0:02

Hello, and welcome to the noon conference hosted by MRI

0:06

Online. In responses to the changes happening around the world right now

0:10

and the shutting down of in-person events, we have decided to provide free

0:13

daily noon conferences to all radiologists

0:16

worldwide. Today, we are joined by Dr.

0:20

Gomez. He is an academic radiologist with an interest in

0:24

musculoskeletal image-guided interventions and education.

0:27

He is currently the residency program director and

0:31

MSK section chief at UT Health San

0:34

Antonio. A reminder, there will be time at the end of the hour

0:38

for a Q&A session. So on your screen, if you can please

0:42

find the Q&A feature to ask your questions, and we will get to

0:46

as many as we can before our time is up.

0:49

So it's okay to go ahead and enter your questions throughout the

0:52

presentation. That being said, thank you so much

0:56

today for joining us, Dr. Citron. I'll let you take it from

1:00

here.

1:01

All right. Well, thank you all. Thank you for being here in this

1:05

virtual lecture. Thank you to Dr. Collins and the MRI Online team for the

1:09

invitation.

1:10

So,

1:11

today we're going to talk about the basics of bone imaging and how bone

1:15

physiology affects the imaging. It's more of an introductory lecture, but

1:19

I think it's really important and also a good refresher

1:23

for even experienced radiologists of how to better understand

1:27

how the physiology of bone affects imaging and what we see.

1:32

So, in our overview, we're going to talk about a basic

1:35

approach to bone imaging studies.

1:38

I think we can only explain this well

1:42

if we explain the eternal battle of the osteoclast

1:46

and of the osteoblast in the bone and how that presents

1:50

as a lytic or a sclerotic lesion. We're going to talk about the life

1:54

of the border, and I'm sure that in prior bone tumor

1:58

conferences, you've heard a lot about the border.

2:01

Then we're going to talk a little bit about the location of the pathology and why

2:05

it's that important in our differential diagnosis, specifically

2:09

identifying if a lesion is within the bone or is within the

2:13

articulation. Then we're going to talk some about cortical

2:16

lesions,

2:18

and very briefly on how to differentiate between

2:22

medullary lesion.

2:24

Hopefully, at the end of the conference, you can put it all together and knowing

2:27

all this

2:29

important

2:30

things that we see to help our differential diagnosis and

2:34

differentiate lesions between acute, chronic, and indolent.

2:38

So just to start, I know it's a cliché that people always say

2:42

that we radiologists are detectives because we need to take a

2:46

lot of pieces of a puzzle and put it together to come

2:49

to arrive to the best diagnosis possible.

2:53

But it's true. As I practice radiology through the year, I realized that the

2:56

best radiologists are the people who are able to put every information that they

3:00

have at hand and try to make sense of it for a better diagnosis.

3:04

And in bone, like in any other

3:07

region of the body, age is important.

3:09

The skeletally immature versus the skeletally mature

3:13

patient. The distribution, I call the mono versus poly, if it's

3:17

monostotic or polyostotic, one lesion or multiple lesions, and we

3:21

talk about the articulation. If something is monoarticular or polyarticular,

3:25

maybe something infectious, maybe something systemic, all these things give us

3:29

clues. And the bone is important. Lesions of the axial

3:32

skeleton, the spine, pelvis versus the appendicular skeleton.

3:36

There's a important differential diagnosis for each.

3:40

And even inside the bone itself, lesions in the

3:43

diaphysis, metaphysis versus epiphysis helps us in the differential

3:47

diagnosis. And the soft tissues are important, from the

3:51

radiograph to the MRI.

3:54

So I use this film, I've used it for years.

3:57

And the reason is because back in the day when we used to give board reviews to

4:01

the residents, I would show this image to the residents, and most of

4:05

them will usually jump right away and start describing a

4:08

lesion of the proximal ulna because there is a big

4:12

lucent region here in the proximal ulna.

4:15

And we're going to come back to this image, but this is an image that I

4:19

think put everything together that we're going to

4:23

describe and teach today.

4:26

But just in general terms, we can also see that there is a big

4:29

effusion in this elbow. There are also changes

4:33

at around the trochlea, distal humerus--

4:36

Sorry, around the capitellum and around the trochlea,

4:39

and as well as the radial head. But we'll come back

4:43

because what we want to describe after this conference is what is going

4:47

on here is this a problem of the bone itself?

4:50

Is this a problem of the articulation?

4:52

Are the lesions or erosions that we've seen, are they chronic, are they

4:56

acute? And try to piece things together.

5:00

So the first thing we're going to talk about is the eternal

5:03

battle for supremacy of the bone of the osteoclast versus

5:07

osteoblast. This is a funny image here that I have.

5:10

I

5:13

took it from the internet. I tried my best to find

5:17

who created the image to give credit, but it's everywhere in Reddit,

5:20

and I did not produce the image. But I did try my

5:24

best to get who produced this, but it's all over the

5:28

internet. But it's a good image because if this brick wall is the bone,

5:32

the normal bone, as you know, you have the osteoclast, which is going

5:36

to cause resorption of the bone, and the osteoblast, which produces bone.

5:40

It's putting bricks on the wall. And in a normal state, they live in

5:44

balance. There is constant remodeling of the bone,

5:47

but it is a balance effort between the osteoblast and the

5:51

osteoclast. However, when we have aggressive tumors,

5:55

infection, osteoporosis, the osteoclast just

5:58

become very strong, almost like using dynamite, and they

6:02

explode the bone, creating large lytic lesions or tumors, and the

6:06

osteoblasts just cannot keep up. And just

6:10

in terms of learning and to generalize

6:14

this important phenomenon, we're going to just say

6:17

thatOsteoclastic activity is

6:21

activated by increased vascularity.

6:23

Now, keep in mind that osteoclastic activity is activated by many

6:27

things, but what we see in radiographs and in

6:31

radiological studies is best explained if it's increased by vascularity,

6:35

which is one of the main causes of increased osteoclastic

6:39

activity.

6:41

So remember, osteoclastic activity activated by increased vascularity

6:45

eats up the bone, creating lytic lesions.

6:48

The osteoblasts will produce bone

6:50

and will try to stop the osteoclasts, because as you know, in inflammation,

6:54

tumors, and many disease processes of the body, it just

6:58

causes increased vascularity. So what are we going to have

7:02

when these people start fighting each other?

