Anatomy and Physiology Chapter 6 Part B: Bones and Skeletal Tissue Lecture

0:00So we're going to be starting u or

0:02continuing actually with chapter six. Uh

0:05this is a part B on bones and skeletal

0:07tissue. So um now

0:12for bone development the terms

0:14osteiogenesis and o uh oification

0:17they're are synonyms so they're used

0:19interchangeably. Uh this describes the

0:22process of bone tissue formation.

0:24Now in the embryo uh this process uh the

0:29process of ocification uh it leads to

0:31the formation of the bony the bony

0:33skeleton and this starts at uh the two

0:36month uh the two month mark. So right

0:37around the second month of uh

0:39development uh and remember this is

0:41called prenatal development. Okay. So

0:43prenatal means you know before birth

0:45postnatal post means after birth after

0:48birth. So post-natal bone development,

0:50bone growth, it continues uh well into

0:53early adulthood. U

0:56the process of bone remodeling and bone

0:59repair is ongoing. It's lifelong. Uh so

1:03again even after postnatal bronco goat

1:05stops uh remodeling continues throughout

1:08your life. Uh it doesn't end.

1:13So uh the formation of the bony skeleton

1:16at up to about 8 weeks the fibrous

1:19membrane and highening cartilage of the

1:20fetal skeleton they replaced with bony

1:23tissue.

1:24So when the uh the the the bone when it

1:29develops uh by replacing

1:34uh highen cartilage we call that uh

1:37endocchondrial oification. Okay. And uh

1:41the bones they're they're they're called

1:43cartilage or endocchondrial bones. All

1:46right. Now the other type is this in

1:49membranous oification. As the the the

1:51name implies this uh type of bone

1:54development occurs from the uh the

1:56fibrous membrane. And these bones are

1:59called the membrane bones. Now the

2:01difference between these two we're going

2:02to be looking at in in detail in a

2:04little bit but in a nutshell most of the

2:05the flat bones these are these uh

2:07intrammebranous ocification the these

2:10bones develop through intram

2:11intrammebranous ocification while the

2:13majority of your the bones that make up

2:15your lungs and the long bones they tend

2:16to be uh endocchondrial uh uh developed

2:19by endocchondrial ocification.

2:23For endocchondrial oification this

2:26excuse me this forms just about all your

2:28bones in your body that's below your

2:29skull. The exception being are your

2:31collar bones, your clavicles. Uh it

2:33starts uh in the later part of the

2:35second month of development and

2:39it uh it uses the the the the previous

2:42bones uh this highen cartilage uh that

2:46was formed earlier on as a model or

2:49pattern for the bone construction. uh

2:51it's more complex than intram membranous

2:54ocification because the highen cartilage

2:56it has to be broken down uh in order for

2:58the ocification to proceed. Uh we're

3:00going to be looking at uh we're going to

3:02be talking about both these things in

3:03details as we move forward. But uh this

3:06process it starts um at a primary

3:10ocification center. Okay. And this is

3:12this prim primary ocification center is

3:15found in the center of the shaft of the

3:18bone.

3:20So what happens is blood vessels they

3:22infiltrate the paricchondrium and once

3:25that happens it converts it into a

3:27perryioium. Okay. So once you get blood

3:30vessels coming in it brings life. In

3:32other words it kickstarts uh this uh the

3:35the this uh bone formation process this

3:38oification process. The meenyal cells

3:41they uh specialize into the osteoblasts.

3:44And remember these osteoblats these are

3:46the bone building cells.

3:48Now that you know you've got these

3:50messenal cells that are you know

3:52starting to specialize into osteoblast

3:54and you got the the the blood vessel

3:56that's come in there and all the

3:58processes kicked off. Let's look at how

4:00the next steps occur. What happens next

4:03afterwards?

4:05So there's five steps that are in the

4:07process of oification. The very first

4:09thing that happens is this. The

4:11osteoblasts uh they start secretreting

4:13osteoid against that hymn cartilage

4:16diaposis. And what this does is that the

4:19the bone now becomes encased as are

4:21being pushed out. Now once once that

4:25happens that freshly formed layer of

4:27bone that's what's called the pio pio

4:30bone collar. Okay. So the next thing

4:33that happens is this step number two.

4:37So as the collar forms the condraides

4:39that are found within the shaft they

4:41enlarge and they signal the the

4:42surrounding cartilage matrix to calcify.

4:45Now because the the cart cartilage

4:47matrix is now calcified nutrients they

4:50can't diffuse through so it's

4:51impermeable uh and then what happens is

4:54the condraittes they end up dying

4:55because it's you know they're not able

4:57to get their nutrients and then

4:58eventually the entire matrix starts to

5:00deteriorate.

5:02Now this when it starts deteriorating it

5:04ends up opening up cavities. Uh but

5:07however now the highen cartilage uh it's

5:10stabilized by the the collar bone that's

5:12there. Okay. It's not going to just fall

5:13upon each fall down. But now remember

5:16this is just happening in the shaft.

5:17Okay. Now other parts uh in the

5:20cartilage that's still healthy and it's

5:22going to continue to grow. Uh usually

5:24what happens how it's going to grow is

5:26that it's going to get longer. So it

5:27starts it's going to elongate. Uh but at

5:30this point all the changes taking place

5:33within that shaft. So now we go on to

5:36the third step number three.

5:39So the the cavities we had from the

5:42previous step they start getting invaded

5:44by perryioial buds. Now these perryio

5:47buds they contain the nutrient arteries,

5:49veins, lymph vessels, uh nerve fibers,

5:52red marrow, osteoblast and osteoclass.

5:55Now these osteoclass this they start

5:58partially eroding the calcified

6:00cartilage matrix and the osteoblast they

6:03start secretreting osteoid around the

6:05remaining fragments of alen cartilage.

6:07Now when they do this it starts forming

6:09bone covered uh cartilage tbacula

6:12and that's how you end up with spongy

6:14bone. Now for the fourth step as a

6:18primary oification center enlarges

6:20osteioclass they break they break down

6:22that newly formed spongy bone and when

6:24they do this it opens up a medularary

6:25cavity in the center of the diaphosis.

6:27Now up until uh the ninth week

6:31the epiphosis is only it's made up of

6:33only of cartilage and highland cartilage

6:35model it continues to elongate by the

6:37division of the the cells at the

6:39epiphosis. Now oification it ends it

6:42chases this cartilage formation along

6:45the length of the shaft as cartilage

6:46calcifies it gets eroded and then and

6:49then it's replaced by these uh by bony

6:51spicules on the epiphysial surfaces uh

6:54facing the meillary cavity. So this is

6:56how you we we start seeing this uh

6:59secondary oification

7:01centers to appear.

7:04So uh in the fifth step what happens

7:06what's happening is this the the

7:09cartilage in the center of the epiphosis

7:11it calcifies and it deteriorates. When

7:13this happens it opens up cavities that

7:15allow the perryio buds to enter. Now

7:17what's going to happen at this point is

7:19the same thing that happened in step

7:20three over here. uh because remember you

7:23got blood vessels, nerves, red mineral,

7:25osteogenic cells and osteoclass. So

7:27essentially what happened over here is

7:29now going to uh

7:31almost the same thing is going to happen

7:32over here. The exception being is this

7:34though. Um there's not going to be a

7:38bone marrow that's formed. Okay? You're

7:39not going to get a a medularary cavity.

7:41Instead, you're going to end up getting

7:42all spongy bone over here.

7:46So uh the bone tacular pair and then you

7:49have spongy bone at this point. Now um

7:52with secondary ocification uh when it's

7:55complete highland cartilage it remains

7:58only in two places okay on the uh the

8:01epiphysial surface as articular

8:03cartilage and at the junction of the

8:05diaphas and epiphosis where it forms the

8:07epysial plate.

8:11So in this picture what you what we have

8:13going on is this the osteoblast they're

8:16starting to secrete the osteoid and then

8:17what you end up having is uh you're

8:19starting to get this bone collar that's

8:21forms over here. All right and this is

8:23kind of what's keeping this entire

8:25structure in shape. Okay it's pre

8:27preventing it from falling collap

8:28falling upon itself. Uh and then you

8:31have this primary oification center also

8:33that you start to see. Now moving

8:36forward past week nine what we having is

8:38this the cartilage in the center of the

8:41diaphosis it's starting to calcify okay

8:43once it starts to calcify it starts to

8:46make this cavity now this third step is

8:49this when you start getting these

8:51cavities now you have room for these uh

8:54uh the the the perryioial buds to come

8:58and invade. So now what do you have? You

9:00got blood vessels coming in and nerves

9:01and then you have these osteoblast and

9:03osteoclast. So in other words at this

9:05point now the thing things are going to

9:07start uh you're going to start seeing

9:09the dramatic change over here cuz now

9:11you just got the lifeline of blood

9:13vessel. Okay remember blood all the the

9:15everything gets transported through

9:17blood through the blood vessels. So now

9:19let's see what happens next.

9:22In the fourth step what you see is this.

9:25Notice that uh you you have a cavity

9:27that forms now because remember the

9:28osteoclass they came in they start

9:30chewing away all the tissue that was

9:32there. Now we have osteoclass again you

9:34got the blood vessels that further start

9:35to uh to to expand and they start

9:37creating this capillary.

9:40Um also you're starting to see these

9:43secondary oification centers. They're

9:46not quite developed yet. That should be

9:48in the they start to to form over here.

9:51However, when you go to the fifth stage

9:53over here and this will happen uh this

9:56will happen after birth or sometimes

9:58right before birth this is when these

10:01epiphosis they will oify. So now the

10:05main difference is this uh at this point

10:09is that uh you end up getting

10:12these blood vessels. So when these blood

10:14vessels they enter then you end up you

10:17get you get the the spongy bone that

10:19starts to form over here. Now the main

10:20thing over here is this that over here

10:24where we had the the uh uh when the pios

10:28entered same thing happened you have the

10:30parasal buds enter over here also

10:31however over here it form the medularary

10:33cavity but at the epiphosis you're not

10:35going to get these cavities forming

10:36you're just going to end up with spongy

10:37bone okay so uh now once that happens uh

10:42once the epiphosis it calcifies only

10:44place you're left with with cartilage is

10:47at the uh the uh epicial plate and at

10:51the end of the bone. Uh so it's

10:54articular cartilage over here and then

10:56it's uh the the epicial uh plate

10:59cartilage over here and over here. Okay.

11:02So remember these are the epiphosis. The

11:05epiphosis is the area between the uh the

11:09uh the epicial plate. It's the it's the

11:11area it's what separates the epiphysis

11:13from the diaphosis. Okay.

