36: Exam Review

September 19th, 2014

Diagnosis and Treatment of Oral Diseases-- Lectures #36 – Histopathology of the Dental Tissues as Relates to Caries II, Review Session – Dr. Wolff

Can you hear me in the back of the room?Any questions from the audience at this moment you want to know about tooth decay? Yeah? [Student question: How long does it take for the stains to appear with the chlorhexidine?]So the question is, how long does it take the stains to occur with chlorhexidine? The bad problem is, quick. The stain is actually bacteria in the plaque dying. And staining in the plaque, dying. It’s ugly. So the CPC that you also see in the Crest products is also implicated in the staining. So if you actually get an effective killing of everything, you get some staining at the surface. And the place that stains the worst is at the gingival margins. You put a restoration, you get this black line and you can’t get that clean, no matter what. And it starts very quickly its dependent on what you eat and how. I’ve seen chlorhexidine stain in patients, we use chlorhexidine after we put implants in places in patients because they can’t brush in that area, it’s sore, and we actually have them clean with chlorhexidine to keep the bacterial counts down. It’s probably all voodoo but it’s what I was taught when I was taught how to place implants. Those patients come in with stain on their teeth in two weeks. You want to get them off of it as quickly as possible. It prophys off easily if you see them rapidly but after a couple of months you can’t blow the stuff off with a sandblaster. Any other questions?[Student question: what about on the tongue?]The tongue? Placing chlorhexidine or brushing with chlorhexidine on the tongue? [Student question: will it stain the tongue as well?]It will stain everything the same way, the tongue has abrasion on it which you tend to want to clean off the tongue a bit. I can’t say – you haven’t seen any staining on the tongue because of chlorhexidine, have you Kenny?[Dr. Allen: No, I’ve only seen it on the teeth]Yeah I have to tell you, I haven’t seen it on gingiva or the tongue. Even on my cancer patients that don’t have saliva, the tongue doesn’t change. I actually use it when they start to complain that their tongue is getting slimy and hurts. So there are times when you need it.

Any other questions? Yes?[Student question: If you have caries in the last three years do you have high risk caries rate, or is it only in the past year?]Ah ha!!!![Student: Because you said both!]We had said both!!!!! And it actually fits properly. The research shows that you’ve had active caries in the last three years, you are – I’d have to go back and look at – it was something to the you are a thousand times more likely to get caries in the next three years. I’d have to go back and look at it, it is a Featherstone paper. Its wonderful data. The problem is it hasn’t been well defined how long you have to be caries free before we can drop you out of the high risk category. So what we have adopted, because there is very significant expense associated with high risk maintenance, is a lower cost knock down after one year. So your first year you’re high risk. If you have another caries, you’re high risk. If

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you come in after one year and everything is staying the same, we’ll talk about dropping down to a lower risk. And we don’t make you low risk, we make you moderate risk. So the difference between our risk assessment and the Cambra that’s been published in the Dental Journal, which I think we made available to them? No? Well, make sure that you get it available. We were co-authors on it. They actually have advocated for four levels of risk. I don’t have enough room for this to divide this in such micro. So when you look at the highest risk, I have everybody coming in on three month intervals for fluoride, I have everyone coming in using a home fluoride supplement. I have them using a calcium supplementation of one form or another. I don’t mean tums type calcium supplement. I mean calcium containing toothpaste in a effort.. what I’m doing and I’ll show you on the slides in a minute, I’m using methods that have weak evidence, but because your disease is so likely to occur, I’ll use everything in the kitchen sink. When I get to the person that’s got caries AND no saliva, I’ll even throw my anti-microbial on top of it. But you’re high risk. I have difficulty saying “high risk” and “super high risk.” Honestly, my cancer patient, my Sjogren’s patient, those are my super high risk patients. After a year, I’ll knock down that high risk patient to the moderate risk category which still has them using some sort of home fluoride. Maybe or maybe not using a calcium supplement. But we are willing to take down some of the high expenses. I’ll move them from four visits a year for fluoride varnish down to two or three and watch them from there. And the reason why we need to measure severity of disease is we need to know whether or not it is advancing. I need to know how the decay is advancing.

