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<v ->Okay, we've come to the exciting part

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of this particular lecture,

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because you know as you look back today

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over the lectures that I've given,

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we started with transient osteoporosis.

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We moved on to show frequent

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associated transient painful marrow edema.

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We went on to osteonecrosis,

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and then we showed you a cases

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where maybe it wasn't osteonecrosis,

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perhaps we were dealing with insufficiency fractures.

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We then covered some of the insufficiency fractures

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and indicated how similar they might be to osteonecrosis.

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So what I'm gonna try to do in the next 10 minutes or so,

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is I'm going to try to tie these together,

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show you how perhaps we can tie together

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these three entities,

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transient osteoporosis/marrow edema,

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osteonecrosis, and subchondral insufficiency fracture.

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And I'm gonna introduce you

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to a term you may not have heard,

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but if you go ahead and query it on the internet,

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you'll be amazed how many hits that you will see.

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So let's start with this.

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The pathogenesis of transient migratory

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or non-migratory osteopenia/marrow edema is not clear.

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And in the second paragraph here,

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I'm indicating all the possible entities

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that might explain why in fact we deal with this condition

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of osteopenia knee or a joint

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associated with marrow edema on MR.

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There is increasing evidence that this particular phenomenon

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relates to some sort of stimulus

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that produces a cascade of events,

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and I'm gonna show you that cascade in a minute,

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that results in transient osteopenia, okay?

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And that this particular pathway includes something

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that as of about four or five years ago,

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I had never heard of,

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it's called Regional Acceleratory Phenomenon,

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and I'm gonna abbreviate it, RAP.

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Easy to say, it'll shorten this talk by about five minutes.

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Well, at the time I began to hear about it, I did a search.

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And when I did this search,

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and this is a number of years ago,

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there were almost 4,000 results of this RAP phenomenon.

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And it was of interest to me that a many of those results

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were in the dental literature explaining changes

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that occur in the mandible and maxilla

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after for example, a tooth is pulled,

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what is the reparative response that occurs.

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So kind of to let you know at the beginning,

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just a general idea of what RAP is,

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think of it as an SOS response.

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It's a reaction of a tissue to a noxious stimulus

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that then increases the healing capacity

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of that tissue, okay?

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And there's insult to that tissue could be trauma,

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it could be infection, it could be tumor.

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So it is RAP that leads to the callus formation

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and the proper bone union,

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rather than a non-union following a fracture.

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It's this particular phenomenon, okay?

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And what it relates to is something that affects

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what is known as the basic multicellular unit (BMU).

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You learned about this in medical school.

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You may not have thought about it very much,

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but that BMU, that unit,

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is a team, a wandering team,

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composed of osteoblasts, which as you know produce bone

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and osteoclasts which resorb bone.

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And the process they produce at the site of injury

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is osseous remodeling, right?

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It is a balance pattern of bone formation

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and bone resorption.

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There is strong evidence that the stimulus

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that activates RAP

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is repetitive loading and unloading a bone.

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When you think of the transient marrow edema

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that migrates or is stationary,

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is generally in the lower extremity

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that we are talking about.

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Most of the stress fractures that we see

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are in the lower extremity.

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There is in fact repetitive loading

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and unloading a bone within that lower extremity.

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So some noxious stimulus likely loading

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and unloading a bone activates RAP.

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Now there may be other stimuli as well.

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I just don't know what they are.

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So let's follow the sequence of events.

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Repetitive loading or unloading a bone leads to microdamage,

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the degree of which has been well shown

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is dependent upon a lot of things,

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the magnitude of the load, the number, rate,

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frequency, duration, distribution,

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and polarity, direction of the loading cycles

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and the quality and quantity of the bone

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at the site that the load is being applied.

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Prolonged or exaggerated RAP levels

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leads to an inflammatory response in the bone.

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This increases the permeability of the capillary bed,

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producing hyperemia, which we've now added to our equation.

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This leads to increased bone turnover

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and marrow edema-like changes,

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elevating marrow pressure.

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So, so far, we've gotten this far.

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Hyperemia leads to loss of bone

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in the form of various patterns of regional osteopenia,

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which are closely associated

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with marrow edema-like abnormalities.

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And I think the edema occurs

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prior to the regional osteopenia.

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RAP and other unknown stimuli

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may also trigger complex regional pain syndrome.

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So we're gonna add that to our equation, okay?

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And it's accompanied by hyperemia

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and has been likened to other forms of regional osteopenia.

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And in addition, there is data that support

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the association of generalized and regional osteopenia.

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Up to this point, all of what we have talked about

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lead to findings that are reversible.

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But then, in some persons,

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additional irreversible abnormalities

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may subsequently appear.

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The next step is, is that the generalized

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or regional osteopenia can predispose

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to subchondral insufficiency fractures.

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These are invariably accompanied by marrow edema.

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Subchondral insufficiency fractures shown here

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can lead to bone collapse

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as well as focal regions of osteonecrosis,

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although there are a lot of other causes

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of focal or widespread osteonecrosis as well.

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These last findings may be,

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but are not invariably irreversible.

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Think back to one of the articles I showed you from Belgium,

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where they tried to figure out

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when they were looking at cases of osteonecrosis

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or something else,

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remember in the knee,

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whether or not they were dealing

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with irreversible or reversible findings

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that something else was likely

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to subchondral insufficiency fractures

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which may not be irreversible,

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long as there is not collapse

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of the subchondral bone plate.