11:20Now we're going to be talking about uh

11:22intramebr intramebranous ocification. Um

11:27so intrammous ocification it begins

11:29within the fibrous connective tissue

11:31membrane that's formed by the mezenymal

11:33cells. Now remember these messenymal

11:36cells uh they are able to specialize

11:38into other type of cells just like we

11:41saw in the in the previous uh in the

11:44previous scenarios with the

11:46endrochondrial ocification. Uh so we're

11:48going to be seeing a lot of that

11:50somewhat similar stuff going on over

11:51here also. The process is relatively

11:54similar uh and we're going to be talking

11:56about that. But uh now uh before we get

11:58to that keep in mind that end

12:01intramembrane classifications it forms

12:03the bones of your skull your clavicles

12:06in addition to that your jawbones also

12:07your mandible. Um so the four major

12:11steps that are involved are as follows.

12:14Now ocification setters they formed when

12:16these messenymal cells they start to

12:18cluster and then they they start to

12:20aggregate

12:22and then uh they specialize into these

12:24osteoblasts. All right. So as they uh

12:28once they specialize into osteoblast at

12:31that point they start secretreting

12:33osteoid. So this remember this osteoid

12:35is going to end up being the matrix. So

12:38uh once that osteo is secreted then

12:41after some time passes it starts to get

12:44calcified uh by calcium and other

12:46mineral salts that come in. Now the next

12:49step uh number three what happens is the

12:53woven bone is forming at this point. Now

12:56this happens when the osteoid is laid

12:59around these blood vessels. So these

13:01osteoids when they and what you have are

13:03these these um these primitive

13:07embryionic blood vessels. So when these

13:10osteoids they start laying themselves

13:11around it then you end up starting

13:13getting these bones that form around

13:15these blood vessels. So and these bones

13:17are are called these tbacula right and

13:20this is going to be essentially what you

13:22end up having uh to be the remnants of

13:24this spongy bone. Um now

13:28at the same time as this is going on

13:30what's also happening is the outer layer

13:32of the of the woven bone it forms the

13:34perryioium.

13:36Now what's going to happen is this in

13:38the next step is that laminal bone it's

13:41going to end up replacing uh these woven

13:44bone and the red bone marrow starts to

13:46appear.

13:48So let's look at what happens

13:49graphically of the previous steps that

13:51we just went over. So in the very first

13:53center what's going to happen is this.

13:54you have these messenymal cells. Now

13:56these messylchymal cells they end up

13:58specializing into these osteoblasts. All

14:02right. Now when the after these the

14:04messy cells they turn to this osteoblast

14:06they start to aggregate they start to

14:08cluster up and when they start to form

14:10they when they start clustering up this

14:12is when you end up uh getting what we

14:14call this oification center. Okay. Now

14:16in the second step what happens is that

14:18these uh the these u uh these uh uh

14:22these osteoblasts you can see over here

14:25that they're starting to secrete this uh

14:27these osteoids. Okay. Now these osteoids

14:30you see you saw over here that they

14:32started to secrete this. However, it's

14:34over here that there's further secretion

14:35that takes place and then uh what ends

14:38up happening is uh uh it start the as

14:42the calcium and other mineral salts they

14:44start to come in uh these osteoids they

14:47start to harden up. So in other words it

14:48starts to calcify. Now the other thing

14:51that you see over here is this in this

14:53uh in this uh picture over here. Now in

14:54step two

14:57the some of these uh two of these in

14:59this uh case right here two of these

15:01osteoblast they ended up coming to the

15:03center and now what ends up happen what

15:07ended up happening is this as this u the

15:10the ground matrix as it calcified these

15:13cells they turn into or they they were

15:15further able to specialize and turn into

15:17osteoccytes. Now these are the cells

15:19that are eventually that's going to

15:20maintain uh this uh this bone cell.

15:23Okay.

15:26Now in the third step, let's see what's

15:29going on over here. Now in the third

15:32step, what's going to happen is this.

15:34Notice what we have going on over here.

15:36So the the one of the main things that

15:38we see that's different from here to

15:39there is now we're starting to see uh

15:41these uh cavities that are forming. In

15:44addition to that, you see these blood

15:45vessels that are coming in. All right.

15:47Now these osteoids that have been

15:50accumulated that are laid down between

15:53the these embryionic blood vessels they

15:56start to form these uh these tbacula.

16:00Okay. Or in other words what we call

16:01this woven bone which is essentially

16:04going to end up being the spongy bone.

16:07So the vascular mezzenine uh condenses

16:10on the external face of this woven bone

16:12and it ends up becoming the perryostium.

16:18So in the next step again you can see

16:21over here what's happening this mezenine

16:24uh is uh now it's turned into this

16:27fibrous perryostium.

16:31Now uh the osteoccytes that you have

16:34that are uh at the edge of these the the

16:36the tbacula uh so again the trabacula

16:40that's just deep to the perryioium they

16:42end up uh turning into these laminal uh

16:46into the the the lamalar bone okay so

16:48they further again through the process

16:50of remodeling they end up specializing

16:52and they turn into this lamalar bone

16:54that you see here or the compact bone

16:56now the the spongy bone the diplo uh

16:59it's made up of these

17:00what we call the tbacula. All right. And

17:03what it is essentially uh it ends up

17:05forming these compartments that go

17:06around these blood vessels and that ends

17:08up becoming this red bone marrow or the

17:11red marrow.

17:18So in postnatal bone growth so um after

17:22you're born again during infancy and

17:24youth long bones uh they grow

17:27lengthwise. So they lengthen entirely by

17:29interstial growth of the efficial plate

17:31cartilage and then it ends up getting

17:33replaced uh by bone. Uh so all bones now

17:37when we're talking about how they grow

17:39in diameter and thickness this happens

17:41through appositional growth. Now bone

17:44growth uh it stops during adolescence.

17:46Towards the end of your adolescence this

17:48is when this is when it stops. uh in in

17:51boys it's usually around the age of 21

17:53and then in in in girls or in women it's

17:55at the age of 18. However, some of the

17:59facial bones they continue to grow

18:01throughout your life.

18:03So let's take a look in uh growth in the

18:08the length of long bones. Now u this uh

18:13uh these events uh in longitudinal bone

18:16growth they mimic a lot of the stuff

18:18that goes on in endocchondrial

18:20oification. Now in order for interstial

18:22growth to occur uh you need to have uh

18:25the epical cartilage within the epical

18:29plate. Okay. So the epitheal plate it

18:32maintains a constant thickness. Uh now

18:35how it does is is that the rate of the

18:37cartilage's growth on one side gets

18:39balanced out by the bone replacement on

18:41the other side. Now we're going to be uh

18:44as we go through these steps you're

18:45going to understand what this means and

18:46how this occurs. Uh but there's five uh

18:50zones within this epical plate. The

18:52resting zone, proliferation zone,

18:54hypertrophic zone, uh the calcification

18:57zone and the oification zone.

19:01So the very first part now uh the

19:04resting zone now this is a part of the

19:08the area of the cartilage that's on the

19:10epicial side of the plate. Okay. So what

19:14now one of the things that you guys need

19:16to to understand is this. Do not forget

19:18the terms. When we're talking about the

19:20epiphosis we're talking about the ends

19:22of the long bones right and when we talk

19:23about the diaphosis we're talking about

19:25the long part. Okay the area between the

19:28epiphosis. Now remember when long bones

19:30what do you have? You have the ends. So

19:31the ends are the epiphosis and the

19:33middle part this is the the diaphosis.

19:35So now uh what they're talk what they're

19:37saying over here is this the cartilage

19:41that's on the the let's look at a

19:43picture before we go over here so you

19:44guys have a better idea of what's going

19:45on. So when you look over here this is

19:47the the the epiphosis right over here.

19:49Okay the this epicial plate. So now the

19:52cartilage and this is what they're

19:54talking about when you're talking about

19:55the cartilage that's facing the

19:56epiphosis side. So that's up here and

19:58the car that's facing the diaphosis

20:00side. This is the part down here. So

20:02remember this is the facial plate and

20:04this is the area that we're talking

20:05about now. So let's go back up over here

20:07now back to number one. And uh so what

20:11they're saying is that uh yeah the area

20:13of cartilage on the epiphysic side of

20:15the plate is relatively inactive.

20:20However, the cartilage that's facing the

20:23side of the diaphosis. Okay. uh this is

20:27uh in this zone it's not uh inactive.

20:31This side is actually dividing quite

20:33rapidly. Now this is this represents a

20:36different zone and this is called the

20:38proliferation zone or the growth zone.

20:41So let me let's go back to this uh to

20:43that slide over here. Now this is the

20:44part that we're talking about this

20:45resting zone. This up over here okay

20:47this very top part. But now when you

20:49look over here, this is this very active

20:51zone, the the proliferation zone. And

20:54these cells over here, they're they're

20:55they're undergoing mitosis. This is a

20:57very it's a highly motic area.

21:03So as these cells are dividing, they

21:06start to to accumulate in stacks. So it

21:08kind of looks like stacks of coins. Now,

21:11as this is happening, uh the di the ends

21:14of the bones are starting to get pushed

21:16away. So what's happening is is that u

21:18the diaphosis is lengthening. So as more

21:20and more cartilage is being the these

21:22cells are are being added which takes us

21:25to the next next part of the of the of

21:28this the next zone zone number three.

21:33So as the the condraittes in the

21:35proliferation zone as they continue to

21:37divide motically and uh you end up

21:40getting this lengthening

21:42taking place uh within the cartilage the

21:45older condraittes that are now closer to

21:47the diaphosis they start to uh to get

21:51big they start to enlarge. Okay. And

21:54when this happens uh this is starting to

21:56set up uh the neuh everything for the

21:58next stage because as they're enlarging

22:02uh they're um the the lacun for these

22:06condra sites they start to erode. All

22:09right. Now this leaves these large

22:11interconnecting spaces. So when you look

22:14at the next page the stage the

22:16calcification

22:17zone uh the surrounding cartilage matrix

22:20it calcifies and these condraides they

22:23die they deteriorate. Now you have and

22:26this is why we call it this

22:27calcification zone. So this leaves these

22:29long uh these spicules of calcified

22:33cartilage at the epiphosis diaphosis the

22:36junction. So what's going to happen now

22:39uh in this next zone this oification

22:42zone uh at the spaces from our previous

22:45step uh they get invaded by uh marrow

22:50elements from the medularary cavity. Now

22:52the carospicles they get partly eroded

22:54by the osteoclass and then they ended up

22:57getting quickly ced with new bone and we

22:59call this new bone the the the woven

23:00bone by the osteoblast. Ultimately it

23:04gets replaced by spongy bone. The

23:06spicial tips they eventually get

23:07digested by the ICU class. Uh this way

23:11you end up getting a medularary cavity

23:12that also grows longer as the long bone

23:16starts to lengthen during growth. Uh the

23:19the epicial plate it maintains a

23:21constant thickness because uh the rate

23:23of cartilage growth on its epiphosis

23:26facing side ends up getting balanced by

23:28the replacement with the bony tissue on

23:30the diaphosis facing side.

