23/24: Diagnosis of Caries

Transcribed by: Atiya Bahmanyar August 12, 2014

Diagnosis and Treatment of Oral Disease

Introduction to Cariology/Diagnosis of Caries

[mumbling with the AV guys and Dr. Wolff]

Yeah something got tripped. I’m powering up right now. Student: I heard you were handing out candy

[Mumbling]

Dr. Wolff: What’s tomorrow?

Introduction to Caries, Caries Management and Caries as a Public Health Issue[Dr.Wolff]: The remote is working but the pointer is not. It’s not bad, it’s too weak. Ummm. So your class is actually the first class that’s heard something about caries as their operative dentistry class, and that’s great. We’re going to try to build upon that. So we’re going to spend a little bit of time working towards that, um, as we go through the process. Today I’m going to talk a little bit about the whole scope of what this course is going to include as well as some very specific learning objectives. The very first of which will actually be getting you to understand how to diagnose caries, what’s the physical diagnosis and what process we’re going to do. You’ve already received, the 14 of you who attended Dr. D’s lecture. You’ve already received presentation on, and for those of you who are listening to the tape, I hope you listened to his before you got to mine, so that you hear me say only 14 attended, but neither here nor there. That’ll be my last sarcasm and since you folks were good enough to be here and eating all the candy that was brought for you.

[Students: Woo]

[Dr.Wolff]: Go get that candy off the table. Umm. But they’re probably sitting in their living room…oh, nevermind. I’m going to concentrate and get you guys out of here. Umm. Caries we would imagine, so when I entered dental school in 1977, the very first presentation I received was from an epidemiologist who told me that caries would be gone by the time I graduated. Sealants had been invented, and fluoride reached its apex in usage throughout the country. It was all over, and sometime right around you know 10 years into practice, caries would not be an issue. Were that only the case. It wasn’t even close to being the case. And dental caries today is actually a growing disease with more and more issues associated with it. Today we’re going to, I was going to set up my twitter account and you could tweet me if you had a question and wanted to ask it.

About the Course[Dr.Wolff]: This is such an intimate group spread out over a very large area of listening, normally I would consider this a living room group. Please, raise your


hand, do the speak up thing and ask the questions. If you need to email me a question, please email me a question. Don’t isolate this, um, as most of you know, I have a daughter who went through dental school. Um, or is going through dental school right now- in her second year she was studying for an examination in the DOD course, where as she was studying- she came across an old copy of an examination through whatever method, um, and the class was arguing in facebook as whether or not this patient had a high or low caries risk. And it was kind of interesting, she’s busy cursing out her computer while listening to me on tape while rather than listening to me the original, she did not go to class either. But listening to me on tape, taking notes, going through the process and cursing the facebook process that’s going on in the class. They’re all idiots, dan-na-da-na-dah. Now it’s interesting because I sit in the evening and my email is always open and running. I’m always working, I love what I’m doing, I’m always working. Now, the class was arguing as to whether or not a patient who had caries that was treated a year before and was restored, and there’s now current caries in the mouth is still a high caries risk patient. And what facebook voted, was that that patient was a low risk because the patient no longer had caries in their mouth. What Samantha actually new, was that the rule said if you had had caries in the last 3 years that had been treated, you’re still a higher caries risk patient and no matter what metric you use within the last year, absolutely you’re still a high risk patient. So she votes for the high risk, everybody comes back and says no, there is no caries in it it’s low risk. They’re arguing back and forth, and I finally go what’s going on there, I can’t take it. She’s sitting at the dining room table with this throwing things around and getting annoyed and she says- I didn’t want to tell you but there’s a copy of the old exam floating around and the class has a debate about one of the questions on it- they said it’s low caries risk- I said what do you think? And she says I think it’s high caries risk. Why do you think it’s high caries risk? And by the way Samantha, it’s a brand new examination I don’t care that you have the old exam, you don’t have to hide that from me. They weren’t supposed to, but it was a brand new examination. So she types back on facebook, that I have it from a good source that the patient is high caries risk. And a student in the class answers on facebook ‘he’s wrong’. So I write an email to the entire class minutes later, because I don’t use facebook nor am I invited on your facebook page, that the patient is high caries risk because somebody asked me a question and the answer is and I make a public answer to every one on the email thread, then it was the class of 2015- the patient is high caries risk because of…

Now it’s an interesting and bothersome thing to me, because you folks were studying using facebook, which is great, but you could have gone to the source. A. you could have gone to the sheet which actually says 1 year, heaven forbid someone actually pulls out the sheet that says caries risk as part of the course. But outside that, someone could have asked the question of a course director or a course lecturer and gotten the right answer. So when you don’t probe the faculty, you’re making a mistake. Not all faculty answer their emails all hours of the day and night. Feel free to send me an email, feel free to ask me questions- and you’ll get the right


answer. So as we look at this patient, and this is my famous lside, I love this slide, it’s got lots of stuff on it.

NYU| DENTISTRY (First caries slide)[Dr.Wolff]: So we see here the caries right at this spot (arrow) I have to ask this question, when we do that to this patient and we treat this tooth, have we actually cured the patients caries? Why?

By restoring this tooth[Dr.Wolff]: The risk factors are still there. So caries cavitation is the outcome of the disease, not the disease. And, uh, cavitation I should say, I got that a little messed up. Cavitation is the outcome of the disease, not the disease. So for many, many decades, treating this hole was a surgical intervention, and when we finished the patient was cured, or so it was thought. How many people have ever had a restoration ever placed in their mouth. Any of your dentists ever given you fluoride after you’ve gotten that restoration. Told you that you need to use fluoride routinely as a preventative factor cause you’re at risk for developing caries. That’s the key!

Treatment of the disease requires [Dr.Wolff]: So upstairs, routinely we have these patients getting all sorts of restorations in their mouth and dentists make the recommendation, brush, floss, and cut down on sweets. We’ve already had the discussion last year flossing and cutting down on sweets doesn’t reduce tooth decay. Anyone want more of that chocolate? Yeah, I know it’s circulating around somewhere up there. If you need more, go pick some up, your strep mutans needs a good feeding right now. Risk reduction turns out to be the most important factor, and when we look at this radiograph we see lots of areas over this radiograph that’s telling us that the disease is in multiple processes.