7:06

How are we going to see that on the radiographs?

7:07

We're going to see that in the borders.

7:10

And the well-defined borders, it means that the

7:14

lesions are less aggressive and the osteoblasts are able to

7:18

get a response to this growing resorption of bone in an

7:22

adequate time and manner, and the borders can be sclerotic and non-sclerotic.

7:26

And when there are ill-defined borders, it means that the dynamite is just

7:30

too strong, the explosion of bone is getting everywhere, and the

7:34

osteoblasts just really are not having a chance to get a response.

7:37

So those are the ill-defined borders, which we define as a wide zone of

7:41

transition, a primitive pattern, or moth eaten.

7:44

I'm sure that you have all heard all these terms.

7:49

So this is a very important slide, and the importance of borders.

7:53

This is probably one of the most important slides in the whole

7:56

conference. So we have lesions here in the left of the screen

8:00

from less aggressive or no aggressive

8:03

to the right of the screen who are very aggressive.

8:06

So

8:07

in the first film here, we have a peripheral lesion within the

8:11

distal tibia that has well-defined

8:15

and sclerotic borders. So it's a lucent

8:18

lesion, but the borders are well-defined.

8:21

You can take a pencil and draw a line on top of that

8:25

border because it's well-defined and it's thin.

8:28

This means that this lesion is most likely inactive.

8:31

This is a non-ossifying fibroma, a don't touch lesion, and a

8:35

lesion that is mostly inactive. There is no really increased

8:39

vascularity or any physiologic activity within the

8:43

lesion. So it's being stopped by the surrounding normal

8:46

bone.

8:48

If we move to the next image, we have a CT coronal

8:51

reconstruction of the tibia. And what do we have here?

8:55

We have a lucent lesion, much like the one in the left.

8:58

However,

9:00

the borders are well-defined, but the

9:03

sclerosis about the border is thick.

9:07

So this is

9:08

less

9:10

benign or a little bit more aggressive. So what does this mean?

9:14

So it means that this is a Brodie's abscess, which is subacute

9:17

osteomyelitis. So obviously, it's an active lesion within the

9:21

bone. We have the granulation tissue here, the penumbra

9:24

sign, but the border is thick because the lesion is

9:28

still active, but it's indolent. It's not really

9:32

extremely aggressive. So as you can see, as you

9:36

go away from the lesion, the border becomes less sclerotic.

9:39

Just think about it in a way that the osteoblasts are

9:43

trying to stop this lesion by creating bone and creating a

9:47

barrier against the osteoclastic activity, and

9:51

think about the less sclerotic as we move away from the lesion as

9:55

recruitment of osteoblasts, just osteoblasts trying to come to the fight if this

9:59

a war, and they're trying to help the osteoblasts that are in the front line.

10:04

So then we move

10:05

to the other image,

10:08

and here we have a giant cell tumor that is a lesion of the

10:11

epiphysis, a bone in the epiphysis.

10:14

And here we can see that the borders are well-defined but are

10:18

not sclerotic.

10:19

So once you don't have a sclerotic border, then it becomes a little bit

10:23

more aggressive because the osteoblasts are not having

10:27

enough time or resources to mount that reaction and

10:31

start building bone around this growing lesion to

10:35

stop it.

10:37

But the borders are still kind of well-defined.

10:40

So this is an intermediate aggressive lesion.

10:43

So sclerotic borders, it means less aggressive.

10:46

And as you move to the non-sclerotic borders, it means

10:50

non-aggressive. And then we have the last

10:54

image here. We have a lesion at the proximal tibial

10:58

diaphysis. This is an Ewing sarcoma, a very aggressive and

11:02

bluster lesion. And note that in this lesion,

11:05

there is no beginning or end to the lesion.

11:08

You cannot trace a line around the lesion.

11:11

You cannot precisely say where is the beginning or where is the end

11:15

of the lesion. This is what we call a wide zone of

11:19

transition with a primitive pattern.

11:21

So this is so because the lesion is growing so fast

11:26

that the osteoblasts have no chance whatsoever to build

11:30

bone and try to stop this lesion. So this is a lesion where the

11:34

osteoclasts have all the dynamite. It's exploding everywhere.

11:37

The osteoblasts are flying away and have no chance to mount a

11:41

response and build a border or a fort to stop the

11:44

progression. So very important image.

11:47

We go from less aggressive to non-aggressive and how the border will

11:50

describe the physiology of what's going on.

11:55

But like I said before, a radiologist needs to put all the

11:58

information that they have and try to make a diagnosis. So what's going on here?

12:02

We saw here a pediatric nurse, 17-year-old

12:06

patient came to the clinic with pain, and we saw

12:10

a lesion, and I was like, "Well, it seems that it's

12:12

well-defined."However,

12:16

the borders are not really sclerotic.

12:18

And we're like, "Well, is this a bone cyst?

12:20

I mean, it's just something non-aggressive, but something intermediate."

12:25

So we ended up doing images. And I just want you to know that this, as you

12:29

see in the axial image, MRI image here, this is an MR

12:32

arthrogram T1 with fat suppression, as we do all arthrograms.

12:37

And we see that this lesion is well-defined and has created a

12:40

cloaca, or a tract from the lesion to the soft

12:44

tissues, and there is a soft tissue component.

12:47

We biopsy this, and this ended up being a Brodie's abscess with a

12:51

cloaca, an extension into the soft tissues with

12:54

decompression. And you can see here the penumbra sign on the T1-weighted

12:58

images, which is that peripheral granulation tissue.

13:02

And the

13:03

reason I bring this study is because as we

13:07

saw on the other image, the Brodie's abscess have very thick sclerotic

13:11

borders. But in this case, what happened here?

13:14

There is no more need of the osteoblasts to start

13:18

trying to stop this lesion because the lesion decompressed.

13:21

There is no more pressure, there is no more growing of this lesion because the

13:25

lesion is just decompressed to the outside, and the

13:29

osteoblasts don't have that need to just come back and try to stop the

13:33

lesion. So at the end of the day, you have to put all things together.

13:36

This was a challenging case, but it's a good case to explain the

13:40

behavior of the borders.

13:43

Also very important in terms of the bone, the trabecula

13:47

defines the architecture. We know in radiology

13:51

that we're all about the architecture of the tissues that we're dealing

13:55

with. In mammography,

13:57

in chest, we see a spiculated mass, and it means that it has

14:01

complete distortion of the architecture that we're dealing with, and

14:05

we consider those lesions to be highly aggressive and malignant.