There was another question?[Student question: With the chlorhexidine rinse, versus the varnish, is the varnish more site specific?]The answer is the varnish is much more site specific. Varnish literally became available this year in the United States. It was illegal in the US before. The answer is we are probably going to change the concept of going at where the caries is and treat the caries, I’d love to try treating the caries with a stamp. That makes a lot more sense than smearing it all over.

[Student question I couldn’t properly hear about changing a patient’s risk assessment from high to moderate after one year.]If it stays the same for a year, they were high risk. She had [asked about] someone who had caries. If I had someone who had caries and I managed to control it and they are not getting new, we’ll knock them down after a year to moderate risk. It will take them three years before we put them back at low risk. Kenny, is that different then about what you taught?[Dr. Allen: No][Student: No, what you taught was that if it is the same then it was high risk]If it was the same…[Student: If it hadn’t, if it still remained the same it was - ] Oh so you’re asking if you had people with early lesions that just developed?[Student: no… (sorry I can’t hear the recording here due to some background noise near me)No I’m asking you how that person that had early lesions isn’t up in the high risk. How did that patient arrive in high risk if you diagnosed them as having new lesions? They’re high risk.

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[Student: So they’ll remain at high risk?]I’m saying that if I’ve been able to prevent them from getting worse, ok, I’ve got these early lesions, I’ve monitored them for a year, I’ve taken bitewings, the bitewings haven’t revealed any advancement of it, the patient is using the fluoride, their hygiene is correct, we see a decrease in activity by virtue of – How do I measure activity??? You’re going to have to give it to me, I’ll guarantee it’s a test question! Oh, got your attention. I got bad news, I don’t write the test questions, I don’t care. [Student: ICS?]No! Yes? Help me out? Looking at a radiograph and seeing whether it’s advanced in a radiograph. How do you classify caries in a radiograph? Give me the classifications of aproximal lesions! E0, E1, E2, D1, D2, D3. Or pulp. Ok, that’s aproximally. How do we describe activity in a different fashion? It could be arrested, but how do I know whether or not it’s arrested? How do I know whether it’s active on the surface or not? You’re not allowed to touch it so you don’t know it’s leathery. Color is helpful but not necessarily. [Student: blow air on it?]AND?[Student: water?]No, no, no, you were in the right location. You’re drying it with air AND? See if it is frosty. Frosted surface indicates that we have continuing demineralization and remineralization. That patient stays at high risk. There hasn’t been a change. They were at high risk, they stay at high risk. You listening? Did you understand what I just said?[Student with original question: Yeah I’m listening, I’m trying to find the thing that he posted for you]You can find the thing. You know, if I didn’t help write the book on it, I’d be ok. I’m telling you that a contradiction in what is written somewhere, it is an error. You are never raised from middle to high because an inactive lesion on the surface has not progressed, and it’s been there for five years. You’re never raised. It’s the active lesion. You examine a patient and see a new, active lesion, demineralization. A fifty year old comes in with those lesions that are just touching the enamel, I look at his radiographs from a year ago, he’s got these lesions from just touching the enamel, low risk, high risk, or medium risk? Why? They were there a year ago! If I look and they were there ten years ago, is this person at risk? No! They could be low risk. I have to look for something that is indicating that the demineralization is active. That goes to the discussion about charting activity that we had a couple of weeks ago. In a quiescent lesion does not make – it’s not purely looking at a radiograph, it’s not purely looking at the surface of the tooth. A white spot doesn’t make this an active lesion. It’s a white spot with activity. You’ve got to wrap this together. It’s not a single – you’re taking a snap shot and making a decision, high risk, low risk. Yes?[Student with original question: that’s how we were taught]Who taught you? [Student with original question: So how would you place a patient into moderate risk? ICDAS, is that how you would do it?]I don’t use ICDAS. Please review your lectures.[Student with original question: Ok so what you’re saying is that when the lesion is active, you put them into high risk, yes?]If there is an active lesion they are high risk.[Student with original question: So how does a patient go into moderate risk?]It’s no longer active, it can’t stay active. It has to go into inactive. If in one year, they have not developed new lesions and it’s become inactive, they go into the lower risk category. And we measure activity, we started out, she had frosting, he gave me radiographs getting worse, there’s another way, how do I tell interproximally, aproximally, whether the patient