23:34Now, we're just going to go and look at

23:36everything that we just discussed with

23:38this picture, and it's going to better

23:39help explain what we just talked about

23:41in those steps, you know, in those five

23:43or six slides, however many slides that

23:44we had. So, remember this is the

23:46epiphosis. This is the diaphosis, okay?

23:49The junction between the epiphosis and

23:51this diaphosis over here, you have this

23:54uh the this epicial plate, okay? And

23:58remember you have to have you have

23:59cartilage over here

24:01between these two well within this area.

24:04Um now no cartilage this is not going to

24:06happen. Um now so we're taking looking

24:09at this magnifying this. Now the other

24:12thing that you notice is notice there's

24:14only four steps here but remember there

24:16was five. Um they kind of screwed this

24:18slide up a little bit and some of the

24:20information in my opinion is not very

24:22accurate uh or you know it's it's not

24:25very clear. So this should be number

24:28one. This should be two, three, four and

24:29five.

24:31Now remember in the first stage in in

24:34number one this resting uh in the

24:36resting zone or the resting cartilage is

24:38uh this kind of looks like highland

24:40cartilage also if you kind of if you

24:42look at it it resembles that. U now this

24:46uh resting cartilage over here it helps

24:47secure the the epiphosis to the epicial

24:50plate.

24:52All right the the the epicial cartilage

24:54to the epicial plate. Now, uh, also some

24:59of these cells that you find here, the

25:00condraittes, they're going to help

25:01contribute to what's going to go go

25:04what's going to take place in number

25:05two, okay? At the proliferation zone.

25:07So, in in step two, the condraittes

25:12over here, they're going under they're

25:14undergoing mitosis, okay? Rapidly

25:17undergoing mitosis. Um and as these

25:19cells are dividing, okay, they start to

25:24align themselves into columns. So they

25:26kind of resemble these stacks of coins.

25:28And these stacks, they they they run

25:30parallel to the diaphosis. Now, because

25:33of this, this is how this bone is

25:35lengthening at this point. All right?

25:37Now, now in the third step, uh what's

25:41happening is these old older stacks that

25:43we've had. So if you look over here

25:45again, these are these cells and there's

25:46a stack here. There's another stack

25:48here. There's a stack over here. So

25:50these are these stacks that we're

25:51talking about.

25:53So as these are lengthening, what's

25:55happening is this part is getting pushed

25:56upwards. All right. So this is getting

25:58this part is getting further away from

26:00the the the epiphosis as it starts to

26:03lengthen. All right. Now as this is

26:06occurring the older condraittes over

26:08here in step number three, they start to

26:12enlarge. So you can see over here what's

26:13happening. The cells are starting to get

26:15really big. they're start to hyper you

26:17know they're hypo hypertrophy over here

26:20now

26:21so also at this point in step in the

26:24third stage uh these cells are not

26:26dividing anymore right so all the thing

26:28that's happening is that they're growing

26:29in size uh at the same time uh the lacun

26:34they're starting to get thin right so

26:37they're starting to erode uh when you go

26:40down to the next stage four in step four

26:46So step four, if you look over here,

26:48there's only roughly two three roughly

26:51between two to three cell layers

26:54thick. This is how much uh how large

26:57this area is. So you're going to find a

26:58few layers of cells over here in the in

27:00the in the the fourth stage. And

27:02remember this is called the

27:04calcification zone. So already we had

27:06the the in in the in the previous step,

27:08we had these cells that are starting to

27:09get big. They're starting to enlarge. Uh

27:10they're luin they're starting to get

27:12eroded out. Well, now this is setting up

27:14the stage for this uh for the fourth

27:16part.

27:18At this point, what's happening is uh

27:20the mineral the calcium is phosphorus

27:22they're trying to get deposited now. All

27:23right, this is what's happening.

27:24Calcification uh this is why you call

27:26the calcification zone. So the matrix it

27:29calcifies uh the cells they're in the

27:32process of starting to die out. Now when

27:35you get to the fifth state step over

27:37here, the oification zone, the cells are

27:40dead over here. All right, the cells are

27:42dying. uh the walls the they're broken

27:45down between the luquin uh in these

27:47columns and now we have these spaces uh

27:49in over here that are formed if you can

27:52see the spaces over here now right over

27:54here. So what's going to end up

27:56happening is this within these spaces uh

27:59they get invaded by these capillaries in

28:02these osteopenerator cells. So these

28:04osteopenerator cells they give rise to

28:07either osteoblast and osteoclast. Now

28:10the osteoblast they're going to start

28:12laying down the new bone matrix. Okay,

28:14that's going to be uh eventually gets

28:16turned into the oified zone and the

28:17osteo class they start breaking down. So

28:20the the spicles that we're talking about

28:22uh from the previous uh steps they ended

28:24up getting broken down by the

28:25osteoclass. Right? So this is

28:28essentially what's going on uh in this

28:32uh this step or how this uh these five

28:35steps grow in the lengthening of bones.

28:38Okay. So you got nothing much going on

28:40over here in this in the first uh step.

28:43Okay, this resting zone except you know

28:45you have those condraittes that are

28:46helping to um the the second st the

28:51cells that you find over here uh they're

28:52kind of assisting them but nothing much

28:55is there. Remember their main job is to

28:57help secure the the fifths the to the

29:00plate. Now in this se this step once

29:03again remember what's going on is these

29:05cells they're undergoing mitosis right?

29:07So they're they're dividing constantly.

29:09As they're dividing, they form these

29:10stacks or these long columns. And as

29:13these columns get larger, it moves uh

29:16the it moves the the cartilage further

29:20away from the the epiphosis. So now

29:22you're getting the the lengthening in

29:23the bone that that's happening. So as

29:25you get more and more cartilage that's

29:26forming over here, it's going to

29:28eventually get oified. All right? So

29:30this is what what they're talking about.

29:32As more cartilage is laid down, the

29:34ocification occurs. you get more

29:35cartilage and then more more

29:36ocification. So let's just kind of go

29:39down again. This is how this bone is

29:41going to lengthens.

29:43So uh the the next step the third step

29:46which is number two over here u the

29:49cells now these stacks you see what's

29:50happened to them they change in shape is

29:52starting to get big. The lucquinate is

29:54start to thin out. They're starting to

29:55deteriorate. So in the fourth step as

29:58these lucinia are deteriorating what's

30:00happening is that the the these

30:03the cells they've enlarged the lucin

30:06starting to thin out now uh the salts

30:09are starting to come in okay the the

30:10minerals are coming so the

30:11calcifications is taking place at this

30:14point these the the condraides they're

30:16completely die out okay they're

30:18completely dead the matrix is

30:20deteriorating uh uh at this point and

30:24then in the fifth step finally you get

30:27the blood vessels that start to come in

30:29and now you got osteoblast and

30:30osteoclass. They start coming in and

30:32they start laying down and breaking

30:34about uh breaking about the old matrix

30:37and building up the new matrix uh laying

30:39down the new bone. Right. Uh

30:43so as this uh the next slide as it says

30:46uh towards the end of adolescence the

30:48condroblasts uh they they're not

30:50dividing as often. Okay. So that their

30:52activity decreases uh the plates start

30:54to thin out and then it gets replaced by

30:56bone. So at this epicial plate closure

30:59this happens when the the epiphosis and

31:01the diaphosis it fuses. Now when does

31:03this end? So in other words when does

31:05bone lengthening stop? Well in men and

31:07female in males and females it's a

31:09little bit different. Females it occurs

31:11a little bit earlier. So right around

31:12the age of 18 uh you'll notice that uh

31:16in females they will not grow anymore.

31:17So, uh, in males now, this usually

31:21occurs right around when they're 21

31:23years of age. So, at this point, you're

31:25not going to see any more growth. So,

31:28uh, again, uh, if you how do you find

31:30out for sure if if you're going to grow

31:31or not? Remember, not everybody's,

31:33remember, it says usually occurs around.

31:34If you go get an X-ray, all right, and

31:36they take an X-ray, the radiologist,

31:39they can tell if these uh the if this ep

31:43there's closure at the the epicial

31:44plate, all right, or not. So, if there's

31:46still cartilage there, that means, you

31:48know, you're still going to be growing.

31:50If there's not, if it's closed, that

31:51means, you know, you're not going to

31:52grow anymore. In other words, that's the

31:53end of the line. You're not going to get

31:54any taller.

31:57Um, so yeah, females right around 18,

31:59they stopped. They're not going to get

32:00any taller. So, if you're 18 years old,

32:02you're past 18, you think, you know,

32:04you're going to grow more, you're going

32:05to get taller. Chances are, probably not

32:07going to happen. Um, uh, same thing for

32:10for uh for men. If you're right around

32:12the age of 21, most likely you're not

32:14going to grow anymore. Uh that that's

32:16it. You've reached the end of the line.

32:18So the growth and width uh bones as you

32:22already know bones grow in width uh

32:25through appositional growth. This occurs

32:28throughout your life. Now bones will

32:30thicken in response to an increase uh

32:32stresses from muscle activity or from

32:35additional weight. uh osteoblasts that

32:37we find beneath the perryioium they

32:39secrete the bone matrix on the bone on

32:42the external bone and osteoclast they

32:44remove the bone on the endostial surface

32:47okay from within the bone. Now usually

32:49what ends up happening is more bone

32:51building uh takes place then bone

32:54breaking. Uh so this ends up leading to

32:57thicker and a stronger bone and again

32:59this is it's also it helps that it

33:01doesn't end up being too heavy. uh at

33:04the same time you end up getting

33:05remodeling taken in the same place. So

33:08if you look over here what's happening

33:10is uh okay so bone growth now what are

33:13they saying over here uh so bone yeah

33:16the bone gets replaced by cartilage over

33:18here for bone growth okay when it's uh

33:21when bone grows of course um and uh yeah

33:26you get cartilage grows over here on

33:28this end bone replaces the cartilage

33:30down over here uh bone replaces the

33:33cartilage over here now in bone

33:34remodeling what's happening is the

33:36cartilage stays here. Okay. Uh the

33:39cartilage is not growing. So where he

33:40has cartilage growing over here, you

33:42don't have that over here. No cartilage

33:44and bone remodeling. The epicial plate

33:46is right over here. Again, they're both

33:48the same. Uh now, uh appositional growth

33:53now. Yeah, you can see over here it's

33:55adding bone over here. So again, now

33:57what's happening over here? The bone is

33:59starting to widen out. All right. Now,

34:02uh the bone that was inside, it ends up

34:05getting resorbed. Okay? egg gets broken

34:07down. So as bone is being broken down

34:09here, it's end up getting laid down

34:11outside. Okay. So this is how we're

34:12talking about bone uh thickening and

34:14remodeling. You end up getting uh the

34:17old bone eaten up from in from within

34:19and the new bone getting added from out

34:21from the outside the outer part. Okay.