14:10

But in the bone it's different, and that is because the

14:13

trabecula is what defines the architecture.

14:16

So we have here a bone island, and as you guys can see, it has small

14:20

spiculated borders.

14:22

And in the bone radiology world, spiculated borders means that it's

14:26

benign in a sclerotic lesion, and that is because the

14:30

lesion is growing in and about the trabecula, but

14:34

without destroying them. So it's a good thing to remember that in the

14:38

bone, trabecula defines architecture and lesions that grow

14:42

about the trabecula without destroying them are usually

14:45

benign, like the bone island. Which is very different from breast and

14:49

chest, and when we see a spiculated lesion, it means aggressive and

14:53

malignant.

14:55

So what would you say here? We have a primitive

14:59

pattern. We have two views, AP and lateral of the tibia, and we have

15:03

a primitive pattern that is in the cortex.

15:05

We're going to talk a little bit about the location of the lesion a little further

15:08

on in the conference.

15:10

But I have two teaching points in this

15:14

case. First, that the primitive pattern is within the cortex,

15:18

so all this characterization that we see on the bone,

15:22

it's not only for the medullary cavity, but also the cortex.

15:26

Primitive pattern, wide zone of transition.

15:29

You cannot see where this lesion begins and where it

15:33

ends. So as we described previously, this is an aggressive lesion.

15:37

It is behaving aggressively. It is actively vascular.

15:40

It is actively growing. And there is no

15:44

signs in the radiographs that will let us know that the bone

15:48

is actually stopping what is going on.

15:51

In an MRI, we see the cortical lesions with a lot of surrounding

15:55

edema in the soft tissues. And in the medullary cavity, we have

15:59

T1, T2 with fat suppression, and T1 fat suppression

16:03

post-gadolinium.

16:04

And it ended up being a little abscess within the cortical bone, so a

16:09

intracortical osteomyelitis. But

16:13

the second teaching point that I want to make to you guys today is

16:16

this.

16:18

Notice that in the radiograph, the border of the lesion is

16:22

ill-defined. However, in the MRI, the

16:26

border appears to be well-defined.

16:28

And the importance of this is I know you've heard on and on that you should

16:32

never read lesions of the bone without

16:36

correlation with the radiograph.

16:38

And that is because MRI is not good at all to be

16:42

able to define and describe the borders in terms of

16:46

explanation of the physiology going inside the

16:50

bone.

16:51

That we do with radiographs or CT, and

16:55

mostly with radiographs. So that is the importance of radiographs

16:58

for the osteoradiologist.

17:02

So also remember that the soft tissues sometimes attack the

17:06

adjacent bone, usually because something in the soft

17:10

tissues that is adjacent to the bone increases the

17:13

vascularity and inflammation and affects the bone, the

17:17

periosteum, which we're going to talk a little about.

17:19

So notice that in this ulnar styloid process, there is a region

17:23

of small erosion and resorption of the cortex.

17:27

So the first thing you think, "Well, this is RA," right?

17:31

Because early RA can show rheumatoid arthritis with

17:34

small erosions of the ulnar styloid process.

17:38

But in this case, we had a guy who was playing a lot of golf.

17:41

The doctor told him to stop playing golf.

17:43

He didn't want to play golf, and he had a longitudinal tear of the

17:47

extensor carpi ulnaris tendon, which is compartment six

17:51

of the extensor tendons, and had developed a lot of

17:55

synovitis around the

17:58

tendon.

18:00

So all this is just synovitis around the tendon.

18:02

And that synovitis is very vascular.

18:04

And that increased vascularity ended up creating and activating the

18:08

osteoclastic activity of the periosteum around the ulnar styloid process.

18:12

And you know what? That is the same thing we will see in RA.

18:16

We will see attackedautoimmune attack

18:20

of the synovium in the tendon sheath, and it will end up creating erosions of

18:24

the adjacent bone. So we can also see processes in the

18:28

bone associated to surrounding soft tissues,

18:32

and the characterization goes the same.

18:34

So another example,

18:36

a very classic example of gout,

18:40

just a magnified region of this lesion.

18:42

This patient has a lot of osteoarthritis, but also has this

18:46

paraarticular erosion. The joint space seems not to

18:50

be too much involved besides the degeneration.

18:53

We see this big lesion here, and that's because of the facial gout, right?

18:57

As you guys know, tophi around the articulation

19:01

cause chronic pressure erosion on the bone.

19:05

And as you can see, it's the same description.

19:07

We can tell that this erosion is chronic because it's well-defined,

19:11

and it has very well-defined sclerotic borders that are thin.

19:15

And we also have the overhanging edge because the bone is trying to engulf

19:19

this

19:20

tophi that is creating this reaction on the

19:24

bone because of the chronic pressure.

19:26

So something in the soft tissues that is causing abnormality of the bone.

19:31

So now let's talk about abnormalities of the bone versus

19:35

abnormalities of the articulation. This is very important.

19:39

I think that when you see any lesion at the end of the bone,

19:42

the first thing that you should think about and decide

19:46

is if the problem is centered in the articulation

19:50

itself and consequently affecting the adjacent

19:54

bone, or it's a lesion at the end of the bone

19:58

that may have extended into the articulation.

20:01

And that is an important

20:03

thing to differentiate, mainly because abnormalities of the

20:07

articulation, the differential diagnosis is very different from

20:11

abnormality of the bone. There are a few tumors of the

20:14

articulation, but that is far in between, and of the bone, there

20:18

are many. So an articular process, we should see,

20:22

obviously, joint distension, which is usually caused by an effusion or

20:26

synovitis, inflamed synovium, acute or chronic.

20:30

And the pathology extends on both sides of the articulations, which

20:33

sometimes we cannot definitely see on radiographs, but usually we can

20:37

see better on cross-sectional imaging.

20:42

So if it's in the bone, it's usually a well-defined lesion that does not

20:46

extend beyond the subchondral bone.

20:47

Not the subcortical bone, but the subchondral bone that extends into the

20:51

articulation.

20:53

So let's see this image. We have a shoulder radiograph here,

20:57

and we see this lesion, and this one is very, very, very obvious.

21:01

So what do we see here? We have

21:04

a large soft tissue component that appears to be arising from

21:08

the acromioclavicular joint, right?