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is keeping that area clean? It’s on the slide? Gingiva that’s right. What does the gingiva look like if they are not keeping it clean? Red and inflamed. Disease activity. If they still have an active lesion they are still high risk. If the lesion is gone – the lesion can still be there but it can’t be active. You can knock them down. What is the caries risk on this patient? [Slide 59]. What’s that? Ok, it was like this three years ago. [Class says low risk]. Yeah I’m not sure I’d make the bold statement of dropping them totally to low risk, because they have a history of activity. All of these black lesions are arrested caries. I’ve already told you, why don’t we see caries up here? Yes, that’s right, it’s a denture. You don’t get tooth decay on dentures. All this schmutz you see up here is just stain, it’s not caries. But this stuff here, this black, that’s caries. The question is now, if I saw a light color to it, if I saw frosting on the enamel next to it, that’s activity. If I see gingivitis, I mean, look at the gingiva here. That’s a pontic (?) by the way. This guy has no disease activity going on here. He’s keeping it relatively clean, it’s hanging out, it’s old, it’s been here for a long time, do you want to go in there and redo all this work? YES, because you’ve got a Mercedes payment, but NO because of caries. You know, you have to make that decision. Patient came in to me and had like all these black spots on here, I would treat this because it is an aesthetic concern for the patient, falls into what Dr. Vogel refers to as “being broken.” The patient doesn’t like it! My teeth are ugly! I’m taking care of someone next week who has exactly this scenario. It didn’t bother her until it was time for her son to get married. Now she doesn’t like smiling and having black on the teeth. Its an esthetic concern. It’s not associated with active caries. Today we treat this differently, we try to control the environment. Do we have other questions? Do you want to read it to me, do you want to put it up on the stage? (referring to the student with the questions on the previous page). Put it on the stage and I will explain it to you. You’re not listening or – put it up![Student: No, I’ll ask you after.]Do you think these people aren’t confused?[Student: No, it seems that everyone else is frustrated. No! With me, not with you!][Class laughing]Is anyone frustrated with him? Hands down because questions are appropriate!!![Student: If it doesn’t pertain to other people then there is no point in me - ]Does everyone else got it, or is there confusion? Because I’d rather settle it. That’s the value of being in a classroom. I’d rather settle it and get you to understand it, than let you go home. Let’s settle it because I want to see what this is! Bring it on!!!! Bring what you got, and I’ll project it!!! This isn’t an embarrassment! (Clapping as student heads up to the stage). Are we looking at the caries risk assessment form? It’s easy to explain. First, there are multiple versions of the caries risk form that are out there. Some have not been updated.

Ok, I’ll take another question in the meantime![Student question: You mentioned before, I think in the first lecture, that chlorhexidine isn’t the best because while it kills bacteria, it actually causes more harmful bacteria to -]Well, no, no. So the answer is yes, I did say that, I still agree with that. You have to stay on it and Dr. Featherstone’s protocol was staying on it for a month and then going to it once a week every month. So essentially what he was doing was trying to wipe it out and then it comes back again. Keep killing it down – the idea behind the stamp is to go in there and eradicate that particular bacteria and let healthy bacteria come in. Do monitoring of the bacteria, and if you can actually get the flora to become non-Strep mutans it would stay

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permanently. The chlorhexidine is a general kill. It kills about 80% of what is in the mouth right off the bat. The stuff that happens to stay, stays in nooks and crannies, it includes the Strep mutans, the lactos, all the things that we hate, still stay there and grow back real quickly. It has, by the way, been shown to be effective in anti-periodontal disease – as a perio med. I mean, I don’t want you to get that it does nothing, it gets in there and it kills some of the slower growing bacteria. The rapid regrowing bacteria are the most difficult for us to deal with. [Student: I don’t understand the exact mechanism, but I assume from the class talks about antibiotics that would cause resistance, and that might not be ideal - ]So, resistance is whether or not, you do shift the flora. It’s not necessarily a question of resistance. So resistance is you give an antibiotic, it kills all but the bacteria that are not susceptible to that antibiotic. And the ones that remain keep growing, they are not susceptible. It’s similar except this is a broad – spectrum kill. And it is an ineffective kill. It doesn’t kill 100% of. And it’s not killing it because this one is resistant and this one’s not. It just didn’t get to that bacteria at a high enough concentration, at a high enough availability, stay there long enough. So that guy got lucky and got it, you were sitting on the surface, you die. Ok, so its not the antibiotic mechanism that all the bacteria get exposed to it and only those that are immune to that antibiotic survive, now the next generation grows up being immune. So it doesn’t necessarily – but what it does do is favor the most rapidly regrowing bacteria. By wiping everything out and taking the competitive inhibition away, it allows the ones that are still left there to reproduce rapidly once you take away the chlorhexidine. So Featherstone’s idea is just to keep coming back with chlorhexidine and beating it down again. And in fact in my cancer patients, like I said, the ones that have had head and neck radiation, we do just that. We do varnishes, we follow them up. We beat it up aggressively, because they can’t even tolerate slight, they have no remineralization capability because they have no saliva. Any other question? Yes?