34:26So we've said that bone growth occurs up

34:28and again throughout your you know from

34:30infancy all the way into your

34:32adolescence. So right up until about 18

34:34to 21. uh you know your bones stop

34:37growing the the the epicial plate is

34:39formed you're not going to grow anymore.

34:41Now what you have to understand is this

34:43bone growth is very uh

34:48very smartly uh controlled by a handful

34:52of hormones okay that are that are all

34:54more or less working together. So during

34:56infancy and your early childhood the

34:59most important hormone is growth hormone

35:01u and this stimulates the epile plate

35:03activity. All right. The second hormone

35:06is this thyroid hormone. Now this

35:07thyroid hormone. It works in conjunction

35:10with growth hormone. Okay. So it

35:12modulates the activity of growth growth

35:14hormone making sure there's proper

35:16proportions. Now the next hormone

35:20testosterone uh and uh the these are

35:22also known as the the sex hormones. So

35:24in males we're talking about

35:26testosterone. In females we're talking

35:27about estrogen. Okay. So uh this

35:31promotes adolescent growth spurts. All

35:34right. And also uh this hormone towards

35:38the end of uh towards the end of

35:40adolescence uh it ends it starts the uh

35:44the epicial plate closure from occurring

35:47also. So it ends the growth this uh

35:50testosterone. Now having uh too much or

35:53too little of uh of any of these

35:55hormones can cause uh among other things

35:59abnormal skeletal growth.

36:03Now so between 5 to 7% of our bone mass

36:07is recycled weekly. So spongy bone gets

36:10uh replaced between 3 to four years.

36:13Compact bone gets replaced about every

36:1510 years. Now bone remodeling it's what

36:18it consists of is both uh bone deposits

36:21and bone resorption. In other words,

36:23you're building bones and breaking away

36:25bones. Resorption means to break away

36:28break away and uh deposit means to

36:30build. Okay, building and breaking bone.

36:32So this happens at the surface of the

36:35the the perryioium and the endostium. Uh

36:38so when we're talking about remodeling

36:40units so these are packets of adjacent

36:43osteoblast and osteoclass that are uh

36:46remodeling that uh coordinate this

36:48remodeling process.

36:52So um

36:55let's talk about bone deposit now. Now

36:58uh bone deposit this is going to happen

37:00whenever there's injury to the bone or

37:02uh uh the bone needs to be strengthened

37:05further. Okay. So again if you you're

37:07starting to build more muscles more

37:09stresses on the bone then you need to

37:11have more deposit taking place. Now for

37:13optimal deposit to occur you have to

37:15have a good diet as well. So a diet

37:17that's good and rich in high in proteins

37:20and in vitamins A D and C and also you

37:23want to have a lot of minerals. So you

37:24want to have enough calcium and

37:26phosphorus of course. Okay. Among that

37:27you want magnesium magnes also amongst

37:31again many many many other minerals. So

37:34again you have to have a very good

37:35healthy diet for to to uh you know

37:40that's required in order for this bone

37:42deposit to occur. So also when you look

37:44at uh people that are bodybuilding um

37:47you know or you know they want to get

37:48muscles one of the things that they have

37:50to look at is worry about is also to to

37:52get first of all a very high uh calorie

37:57diet. But uh amongst that high calorie

37:59diet they need well when we get to the

38:01chapter muscles you're going to

38:02understand uh they need to have a lot of

38:04amino acids. So a very high protein diet

38:06but in addition to that they have to

38:08have uh their vegetables as well and one

38:10of the reasons they need to have a lot

38:12of vegetables in their diet is because

38:15the vegetables they are sources for all

38:17these minerals and vitamins.

38:20Uh so moving forward uh yeah so the new

38:24bone mot matrix it gets deposited by

38:27osteoblast.

38:29Okay. Now um so the

38:32yeah the new the the bone matrix that

38:34are deposited by the osteoblast they get

38:36marked by a presence of a seam that we

38:39call an osteoid seam which is

38:41unmineralized band of gauzy looking bone

38:43m matrix. Um uh so between the osteoid

38:47seam and this older uh mineralized bone

38:50you have this abrupt transitional uh

38:52zone that we call this calcification

38:55front. Now because the osteoid seam is

38:58always of constant width and the change

39:01from unmineralized to mineralized matrix

39:03is sudden. It looks like that the

39:05osteoid must mature for roughly a few

39:09weeks before it's actually able to

39:10calcify. Now

39:15uh

39:16how long it takes to calcify that's kind

39:19of tricky. Okay. But what we do know is

39:21that we have to there are triggers. So

39:24what the question is this what are the

39:26triggers for calcification to occur.

39:29That's the correct thing to ask. So this

39:31is what they what you know what do we

39:33believe are the triggers uh for uh the

39:37the calcification to occur. First of

39:40all, it could be uh mechanical signals.

39:45An increase in the concentration of

39:46calcium and phosphate ions for hydroxy

39:50appetite formation. That could be a

39:52trigger. The other thing to think about

39:53is our matrix proteins that bind and

39:56concentrate calcium. In addition to

39:58that, proper amounts of the alkaline

40:01phos phosphatase. Okay, this is an

40:04enzyme that's required for min

40:05mineralization to occur. So when we're

40:07talking about bone resorption, we're

40:09talking about bone breaking and bone

40:11resorption is a function of osteoclast.

40:14Now uh what we find over here is this uh

40:18these osteoclast

40:20uh we find them clinging to the bones

40:22and when they cling on they kind of they

40:25end up forming a fold as they move along

40:27uh the the surface. As they're moving

40:30along they end up digging depressions or

40:32grooves as they're breaking down uh the

40:34bone matrix. Now from uh they're also

40:38secretreting a couple of different uh

40:41chemicals. The first thing that they

40:43they're secretreting are lysosomal

40:45enzymes and protons and this helps break

40:47down the matrix. The other thing that

40:49they secrete are is hydrochloric acid

40:51and this converts the calcium salts into

40:54into a soluble form that that gets

40:56passed easily into the solution.

41:00Um now osteoclass they're also

41:03fagiciides

41:05uh demineralized matrix and dead

41:07osteiocytes. So the digestive products

41:09uh they get transcytos across the cell

41:12and released into the inter intersticial

41:15fluid. From the interstial fluid it'll

41:17then go into the blood. Uh once

41:19resorption is complete osteoclass they

41:21end up dying. So they under they end up

41:23undergoing aptosis or again it's cell

41:26death program cell death. So you know

41:28these cells they end up committing

41:29suicide. Think of it like that. The

41:32osteoclass

41:33they activation includes a couple of

41:36things. Uh first thing one of the things

41:38that it involves is u a protein that

41:41secreted by uh the the tea cells of your

41:44immune system. In add in addition to

41:46that uh parathyroid hormone also plays a

41:49role in activating these osteoclasts.

41:53So remodeling is go is occurring

41:56continuously in the skeleton. Um it's

41:59regulated by genetic factors and also

42:01two control loops. Uh one of them is a

42:03negative feedback hormonal loop that

42:06maintains uh calcium uh homeostasis in

42:08the blood. The other it involves uh

42:11responses to mechanical gravitational

42:13forces that are acting on the skeleton.

42:15Now you have to understand that calcium

42:18is very important. uh it serves so many

42:20functions in your body uh in many

42:23processes such as nerve transmission uh

42:25muscle con contraction, blood

42:27coagulation. So for the in order for

42:29clotting to take place you need to have

42:31calcium uh in order for muscles to

42:33contract you need calcium also. And

42:35again for nerve transmission you need to

42:38have uh calcium. Now in certain

42:40individuals for example uh that are

42:43maybe experiencing certain types of

42:46depression. Now one of the underlying

42:48factors may be a depleted amount of

42:50calcium. Uh also when you look at u uh

42:54athletes uh baseball players, football

42:56players, basketball players also uh when

42:58people are running or when people are

43:00are lifting weights uh one of the things

43:03when when they're drinking uh Gatorade

43:05for example or again these uh sports

43:08drinks, one of the things that that uh

43:10that uh these sports drinks are

43:11fortified with is calcium. uh because

43:14again your body needs that calcium to

43:16contract the muscles. When you're

43:17exercising there's a lot of muscle

43:18contraction going on. Um so in addition

43:21to that uh your glands and nerves uh ner

43:24nerve secretions they're also utilizing

43:26calcium. Even cell divisions utilizes

43:29calcium.

43:30Now the interesting thing is that uh 99%

43:34of the calcium uh is found in bone. And

43:38what is that amount? That's anywhere

43:40from two a little bit over two and a

43:41half to three pounds. Okay, so that's

43:43between 1,200 to,400 grams. Uh that's a

43:46lot. Uh that's, you know, it's quite

43:48significant. Uh what happens to calcium?

43:51How does it get absorbed? Well, calcium

43:53is absorbed in the intestines. Uh

43:55however, your body needs vitamin D in

43:57order to absorb calcium. So when you go

44:00to the store and if you're looking at if

44:01you're looking at supplements to uh such

44:03as calcium supplements, you'll see that

44:05majority of the time they're they're

44:07sold as a a combination of calcium and

44:09vitamin D.

44:13So when you look at the hormonal

44:14controls uh parathyroid hormone, this is

44:17produced by uh the parathyroid glands in

44:20response to do in response to low blood

44:22calcium levels. So when your blood

44:24calcium levels drop, it stimulates the

44:27your body releases this parathyroid

44:28hormones and the parathy thyroid

44:30hormones. It stimulates the osteoclass

44:33to start breaking down the bone matrix.

