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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.

>> This video is on bone

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B2 中高級 英國腔

BIO160 預覽視頻 第8講--骨骼與鈣質 (BIO160 Preview Video Lecture 8 - Bones and Calcium)

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    李佳憶 發佈於 2021 年 01 月 14 日
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