[Student question: I’m still unclear about how fluoride works how you ingest it. I think it’s well explained the purposes of fluoride because -]I got stuck reading (looking at what the student who went up to the stage projected). Because, Kenny if that’s what’s on the form..[Dr. Allen: That’s an old one.]That’s an old form?[Dr. Allen: What’s the date on it? The one that’s on, that I posted, is different than that.]Yeah that shouldn’t be there. That is a wrong form. That form has been removed.[Student: So this bottom part, it doesn’t exist?]No, actually if they stay,[Student: This is from Dr. Glotzer here]Then he gave you an old form. And that’s why I said, you have to bring up the question. We have lots of forms, he may not have realized this is an old form.[Student: So this is wrong then?]This is currently wrong. Two years ago, this was considered correct. [Student: So how does one become moderate risk in the first place? You can’t be diagnosed as moderate risk first]Correct. Well, no, no, no. That’s not true. Scroll down. Right over here, this is what gets you in right off the bat. Patient comes in, they’ve got xerostomia in their mouth.

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[Student: Other than salivary..]No, other than severe salivary reduction. Xerostomia, I’m taking a bunch of drugs, my mouth is dryer. They wind up with moderate risk. How do we treat moderate risk? It could be prevident 5000, I told you there is another alternative to it, that’s the OTC mouth rinse. Either of them will work ok. That’s the type of treatment that we give them. So we get them on a supplemental fluoride. In that patient. What happens if they get caries? High risk. Ok. Over here, what’s the recall rate on this? Six months. If this person comes back at three months, getting fluoride varnish, three months they are getting an in office fluoride, the MI paste, they could be a meth addict, that’s one of those real disasters. See how important it is to ask the question? Because all of these people would have been confused forever because there are multiple forms out!! We changed the form multiple times over the last, we had a form out before John Featherstone in San Francisco had a form out. And it has changed and been modified based upon the evidence that is available. [Student: So do they move down the risk?]What we did is we allow them to move down, it takes them three years to get down here (to low). You’re going to have to show me three years of not getting caries. And I have to tell you, from a personal story, somebody in my family, who is high risk because she had all of these lesions and I’m remineralizing all of them, she dropped down to low risk abra cadabra, one of the lesions advanced over time. So you can go back, you have to take those radiographs at a reasonable interval, and keep checking the patients. So the keys for me here actually turn out to be these items. The bitewings, the number of visits, the patients have to undergo, the recall interval. When I’m doing fluoride, and what I’m doing in here, you manage the patient. So as you look at this, I keep working on the patients that are moderate risk and recall them every six months, fluoride varnish every six months, working on patients with tooth decay, I’m giving them fluoride varnish every visit they come in, they are scheduled for three months, they get a fluoride home that they have to be using and there I do head to the prevident 5000plus. I give these patients, generally when I’m here, I’ll go to xylitol before I’ll use chlorhexidine and that’s really pure whatever fits me inside feeling better. There’s no specific reason. Everybody gets dietary advice, that does nothing. There’s been no evidence – if I could tell you, cut down on sweets to prevent tooth decay, there would be nobody overweight in this world. Think about it, you can step on a scale tomorrow and know that you ate less calories. You’re going to have to go for 1, 2, 3, years eating less sweets. Not less sweets, really, very few sweets to reduce tooth decay. What’s a chance a human being has that mindset, I’m gonna prevent decay, I’m never going to touch any sugar again. Not happening! And that’s why dietary advice sounds like a great thing! But the truth is it doesn’t particularly work. But topical fluoride as it says every visit, calcium supplement, sugarless gum to stimulate saliva xylitol is better than non-xylitol in that case. Hygiene, flossing and brushing, I told you, you don’t need much. Flossing, brushing with a fluoride toothpaste two, three times a day is a great idea. And that’s how we go manage that. Any questions on caries risk?[Student question: (Couldn’t hear exact question, but she was asking if the most updated form is what we will have access too in clinic)]Yes. It should be. You know the problem with the clinics upstairs is the version will be the one on the computer, and that is because I am the one putting it on the computer. The problem with forms is these things hang out in the ethos for very long periods of time. And instructors can make a mistake and hand out the wrong one, they can even teach the wrong

