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<v ->We're gonna finish up this first session

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by talking about the pathogenesis of osteonecrosis.

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And let's just look at a few factors.

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The literature would tell you, there are a lot

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of possible factors that I've listed here,

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six or seven of those,

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many of these include vascular compromise

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or intraosseous hypertension.

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So certainly that type of alteration

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can produce a propensity to develop marrow ischemia.

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Now, one of the interesting observations is the shape

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of the bone and the size of the marrow chambers may in fact,

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be important in predicting the sites of osteonecrosis.

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In general, when you think about all the sites

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that are involved with avascular necrosis

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or osteonecrosis of an epiphysis,

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we think of convex surfaces,

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the femoral head, the humeral head,

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the femoral condyles, the lunate.

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I mean, all of those are areas that are convex.

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Here I show you classic necrosis in the femoral head

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and numeral head, but the same thing about the capitate,

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the proximal poles involved convex,

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the proximal portion of the scaphoid,

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which is convex, the tailored dome convex.

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So it's kind of interesting that it predominates not

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on concave surfaces, but on convex surfaces.

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So if we go back to the trabecular architecture

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of a convex surface on your left

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and concave surface on the right, we see some differences.

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Those of you who have attended the entire course

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maybe remember a few comments

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that I made about this on day one.

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I indicated that when we deal with an articulation

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and has a convex and concave segment

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the tensile forces are greater on the concave side

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and the compressive forces are greater on the convex side.

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So the subchondral bone plate a lot thicker

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on the concave side than on the convex side.

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And the other point I made when you look

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at the trabecular chambers, and we're gonna talk

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in great detail about those later on,

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but the trabecular chambers are larger, wider

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on the concave side

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and they're much more narrow on the convex side.

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And it may be that sort of architecture

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that predisposes the convex side

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or convex surfaces to osteonecrosis.

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Well, let's look at it in a different way.

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Do you remember that I indicated that

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when deal with articular surfaces,

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they are not the spheres, but they are ovoids and egg shape.

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So let's look at this egg,

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and let's look a little bit at the surface of the egg.

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Let's go ahead and cut that apart.

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And if we did that, beneath the subchondral bone plate

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we see these chambers consisting

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of vertical and horizontal trabecular.

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Well, talk about those later as the walls of these chambers

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and typically in the middle, the marrow

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which in general in the adult

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is mainly fatty marrow rather than atopic marrow.

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So what occurs when forces are placed

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while on that surface, the cartilage?

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The forces extends through the cartilage,

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it reaches the subchondral plate

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and then extends down into this trabecular architecture.

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And what it can do is in fact, produce forces

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not only in the trabecular, but within the marrow chambers.

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It can pressurize those marrow chambers,

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and that pressure within those marrow chambers

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can lead to damage to the trabeculae.

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And that damage with increased pressure

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in the chambers can lead to osteonecrosis.

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The second factor clearly in the pathogenesis

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of osteonecrosis has to do with the vulnerable blood supply.

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If think of this for example, with the scaphoid,

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there is retrograde vascularization.

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The blood flow enters more distally typically

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from a dorsal more than a volar region

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and then the blood vessels extend toward the proximal pole.

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So that explains why that is the proximal pole

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that more commonly is involved in osteonecrosis.

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Furthermore, we often talk about one

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of the causes being arterial occlusion

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from a variety of causes itself.

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Now, one of the problems we run into

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is diagnosing posttraumatic osteonecrosis of the scaphoid.

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So I just wanted to briefly give you some rules.

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What I'm showing you here are T1 rated images, this column,

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T2 fat suppressed images in this column,

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T1 fat suppressed intravenous gadolinium images

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in this column, and then the T1 fat suppressed images here.

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So when we go ahead

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and we look at the normal situation shown in this row,

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typically we see high signal intensity on T1

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and slightly high signal of the proximal pole

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on T2 fat suppress and of the entire bone

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on T1 on fat suppressed intravenous gadolinium image.

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If we look at the classic findings

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of avascular necrosis involving the proximal pole

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of the scaphoid, the rule is low signal intensity

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within that pole.

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We see low signal intensity on T1 on T2 fat suppress

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and on T1 fat suppress gadolinium enhanced images.

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And then we end up with other patterns that are not certain.

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Are they normal?

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Is it ischemia?

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Is it necrosis?

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For example, as is shown here in this row,

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low signal intensity of the proximal bone on T1

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but high signal on T2 fat suppressed and variable signal

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on T1 fat suppressed intravenous gadolinium.

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That is not certain

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whether it is going to be avascular necrosis.

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So let me show you first,

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a classic example of osteonecrosis involving

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the proximal pole of the scaphoid.

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I show that here with T1, with T2 fat suppressed

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and with gadolinium and you'll note, in fact,

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in all of these there is low signal involving

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the proximal pole of the scaphoid.

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Classic avascular necrosis.

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Let me show you an example where in fact

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we can't be certain.

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As you look at these images

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which include not only radiograph CT, T1, T2 fat sad

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T1 fat sad, and here the gadolinium,

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low signal the proximal pole on T1,

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high signal on the T2 fat suppress

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and areas of low and high signal

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on T1 intravenous gadolinium.

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And this is not certain.

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This may represent some focal osteonecrosis

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within the proximal pole,

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but we can't be certain in that case.

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Here's another example

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where you can't be certain, all right?

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Slightly low signal of the proximal pole on T1,

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high signal on T2 fat suppressed and low signal on T1 IV Gd.

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I know we'd like to call this necrosis

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but actually we can't be certain

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with this pattern of signal intensity.

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And then finally, just a couple words that there is a belief

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that it's not the inflow of blood

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that when compromise produces the osteonecrosis

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but more important is obstruction of vascular outflow

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which produces intraosseous hypertension.

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In order to understand that,

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you have to understand sinusoidal capillaries

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and this is what they look like.

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This is a special type of capillary with a wide diameter.

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It's found in certain sites I've listed them there,

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which include the bone marrow,

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and these capillaries have holes

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or fenestrations within them.

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They're discontinuous along their course.

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They have great permeability and allow molecular exchange.

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So these are the type of capillaries that we see.

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Peter Simkin who is a well known rheumatologist,

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pointed out the importance of obstruction

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of the vascular outflow.

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He said here for example,

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the subchondral bone contains chambers composed

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of marrow fat, trabecular walls,

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and one or more of these vascular sinusoids.

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He said, when you load the joint with axial loading,

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the marrow chambers are compressed,

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pressure rises and interstitial fluid

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is driven into the sinusoid and flows from the arterial

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through the sinusoid into the veins.

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In pathologic conditions, the venous outflow can be blocked

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by intraluminal thrombosis as in sickle cell anemia

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or extrinsic pressure related to fat hypertrophy

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even fat that enters into the bloodstream.

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And this can in fact cause upstream blood flow

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and even intervascular fat,

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and finally with joint unloading, the fat may lodge

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in the vessels resulting in osteonecrosis.

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So a skin that would suggest it's the obstruction

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of vascular outflow rather than the obstruction

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of vascular inflow that may explain osteonecrosis

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in a number of conditions.

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We've reached the end of segment one

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and I'm gonna turn the program

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over to Abella to discuss his first cases.