NYU| DENTISTRY (Second caries slide) [Dr.Wolff]: Caries was born, the discussion, the early era of caries. How many treatments did GV Black have to control caries? One. It was restorative therapy, it was actually amalgam, they did have silicates, cements, um, available, um. But it was surgical intervention, there were no drug interventions and did they know, when he first wrote did they even know what causes caries? We’re going to talk a lot about risk assessment, do you do risk assessment or? No, I do risk assessment. The risk assessment lecture is very important …

Risk Assessment [Dr.Wolff]: …and it’s not mechanical that you need to understand. It’s your ability to discuss this with the patient. Who gets caries and whose fault is it? It’s the patient’s. You’re there to educate them and guide them and give them the best methods of preventing it, but they own the disease! And you have to do everything in your power to make sure that they understand that it’s in their hands. So if we go


ahead and look at this particular patient, this particular patient has this toothache of 3 days what do we see on this tooth?

35 year old female [Dr.Wolff]: distal of tooth…

NYU| DENTISTRY (Third caries slide) [Dr.Wolff]: …number 30 has caries probably, distal on 28, definitely on 28 and probably on 29 all have what look like…when did this start? Is caries a rapid disease? Not typically. Could be, but when we say rapid, we are talking about months or years, not days. That’s rapid, is months or years. This is an ongoing disease process that has the opportunity to do 3 things, get worse, arrest, or get better. They use fluoride, they brush their teeth 2x a day, and they use dental floss, yet they’re still developing the disease and we have to understand what the risk factors are for the patient and how to control them.

Why do I get cavities, but my sister never does?[Dr.Wolff]: Caries comes from the latin word, um it stands for rot or rotten.

What is Dental Caries? [Dr.Wolff]: It came out of medieval Europe and it comes from medicine, and it was actually gangrene that they were referring to. Um, so they used to call it um the rot, when the bone became infected. Rotten teeth are the signs of a disease which is called dental caries it’s a very simple disease. New textbook by Rory Hume and myself, will be coming out in the fall, we’ll see to it that you have it available on vital book. Um, we spend a good deal of time talking about the history and understanding because where you are right now is in the (something) of change in therapy. Before you finish dental school, there will be therapies to arrest active caries in almost all circumstances that will be acceptable and viable in dental practices, and this is going to radically change the way we approach dentistry. It’s one of the most common diseases and they like to refer to this as being more common that asthma and resulting- you know, the truth is very few people die of dental infections. Lots of people die of asthma, so we need to recognize the magnitude of the disease is much much greater. It’s the most important cause of tooth loss in adults, or younger people. 20% of the population has 60% of the decay; where are they on the socioeconomic strata? Here’s lookin at ya.

Disease Distribution[Dr.Wolff]: I just found out we had a simpatico thing with diet coke. She has that giant can, we won’t go into that. So the lower economics is that is there something genetically in lower economics that make them more likely to get tooth decay?? I just had this discussion actually with a director of dental clinics in Brooklyn less than an hour ago. Anything genetic that we find in lower socioeconomic? Tell me something else that tracts with that? Diet? That’s true. Now Dr. Caufield likes to refer to malnutrition, now, malnutrition is a lot of things. What does mal mean? There ya go. It is bad nutrition. It may even mean a deficient diet in certain areas


and certain items, like vital nutrients. But, it’s not the malnutrition that we currently or frequently attribute to, um, starving. It’s not that type of malnutrition that we refer to. SO if it correlates with mal, malnutrition, it correlates with education in all respects. SO going to a bodega that’s selling food in an area that’s lower SES we see processed foods going out of there we see high carbohydrate foods going out of there, easy items to eat and cook and that influences their malnutrition and their likelihood of getting caries. But what’s interesting is 10% of the population receives 65% of the restorations, but it’s not necessarily the people with all the caries.

Distribution of Insured Restorative Services [Dr.Wolff]: Where are the 10% actually residing? They actual reside in a better SES population that’s actually receiving much more of the care and much higher utilization of their insurance

Distribution of Insured Restorative Services (with graph) [Dr.Wolff]: So we’re just in this Medicaid practice or capitation practice in Brooklyn and he was saying I would love to get my patients in 4x a year for fluoride patients. We wouldn’t worry about that at all. He says I couldn’t get them to come in 4x a year for anything. I have nurses chasing after them to get stool samples, to do blood and stool because that’s an outcome measure that the insurance companies use. I have people chasing after them to talk about the tobacco cessation. It all stems back to the education, or the lack there of, that health is something that can be improved by prevention and that comes back to this risk assessment management. So the wealthier people are using 65% of the restorative dollars that are spent on delta dental. They automatically have a job, and it’s not the low socioeconomic group. Another problem that we have is that we’re going to deal with old teeth. We’re going to deal with old people that didn’t exist, old teeth that never existed because we’re getting better in perio control.

We are getting older![Dr.Wolff]: This is an oncoming crisis. Aging and dental health. We’re going to talk about some items related to saliva. That’s going to be, I think that’s not for a while. You know this 1000 medications…

Effect of Medications[Dr.Wolff]: It’s actually more than 1000 now. Sreebny was one of my mentors in my pHd program and what was very interesting it was very simple study. He sat with a book called the physicians desk reference. It was something with paper inside of it. He sat with a book and looked at every single medication and just counted up how many of these had the side effect xerostomia and what’s amazing is that in this PDR there are today using computer searches and medical prescription guides, it’s actually measured in the 1000s. Lots of our patients are taking polypharmacy that results in dry mouth and it coan be over the counter or um prescription in nature. We’ve managed to decrease decay in our young population. Our older population we have real significant issues, even today, with large amounts of decay.