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one! The current one that is out, this is pretty much the uh, I don’t think that the risk factors have changed on this. [Dr. Allen: I think that’s incorrect there, the radiograph. We now use an interval at where appropriate, not just four bitewings]Yes, yes it should say “when appropriate.” So I have a question, somebody tell me why pit and fissure protocol is all the way over there. And do pit and fissures put you in the high risk? This is a tricky one folks. Pit and fissure caries, even if it is on an anterior tooth. Does that put you at high risk? You’re at high risk – well, let’s ask a different question. Does fluoride, cutting down on sweets, xylitol, fluoride varnish, calcium, reduce tooth decay in the occlusal surface? Just slightly. Real, tiny increment. I would be a liar if I said it didn’t have an effect, it does, but just slightly. What has an effect? See if you put a sealant on it, a patient that had active caries and would be called high risk until they had the sealant put in, is at high risk. Once you put the sealants on, you go from being high risk to whatever everything else is in the risk categories. If you are having smooth surface demineralization, the bad news is you were born with deep grooves that weren’t coalesced, you get caries. Not your fault. As much as you’d like to blame them for not - for getting decay, it’s not their fault. You instantly get out of the high risk category the moment you put the sealants in place. So I’m not recommending someone who gets occlusal caries get MI paste, fluoride varnish, 4 times a year, bitewings, that’s not what made you high caries risk. Your anatomy did. So we actually did this differently than every other school in the country. We are right, they are wrong. Well actually, a number of the caries scientists have started hearing the wisdom and changing their thoughts on it. I just had obnoxious long enough for them to finally think about it. Caries, if all you have is in the occlusal surface, may not be the patient’s fault. It’s the fault of the anatomy, and we have a way of correcting that. Once we correct it is the patient at high risk? If everything else is good, if they have no redness of the gingiva, they have no active lesions, they are keeping everything clean, they control their sugars, they are fine, they are low risk. There is no reason to bump them up. They are high risk until you put the sealant on.

So this is actually a wonderful publication that has just recently come out, I was honored to be a part of this process. But this actually, if you use this as your guide to patients, you’ve got it nailed. You’ll understand in everything that you do, how to make your decision. Now I have to tell you my faculty don’t all have it yet. Many of them understand it, live it and do it, but after 30 years of private practice and having learned GV Black, some of them just can’t kick the habit. It’s tough. Yeah?

[Student: You never answered my question.]Oh, I don’t remember your question! [Student: Well, my question was, in class it was well explained how the topical effects of fluoride work, but you talked about ingesting fluoride tablets. How is the fluoride getting to the tooth?]So it gets into the blood stream. So the question was, how does systemic fluoride effect the tooth. So when we drink fluoridated water, we get a very low concentration of fluoride through the mouth. You may get some fluoride in the plaque and we believe there may be some minor fluoride effect there. We’re really not sure. If I put 1ppm coating on your teeth, they haven’t been able to show caries reduction in young children. In older children they

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have, in young children they weren’t able to. On the flip side, when we ingest up to 1ppm, it goes into the blood stream, it gets incorporated into the – because fluoride has a high affinity for calcium, gets incorporated into all calcifying tissues at that time. Bone, and tooth. And that calcification, actually, that’s probably where you get a true hydroxyapatite crystal. We know it forms hydroxyapatite. If you put fluoride into it, you see fluorapatite in tooth. We don’t see fluorapatite at the surface of teeth as easily when you brush fluoride on the surface. And what that did, and that’s the original studies that showed how fluoride worked, it lowered the critical pH. So tooth started to dissolve at 5.5, natural tooth. Natural dentin, 6.2. If you fluoridate it, it drops as much as a full pH, 1.0, which is a lot. It’s a big value. But it drops somewhere between 5.5nand 4.5 before it starts to dissolve. It’s pretty remarkable. And that is if you incorporate it into the crystal. If you get it on the surface, that also prevents that dissolution, but not by the same mechanism, there are probably a couple of mechanisms. Yeah?