44:34As is breaking down the bone matrix,

44:37calcium gets liberated into the blood

44:39and this raises your blood calcium

44:41levels. Um so parathyroid uh hormone

44:44secretions they stop when uh the the

44:47levels of calcium levels have been

44:49reached when they're within that range

44:51that we talked about earlier that 9 to

44:5311 milligrams per deciliter range. Uh

44:55once that is reached then the the loop

44:57stops um your body stops secretreting

44:59this uh the the hormone. Now calcetonin

45:03uh is produced by paraphilicular cells

45:05of your thyroid glands. uh these are

45:07called sea cells and this is uh they

45:09also get secreted in response to to

45:11levels of of high levels of blood

45:13calcium levels. Um so calcetonin uh

45:17again its effects are negligible but uh

45:19at high pharmacological

45:22uh uh doses it does seem appear to to

45:27decrease blood calcium levels

45:29temporarily. Now whether calcetonin uh

45:32has an effect in the body it's not very

45:35clear. Uh the old school thought was

45:37that yes it was but again you know now

45:39they're thinking that you know it's

45:41probably doesn't have much to do with

45:42it. Uh but then then again again they're

45:45still figuring out you know what is this

45:47uh hormone for but it does have the

45:49potential to uh decrease uh high levels

45:54of calcium.

45:57So when you're looking at this side over

45:58here uh essentially this is showing that

46:00there there's a negative feedback going

46:01on here. So remember calcium homeostasis

46:04of blood it needs to be between 9 to 11

46:06uh milligrams per 100 milliliter range.

46:09All right. So when the blood calcium

46:12levels fall okay when you have an

46:14imbalance again so the stimulus is what

46:16the fall falling of uh blood calcium

46:19levels it will cause the parathyroid

46:23glands. Remember these parathyroid

46:24glands are found on the posterior aspect

46:25of the thyroid gland. It causes them to

46:28secrete the parathyroid hormone.

46:29parathyroid hormone uh is going to end

46:31up uh triggering these osteoclasts to

46:35start breaking down the bone matrix.

46:37When the bone matrix is broken down,

46:38calcium gets liberated into the blood

46:40and the blood calcium levels go up. So

46:42once the blood calcium levels go up,

46:44then you uh it's balanced, your body

46:46will stop sending signals for these uh

46:48parathyroid glands to secrete their

46:50hormone. Um so what's important to

46:54understand there is even small changes

46:56in blood calcium levels can have severe

46:58neuromuscular problems if you have too

47:01little calcium. So when you look at this

47:03term low calcium levels so emia

47:05hypocalcemia emia the suffix means blood

47:08condition kelk means calcium and hypo

47:11means low. So low calcium condition

47:14blood condition of low calcium uh what

47:18this will cause is hyperexitability.

47:20Okay. in uh neuromuscular

47:23tissue.

47:26Hypercalcemia, high levels of calcium,

47:28this causes no non-responsiveness in

47:30neuromuscular uh tissue. Uh now when you

47:34have high sustained high blood calcium

47:36levels, this will lead to deposits of

47:38kidney uh calcium salts in the blood

47:40vessels or kidneys in other soft organs.

47:43So this is going to impair function of

47:44these organs and in the case of kidneys

47:46for example, it's going to cause stones

47:47to start forming.

47:50Uh so other uh controls uh hormonal

47:53controls uh in calcium levels so they

47:57include uh uh

48:01leptin uh the hormones leptin and

48:03serotonin. So uh leptin um

48:08so this is hormone that's released by

48:10atapost tissue. Okay. By so your fat uh

48:12it plays a role in bone density

48:14regulation it by inhibiting uh

48:16osteoblasts okay from uh doing their

48:19jobs from bone building. Uh the other uh

48:24hormone okay or is serotonin okay

48:27serotonin actually it's a it's not a

48:29hormone I'm sorry serotonin is a

48:30neurotransmitter. Now this

48:33neurotransmitter uh it's responsible for

48:36mood levels uh also is sleep cycles. It

48:39affects your sleep uh and it also

48:41interferes with osteoblast activity. Uh

48:44serotonin it's made in your small

48:45intestines and is secreted into the

48:48blood after you have a meal. Uh it could

48:51inhibit bone turnover. Uh so u bone

48:54calcium it gets locked in when new

48:57calcium is flooding into the

48:58bloodstream. Um so uh

49:05responses to mechanical stress. Now,

49:08so bones they reflect stress uh stresses

49:12they encounter. So bones are stress when

49:14weight bears on them or muscles start

49:16pulling on them. So when you're starting

49:17to lift up really heavy weights uh again

49:20or you know again you're just exerting a

49:22lot more uh you're doing a lot more

49:24labor, a lot more work uh this is going

49:26to cause uh stress on the bones. Okay?

49:29Because remember what's happening is the

49:31muscles they're pulling on the bones.

49:32Now Wolf's law it states that bones grow

49:35or they remodel in response to demands

49:38placed on them. So stress is usually

49:40offc center. So bones they they tend to

49:42bend. So bending it compresses one side

49:46while it stretches the other side. Now

49:50the diaphosis is thickest where bend

49:53where bending stresses are the greatest.

49:56Okay. So the diaphosis is thickest where

49:58the the stress of bending is going to be

50:01the most. Now bone it can be hollow

50:04because compression and tension they

50:06tend to cancel cancel each other out in

50:09the center of the bone. So when you look

50:11at this diagram here now what they're

50:13showing you is this. So the tension is

50:15here and the compression is over here.

50:16So the greatest amount of compression is

50:18over here and the tension is going to be

50:20more most over here. In other words,

50:23this part is going to be stretching out

50:24the most and this part is going to be

50:26compressed the most. It's going to be

50:27pushed down the most. Okay.

50:30Um

50:33so uh yeah let's see so wolf law also

50:37explains that the hardness right right

50:40or being right or left-handed hardness

50:42results in thicker and stronger bones of

50:44the corresponding upper limb. Uh curved

50:48bones are thickest where most likely to

50:50buckle. Uh the tbecula uh form uh

50:54trusses along the lines of stresses. uh

50:57large bony projections they occur where

50:59heavy active muscles attach. Uh so again

51:02when you're talking about these large

51:03bony projections uh these trocanters for

51:06example uh again where when you have

51:08muscles that are very uh when you look

51:11at some of these bones uh and uh again

51:14one of the things when you look at it

51:16you know if you want to differentiate

51:17one bone from another bone uh versus men

51:20versus women the bulk of the time

51:23majority of the time when you see these

51:24trocanters that are very well defined

51:27again these bumps that are very well

51:29defined that are much bigger you know

51:31the rough different appearance. This

51:33usually tends to be that of males.

51:35Again, when men again historically uh

51:38especially when you're looking at uh

51:40again skeletons from going back, you

51:41know, hundreds of years ago, uh when

51:44where men did most of the hunting and

51:45and uh you know, when women did most of

51:48the gathering. So, when you look at

51:49hunters and gatherers, for example,

51:51again, when men, they were out there

51:52doing the hunting, they're lifting

51:54really heavy things, they're doing most

51:55of the building. uh and you look at

51:57their bones today, you'll see that, you

51:58know, they're much much much more

52:00defined when you look at these bumps,

52:02for example, these projections. And

52:03that's from where these muscles attached

52:06to them. A lot more muscle attached to

52:09them. Uh so, uh you're going to see this

52:12and it helps archaeologists

52:13differentiate.

52:15So, like they say, weightlers, they have

52:17enormous thickening thickening site,

52:19muscle attachments sites uh of most of

52:22the muscles uh that they're using. uh

52:24the bones of a fetus and bedren people

52:27they are futureless you're not going to

52:28see anything why because there's no

52:30stress on them okay lack of stress

52:32you're not going to see anything uh

52:35so mechanical stress it causes

52:37remodeling by producing electrical

52:39signals when bone is deformed so

52:41compress and stretch regions they're

52:43oppositely charged compression and

52:46tension it changes fluid flow within the

52:48canaluli which may also stimulate

52:51remodeling so hormonal controls They

52:54determine whether uh and when remodeling

52:56occurs in response to changing blood

52:58calcium levels. But mechanical stress it

53:01determines where it occurs. Right? So

53:03keep this in mind.

53:05Hormonal control is just going to say

53:07all right do we need uh remodeling to

53:10occur? Yes or no. Mechanical stress is

53:12going to say okay you need it over here

53:14on this spot or you need it over there

53:16on that spot. Okay this spot needs to be

53:18remodeled much more than some other spot

53:20does because there's a lot more stress

53:22over here. this part of the bone is

53:24being used a lot more than some other

53:25part of the bone.

53:28So let's talk about bone fractures now.

53:30So fractures they're just breaks in the

53:33bone. Now during your youth most

53:35fractures result from trauma. So or you

53:37know for example you might be playing

53:39basketball. So like sports injury or

53:41football or basketball uh sports

53:43injuries uh you know maybe you have a

53:46fall or that'll break cause a fracture

53:50uh perhaps a car accident uh or end up

53:53uh again you get into a fight in some

53:55type of an altercation uh that could

53:57result in in you know uh in a in a

54:02fracture. Um in old age uh the fractures

54:08they don't really usually you know occur

54:11from or not necessarily occur from uh

54:14from trauma but they a lot of times uh

54:18end up resulting from weakness of bone

54:20okay because the bone is getting too

54:22thin okay due to bone thicken uh

54:24thinning. Uh now one of the reasons this

54:28may happen uh again there's genetic

54:30factors uh again hormonal factors that

54:33we talked about but uh other one of the

54:36one of the reasons that this may happen

54:38is uh from a lack of movement and also

54:41this could happen uh from uh bad uh uh

54:45you know insufficient uh nutrient intake

54:48as well. So uh especially when you're in

54:50your in your younger age it's important

54:52to get enough calcium in your diet. uh

54:55because that's gonna affect uh you know

54:57how you're going to be when you're much

54:58older. So you know you all should be

55:00eating you know at least a glass of milk

55:04a day. You should be drinking a glass of

55:05milk or yogurt or some cheese or again

55:08uh foods that are high in calcium. Uh

55:11it's important to have and that's going

55:13to help you later on down the line as

55:14you get older. Again that doesn't mean

55:16you can stop. You need to continue to

55:17eat uh you know drink some milk or have

55:20some yogurt. Again the the example is

55:23milk milk and yogurt because these tend

55:24to be foods that are high in in the uh

55:27the amounts of uh of calcium

55:31uh that's present in an inner serving.

55:33Um now

55:36let's look at fractures. Now when you

55:39break a bone again that's called a

55:40fracture. So um yeah so that was already

55:44been established. So how you classify a

55:47fracture? Uh well three criteria we can

55:50use. So, what is the position of the

55:53ends of the bone after the break occurs?

55:56So, we're talking about are the ends of

55:58the bones still in position? If it is,

56:00then we say it's non-displaced. However,

56:03if the ends of the bones, they're not

56:05aligned anymore, then we're saying that

56:06it's a displaced fracture. All right?