21:12

And what else do we have? We have these big erosions

21:16

on both sides of the acromioclavicular joint.

21:20

So even though the distal clavicle appears

21:24

expanded and almost appears like there is a mass in there, we

21:28

can confidently say that this is an articular process and not a

21:32

process of the bone itself. And the differential diagnosis will vary

21:36

tremendously. We're not going to say, "Well, there is a tumor of the distal

21:39

clavicle." There is not. This is more an erosion of the distal clavicle,

21:42

and this is a case of PVNS of the AC joint, which is not too

21:46

common, and it's causing these chronic erosions around the

21:50

articulation. So a good way to try to differentiate

21:54

between two, and this has all the things that you need.

21:57

Joint distension,

21:59

erosions or abnormalities of the bone at both sides of the

22:03

articulation.

22:05

Now,

22:07

not everything is perfect, right?

22:08

And we have to put, again, all these pieces together that we see on the

22:12

radiograph and clinical picture to come to the best

22:15

diagnosis. So in this case, are we having an articular problem or

22:19

are we having an osseous problem? So here on the

22:23

image on the right, we see a lot of small sclerotic lesions

22:27

centered mostly about the articulation at the hip joints,

22:31

symphysis pubis, sacroiliac joints bilaterally.

22:34

But what's going on with the articulation?

22:38

Nothing is going on. It's normal. We don't see erosions.

22:41

We don't see bone destruction. And yes, we have lesions that are

22:45

on both sides of the articulation, but the articulation is normal,

22:49

so not all the pieces are there. So this is an osseous problem that happens to be

22:53

polyostotic. These are multiple bone islands called

22:56

osteopoyikilosis, just a benign condition.

23:00

Similar to the case on the right side, we have all this

23:03

lesion at the distal femoral metaphysis, proximal tibial

23:07

metaphysis, and even the fibula. Lesions that extend from the medullary

23:11

cavity face away from the articulation, classic osteochondroma.

23:15

But how about the articulation itself? The articulation is normal.

23:19

The subchondral plate is intact. We don't have any evidence of distension of

23:22

the joint or joint effusion. These are lesions that are on both sides

23:26

of the articulation but that do not affect the articulation and commonly seen

23:30

with systemic processes such as osteopoyikilosis or multiple

23:34

hereditary exostosis.

23:38

So how about this case? So we have right and left elbows, and

23:42

our clichéd detective radiological radar

23:46

just

23:48

comes on, and we can say, "Well, man, we have a bilateral

23:51

process, so this is probably a systemic process.

23:54

This is probably something that is affecting a lot of the

23:57

articulations." And in this case, almost seems like it's symmetric.

24:01

But what do we see here? We obviously see that there are big

24:05

erosions at the end of the humerus, both at the capitellum and trochlea.

24:09

There is chronic resorption of the proximal ulna

24:13

and as well as the radial head. There is almost subluxation and

24:17

dislocation of the elbow joint bilaterally.

24:20

So we see that the borders that we see in this erosion are

24:23

well-defined and sclerotic, that you can trace with a

24:27

line. So this is an active process.

24:29

We know this is chronicBecause of the behavior of the bone and

24:33

what we see in the radiograph, we know that this is a chronic process.

24:37

But we also know that this is an articular process

24:40

because there is destruction of the bone on both sides of the

24:44

articulation. So this is a patient with chronic hemophilia that

24:48

has been treated, and there has been a destructive arthropathy related to the

24:52

recurrent hemorrhage.

24:55

As just a confirmation with the MRI, we see the T1 and T2, and we

24:58

see all the susceptibility artifact inside the joint, which is related to

25:02

hemosiderin deposition. And we also can see the big erosions

25:06

that we see here. So a lot of the clues that we have, and we can come to the

25:10

diagnosis if we

25:12

take the findings in step and try to piece them together

25:17

in a way that makes sense.

25:21

So let's talk about this. So this is a classic finding.

25:23

We have a pelvis frog's view here, and on the right

25:28

femoral head, we have diffuse increased sclerosis

25:32

of the femoral head.

25:35

And we have this kind of

25:37

serpiginous line right at the subchondral bone with a little region

25:41

of air and subchondral collapse. Clearly, the crescent sign, very

25:45

classic for avascular necrosis. So this is a problem at the end of the

25:49

bone, classic at the end of the bone, avascular necrosis.

25:52

This is no tumor. This is nothing.

25:56

This is not cancer, obviously. But then the articulation looks fine.

26:00

There's the subchondral plate of the acetabulum looks

26:04

fine. There is no dysplasia. There is no distension of the joint anywhere.

26:08

It just looks perfect. So it's a classic subchondral bone

26:12

abnormality, and we can see it very clearly in

26:15

MRI. But the point is that when you have a

26:19

mechanical problem at the end of the bone, it is not an articular

26:23

process, but it will eventually be an articular process like we see here on

26:27

the right, a chronic Legg-Calve-Perthes, chronic avascular necrosis of the

26:30

femoral heads because of secondary osteoarthritis and

26:34

degeneration. Once you have an abnormality of the subchondral bone that

26:38

affects the mechanics of the articulation, it is

26:42

inevitable that you're going to develop osteoarthritis.

26:45

And in this case, it's even more interesting because it happened

26:49

when the skeleton was immature, and we have evidence of

26:53

this plastic acetabulum shallow and

26:57

abnormalities that happened before the closure of the growth

27:00

plate. So subchondral bone changes can

27:04

also cause

27:06

articular changes, either by direct extension or just

27:10

by secondary osteoarthritis because of abnormal mechanism.

27:14

So let's try again. We have a shoulder radiograph here and

27:19

obviously in external rotation.

27:22

And similar to the prior radiograph that we saw of the hip, there

27:26

is flattening of the humeral head.

27:29

And we say, I present this to... I

27:35

know the diagnosis already, which is easier.

27:37

But there is flattening of the humeral head, and most people think, well,

27:41

there is some avascular necrosis.

27:44

But if you look closely here,

27:47

there is some irregularity of the glenoid, and most importantly, there is

27:51

high density within the axillary recess, which means that the

27:55

glenohumeral joint is distended, and it's distended with

27:59

something that is high density. It almost looks like calcium.

28:02

Then you think, can avascular necrosis cause

28:06

increased calcium on the joint? Probably not.