[Student question: (can’t hear it at all)]There’s actually some work being done looking at Tums. Do something, use something that creates bicarbonate, with calcium in it at the same time. I didn’t say that this was the only way to do it. We’re just talking about what’s currently available. There is a good discussion about chewing Tums after eating. It just hasn’t been done. You want to do it with me, I’ll make you patent holder. You and I can become multibajillionaires. Don’t make a joke. I mentor is getting about 8 million a year off the patent I did as a graduate student. Oh you don’t want to do any of the work?? Well we won’t know the outcome until you go look at it. There are people that are currently recommending Tums, but I can’t give any advice on it, I haven’t seen anything on it.

[Student question about using triclosan, couldn’t hear the full thing]Well there’s no scientific evident that’s actually had a health outcome associated with it. [Student: Dean Marrus is very adamant against it.]He may be adamant about it but there’s still no science. The current discussion – you can be adamant about something. I’m sorry about it, I get tons of Colgate demo tubes. If you want some feel free, I’d be happy to give you some. You get Colgate toothpaste here. The problem is, there’s been no scientific evidence that there had negative health outcomes associated with the concentration in toothpaste. There have been in other items. I’m conflicted in what I can say with association – I have legal conflicts with what I can say on the Colgate stand on it. I can tell you, they are very comfortable with the literature. They are very comfortable with the literature.[Student: So is it’s the concentration that is the issue?]Yeah, it’s the amount of triclosan that you take. There’s some discussion about whether all the triclosan that we are using is – the big issue was triclosan in hand soaps. High concentrations in hand soaps, killing bacteria, getting bacterial shifts and change in flora, but the latest concern has been over the carcinogenicity of it. They are concerned about all triclosan and where it is showing up.

[Student question: Since all of your favorite students are here and you are offline, I think we are all dying to know what kind of things to focus on for the exam]

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I can certainly tell you that you are going to need to know that caries risk assessment form that we went over quite extensively. The recall rates, the radiograph rates, the fluoride regimen rates. You’ll need to talk about the use of fluoride in patients, and where and when. You’re going to need to talk about adjuncts and when you’re going to be able to bring in an adjunct, you go ahead and do it. Oh you want to know the answers? A, write this down, C, F, I’m sorry I can’t help it. The obnoxiousness is my mother’s fault. My father, a nice, mellow guy. Mom, she has all of that sarcasm in her and all of that. So I blame it on my genetics. You have to have something to talk to your psychiatrist about. Any other questions? Dr. Allen, anything else you recommend, because I don’t write questions…[Dr. Allen: That’s a very good starting point.]You’re in the ballpark if you follow where I was. It follows that trend, what does saliva bring to the situation and how, is Strep mutans the only bug you need to worry about at night, what about circadian rhythms. Or we can go on microphone and give them some things to study that – I would read the paper by Adi. I can be so nasty. I told you who was the cause of that? Mom, I told you.

[Student question: You said that for(hard to hear, I wrote what I thought he said) once you put sealant on the prep they become low risk. Do you still recall them every three months or do you lower the recall?]I don’t do any change to the patient’s recall rate. And it goes to the principle of, once you’ve cured that site, if you believe if that that site became – which, by the way, you need to know we don’t use ICDAS anymore as our classification. You need to be able to understand how ICDAS fits with our current classification with early, moderate, and severe. ICDAS is more extensive than we are currently using. I would remember that. You need to understand why an ICDAS 2, 3, 4, even an ICDAS 5 that requires me to do surgery a moderate or severe, cavitated to the dentin, I do the surgery on it, I look at the rest of the teeth, I say they are at high risk, once I’ve sealed them, that occlusal risk disappears. What happens if you seal in caries? Nothing. You’re better off. So this slide actually, go through the slide that’s there. This stuff here, its all in the stuff I gave you. You got the pearl for being here, it was worth the ten minutes not to, what else would you have been doing, sleeping or something? Are you taking pictures? I’m ready, take the picture! Are you videoing me???? If this winds up on YouTube, I’m telling you, I’m coming after you! I will unleash the full power of NYU. No even worse, I’ll make you miserable and keep you here for extra years! More tuition and YEARS here, you’ll pay for it!! I promise you! [Student: Well, we still use ICDAS in Dr. Glotzer’s course to classify caries]He taught you the ICDAS method. I’m telling you what you are going to use in clinic. What’s that, so ICDAS was the basis if you attended my lectures! ICDAS was the basis of the classification that you are going to use in the clinic. So you will understand that an ICDAS 3, 4, is a moderate lesion, and an ICDAS 5, 6, is an extensive lesion. An ICDAS 1, 2, 3, are initial lesions, early lesions. So learning the ICDAS doesn’t mean that the classification system we are going to use in clinic doesn’t fit.