56:09Also, we talked about uh the

56:11completeness of the break. If the break

56:14is all the way through AC, all the way

56:16through the bone, we call that a

56:18complete fracture. If it's not all the

56:21way through the bone, then we call that

56:22an incomplete fracture. The third thing

56:24is uh we talked about if there's any uh

56:27skin penetration uh involved in the

56:30fracture. Uh if there is so if the bone

56:34is sticking out of the if the bone is

56:36sticking outside of your skin, then we

56:38call that an open fracture or a compound

56:40fracture. Uh if the bone is not sticking

56:44out of the skin and is still, you know,

56:46enclosed, in other words, you don't see

56:47any blood. uh if you broke your arm,

56:49there's no blood on the outside, then uh

56:52that's we call that a closed fracture.

56:54So a closed fracture again that's when

56:57there's no penetration of the bone

56:59through the skin that takes place. Uh so

57:02uh in addition to that you can also

57:04describe these fractures by the location

57:05of the fracture, its external appearance

57:08and the nature of the break. So when you

57:10look at these next slides uh this is

57:12called a communed fracture.

57:15So the bone fragments into three or more

57:17uh pieces. Uh

57:20so you tend to see this in in older

57:23people uh again whose bones are they

57:25tend to be you know not as strong as

57:27before. It's a little bit more fragile,

57:28more brittle. Now compression fractures.

57:30So this happens when the bone gets

57:32crushed. So the example they're giving

57:34you over here, they're showing you in in

57:35the vertebrae over here. So you have

57:37these crushed uh vertebrae. Uh so this

57:40is a compression fracture. So again

57:42common in porous bones. So osteoporotic

57:44bones or you know bones that are subject

57:47to extreme trauma is in a fall.

57:50Um then you have u a spiral fracture. So

57:54this is showing you that again this

57:55fracture is occurring in a spiral. It's

57:57a ragged break that occurs when

57:58excessive twisting forces are applied to

58:00a bone. So it's very common in in sports

58:03injuries. You'll you you'll tend to see

58:05this uh epiphysial fractures. So what

58:09happens over here is the the epiphosis

58:11it separates from the diaphosis along

58:13the epicial plate. So here we go.

58:16Remember this is a a long bone and right

58:18over here you have this fracture that's

58:19taking place. So notice that this is

58:21part is displaced. Uh so again tensor

58:24curve where cartilars are dying and

58:25calcification of the matrix is

58:27occurring. Then you have sometimes you

58:29see this a depressed fracture. So broken

58:33bone portion is pressed inwards. So this

58:36is very typical of skull fracture. So,

58:38you know, you take a hammer, you hit

58:40somebody in the head with a hammer, that

58:41could be a, you know, could lead to a

58:43depressed fracture. There's also

58:45something that's called a green stick

58:46fracture. Now, green stick,

58:49you tend to see this in children. It's

58:50very common. Uh, so the bone it breaks

58:53incompletely. Okay? So, it's an

58:54incomplete fracture. But much of uh much

58:57in the way a green twig breaks it, you

59:00know, that's what it looks like in

59:01appearance. Uh, so what happens is if

59:04you look over here, uh, one side of the

59:05shaft is broken. Okay. And the other

59:08side, it bends. Can you see the bend

59:10over there? So, this is a a green stick

59:15fracture.

59:17So, when we're talking about fracture

59:19treatment and repair, uh couple things,

59:23handful of things need to happen. So,

59:24one of the things when you're treating

59:26it involves reducing uh the the amount

59:29of uh bone that uh needs to be for your

59:32body to repair. So uh in other words,

59:35you want to realign the ends of the

59:37broken parts as close as possible

59:39together. You want to realign them uh

59:41bring them back together uh as best as

59:43possible. Now this can happen uh in two

59:47different ways. Well, sometimes if

59:49there's not if the break is not very

59:52bad, there's not too much of a

59:53misalignment and again it depends on the

59:55bone and where it happens. Uh but uh

59:57that could be realigned through a close

59:59reduction. So the doctor, the

1:00:01orthopedist, they're going to manipulate

1:00:03uh you know the muscles and and the bone

1:00:06to back into the correct position. Uh

1:00:09the other option is uh you know it

1:00:11cannot be done through phys external

1:00:13physical manipulation. It needs to have

1:00:16uh it's it requires surgical uh

1:00:18correction. So they have to cut you open

1:00:21and then they have to insert pins,

1:00:23wires, screws to secure the ends the

1:00:25broken ends of the bones. Now the once

1:00:29you know you've uh reduced the fracture

1:00:33what needs to be done is you need to

1:00:35immobilize that bone. Okay. And imil

1:00:38immobilization is usually done either by

1:00:40cast or some type of attraction device.

1:00:42And again you need this for healing. Uh

1:00:44because if you don't have this cast or

1:00:46attraction in place the bones are likely

1:00:48to move out of place again. If if that

1:00:51happens then it's not going to heal as

1:00:52quickly. It's going to take a much much

1:00:54much longer time to to heal. In addition

1:00:56to that, there's going to be a lot of

1:00:58pain. Uh in addition to the pain, uh the

1:01:01bones, they're going to uh be uh

1:01:03disfigured. Okay? Uh and that's going to

1:01:06affect that could affect how that uh

1:01:10limb is. If it's a limb, for example,

1:01:11it's going to affect how it's going to

1:01:12function. You may not regain full uh

1:01:14full function or full or full range of

1:01:17motion. For example, if it's an arm or a

1:01:19leg. Now, the time needed for the repair

1:01:21depends on how severe of a fracture you

1:01:24have. uh which bone is broken and also

1:01:27it affects uh you also also consider the

1:01:30age of the patient. So younger people,

1:01:32children for example, they tend to to

1:01:33heal much quicker than uh somebody

1:01:36that's in their you know 50s or 60. Also

1:01:39um you know your diet, your nutrition,

1:01:42what your overall health is also affects

1:01:45how fast or how well uh you're going to

1:01:48heal. Um if you're a smoker, you're

1:01:51abusing drugs, that's going to severely

1:01:53it's going to take you know affect how

1:01:55your your outcome is. It's going to take

1:01:57much longer to heal.

1:02:00Now factory repair it involves uh four

1:02:03major stages. Uh number one being a

1:02:06hematoma formation. Number two is a

1:02:08fibro fibro fibrocartilagynous

1:02:11callus formation. Number three is a bony

1:02:14callus formation. And then four is

1:02:16finally remodeling. bone remodeling.

1:02:21So

1:02:22the very first step the hematoma for

1:02:24formation. So uh when you get a a

1:02:27fracture in the in the bone you end up

1:02:29getting blood vessels that are torn.

1:02:31Okay. So these blood vessels they start

1:02:32to bleed now. All right. The blood is

1:02:34not flowing within the tubes anymore. So

1:02:36the blood starts flowing all over the

1:02:38broken site. So it's hemorrhaging. It

1:02:40forms a

1:02:42a big clot. Okay. And that that clot

1:02:46that's formed is what we call that

1:02:48hematoma. Now this ends up swelling up a

1:02:52lot. You end up uh getting a lot of

1:02:54inflammation over here at the site. In

1:02:56addition to that, it's extra very

1:02:57painful. All right? Whenever you have

1:02:59swelling uh take place, it starts

1:03:03pushing down on the nerves. All right?

1:03:04And whenever you get nerves that are

1:03:06pushed, that causes pain. Uh in addition

1:03:09to that, remember you have nerves that

1:03:11you know you had a bone that tissue has

1:03:12been broken. So the nerve endings are

1:03:14also been damaged. So that causes the

1:03:17the you know that'll cause pain uh too.

1:03:20Um so over here in this picture you this

1:03:23is the bone and notice that you have a

1:03:25blood vessel over here and a blood

1:03:26vessel over here and now they're no

1:03:29longer connected. So what happens

1:03:31instead of the blood flowing nicely

1:03:32within this it ends up spilling all

1:03:35about. Okay? It floods this entire area.

1:03:37And this blood that's now that you know

1:03:39that's that's gone out of the the the

1:03:41the tubes and now is within uh you know

1:03:45this uh bone tissue is what we call uh

1:03:48it's formed into it's formed into a

1:03:50hematoma. So this blood when it once it

1:03:52leaks out of the blood vessels it clots

1:03:54and once it clots it forms this

1:03:55hematoma.

1:03:58So what happens next is that usually

1:04:00within a few days handful of events it

1:04:03leads to the formation of soft

1:04:04granulation tissue that's uh called a

1:04:07callus or soft callus. Now capillaries

1:04:10they grow into the hematoma and these

1:04:12fagocitic cells they invade the area and

1:04:14they start the cleaning up process. So

1:04:16they start cleaning getting rid of all

1:04:17the debris that's there. So at the same

1:04:19time you get fibroblast and osteoblast

1:04:22that come into the the fracture site uh

1:04:24from the nearby perryioium and the

1:04:26endocium and they start uh to

1:04:29reconstruct the bone. The fibroblast

1:04:31they start uh producing collagen fibers

1:04:33that'll span the the the break and they

1:04:36connect the broken ends uh and some uh

1:04:39some of these uh they differentiate into

1:04:40condro blasts that secrete the cartilage

1:04:43matrix. So within this mass of repair

1:04:45tissue, osteoblasts they start forming

1:04:48spongy bone but but those that are

1:04:50farthest away from the capillary supply

1:04:52they secrete an externally bulging

1:04:54cartilagynous matrix and this uh

1:04:57cartilagynous matrix. It later it

1:05:00calcifies. So this entire mass of this

1:05:03repair tissue is now called this fibbral

1:05:06cartilagynous callus. So again this is a

1:05:09splint uh it acts as a splint uh between

1:05:11the broken bones.

1:05:13So in this drawing you can see what's

1:05:15happened is uh that uh where the

1:05:18hematoma was you've had these blood

1:05:20vessels that are starting to grow in it

1:05:21starts to clean up all that uh the the

1:05:23the clot that was there. Uh and you have

1:05:27now you can see this external callus and

1:05:29internal callus. Uh so over here also

1:05:31you see the blood vessels been uh

1:05:33repaired. Uh so essentially uh again

1:05:36what happened was uh in this step is

1:05:39that um uh so these fibroblasts and

1:05:44osteoblast all right they ended up

1:05:46coming over to the site they start

1:05:47laying down this uh uh this uh the

1:05:49fibrous tissue and the cartilage there.

1:05:51So this is what this what's acting as a

1:05:53splint as a temporary splint. Uh and

1:05:55then when we go into the next steps

1:05:57you're going to see what's going to

1:05:59happen at this point. But remember uh

1:06:02this is quite clever. It's amazing.