28:09

So this is a case of Milwaukee's shoulder, which is a

28:13

destructive arthropathy related to hydroxyapatite deposition

28:17

within the joint itself. And it is so destructive because this

28:21

foreign objects of calcium cause so much increased vascularity that you pretty much

28:24

destroy the bones that are

28:28

adjacent to the articulation that the differential diagnosis is usually charcot

28:32

arthropathy related to syringohydromelia

28:36

or even Gorham's disease, which is a vanishing bone disease.

28:40

But we can see in this case that because the joint is distended with

28:44

calcium, all this destruction is related to the articular process and not

28:48

the process that we see in the bone extending into the articulation.

28:51

So putting all these things together is important.

28:56

So let's go back again and try to put this all together with the

28:59

radiograph that we saw at the beginning.

29:02

So we have the AP and lateral view of the elbow,

29:05

and there are several things that we see.

29:08

The first one, there is the anterior sail sign, which means that

29:12

there is a big effusion here, that all this is

29:16

distension of or effusion or synovitis, distension of the

29:20

joint.

29:21

We also

29:23

see this erosion here

29:27

at the proximal ulna that has well-defined sclerotic borders.

29:32

However,

29:33

we also can see this other big erosion here where the

29:37

borders are less well-defined as compared to the ones

29:41

here. And we also see in the AP

29:45

view that there is some resorption of the bone at the

29:49

peripheral capitellum as well as the trochlea.

29:52

So if we put all this together, we can say with the radiograph, there is distension

29:56

of the joint and destruction of bone on both sides of the

30:00

articulation. In this case, the three sides of the articulation.

30:03

So we say, well, this is an arthropathy.

30:05

This is an articular process, something that is causing inflammation of the

30:09

joint. And now we have to think, is this something acute, chronic?

30:12

What is going on? But we can see that some of the erosions have

30:15

well-defined sclerotic borders, which tell us that there is some

30:18

chronicity to it, to the process. But other

30:22

borders show no sclerotic borders.

30:25

So it's like an intermediate. So this is what we call an

30:29

indolent processAnd when we see this, we're thinking about PVNS,

30:33

tuberculosis arthritis, all those arthropathies that are in

30:37

between, or you can even say a treated or

30:40

partially treated inflammatory arthropathy.

30:44

In this case, we have the MRI, we have the T1, T2 fat-suppressed

30:48

images, and T1 fat-suppressed with gadolinium.

30:52

And we see that there is extensive

30:55

synovitis here. All this stuff is just synovitis all around the

30:59

joint and not really much fluid. Then with

31:03

the contrast, we see thick enhancement of the synovium just

31:07

above the bone. We see the region of low T1 signal intensity in

31:11

the erosion, which means sclerosis.

31:13

So this ended up being tuberculosis arthritis, which is an indolent

31:17

inflammatory infectious arthropathy.

31:21

But I think it's a good case to differentiate between

31:24

articulation or the bone, and also to evaluate the borders of

31:28

the lesions that is creating and how does that help us come to a better

31:31

diagnosis and narrow our differential diagnosis because of

31:35

what we know of the behavior and physiology of the bone.

31:41

All right. So briefly, we're going to discuss here. So where is the lesion?

31:45

So we have here the

31:47

leg, the tibia fibula.

31:49

We have seen this radiograph already,

31:52

and I know you guys seen a lot of memes nowadays about the

31:56

importance of two views. I think medullary lesions are kind of easier

32:00

to see. You see them on both views, and you can see that there

32:04

is extension or affecting the medullary cavity

32:08

or it seems to be in both the AP and lateral view.

32:11

There is something in the

32:14

cortex. When you see the AP view, you cannot really

32:18

tell if it's in the cortex of the medullary cavity.

32:21

Obviously, in the lateral view, it's pretty obvious that the

32:25

lesion is in the cortex. However, something that you want to keep in mind,

32:29

the lesion, the bone, obviously is a cylinder.

32:33

And that said, it can affect any part of the cylinder, but most of the

32:37

cortical lesions will be in one side of the cortex, either the posterior,

32:41

anterior, lateral, or medial. So that said, you can

32:45

see that the cortex here adjacent to lesion is usually

32:49

intact. I wouldn't take that as, "Okay, this is a

32:53

hard sign of a cortical lesion," but it does help. It does help.

32:57

If it was a medullary lesion, you would see that it will extend more to the

33:00

cortical region.

33:02

So now we're going to end up the conference talking about lesions in and about the

33:06

cortex because I feel it's very important, again, to narrow your

33:10

differential diagnosis. So we're going to talk about lesions

33:14

within the cortex and how we can differentiate that from other lesions

33:18

in and about the cortex. What are the findings that we can see that help

33:22

us in that differentiation, and we're going to explain what that cortical

33:25

thickening means and how we can identify it better.

33:28

Lesions or abnormalities that affect the inner surface of

33:32

the cortex, which is the endosteum, and that is seen with endosteal

33:36

scalloping. And then lastly, the outer surface of the cortex, which is the

33:40

periosteum, and we call that a sclerosis.

33:43

And also you can have periosteal reaction.

33:46

So endosteal scalloping is

33:50

the term that we have to describe

33:53

a pressure chronic erosion of the

33:56

endosteum. Right? So we have here a patient with

34:00

multiple enchondromas in the body. That's Ollier's disease.

34:04

And we see that this lesion of the medullary cavity expands

34:08

the bone. And because it expands the bone in a chronic, slow

34:12

way, it kind of creates that scalloping in the

34:16

endosteum. The thicker the cortex, the more obvious that is

34:19

going to be the endosteal scalloping.

34:22

The reason why I have this as an example is

34:25

because enchondroma is a quintessential lesion to be

34:29

described as endosteal scalloping, which is that you have the

34:33

cortex and you have this

34:35

kind of pressure

34:37

erosions or concave lesions about the inner aspect of the

34:41

bone. And it's classically seen in enchondroma, but it will happen

34:45

with any slow-growing lesion of the medullary cavity that it

34:49

happens to expand or be expansive.

34:52

Now, if it was an aggressive lesion of the medullary cavity that

34:55

affects the endosteum, you're not going to see this, right?

34:58

You will see cortical breakthrough and cortical

35:02

destruction, which is a term that we use a lot in our

35:05

radiographic reports. There is no cortical breakthrough or there is cortical

35:09

breakthrough. So endosteal scalloping we see in lesions that are

35:12

non-aggressive and give time to the bone to create that pressure

35:16

erosion with well-defined borders.