[Student question: you had a slide where the lesion… (couldn’t hear anything after that)]Actually, if you look at that surface, it was one break in the surface. And the caveat that’s changed from ICDAS is that you need to look at bitewing radiographs to see whether or not there is any evidence of decay below the dentin. And if there is, you have real problems

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because caries under the dentin is a fairly extensive – caries under the occlusal surfaces of the dentin is a fairly extensive amount of disease. Let me just make sure there’s nothing here I wanted to make sure you got. You gotta know this. I’m tired of somebody saying, let’s put a restoration in here! There’s a life expectancy of that restoration. Watching is malpractice. It’s not treatment. If you think there’s an early lesion, if you think it’s active, put them under treatment! We need to treat this now in case the patient doesn’t come back again. Faculty will tell you that. Look them in the eye and say, I don’t think Dr. Wolff is going to agree with you. Should I give him a call? No, don’t do that, that is obnoxious, you will probably fail the rest of dental school. But I would have an intelligent discussion with that faculty member at that time about why you believe this is not an active lesion. About why you believe this should not be aggressively treated. Or, that you want to treat it in a different fashion. You want to treat it with remineralizing agents. These are the important things that you need to work on. Drilling and filling doesn’t cure it, prevention does not yield immediate results, prevention may lead to more permanent improvements, and it is evidence based. All of these things do come as evidence based. This is the key. All of these things were surgical in this school 9 years ago. Every one of these lesions would get cut open. Today, we’re starting to talk about whether we should use a non-surgical technique here. We aren’t there yet. I’m telling you, five years from now, I think we’ll be teaching the children that sit in these seats, remember they are children to you now. They’ll be grown up by then. We’re teaching them to do something different for this. I don’t think we are going to keep drilling these holes. There will be more aggressive treatment. And they YOU will be one of the faculty members at the school who look at the students and say “well, let’s drill this before it gets worse.” Where do you think those faculty came from?! They were you 20 years ago! They listened to a me on the stage 20 years ago and I looked at that and said, you have to restore that while its conservative. But the rules have changed! The rules on caries risk assessment have changed in a matter of years. [Student: Can we graft teeth yet?]Can we graft teeth yet? Well we actually call that a composite. Dr. Allen, did you learn how to use composite in dental school?[Dr. Allen: Yes, adapt it]Were you able to, so the reason I asked Dr. Allen, Dr. Allen and I were probably separated by about five years in school. Did you use a polymerization light in school?[Dr. Allen: No]Ok. I went to dental school, I put composites in with ultraviolet light. That was latest thing. It had to be put in under 1mm increments because it wouldn’t set under the UV. But I was now able to control the set. He was able to do it with putty putty mix and stick it in the hole, I did it with UV, today we do it with – yes, do I believe that there will be a method of grafting, probably not. Growing, manufacturing, doing, you bet. This remineralization is the earliest form of that type of repair. [Student: Why? Why do you need to replace the whole tooth when -]I don’t need to replace the whole tooth[Student explains further, couldn’t hear]The answer is, it is coming! That methods of growing crystals on teeth, of growing crystals in the caries and, so if Dr Kim (?) was lecturing here, she would tell you take that occlusal surface, open it up and clean it out and let saliva get in.

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[Do we need to know dates and percentages of the studies?]I can’t speak for all faculty that are involved in writing questions.[Student: for you?]Do they need to worry about dates for questions for me? I don’t think so.[Dr. Allen: Not for you but there may be some from somebody else with low attendance]You should be able to put things in sequence. You know, the 1940s, the 1980s, 2000, and understand what constraints GV Black had about fluoride.

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36: Exam Review