Caries Scores by Age Group[Dr.Wolff]: Much less today than we had in the early 80s but we still have a significant amount of surfaces that are decayed, missing, or filled. That’s really good news since I understand most of you have a fairly large tuition debt. That means that you must be able to fix Mr. Cavity. There’s going to be plenty of work out there for your generation and probably for your children’s generation too. But the problem is, what’s occurring down here is a question of whether or not this continues to grow as they get older. Unfortunately as we’ve been able to manage and control in our younger population, and there seems to have been a little boost, you can actually see out here that there’s been an increase in our most recent time frame in caries in the younger population, they’re actually seeing a rise now, instead of it being at 6-19 there’s a rise in the health programs for preventative; we are now seeing a rise in the 19-25 yearolds and in fact this may not be so artificial in the future. I can’t imaging 25, 45 surfaces of caries or restorations in the mouth- that’s a massive number of surfaces. Uh, I’m sorry 45% of populations having more than 20 surfaces of caries that’s been restored in the mouth. So prior objectives were to just diagnose and treat the disease, today the decision has been to prevent the disease as a big portion. Many insurance companies, medical being one of really great examples have made a tremendous effort…

OBJECTIVES OF DENTAL THERAPY[Dr.Wolff]: …to actually pay for prevention and they now are starting to pay for outcome. So we are going to see medical practices throughout the US and world in dental practices following shortly that actually pay for outcomes, reduce blood pressure, reduce number of smoking, and reduce caries will be one of the outcomes that we need to see, and you’ll be paid more. As a matter of fact, it’s being demonstrated on the west coast in the Kaiser group, if you’re group has patients that have lower DMFS each year incrementally when they’re in your practice, you receive a 20% higher reimbursement than you would have had if you didn’t have the higher reduction. So, this is a pay for performance modulus. We are seeing it start to break into dentistry. Kaiser is a large um group that provides dental insurance to large industry on the northwest in the US. It’s just a coming trend that’s going to arrive. We have to remember that restorative technologies are profitable for manufacturers and for practitioners, so a lot of people actually see no reason to do prevention.

REPAIR DEFECTS TO RESTORE FUNCTION[Dr.Wolff]: I’m pushing you guys against the salmon stream, the water stream, to try and get it so you can actually work on prevention as part of your practice. But the biggest psychologic(al) barrier and I saw it yesterday when it was in practice- my patient says Dr. Wolff, I have this little thing in my gum over here. It was a little black spot on the root of their tooth. Black, black, it had been a little bit of loss, and in fact when I look at my records it’s been black and it’s been there for years I don’t know hwy last week they looked at it and said I have an emergency. I looked at it and said it’s arrested decay, we’ve been tracking it for a number of years now. It’s fine, it’s at the gum line, putting a restoration there is difficult and you’ll have issues


associated with it. The patient almost begged me, to please drill it. Now, the interesting thing is, if I don’t like what it looks like- it’s a problem to the patient and we should treat it. We should treat it. But if they’re coming to me to treat it because it’s caries, I can treat it in a different fashion. And in fact for the last decade we have. She’s on home fluoride, she gets fluoride varnish when she sees us 2x a year in the office. Despite the fact that she’s an adult- that’s managing her risk. The comment is treating the spot is not going to make you greater or less at risk for tooth decay. If it’s bothering you visually I’ll treat it- but understand, from a medical standpoint you don’t need to treat it. It’s a different module and a different method of treatment but patients are not exactly into that treatment. So our goal is to promote and maintain an intact dentition throughout life. What’s interesting is if we actually look at caries historically, we saw this very well, 10 teeth with caries, historically very high…

CARIES MANAGEMENT[Dr.Wolff]: …but 3 or 4 when you go look at the before the common era, before zero…

DECAY HISTORY OF MAN[Dr.Wolff]: …You know it was very rare, and what’s the reason for that? Did they not eat sugar? It wasn’t processed- so it wasn’t concentrated to a highly compact fermentable item and there are number of different, and there’s an exception to that- and it’s honey. Naturally processed by bees, but honey was something used by royalty- not commonly available, not to mention you had bees around to get it. We did not, what caused the spike? It was the crusades. Right around the crusades, they came back through the trade routes and brought sugar to Europe. So we had Europe now with processed sugars, Europe that rewarded itself, it was worth much more than gold the first time it was brought to Europe, and very quickly was one of those things- sugar was one of the main reasons Christopher Columbus set sail to find the new world quote unquote. In an effort to find a quicker route to bring this stuff into Europe. So one of the things that was brought back by one of the crusaders was sugars- through one of the spice routes from south east asia into Europe and caries went up radically. Now caries has been around for a very long time. It dates back to the, descriptions date back to the ancient Egyptians. It started out with worms destroying teeth. The worm destroying teeth actually persisted for quite a while.

HISTORY OF CARIES: ACID FORMATION AND DIET[Dr.Wolff]: if you ask your friends and family what causes tooth decay they’ll tell you bacteria eating the teeth- bacteria, just small worms. They don’t realize that there’s an actual process. Um, it’s been described as an evil by which teeth become full of holes and hollow, um which most often effects the back teeth, especially so when they are not cleaned of food particles which decompose producing an acid moisture which eats them away and destroys them so that finally with much pain they rot away little by little. Interestingly they thought it was the decay of food not realizing the bacteria causes the food to decay and it’s the process of bacteria eating


the food. So it was not until the 1800s that people started realizing that the natural process of breakdown generates acids.

“Acid produced as a natural process…”[Dr.Wolff]: It was Miller in 1890 same time that GV Black was writing that actually explained the process of fermentable carbohydrate to certain bacteria they eat it, they produce acids, the acids sit on the outside of the tooth.

“Mouth organisms produce lactic acid…”[Dr.Wolff]: And it was from 1890 until almost 1980-1990 that every body assumed that it was a one way path, that demineralization was the eventuality. And in fact as we describe this eventuality it was always in the direction of fermentable carbohydrate to demineralization. Now, what interestingly occurred is the conversations in the early 1980s…

“Mouth organisms produce lactic acid…”[Dr.Wolff]: …actually highlighted the concept that there was this…

Miller’s acid Decalcification Theory[Dr.Wolff]: …acid balance that went on, and people started talking early in the 40s about this being mediated by saliva as one of the items that will control whether or not you get tooth decay. It turns out a number of factors influenced whether or not we would get decay. So you start looking at people that have absolutely clean teeth, they eat lots of sugars and they don’t get decay.