35:20

So let's talk about this lesion. So we have a lesion in the AP view that

35:23

looks in the middle of the bone, just like the other one we saw.

35:26

There is a little bit of periosteal reaction here.

35:29

But in the lateral view, we can clearly see this lesion is

35:33

within the cortex, right? So what is important about

35:37

this?

35:38

It looks like it's in the cortex, and it is in the cortex.

35:41

And one of the things and findings that we can tell in the

35:45

radiograph is that the cortex of the

35:49

posterior course of the fibula, it is expanded both in

35:53

the side of the endosteum as well as the side

35:57

of the periosteum. So in

36:01

general terms, it expands the bone in both ways, this way

36:05

and this way. So that is very classic of an intracortical

36:09

lesion that tends to expand the bone both at the side of the

36:12

endosteum and periosteum.

36:14

So we did an MRI

36:17

of this lesion, T1, T2 with fat suppression,

36:21

T1 with fat suppression and gadolinium.

36:24

And we see this small intracortical lesion within the posterior aspect

36:28

of the cortex. We can see the thickening of the posterior

36:31

cortex and some enhancement, high T2 signal intensity and

36:35

enhancement, which has a little track and extends into the soft tissues.

36:39

This is also intracortical osteomyelitis that

36:43

happens to show extent into the soft tissues and decompress.

36:46

But it's a purely intracortical lesion, and as you see, the medullary cavity

36:50

is uninvolved, even though the endosteum appears unperceptible at

36:54

this point in the MRI.So this is the sagittal

36:58

view, and again, just to pay attention how there is

37:02

expansion of the cortex in both direction

37:06

because obviously we have this intracortical lesion here in

37:10

the bone that we can see both on the T1-weighted images as

37:14

well as the T2-weighted images with fat suppression.

37:17

Now let's go back and discuss this because it's a good

37:21

teaching point. So we have seen two cases today in our

37:25

conference of intracortical osteomyelitis, and you say,

37:29

"Wow, man, that looks different." And in this

37:33

lesion, intracortical osteomyelitis in the cortex, we have a

37:36

well-defined lesion, and in this one we have an

37:40

ill-defined lesion. And we're just going to go back again about the

37:44

behavior of the bone and what we see in imaging, is

37:47

that the one on the left side, the difference is

37:51

that, same as we described previously, it decompressed to the

37:54

outside. So it looks less aggressive because the

37:59

lesion is not extending through the bone and trying

38:03

to attack more parts of the bone, but it's decompressing through the path

38:07

of least resistance and it's going outside the body,

38:10

and that's why it looks less aggressive.

38:13

The attacking of this lesion is not to

38:17

the bone, but to the outside. So a very good example to explain

38:21

this physiologic

38:22

behavior of the bone and the,

38:25

what is it? The battle of the supremacy between the osteoblasts and the

38:29

osteoclasts.

38:31

So we have another lesion here, a very classic lesion, and again, in

38:34

the proximal tibia. We have thickening of the cortex that

38:38

extend to the periosteum as well as to the endosteum.

38:42

So we say, "Eh, we don't even need the latter." This is a classic

38:46

cortical lesion. There is expansion.

38:48

There is something that's going on here in the cortex because the endosteum is

38:52

being expanded as well as the periosteum.

38:55

We do a CT, and we have a very small osteosteoma, and

38:59

again, we can see that there is

39:03

expansion of the cortex in both ways of the periosteum and the

39:06

endosteum. And as you know, osteosteoma,

39:10

it creates a lot of thickening. We have another case here with

39:14

osteosteoma here, and the thickening of the posterior cortex of the

39:17

tibia is really, really very prominent.

39:20

So it's an intracortical lesion that causes all this thickening.

39:25

So I want you to pay attention to this, just a matter of comparison and

39:28

to better see the difference.

39:32

We have here smooth,

39:35

non-aggressive periosteal reaction, which is related to a chronic fracture

39:39

healing. Now,

39:41

the endosteum here is intact. It's not extending

39:45

inside the medullary cavity,

39:48

but the periosteum is thickened. Right?

39:50

So this is not an intracortical lesion.

39:53

You may think it is, but it is circumferential periosteal reaction, and

39:57

it's affecting the periosteum but not the endosteum.

40:00

It's not causing that expansion of the cortex.

40:02

So that will go away,

40:05

will steer you away from trying to name an

40:08

intracortical lesion in your differential diagnosis.

40:11

So that's an important thing to remember.

40:15

So last but not least, we're going to describe lesions or abnormalities

40:19

that happen at the surface of the bone, the periosteum, the

40:23

outside. So we have four different lesions here that

40:26

somewhat can be in the differential diagnosis of abnormalities at the

40:30

surface of the bone. So we here have a proximal femur, and we see

40:34

this

40:35

lesion here around the bone that we partially see.

40:39

But just remember, this appear to be surface, and look in the endosteum.

40:43

The endosteum look fine. How about the outer

40:47

surface of the cortex? Looks fine as well.

40:50

It's not ragged, right? We don't see any resorption here.

40:52

So a purely surface abnormality. Here on this

40:56

other lesion,

40:58

we have kind of expansion of the bone and almost seems like

41:01

continuation of the medullary cavity.

41:03

We're going to describe each of this lesion, but just as a matter of

41:07

comparison. And here we have a lesion that appears to be

41:10

almost like taking a bite of the bone.

41:13

But again, the endosteum, even though it's been pushed inside,

41:17

appears to be kind of preserved. And then the last lesion, we

41:21

see

41:22

another surface lesion that we can tell, again, because the

41:26

endosteum here appears to be fine.

41:29

But here you can see the very sharp difference between

41:33

the lesion and the periosteum here is more obscure.

41:36

And we have this large cauliflower-type lesion that appears to be

41:40

arising from the surface of the bone.

41:43

So the first one is a tug lesion, so in an enthesis where

41:47

muscles or tendons or ligament originate or insert,

41:50

sometimes they get inflammation or repetitive traction

41:54

and increased vascularity, and this calcifies.

41:57

Just like anywhere in the body, when you have an inflammation, what does it do?

42:01

The inflammation decreases, and then you calcify.

