And also vitamin D is made
when sunlight hits your skin
and converts cholesterol
into vitamin D. Vitamin D though
needs to be activated
and chemically transformed
into calcitriol,
active vitamin D 3.
And that occurs mostly
in the kidney.
So the kidney's job is
to convert vitamin D
to vitamin D 3.
Again, we know calcitriol then
goes and helps bring
up our calcium levels
by targeting our intestines.
But it also targets your bones
to make your bones healthy.
So remember calcitriol
and vitamin D are needed
for healthy bones.
We can see this
because if you ever have low
calcitriol,
you'll have weak bones.
And the bones won't be
properly mineralized.
An example of this is called
rickets or osteomalacia
in adults.
And I think vitamin D is talked
about a lot for health
of other origins as well.
Sometimes when your kidneys are
sick, for reasons
that aren't related
to your bones,
but your kidneys are sick,
they won't make the right levels
of calcitriol
because remember they form the
active form
of vitamin D 3 calcitriol
which then can affect
your bones.
So if you don't have enough
calcitriol,
you won't probably have enough
calcium in your body.
And you won't have correctly
mineralized bones.
Is calcium good for bones?
You hear that a lot.
And of course,
we need to have some calcium
coming in in our diet
because we're peeing a little
bit of calcium
out in our kidneys
and in our pee.
So you have
to have enough calcium coming
in in your diet each day either
from milk or dairy
or certain green leaf vegetables
and other sources in order
to keep your bones healthy.
An interesting example
of calcium homeostasis is
if you look at astronauts
in zero gravity.
In zero gravity, you remember
that your bones don't have the
correct stresses on them
because you don't have gravity.
In that case,
the osteocytes tell your bones
to break down by signaling
to the osteoblast
and the osteoclast.
The osteoclast start chewing
up your bone,
releasing that calcium
into your body's fluid
and into the bloodstream.
And suddenly now when you're
in space, you have these really
high calcium levels
in your plasma
and in your extracellular fluid.
This then affects the little
parathyroid cells
to stop secreting PTH
or lowering their PTH secretion.
When you have low PTH,
if you think
about the body's response,
the kidneys are then going
to figure, well,
I should just pee
out the calcium
because you don't need
to keep it in your body
because you've got too
much calcium.
So you start peeing out lots
of your calcium that's basically
coming from your bones.
And if you're an astronaut,
hopefully, you're peeing
in a little bag.
The other thing is calcitriol
will go down,
and so you won't be absorbing
as much calcium
from your diet as well.
And those things will bring your
calcium levels back down.
And possibly even the low PTH
would hopefully slow
down that bone break down.
But the whole case you had here
was to regulate your body
calcium back to normal.
You'll still have weak bones
though because your bones were
being broken
down by the lack of stress.
There's lots
of interesting bone health
and bone disease issues.
Hopefully, we'll cover some
in class.
But that's it.
This is the end of the video
so I'll see you guys in class.
Bye.