“Demineralization—Remineralization”[Dr.Wolff]: They were missing plaque was part of the formula. Another word for plaque is biofilm. As it turned out, you needed a susceptible tooth, and teeth.

Caries: Multi-factorial Etiology[Dr.Wolff]: What helps influence whether a tooth is susceptible or not? This is the interactive part of the lecture, so I’m going to harass you for a moment then we’ll go back to the screen to make sure you’re awake. Crowding. Okay, so anatomic alterations that make the capture of plaque easier or the cleaning more difficult. The location of the teeth? Hmm. What do you think might influence lower anteriors? What’s that? Saliva. That actually turns out to be the largest mediator. Some other things, where do we most likely get caries? It’s pits and fissures. And what is that? Well it is the occlusal surface, except unless it’s the lingual of a lateral incisor in which case it’s still a class 1 on the lingual surface. A sneak examination but the term class I, but we’re going to eradicate because we don’t really want to talk about that. It’s occlusal surface caries. But, so, um, we’ve got this plaque retained area on the um, does anybody have pits and fissures that aren’t sealed? Do you have any caries in your pits and fissures? Why? They’re naturally sealed. Right. There’s a coalescence of enamel in those areas and they don’t trap plaque. Dr. Caufield spoke about another time of location that helps create caries. Malformation of tooth structure that retains plaque inside it; it acts as a really great, great medium, culture


medium, it’s a dish that hold the plaque there no matter how you brush you cant take that out. SO these anomalies or malformations on the enamel at that surface can actually lead to plaque accumulation that can lead to demineralization in that area. So that’s the tooth susceptibility. So let’s talk about the plaque. What influences the plaque? Hygiene, that’s how much is there. Anybody know any cows that brush? You have a cow that brushes? You always have the one person in class whose cow brushes. The rest of you have cows that don’t brush. I have never personally met a cow that brushes. Any of you have met a cow that has cavities? How is it possible that something that has never brushed, never gets tooth decay? Yeah, it’s actually what we feed it and what bacteria is in the mouth and has the opportunity to grow. We’re going to talk about this mixed bacteria colony in a moment because we’re real advocates of the actual colonies and what they mean(?). Now what they get infected with is another caufield discussion and that vertical transmission from mother to child turns out to have some influence in what causes this and what arises there. Then how we feed it and how we culture it. How thick we allow it to grow, what we allow to occur, because not all plaques are equal and what you get and what your brother and sister get may not, so you got the same vertical transmission, but your grooves and pits and fissures may be better coalesced on you than on a sister. You may keep a little bit better of the plaque, you may have gotten the same stuff from your mother, but there could be minor nuances that differ you both. Now sugar turns out to be the feeder of all this and that is the one that creates- but does any body know anyone that eats lots of sugar but never gets tooth decay? It’s this something else that’s effecting it and that’s actually a real common finding. I have patients that come in and say ‘I don’t eat any sugar’ that’s a lie. They may not eat a lot of sugar, but they don’t eat sugar is probably not the truth, and they still get caries all the time. It’s almost impossible if you eat no sugar at all to get caries. As it turns out, saliva has a giant mediating effect, and I’m sorry of this, op, didn’t mean to go that fast; saliva and what goes on- so we’re going to spend time talking about saliva and how it mediates this entire plaque environment, the sugar environment the tooth environment as far as remineralization to determine whether or not you get tooth decay over time. Now, this plaque turns out to be a very interesting item. Now everyone tends to call it biofilm in this environment. The term plaque no longer exists in anything other than dentistry. Plaque is not a description of a biofilm.

What is Plaque?[Dr.Wolff]: All a biofilm is, is a very complex community, it has all sorts of methods of attaching to the surface, at the same time it’s not a single bacteria. The key here is to understand that it’s a mixed bacteria with lots of things going on inside it. But it gets even wilder. The plaque actually is a place where things occur. The transfer of ions from the saliva surface into the biofilm, the biofilm acts as a reservoir to save it there and then it goes into the pellicle, then eventually into the tooth, or it goes out. This is a slide courtesy of Colgate, I remind everybody I am a consultant for Colgate, associated with the development of tooth paste. Okay? I helped invent a toothpaste that Colgate currently is marketing world wide.


Um. It is important for you to recognize that some of the theories that will be spoken about related to that toothpaste, actually involve modifying the biofilm, not eliminating the biofilm. My bet is before you retire from dentistry, we will stop trying to eradicate biofilm with chlorohexidines or iodines, and we will stop brushing off all our biofilms, but rather help try and maintain a healthy biofilm of mixed bacteria. There are lots of ways that people are proposing this. We will talk about a few of them during the course some of these methods of doing this may be by using probiotics, and others by fertilizing essentially that’s the Colgate technology, if we feed arginine to this bacteria, to this plaque, it goes from being a plaque that contains lots of demineralizing bacteria to a balanced plaque that has remineralizing agents inside it. So as things are transmitted from the surface, it comes from saliva, and controls this flow in and out of the biofilm and heavily influences what occurs inside the biofilm. We can get a more cariogenic biofilm if we just put in things that cause acid formation which results in demineralization.