42:04

That's why 95% of the calcifications we see in our soft

42:08

tissues are dystrophic, which means that they are sequela from some type of

42:12

inflammatory process that the tissue die and

42:16

ended up calcifying. But here we can see the lesion in the CT

42:20

that both the outer surface of the cortex and the

42:24

endosteums are well preserved, and we see this lesion is

42:28

arising from the periosteum, but not affecting

42:32

anything of the cortex. Now it may be difficult to

42:36

say, "Well, is this a myelitis ossificans that it's been chronic and calcified

42:40

there?" There are some times, yeah, it can be in the differential

42:44

diagnosis, but this is, again, we're talking about

42:48

having to be a detective and putting all the clues together.

42:52

Tug lesions goIn the direction of the

42:56

muscle. So if you know your anatomy well and know that any part of

43:00

the bone is where a muscle originates, and the calcification kind of

43:04

goes in that direction or the direction that you expect to see the muscles, think

43:08

of tug lesions. A myositis ossificans or something calcified

43:12

around the bone will be more circular and will not have any pattern of

43:15

continuation with any of the adjacent structures.

43:21

So osteochondroma is not really a surface lesion, but because it

43:24

extends beyond the medullary cavity, I like to include it in this

43:28

differential diagnosis. So we have two broad base

43:33

here in the mid-humerus, and we have a more narrow base.

43:37

So osteochondroma is not a surface lesion, but it

43:41

appears to be arising right beyond the confines of the bone.

43:44

It's non-aggressive lesion. And the clue here is that there is

43:48

continuation of the medullary cavity into the lesion,

43:53

as you can see with little trabeculae here at the proximal

43:57

aspect of the lesion. It comes in different flavors.

44:00

Like I say, a broad base or with a small

44:04

stalk, and may confuse you depending on the view for

44:08

a cortical lesion. But this is a very common lesion, osteochondroma.

44:12

So then we have the next one, the one that looked like somebody took

44:16

a bite. It appears like almost somebody took a bite here of the outer

44:20

aspect of the humerus. And we can see some chondroid

44:24

matrix, and there's a juxtacortical chondroma, pretty classic lesion

44:28

of the surface of the bone.

44:31

But the important thing here is that, yes, it is causing

44:35

a pressure erosion of the periosteum, and this is called

44:40

saucerization. We call this pattern of

44:44

surface concave pressure chronic

44:47

erosion, saucerization. As we already mentioned, when it's in the

44:51

endosteum, we call it endosteal scalloping.

44:54

But if it's in the periosteum, we call it saucerization.

44:57

So the important thing here to note is that,

45:01

besides the chondroid matrix and all that, is that even though that the cortex is

45:05

pushed inward, the cortex remains intact,

45:10

both the periosteum and the outer surface.

45:12

So it's almost like it's been pushed, like almost taking the cortex,

45:16

making it almost

45:17

malleable and pushing it

45:21

into the medullary cavity.

45:23

So saucerization, a juxtacortical chondroma, and of course, we can

45:27

see these tiny regions of chondroid calcification or chondroid

45:31

matrix and give us the diagnosis there.

45:35

And then we're going to talk the last lesion that we saw is this large

45:38

lesion that appears to be arising from the periosteum.

45:42

It looks like a cauliflower. If you see in a test, if you're a resident

45:46

and you ever seen a test, there is a cauliflower-type sclerotic

45:50

lesion. Think about periosteal osteosarcoma, which of

45:54

all the osteosarcomas is the less aggressive,

45:58

compared to the periosteal or telangiectatic osteosarcoma or classic

46:01

osteosarcoma, which are very aggressive.

46:03

So there is obvious osteos matrix production here.

46:07

But for the purpose of this conference, the important

46:11

thing to know is that the endosteum is intact,

46:15

and you cannot see the difference between the periosteum of the

46:19

lesion. So it's a periosteal osteosarcoma, but it actually arises from the

46:22

surface of the bone, but almost always seems like it's extending to the

46:26

cortex. And we have a better here view with the CT scan.

46:30

We have this lesion that looks like a cauliflower that is arising from the surface

46:34

of the bone, and it seems like we have this

46:38

kind of region here. But the important thing here,

46:42

again, is that the endosteum appears intact.

46:45

This is not extending into the medullary cavity.

46:48

It's not expanding the cortex into the periosteum.

46:51

So we wouldn't think this is an intracortical lesion that is expanding into the

46:54

soft tissues because the cortex is of normal thickness, but a surface

46:58

lesion that extends into the soft tissues.

47:01

And this is a very classic finding of periosteal osteosarcoma.

47:06

So I'm going to finish my conference with another abnormality that we

47:09

see,

47:11

not at the surface, but that is important for all of us to

47:15

recognize, and it's the subperiosteal abscess.

47:17

In the pediatric patients, they get hematogenous osteomyelitis like this

47:21

patient has here in the distal tibia.

47:24

And the periosteum is not really that firmly

47:28

adhered to the cortex as compared to the adult.

47:31

And in this case, it went through the posterior metaphysis, the

47:35

infection, and it extended between the periosteum and the cortex here.

47:39

And it creates this large subperiosteal abscess that we see in

47:42

hematogenous osteomyelitis of pediatric or young

47:46

patients. So things to keep in mind is I like to

47:50

talk about this in the surface or cortical lesions because

47:54

it's important to note, and actually it's really hard.

47:57

If it's acute, you'd really almost never see it on radiograph.

48:00

You just see the soft tissue swelling.

48:02

But if they ever ask you on a test or if you have this available in your

48:06

institution, you can see an ultrasound.

48:08

The periosteal sheet is so thin that the ultrasound beam can

48:12

cross it and you can see that abscess.

48:14

So okay, we have the cortical bone here, and

48:18

we have here the periosteum. And all that stuff that is inside

48:22

here is the abscess. All this is the abscess with the debris and all that

48:26

stuff. So we may not be able to see the subperiosteal

48:30

abscess in radiograph, but we can see it on ultrasound as well as

48:34

MRI.

48:36

So that will conclude my conference, and I appreciate you

48:40

listening and looking at my cases. And again, thank you to Dr.

48:43

Collins and MRI Online for the invitation.

48:47

All right. So before we move into the question and answer

48:51

session, on behalf of MRI Online, I want to thank you all for participating

48:55

in this noon conference and remind you that this conference will be available on

48:58

demand on mrionline.com, in addition to all

49:02

previous noon conferences. Tomorrow, we will be joined by Dr.