1:06:04Again, you have flexibility over here

1:06:05also. Um,

1:06:09so now bony the bony callus. So remember

1:06:12this is what we call the soft callus

1:06:14that that formed. Okay. Now the the the

1:06:17next step is we get this bony callus

1:06:20that forms. Now this usually happens.

1:06:24Now first of all this part step two this

1:06:26usually happens within a few days maybe

1:06:28two three days this will happen. Now the

1:06:31bony callus formations this happens

1:06:33usually within a week. All right. So

1:06:35again another perhaps 4 days afterwards

1:06:394 days after we had the soft callus now

1:06:41we're starting to get this bony callus

1:06:42start to form already. So over here

1:06:44within a week you get new tbacula that

1:06:46appear in the fyproarinous

1:06:49uh callus. So the callus is converted

1:06:51into a hard callus or a bony callus of

1:06:54spongy bone. uh the bony cacalis

1:06:57formation it continues for about two

1:06:59months until you have a firm uh union

1:07:02that forms between the the the two ends

1:07:04of the bones.

1:07:07So when you look over here uh you don't

1:07:09have uh the fibrocartilagynous tissue

1:07:12over here anymore or that soft callus no

1:07:14longer present. What you see now are

1:07:15these tbacula. Uh so this is why we why

1:07:19we call this a bony callus not a soft uh

1:07:23callus but a bony callus uh that's of a

1:07:26spongy bone. So the next part uh the

1:07:29next step is the fourth step which is

1:07:31bone remodeling. So this begins uh

1:07:34during bony callus formation and it

1:07:36continues for months maybe two to three

1:07:38months. Uh so access material on the

1:07:42diaphosis exterior and within the

1:07:43medularary cavity is removed. The

1:07:46compact bone is laid down to reconstruct

1:07:48the shaft walls and the final structure

1:07:51resembles the original structure. So it

1:07:54responds to the same mechanical

1:07:55stressors also. So in other words, what

1:07:57you have now is something that's just as

1:07:59strong as your original bone. Uh you

1:08:01know, you've had a full complete

1:08:03recovery.

1:08:05So when you look over here now, uh

1:08:09you know, you had the fracture over

1:08:10here, remember? And now you can't even

1:08:12tell, right? because it's been replaced

1:08:14completely by uh by new bone. Uh so you

1:08:17know this is what we said uh we have

1:08:19bone remodeling that occurs. Uh so again

1:08:22this is a it's an amazing way your body

1:08:24ability to regenerate. Fortunately you

1:08:26have this ability to regenerate uh this

1:08:29type of uh uh trauma when it does occur

1:08:32to bones. Uh unfortunately not all body

1:08:35tissues act this way. So for example,

1:08:38you know, if this happened in in if you

1:08:40have a depending on the which type of

1:08:41nerve you're looking at uh nervous

1:08:43tissue you're looking at uh you cannot

1:08:45have any repair of that tissue or if

1:08:47you're looking at your heart muscle for

1:08:49example. Unfortunately at this point

1:08:52it's uh you there's really is no way to

1:08:54repair heart uh uh heart muscle tissue

1:08:58when it is damaged. But fortunately

1:09:00again because people break bones so many

1:09:03times throughout their life um it has uh

1:09:08it has a a way to repair itself.

1:09:13So again these are just the four steps

1:09:15uh from steps one through four when you

1:09:17have a fracture and you know your body

1:09:19repairs it the hematoma forms. Step two

1:09:22is a fibrocartilagynous callus forms and

1:09:24step three you end up getting a bony

1:09:26callus that forms and step four uh you

1:09:29end up uh having uh bone remodeling that

1:09:33that takes place. Okay.

1:09:37Now we're going to be talking about bone

1:09:38disorders. Now just about every disease

1:09:41that we see that affects the human

1:09:43skeletal system uh the underlying

1:09:45problem tends to be uh the imbalance

1:09:49between how much bone is deposited and

1:09:51how much is being resorbed. Uh three

1:09:53disease that we're going to be looking

1:09:55at are is osteomalacia and ricketetts

1:09:58osteoporosis and page disease. Uh now

1:10:01osteomalacia when you look at this term

1:10:03again oste is bone malaysia softening.

1:10:05the bone softening. Uh so the bones are

1:10:07poorly mineralized. Uh the osteoid is

1:10:10produced but the calcium salts they're

1:10:12not adequately deposited and what ends

1:10:14up happening is you end up having soft

1:10:15and weakened bones and again it's quite

1:10:18painful when uh there's a weight that's

1:10:20starting to be beared on these bones.

1:10:22Now ricketetts it's a it's a it's a form

1:10:24of osteinacia that we see in children

1:10:26and so for example in in you when you

1:10:29look at the legs uh you'll see that see

1:10:31that these are bowed. So again

1:10:33bow-legged this is an example of oste of

1:10:35ricketetts. Uh other bones you'll see

1:10:38deformities as well. Um you'll see bones

1:10:40that tend to be enlarged and they tend

1:10:42to be long. Now what causes this um is

1:10:46usually a deficiency in vitamin D or

1:10:49you're not getting enough calcium within

1:10:50your diet. Uh so again in these children

1:10:54you know you want to start increasing uh

1:10:56you want to put them on on a supplement

1:10:57a calcium and a vitamin D supplement.

1:11:00Now when we see osteoporosis

1:11:03um so this is a handful of diseases uh

1:11:07in which bone resorption exceeds bone

1:11:10deposit. So again you're getting a lot

1:11:12more bone breaking down than getting

1:11:14bone building. Uh the matrix remains

1:11:16normal but the bone's mass it starts to

1:11:19decline. So the spongy bone of spines

1:11:21and necks and uh uh and the neck of the

1:11:23femur these are the moles that are most

1:11:25susceptible. Um so the vertebral and uh

1:11:29vertebral fractures again because

1:11:31remember this is where you're going to

1:11:32find the spine right spine is made up of

1:11:34vertebral bones so you tend tend to see

1:11:36this type of uh fractures within the

1:11:39vertebrae also hip fractures when you

1:11:41see hip again uh very common uh to see

1:11:46uh the osteoporosis and hips. Um

1:11:51so here is what normal bones looks like.

1:11:53Notice how you know nice and strong the

1:11:56the trabacula you see over here are. But

1:11:58in osteotroic bones look what look

1:12:00what's happening. Okay you see all these

1:12:02little holes and stuff that that are

1:12:03present. These are not calcified. So

1:12:06because they're not calcified again you

1:12:07have much much much d less low density

1:12:11uh uh of these uh uh the the the the

1:12:14minerals uh and it's not as hard.

1:12:19So uh again what do you have now is now

1:12:21that these bones are very brittle and

1:12:23you know they can fracture quite easily.

1:12:26Now what's interesting to to to

1:12:29note in osteoporosis is that uh it

1:12:32affects women much more than it affects

1:12:35men. uh 30% of American women between

1:12:38the ages of 60 and 70 they have

1:12:40osteoporosis

1:12:42and this number climbs all the way up to

1:12:4670% in uh by the time uh the women

1:12:50reaches uh the age of 80 uh in

1:12:53additionally 30% of all Caucasian women

1:12:57are uh this is the most susceptible

1:12:58group also okay Caucasian women uh

1:13:00they'll experience a bone f fracture due

1:13:03to osteoporosis so again 30% women they

1:13:06end up having a fracture. So again, the

1:13:08bone it just becomes so brittle. So I

1:13:10don't know, for example, if you take a

1:13:12you step off of a curb. All right? And

1:13:15that can set off that can uh fracture

1:13:17your bone. Um and again the hip bone it

1:13:20tends to to occur more. Now it's not

1:13:22your hip that's actually breaking but

1:13:23again it's that neck of the femur uh

1:13:25which is connected to the hip uh you

1:13:28know the the the

1:13:30head of the the femur goes into the

1:13:31acetabulum of your uh your hipbone. uh

1:13:35your uh so um now hormones also they

1:13:40play a role uh in this. So

1:13:45in women one of the things that they do

1:13:47is uh you know they start uh uh estrogen

1:13:50hormone replacement therapy estrogen. So

1:13:52you know when you have estrogen it tends

1:13:54to to offset uh you know osteoporosis.

1:13:57Uh but again then again estrogen uh you

1:14:01know now there's a whole new debate or

1:14:04you know thing about estrogen and how it

1:14:07could cause cancer etc etc or high doses

1:14:09of it. uh you know my personal take is

1:14:11you know if your body is not producing

1:14:14you know again in in in women uh

1:14:18estrogen levels again they they drop off

1:14:21after a certain age and again this is

1:14:23natural this happens due to nature uh so

1:14:27why go against nature this is my

1:14:28thinking of it uh once you start messing

1:14:30with mother nature you end up you start

1:14:32running into into problems

1:14:36uh so I discussed this already in the

1:14:37previous slide but we'll just go over it

1:14:38again I They didn't know they had a

1:14:40slide for this but um uh so yeah risk

1:14:42factors for osteoporosis uh most often

1:14:46uh you'll tend to see this in

1:14:47postmenopausal women and again it's the

1:14:50women that are affected uh not so much

1:14:51as the men uh so 30% of all women

1:14:54between the ages of 60 to 70 years old

1:14:56are the ones that are affected with

1:14:58osteoporosis and 70% of the women they

1:15:01go up to they're I'm sorry u yeah uh

1:15:04this number rises to 70% by the age u by

1:15:07the time they get to age 80. So an 80

1:15:10year old woman has a 70% chance of

1:15:12developing osteoporosis. Now 30% of

1:15:15Caucasian women will suffer fractures.

1:15:17Okay. Because of osteoporosis. And as we

1:15:20said earlier, estrogen plays a role in

1:15:22bone density. So when levels drop at

1:15:24menopause, women risk higher risk higher

1:15:27risk of developing osteoporosis. Uh

1:15:29again, men less prone uh due to the

1:15:32protection by the effects of

1:15:33testosterone. So testosterone levels,

1:15:35they tend to, you know, stay just about

1:15:38the same. You might not be producing as

1:15:40much testosterone, but again, there's

1:15:42enough testosterone that's being

1:15:44produced in men. Uh, um, so again, men

1:15:47don't have to worry about this too much,

1:15:48but you know, men have other tends other

1:15:50problems uh, aside from that. So,

1:15:53additional risk factors for

1:15:54osteoporosis, uh, if you have a petite

1:15:56body form, again, higher risk of, uh,

1:15:58developing osteoporosis.