Source of Caries Problem[Dr.Wolff]: We can go ahead and use saliva to wash away the acids. Anybody heard any of that theory of washing away the acids? What was that? It’s an advertisement. You see it all around you. It’s in the press, you hear about it. Mouthwash? No they don’t talk about mouthwash if you can’t brush your teeth, what do they talk about doing? Chewing gum after eating. What that is, is primarily a dilution and slightly an attempt to bring more buffering capacity from the saliva to the plaque and actually modify that plaque. So, saliva controls that plaque environment quite heavily and we’re going to talk about the management of the plaque. So we can either result in demineralization…What happens if you brush right after you have a high sugar diet 15-20 minutes after you do that? Because? So the acid has come into the surface, it’s resulted in demineralization. Where do the calcium and phosphates go? Where does the calcium and phosphate go from the tooth? Is it in solution? Or does it go quietly into the pellicle and the biofilm? It can’t get directly into the- because there’s something covering it. You wouldn’t have gotten demineralization if there wasn’t an acquired pellicle and biofilm over the top because I can pour all the sugar into your mouth and if there’s no biofilm there for it to eat and produce acids, the sugar doesn’t cause decay. So if we grew you up in a sterile bubble and you had no bacteria in your mouth at all, is sugar cariogenic? Now I’m sounding like iwork for the sugar industry. It’s not the sugar that’s bad, or it’s not the bullets that are bad, it’s the guns, or it’s not the guns it’s the bullets. You need both together to make this happen. You need both to make this happen. Sugar alone doesn’t cause caries. What occurs there is the sugar fed to the biofilm now results in the biofilm generating acids, the acids attack the tooth surface, the acids slowly dissolve, and what can mediate that? How can I slow the dissolution of the tooth? Well buffering is one, but there’s something very specifically that slows the dissolution of the tooth when exposed to acids. FLUORIDE! That’s one of the 2 mechanisms of fluoride in working to prevent tooth decay. It effects the mineral so that it doesn’t dissolve as easily and we’ll go over that also. So the key is, once you get the calciums and phosphates inside this biofilm, if you were to come and brush it away, there’s a net loss of these calciums and phosphates from the tooth structure, and even the presence of saliva


on the surface, that calcium and phosphate is not easily restored even from the calcium and phosphate from saliva. So saliva is an exceplent buffer, it washes away acids and it contains, it’s super saturated with calciums and phosphates, where do we see proof that it’s super saturated with calcium and phosphate? Calculus! So we get that precipitation, and that’s just remineralization; and that just goes to this balance of whether or not we get remin- or demin- in that item.

Role of Saliva[Dr.Wolff]: Now this is a very classic drawing by Stephan, he actually did this in 1946 it’s called the Stephan curve. We go ahead and we feed um, we feed, the patient some glucose,

At Normal pH…pH 7[Dr.Wolff]: the resting plaque pH, uh, Stephan did this by the way,

Demineralization[Dr.Wolff]: …he took a bunch of dental students who didn’t brush for a week…

Stephan Curve[Dr.Wolff]: …that’s when you can do a lot of research on dental students without paying them or asking permission. Everyone had to participate. Told them not to brush their teeth for a week and then had them all swish with sugar, a glucose solution, then started collecting plaque specimens from each area in the mouth. Over time what you found is, just before the plaque was near neutral, right after within 5 minutes the plaque pH drops, it drops rapidly, it drops below 5.5- an important item because 5.5 turns out to be the critical pH for the dissolution of, of enamel. Anybody remember the critical pH for the dissolution of dentin? 6.2. It’s important because you’ll find that patients that have arresting, saliva flow, but that is subnormal, actually have a resting pH near 6.2 and it’s why we have older patients with dry mouth getting rampant tooth decay. There’s no buffering capacity inside the system. So it drops below 5.5, they start dissolving. If we put fluoride in the system it actually lowers this bar just a little bit. The pH drops, as it rebounds it comes back to stop dissolving and eventually it starts to remineralize. So the top is the repair zone, the bottom is the danger zone, and if we add fluoride to the system we actually lower the critical pH and decrease the um, the likelihood of dissolving the tooth and effecting the mineral. So caries management for a long time said- ‘eat less sweets’. And that was the theory. So after a generation of dentists told you to cut down sweets, it was suddenly discovered that it doesn’t reduce tooth decay- not even a little.

Stephan Curve and Plaque pH[Dr.Wolff]: Why? How much sugar does a bacteria need to eat to reduce the pH? Yeah- micrograms. So- 2 teaspoons of sugar in a cup of coffee- that’s drank over an entire period of a day- results in caries because of the repeated diving of the pH below the critical pH and the rise. So it turned out not to be the actual quantity of sugar, but how frequently – because if we moved this interval closer and closer, you


actually always stay demineralizing the Gatorade with less than 100 calories of sugar, the coca cola with 100 calories in the big glass that’s deadly, not because you drank it once but because you drank it over the course of a day. So the theory of cut down on sweets actually changed. It’s more cut down on the frequency of sweets. Big chocolate cake, 2 cups, eat it in one gulp, is one exposure to sugar. What’s the exception to that rule? Hmm? Diabetes, you die- you know because of all that sugar. Low clearance- sticky foods. How many of you had sticky chocolate? I’m sorry but it’s sticking around. The rest of you had one occurrence and your pH is normal already- it’s been 45 minutes since your piece of chocolate. Anyone want some more chocolate? We’re going to keep your pH down for a few hours. D4s are going to be looking for board lesions shortly, it takes a lot of chocolate to make that happen. We’re going to talk very briefly about materials of tooth structure. By the way, enamel is more resistant to tooth decay than dentin. Anyone want to tell me why? Hmm. What’s that? It’s more mineralized. There’s more mineral in it to start with, and it’s highly organized.

What are teeth made of?[Dr.Wolff]: Dentin comes in tubules. You make tubules- there’s mainly air in the middle of this- tehre’s more surface area to be exposed to the acids. It dissolves more rapidly.

Enamel[Dr.Wolff]: It has less mineral content- less organization- about 1/3 of it is proteins in one form or another. There’s also collagenases associated with decay and other things. Collagenases are activated in the acids, wee quicker breakdown in the surface- we see more rapid decay in dentin. Much more difficult to control caries in dentin.