49:06

Riz Dack for a noon conference on case-based interstitial

49:10

lung disease.So, Dr. Gomez, if you could please

49:14

open the Q&A feature on your screen and answer the questions

49:18

of your choosing.

49:20

Yeah, sure. So I have here, "How can you differentiate

49:23

intracortical

49:25

osteomyelitis versus EG, epidural lymphoma, in the

49:29

pediatric age group?"

49:33

It is difficult. I think intracortical osteomyelitis,

49:37

in fact, we have usually have had to biopsy patients.

49:41

One of the last patients that we saw, the one that even had the track, which was

49:45

very suggestive of a small cloaca.

49:47

We biopsy it because the orthopedic oncologist still had doubts

49:51

that they could be EG. But EG lymphoma, there are several lesions,

49:55

EG lymphoma, that can look like anything, and sometimes you can't

49:59

differentiate it. If the clinical picture doesn't

50:03

contribute to the findings, then sometimes it's just sensitive tissue diagnosis.

50:07

But,

50:08

I would say that they can look similar.

50:11

EG usually is more well-defined, doesn't have any sclerotic borders, and

50:15

within the cortex, it will be difficult to differentiate from osteomyelitis.

50:20

And okay, so it

50:25

says that, "Since metastases are more common compared to primary

50:29

bone lesions, are there any specific descriptive

50:33

signs regarding their borders or location that could help make the difference?"

50:37

So, I think metastasis is more common.

50:40

So if you see a destructive, aggressive lesion in the bone,

50:45

and especially in an adult, if it's lytic, you should always think

50:48

metastasis versus

50:51

multiple

50:52

myeloma.

50:54

I think the history helps.

50:57

Their borders really don't help in terms of metastasis and primary lesion.

51:00

The border only helps to describe how aggressive the lesion is

51:04

behaving, or if it's non-aggressive to aggressive or it's

51:08

been treated or not treated. But as

51:11

itself, the border doesn't really help to differentiate between

51:15

metastasis or a primary lesion. But definitely if you see

51:19

multiple lesions, it's most likely to be metastasis, especially in the adult

51:22

population, and as you say, because they are much more common than

51:26

primary lesions of the bone.

51:32

And I have a question here,

51:34

"May I know what does cortical expansion suggest?" Cortical expansion suggests that

51:38

it's an intracortical lesion. So when intracortical lesion happens,

51:41

it tends to expand or create calcium or bone at

51:45

both sides of the cortex, at the periosteum and the endosteum.

51:50

So, "Do we get sequestrum in intracortical osteomyelitis?"

51:56

You can, but not common at all. And

52:00

sequestrum is mostly in

52:02

hematogenous osteomyelitis,

52:06

and you get that piece of bone that get dislodged and floats in the abscess,

52:10

and it usually requires surgical treatment because the bacteria stays in

52:14

that island, and no blood gets there.

52:16

And obviously, it's much easier to be within the medullary cavity.

52:21

Myself, I've never seen an intracortical sequestrum.

52:25

But I'm sure it happens thinking about the pathophysiology, but I've never seen

52:29

it. I've seen a sequestrum in the medullary cavity.

52:32

"Differentiate between juxtacortical chondroma and

52:35

osteomyelitis."

52:39

Yeah. Osteomyelitis can be hematogenous.

52:43

They're related to direct contact or related to instrumentations.

52:47

There are the three osteomyelitis that we have.

52:50

Juxtacortical chondroma wouldn't be in the differential diagnosis of hematogenous

52:53

osteomyelitis, which is the most common.

52:56

And if it's of context, you will differentiate because there will be some type of

53:00

ulcer or abscess around the cortex that will

53:03

differentiate that. And of course, the borders will probably be more ill-defined as

53:07

compared to a juxtacortical chondroma.

53:10

So let's see. "Does a pedunculated cauliflower-type osteochondroma

53:14

have medullary extension?" Yes. One of the hallmarks of

53:17

osteochondroma is medullary extension.

53:20

There is also an aberrant osteochondral lesion called

53:23

Nora's lesion, but we're not going to talk about that, and it's not a true

53:27

osteochondroma. You should have continuation of the medullary cavity.

53:33

And

53:36

say here, "May I know, is it true that periarticular erosion is

53:39

suggestive

53:41

of rheumatoid arthritis whereas juxtacortical erosion..." Yes.

53:44

So as you know,

53:48

in RA, it's not really periarticular, it's marginal.

53:51

So as you guys know, it happens between the boundaries of the origin of

53:55

the capsule and the beginning of the cartilage that protects the subchondral bone.

54:00

That is called the bare area. And because there is no

54:03

cartilage protection, usually the erosions happen there.

54:07

But it's not really periarticular because it is still within the capsule and the

54:10

articulation, so we call them marginal erosions.

54:13

And in gouty arthritis, you can have intra-articular erosions, but

54:17

the hallmark finding of periarticular erosions with well-defined borders

54:21

and an overhanging edge is related to pressure

54:25

erosions that happened around the articulation but not inside the

54:28

articulation. So

54:30

that's a way to differentiate that.

54:32

We have here, "What is the difference between primitive lesion and moth-eaten

54:35

lesion?" Not really anything. It's just two ways of describing the same.

54:38

I think moth-eaten, the little lucencies are a little bit bigger, and

54:42

primitive lesions are a little bit smaller, but practically, there is no

54:46

differentiation.

54:49

And we have a question, "Do we see sclerotic cortical base mets?"

54:54

Not likely. Right?

54:56

Most of the vasculitis in the bone is in the medullary cavity, and metastases go to

55:00

the bone through the blood flow. So, you will find them more in the medullary

55:04

cavity than anything else. So

55:08

anyways, that was bound to be my last question.

55:12

I appreciate you guys so much to listening to my conference, and

55:16

hopefully we'll meet again virtually or not. Thank you so much for everybody.

55:21

As we bring this to a close, I want to thank you, Dr.

55:24

Gomez, for an outstanding presentation and for your time today.

55:27

Thanks to all of you for participating in our noon conference.

55:30

Again, this noon conference will be available on demand on

55:33

mrionline.com, in addition to all previous noon conferences.

55:37

Please follow us on social media at @mrionline for updates

55:41

or reminders on upcoming noon conferences.

55:44

Thanks again, and everyone have a great day.

55:47

Thank you.