1:16:00If you've been lethargic most of your

1:16:02time, okay, insufficient exercise

1:16:04exercise to stress the bones. So if

1:16:06you're not walking, all right, uh you're

1:16:08not doing any type of exercise, this is

1:16:10going to end up result, you know, it

1:16:11could uh increase your risk for

1:16:13developing osteoporosis. So again, it's

1:16:15very important to walk. Uh go out and

1:16:17walk at least 30 minutes a day, 40

1:16:19minutes a day uh minimum. Not only is it

1:16:21good for your heart health, but is this

1:16:23also good for uh your bones uh for to

1:16:26you know for keeping to saving yourself

1:16:28from uh developing uh osteoporosis.

1:16:31Again we talked about nutrition. So if

1:16:34you have a diet that's poor in calcium

1:16:36and protein uh that's going to uh

1:16:38increase your risk of uh developing

1:16:40osteoporosis. Also uh smoking uh

1:16:43cigarette smoking is awful. Cigarette

1:16:45smoking affects uh bone density also. So

1:16:48again could contribute to osteoporosis.

1:16:51Uh we talked about uh estrogen and

1:16:54hormones how they play role in in in in

1:16:57bone density and bone formation. Well

1:17:00hypothyroidism can also affect uh uh

1:17:03your risk of uh your osteoporosis. Low

1:17:06blood levels of thyroid stimulating

1:17:08hormone in addition to that uh diabetes,

1:17:12malitis all these will affect uh your

1:17:15chance of developing osteoporosis.

1:17:18Again, like I said, if you're not

1:17:20exercising enough, okay, if you're just

1:17:21staying at home, you're not moving,

1:17:23you're bedridden, for example, uh

1:17:26immobility,

1:17:28you know, it increases the risk of

1:17:29osteoporosis.

1:17:32If you're taking certain medications,

1:17:33certain drugs like men with prostate

1:17:35cancer, uh again, that can cause

1:17:39increase your risk factor for developing

1:17:40osteoporosis.

1:17:42Now, how do you treat osteoporosis? So

1:17:44traditional treatments what what they've

1:17:46done again in women it's a good idea

1:17:48again after 50 the age of 50 to start

1:17:52taking a calcium supplement uh with

1:17:54vitamin D. Now remember if you don't

1:17:56have vitamin D the body is not going to

1:17:58be able to absorb calcium. Uh so again

1:18:01especially in Chicago where you know

1:18:03it's uh mostly cloudy and and cold and

1:18:07wintry 10 out of 12 months uh and you

1:18:11may not be getting enough sunlight u

1:18:13because you know your body produces

1:18:14vitamin D by when it gets stimulated by

1:18:18sun. So um again if you're not getting a

1:18:21sufficient sunlight and you need about

1:18:2215 to 20 minutes of sunlight a day. If

1:18:24you get about 15 to 20 minutes of

1:18:25sunlight a day then you should be okay.

1:18:28Okay, you should have sufficient uh

1:18:29amounts of vitamin D. Uh so when you get

1:18:32enough vitamin D, uh your body is going

1:18:34to be able to absorb that calcium. So

1:18:36again, women, they'll be prescribed by

1:18:39their doctors. Uh calcium vit vitamin D

1:18:41supplements. In addition to that, do

1:18:43some exercises, running, running is

1:18:45good, jogging is good. Even lifting

1:18:47light weights, uh that's uh very helpful

1:18:50also. Uh again, hormone replacement

1:18:52therapy. Uh it slows bone loss but does

1:18:55not reverse it. uh it's again I told you

1:18:58there's controversial risk uh I

1:19:01mentioned to you cancer uh again

1:19:03estrogen it's been shown you know it's

1:19:06demonstrated that you know it could uh

1:19:08raise your risks of breast cancer in

1:19:11addition to that heart attack and stroke

1:19:13are among the risk factors for uh taking

1:19:16these uh estrogen uh replacement uh

1:19:19hormone drugs uh so uh I don't know my

1:19:23advice is again talk to your doctor but

1:19:26probably better to try some alternative

1:19:29you know stick with the healthy diet and

1:19:31uh exercise.

1:19:34Now

1:19:37uh bisphosinates these decrease

1:19:40osteoclass activity and your numbers. So

1:19:42it partially reverses osteoporosis

1:19:45within the spine. Uh now selective

1:19:47estrogen receptor mod modulators uh they

1:19:50mimic estrogen without targeting breast

1:19:52and uterus. So again, this is something

1:19:54that they're using. Uh they think that

1:19:55it might be a little bit safer to

1:19:57regress the uh the the the risk of

1:20:00developing cancers in breast and uterus.

1:20:03Denosmob, it's a monoconal antibbody

1:20:06that's shown to reduce fractures in men

1:20:08that have prostate cancer. It also

1:20:10improves bone density in the elderly. Uh

1:20:13so preventing osteoporosis, make sure

1:20:15you have a good diet. Okay? Make sure

1:20:16your diet is high in calcium especially

1:20:19in your in early adulthood. Remember

1:20:22what and how you live your life in

1:20:24during your young years is going to

1:20:26affect as to how you are uh in your

1:20:28later ages. Uh so you know having a a

1:20:31diet that's high in uh calcium, vitamin

1:20:33D and also you're getting adequate

1:20:34amounts of protein. This is going to

1:20:36help prevent osteoporosis. Uh also cut

1:20:39down uh on your consumption of

1:20:41carbonated beverages and alcohol.

1:20:43Eliminate this. This is no benefit at

1:20:46all. uh if there are any benefits they

1:20:49for example some people say oh you know

1:20:51a glass of wine is good for you well you

1:20:53know what uh the harm that is does

1:20:56outweighs the benefits that it provides

1:20:59all right uh so it's it should be

1:21:01avoided it's it's uh it's not healthy um

1:21:04it these things you know among you know

1:21:07all the other havocs it causes in your

1:21:09body uh in bone specifically it leeches

1:21:12minerals from the bone so again it it

1:21:14decreases your bone density Uh also make

1:21:18sure you're getting enough weightbearing

1:21:20exercises. So uh like I said earlier,

1:21:23make go out, you should be walking at

1:21:25least 30 to 40 minutes a day. 40 minutes

1:21:27the more the better, but you know, don't

1:21:29do more. You don't need to do more than

1:21:3040 minutes a day. Go out for a walk. Uh

1:21:33lift some weights. Uh so this is going

1:21:35to help increase your bone mass uh above

1:21:38normal for uh to act as a buffer against

1:21:41age related bone loss.

1:21:44In pad's disease, uh this happens when

1:21:47the bone is made too fast and poorly.

1:21:49So, uh you end up having excessive and

1:21:51half-hazard bone deposits and

1:21:53resorption. Uh so, again, we call this a

1:21:56pasotic bone and what it has is a very

1:21:58high ratio of spongy to compact bone and

1:22:02reduced mineralization. Now, this

1:22:04usually occurs in the spine. You find

1:22:06this in your pelvis bones or pelvic

1:22:08bones, your femur, and your skull.

1:22:10Rarely does it happen before the age of

1:22:1240. They don't really know what causes

1:22:14it, but they're thinking that it may be

1:22:16due to a virus. Uh treatments usually

1:22:19include calcetonin and also

1:22:21bisphosinates.

1:22:25Embryionic uh skeleton, it oifies pretty

1:22:27predictably. Uh so the fetal age is very

1:22:29easily determined when you look at a

1:22:30sonogram or an X-ray for that matter. Uh

1:22:33now most long bones they begin start to

1:22:35oify right around eight weeks when then

1:22:38right around the 12th week you start to

1:22:40see these primary ocification centers uh

1:22:42that are developed. Um so from birth to

1:22:47young adulthood uh at birth most long

1:22:49bones are oified the exceptions being at

1:22:51the epiphyses. Now the ephysial plates

1:22:54they persist throughout childhood and

1:22:56adolescence. And again remember what

1:22:58would we say right around age 18 in in

1:23:00in the females uh you know the the the

1:23:04epiil plate you know it's sealed there's

1:23:07no more cartilage and at around age 21

1:23:09you find that in males well again

1:23:11remember I said it varies so anywhere

1:23:13between 18 to 21 but again in certain

1:23:16cases certain instances it can uh occur

1:23:20up to age 25 so usually by age 25 all

1:23:23bones are completely oified uh and the

1:23:26skeletal growth growth stops. So when

1:23:29you look over here in this photo uh

1:23:32again this is a roughly 12week old uh uh

1:23:35fetus that you're looking at. Uh so you

1:23:38can see the parietal bones. Now the

1:23:39darker areas this is where primary

1:23:40oifications already occurred. Uh this is

1:23:42the tibia. Uh I'm sorry this is the

1:23:45femur. This is the tibia over here. This

1:23:47is the fibula over here that you see. Uh

1:23:50this is the radius. This is the ulna.

1:23:53You can see the digits. Uh these are the

1:23:56this is the the collar bone, the

1:23:57clavicle. This is the the the shoulder

1:24:00blade, the scapula.

1:24:02Uh anyway, you can see the the backbones

1:24:05over here. Some of the backbones. Uh

1:24:07this is a finger, by the way. It's not a

1:24:09back. These are the backbones over here.

1:24:11These are the ribs. Uh and this is the

1:24:13the part of the hipbone.

1:24:16Now, in children and adolescence, bone

1:24:19formation, it exceeds resorption. Okay.

1:24:22In children up to adolescence. um men

1:24:24compared to women uh they tend to have

1:24:26greater mass. Okay, men will have a

1:24:28greater mass than females. In young

1:24:30adults, the amount of formation and

1:24:32resorption is relatively balanced. Now,

1:24:35in adults, okay, what ends up happening

1:24:38is resorption it excretes uh I'm sorry,

1:24:41resorption it exceeds a bone formation.

1:24:45Um so bone density changes over

1:24:47lifetime. Uh they're largely determined

1:24:49by genetics.

1:24:51So a gene for vitamin D cellular docking

1:24:54determines mass early in life and

1:24:55osteoporosis risk at an older age. Bone

1:24:58mass uh mineralization and healing

1:25:00ability decrease with age beginning in

1:25:02in in your 40s. Uh the exception is

1:25:05being the skulls of your bones. Uh bone

1:25:07loss is greatest again in females and

1:25:10within the females and white females uh

1:25:13specifically moreover. So this uh this

1:25:18is it for chapter six. Uh, I hope this

1:25:21helped. Uh, if you like it, please give

1:25:22it a thumbs up. If you have any

1:25:24questions, please leave it in the

1:25:25comments below or you can email me

1:25:26directly. And, uh, please feel free to

1:25:29share, uh, with, uh, your friends. Uh,

1:25:31thank you so much for watching.