Acid Exposed Dentin[Dr.Wolff]: We’ll talk about the caries balance, imbalance, it will be a part of our caries risk assessment. Um, prior to Dr.- um I should have had Featherstone 2006, Featherstone was here, it should be Featherstone Wolff actually, he’s now dean at San Francisco, um, we had this balance, and he had this triangle right in the middle here-

The Caries Imbalance[Dr.Wolff]: and I asked this question, do you believe fluoride and salivary stimulants and antibacterials can actually reduce decay- or actually reduce the risk. And the answer was yes, it reduces decay but you can still get decay around it. SO the problem is- when we have patients that have indicators of decay and decay risk, like active lesions- those patients very rapidly develop decay, we have to work really hard on the other side to pick it up. It’s not a fair balance, your risk is much greater once you’ve demonstrated the likelihood of getting decay and it’s not as simple as putting you on a fluoride. We have to work real hard and we have to educate our patients to understand that. We’re going to talk about the classification of caries. Um. This was not considered caries. I still ask this question of dentists all over the


world as I lecture, is this caries? And they go no. You guys, is this caries? Raise your hand- yes? PLEASE RAISE YOUR HAND! I JUST NEED TO GET THAT INNER FEELING THAT WE TAUGHT ONE THING TO YOU FOLKS! He’s a tough sell over there.

Caries classification of the groove[Dr.Wolff]: Have another chocolate on me. Go ahead.

Caries Classification of the Early Lesion[Dr.Wolff]: Get fat and have cavities. It’s okay. This is the earliest signs of decay. It is the caries process. It’s the same caries process, identical to what is occurring in cavitation. It just hasn’t gotten there yet. GV Black didn’t recognize this as caries. It didn’t exist then. Do you know why? You only had one cure. The 1 cure was to drill it and put a restoration in it. So when he saw demineralization on the margins, he had to cut it out. He had to drill away and get clean margins to put as amalgam in there, which by the way had a life expectancy of less than 5 years. Try that on for size if you’re 20 years old and he’s putting a restoration in your mouth.

Caries Classification of the Gingival 1/3[Dr.Wolff]: This is clearly caries. We will talk about caries in the gingival 1/3.

Root Caries[Dr.Wolff]: Um, they’re both carious lesions aren’t they? That looks brown and soft, it is. This is black and soft isn’t it. Should they both be treated? What’s the difference between the 2? Exactly. This one’s not active anymore. It’s like fallen on top of itself.

Active caries versus arrested caries. So that’s a discussion of our activity. We’ll talk about classification of lesions and how we deal with the discussion of a lesion.

Is caries still a problem?[Dr.Wolff]: Is caries still a problem? You bet caries is still a problem. This the the decay of about 12 year olds , the caries rates for 12 year olds, I want you to look at Australia by the way which has an incredible public health system as far as the delivery of dental care. They’re one of the examples that uses non-dentists to deliver some prevention. And that’s up 12 year olds um, but lets take a look over here…

Dr. Poul Erik Peterson[Dr.Wolff]: at the 44 year olds. They now have 13.9, um, what happened? How do you go from this picture being a very lowest in the world of decay rates- to being at the highest in the world? What’s that? They don’t seek care at the same rate. They went from a public health system that was mandatory for children to no public health system necessarily for adults. Decay rates are sky rocketed they aren’t a big fluoride contry even though there’s a large amount of fluoride toothpaste available. The US is in the moderate, but we see much of the world in the older population with a very significant amount of decay and restored teeth. That’s a major problem- so decay is still a very very current problem. We’re going to talk about the challenges of poor nutrition and access, and lack of education to see if we can


address some of it. We’re going to talk about some of the models of prevention and I did give you this presentation, but we’ll spend more time talking about how or why or what we did to control tooth decay. We need to recognize that decay is a continuum, it’s dynamic, it’s multifactorial, and early caries lesions are reversible in many many many many respects.

Challenges to Oral Health[Dr.Wolff]: Even late carious lesions may be arrested and left alone. A large number of very respected caries researchers talks about today about opening up access to a lesion so saliva can get in there, arresting it with silver nitrate thiamine fluoride, or a number of ways and leaving it alone.

Summary[Dr.Wolff]: So I have a question, what’s the life expectancy of an 85 year old in a nursing home? Less than 2 years. How many of those patients actually need to have a dentist restore their teeth if we can arrest the caries? Probably none. Probably none. We have a mode a treatment today that doesn’t fit the disease frequently and doesn’t fit the disease we’re treating. We’re going to spend a lot of time speaking about it. I’m going to take questions while I boot up the next presentation and I promise I will speak relatively quickly and be done by 4:30. Is that okay? Sure. I really do appreciate, um, your being here, and you know what. I’m going to ask- who has a piece of paper- any of you have a piece of paper. You have a piece of paper? Can you please circulate on that piece of paper your name and net ID have people sign it. If you are at a point break, I will be happy to see to it that you people get the point break if you are there. Now there are 32 of you, if there are 33 signatures in there- no body gets it. Dr. Allen will be the keeper of the paper. Any questions? I was going to post this but I’d probably rather have people listen to the hour and a half lecture and take notes. So. Yeah isn’t that cruel? It is cruel? Not cruel? Oh I should post it? What if I gave it to you? Just you. I have your net IDs. There you have it. We’ll find out who shares it, and I’ll copyright it- and then I’ll find out which of you share it AND THEN I’M GOING TO SUE YOU FOR EVERY DOLLAR YOU’RE NOT WORTH!

Diagnosis and Treatment of Oral Disease

Dental Caries Activity and Diagnosis

Diagnosing dental Caries [Dr.Wolff]: We’re going to talk about diagnosing dental caries here and this is really important. We’re going to look at activity and we’re going to talk about the concept of activity and we’re going to talk about diagnosis. So who’s responsible for screwing all of dentistry and also coming up with all the wonderful things associated with dentistry? No, not Mark Wolff. No where near as good as GV Black, my hero.


And GV Black was the 1 person that had 1 bullet, 1 treatment, and 1 classificaction system for caries based on the fact that he only had 1 method of treating it, so I’m going to treat everything, describe everything the same. So when he looked at this patient- someone please tell me what’s the classification of that caries? Classification Dos- class 2. Hmmmmm.

NYU | Dentistry (GV’s pic)[Dr.Wolff]: Does that classification tell you anything about the depth of that lesion?

G.V. Black[Dr.Wolff]: Does it tell you anything about what surface that lesion was on? Was it on the occlusal surface too or was it just on the distal surface.

Image[Dr.Wolff]: You don’t know. So was that a one surface cavity or 2 surface cavity? By the way, when we count DMFS, how many surfaces is this? TWO! So after patients see the dentist, their DMFS rises more than their D was before. Because part of the process we need to go and treat these is to get in there and actually remove some good tooth structure in the process. It doesn’t tell us about depth, location, activity, it doesn’t tell us much other than how to bill a patient, and that’s all GV blacks classification did. It was essentially a billing classification. And we’re getting away from that concept of a billing classification. It’s still a class II restoration. We’re going to describe the caries to the faculty in different terminology. We are going to use terminology like I have an active lesion that penetrates 1 level on the proximal lesion on the … tooth number whatever.

Black’s Classification of Carious Lesions[Dr.Wolff]: Does the system actually tell you about surface of caries, extent of the caries, I shot that already, and it doesn’t make it possible to recognize that the event of remineralization occurs. So I told you fluoride prevents caries by effecting minerals. It has an effect, did Dr. Caufield talk to you about the amylase reaction? Yeah he did. So it interferes with the amylase reaction- it has an effect on the killing.

Black’s Classifications of Carious Lesions[Dr.Wolff]: It requires some relatively high concentrations. Higher than you’d conventionally see in toothpaste. But when we put fluoride varnish on , part of it’s effectiveness is clearly inhibiting the amylase reaction.

Miller’s Acid[Dr.Wolff]: But the big thing you need to recognize is that we now have methods of taking the calciums and phosphates and forcing them back into toothpaste. We have wide range of products currently available, MI Paste, um, there’s a trical phosphate, there’s a number of different products on the market that contain calcium and phosphate and fluorides, calcium, phosphate and arginine, in an attempt to change the balance of the equation. As we’ve already discussed, you know this is a simple chemical equation. If I put you to bed every night wearing a tray that’s stuffed with


calcium and phosphate and you ate sugar just before you put the tray in- are you going to demineralize or remineralize? I’ve got a tray loaded with calcium phosphate covering your teeth. You’ve got acid on your teeth and no ability of saliva to go in there. Are you going to dissolve the tooth structure? Why? Low pH. Tell me about your, Hassels- what is it? Yeah that equation. If you keep a solution out here of calcium and phosphate- even as we drop the pH can we see a mass action pushing in this direction? No. So what if our strategies for controlling caries is actually to use calciums to prevent the tooth from deminerlizing as well as to push it into mineralizing. After a night a demineralizing with all that stuff on the surface, the minute saliva touches the stuff- it’ll neutralize the acid, and you’ll get almost immediate precipitation into the surface, and that’s pretty dramatic. SO we now start concentrating, not on this one surface here and creating surgical work- but looking at these demineraliztions early and figuring out how to manage them. Looking at the aproximal demineralizations. But in order to treat them and say whether things are getting better or worse- we need to be able to record how severe the disease is.

(He flipped between a number of image slides)[Dr.Wolff]:In 2002 and 2003, a group of cariologists, which I wasn’t a part of at this time but did join them in 2006, looked at a staging of caries that went more than hole or no hole. As a matter of fact, it eliminated the use of the explorer, and said that we shouldn’t be sticking it in surfaces, because that will take demineralized surfaces and break them up. It said rather we’re going to use this on the surface, scratching across the surface to see if it’s rough…

ICDAS[Dr.Wolff]: Listening to hear whether it’s rough, but never pushing into surface to see if it’s soft. That’s actually a real critical decision in here. SO we have these sound tooth structures and at the first visible sign of enamel change it’s not there when it’s wet but when we dry it we see the slightest whiteness and start to chart that. Now as it turns out we start to calibrate examiners to determine the difference between an ICDAS 1 and 2 lesion in the presence of saliva versus absence of saliva and it turns out it takes a very well trained examiner to pick that up. Didn’t turn out to be a very user friendly mechanism, but it’s an effective way for research. Then we have all sorts of discussions of occlusal surface and breakdown of surface and whether or not we have caries of the surface. It turns out to be simple- are we open with the caries in the dentin or extensive caries to the dentin. Do we have areas of demineralization and do we see evidence of it on the radiograph, particularly on the occlusal surface. So tooth 19 has a non-cavitated, ICDAS on the occlusal surface. How do we decide whether or not to surgically treat this? What’s that? So radiographically we don’t see anything here. That’s a good sign. Clinically we said it’s ICDAS 3- which is this ugly surface here, maybe a little breaks in continuity.

List 5 critical decisions…


[Dr.Wolff]: But not a giant hole anywhere. Do you surgically treat this? Do we treat it? So, tell me what our treatment is? Sealant is the most common treatment and sealant, the good news is, if you have a tooth that has active decay you actually arrest the decay for a period of time as long as the sealant is in tact. So it’s not a bad thing to make the mistake and seal something active so that whole oh should I or shouldn’t I or if I don’t treat it it’s trouble, but how do I decide whether or not to seal this patients tooth?

ICDAS[Dr.Wolff]: Do we seal all 6 year molars on 6 year olds? Ah risk, yeah, it’s a risk measurement. So if I come in to you and I’m 55 years old, oh okay and I’m 59 years old, and I have that tooth surface, and you look around and I haven’t had a carious lesion in 10 years in your office. If we looked at it and I said it was an ICDAS 2 last year but an ICDAS 3 this year what does it tell you? It’s progressing. So you have activity evidence. If it’s been an ICDAS 3 for the last 10 years should you be treating it? No, because there’s no activity on it. It hasn’t progressed, and that’s the key. That’s where activity and diagnosis and visual appearance of the lesion come together in a synthesized decision on how to treat the patient. It’s that collision. You can’t take a single snap shot and know for sure. So I look inside a patients mouth, it’s the first time he’s come to see me, he’s 59 years old, he’s never had a restoration and he’s got a mouth full of these. What’s the likelihood that it’s an active lesion? I told you the last hour of lecture, how quickly does caries progress? Has there been enough experience of the tooth at 59 years of age. Yeah it’s been hanging out for 53 years. There’s no hole in it yet. What’s the likelihood it’s an active lesion? Very low. So I get patients that come from my practice, move, I have a very academic practice, I still practice out by stonybrook university. These guys go from my practice out to another area, another practice; the guy looks inside their mouth and goes you have 9 cavities. And they go, Dr. Wolff hasn’t treated me for cavities I nthe decade that I saw him. So there are 2 choices of how this can be. What’s that? GV Black is treating him, in which it gets treated. Or I’m just a slouch, a crummy dentist, a slug. One of the 2, I’m glad none of you had the courage to say that to me. The truth is, I’m misdiagnoser or I’m a very good diagnoser. In fact if you track this over time with a category and you know if it’s getting worse or staying the same you know you have the ability to say that’s a quiescent lesion. Now what happens when he comes in with the first one of these that’s become an ICDAS 5 and I see breakdown into dentin. Same patient 59 years of age has nothing nothing nothing nothing and all of a sudden, one of those teeth break down. What do I do? I treat the tooth that broke down and what do I do? (student says fluoride) we’ll talk about fluoride in a little while because fluoride on occlusal surfaces isn’t highly effective. But sealants on any tooth that I suspect to be at risk starts to become a different diagnosis, because the patient has proven risk by virtue of the change in category. Now hopefully I see an ICDAS 3 then 4 and see the lightest shadow. There’s nothing worse than an ICDAS 3 turning into a 5 because I didn’t treat it when it was an ICDAS 3.

So a very complex matrix gets developed with caries classification and we’re going to use caries classification in school that essentially says you have a sound tooth,


you have a tooth with initial lesion, and these initial lesions are all non-cavitated lesions. Can we have a white spot that’s an active lesion? What does it look like? Have any of you done any bonding on any enamel?

Guiding Principles[Dr.Wolff]: Have any of you done any bonding on enamel? What’s that? Did you do any live tooth bonding? In school? No? did you excavate caries on an extracted tooth. I’ll make sure Dr. Bucklan has you etch and bond them next year. Well yeah no not you, but next years class, unless you want to go back to first year again in which case we can accommodate them. Etching results in what a frosty white area and if you ran your explorer over it, it feels rough. Why does it feel rough, no not etch, what occurred? What does the etch do? I think that’s me dinging I’m sorry. It is me dinging. Can you do me a favor Kennie and run up to blue stone, (someone) is looking for me and let her know that I’ll be done after 5. Thank you. Okay where were we? Why does it feel rough? It removes structure- we dissolved mineral ,we took it away and haven’t replaced it. The good news is when you etch the tooth if you don’t bond to it, saliva precipitates mineral in the surface and it becomes smooth again. That’s the earliest evidence of demineralization. So we can have these initial white spot lesions and we can make 1 of 2 decisions. It’s always non surgical, you don’t cut them, but the question is do we need to do something that helps remineralize or prevents demineralizing or do we just leave it alone and let it take care of its own fate? And activity helps us make the decision for us. When we see even the slightest white spot that’s rough and chalky, we talk to the patient about what? Getting the plaque off the tooth. Talking about the fact that our acids start to demineralized. So even the earliest lesions get treatment, but non surgical treatment. Now these moderate lesions are lesions that we need more help with. Sometimes we use diagnostic aids, I’ll show them to you in a moment, other times we look at the caries risk at both at the lesions activity and at the lesion surface but it’s clearly at the patients risk, um and we have to decide do we do nonsurgical therapy or do we do surgical therapy. So if it’s an active lesion, we take an X-ray we look at it we don’t see penetration into the dentin we are going to use a non-surgical attitude or a sealant to go into that occlusal surface, or we are going to do something to come in there do something really early minimum surgery that we can do without doing major damage to the tooth. Do we choose to do amalgam or deposit. We do that at the time before the prep not before we start the procedure. We think we are going to use composite but if we have to use a different material at the procedure we are capable of using it. It’s very simple when we see cavitation to the dentin, or it used to be. In Europe today D1 lesions are being either sealed or remineralized if on smooth surfaces. They’re not even treating D1 lesions radiographically. We’re not there yet, but it does appear that it’s effective. Standard surgery, minimal intervention at all times. We’re going to be using a sound, initial, a moderate, and an extensive loss for caries, on roots I’m sorry. You absolutely use only 3 classifications. Totally sound, moderate with a loss of surface but not cavitated, or extensive when we see cavitated. Yes? (student speaks) Yes. So fluoride will tend to make it less soluble. I don’t like the word harder, it happens to be that it is harder if you do a micro hardness test, but it’s less soluble is the real issue.


Root Caries[Dr.Wolff]: Um, but we actually look at remineralization as capturing more calcium back into the tooth surface. Measurable amounts of calcium into the tooth surface. What’s that? Dentin or enamel. And we use calcium products or saliva to go do that. We see changes in microhardness also just with pure remineralization, not with the use of fluoride- so we actually get a harder surface with more calcium content. We see it in microradiography, we see increases, we see actual physical measurements with some of the research that we actually do here at blue stone. Yeah? (student speaking). That’s a good question. Can you get enough calcium in there that the demineralized area suddenly looks normal again? Up until a week or 2 ago, I used to show pictures of my 30 year olds maxillary premolar which when she came home from college and was 19 years old all of a sudden she had an early lesion that just touched the dentin. We went for 11 years without any progression of the lesion, I guessed her last radiographs were 2 years ago, so 9 years. Last week, she came in and had radiographs just taken a week ago and had caries so my concept of remineralization has just been totally shot, hah oh no, in real experimentation we stop the progress of the lesion and in fact she stopped the home care and things to prevent the progression of the lesion. Uh, and I wonder if that was a HIPPA violation, ratting out my own daughter. It’s not the one you know so maybe it’s not a HIPPA- who cares. What is she going to do arrest me? Fire me yeah, that’s a better idea. Yeah during the summer when we go fishing and vacation, I’ll invite you to come join me ,it’s okay.

Caries Adjacent to Restorations (CAR)[Dr.Wolff]: So caries adjacent to a restoration. Has anybody heard of the term recurrent caries? That’s what every one of my faculty call it. How would you feel about a faculty member doing a restoration on your tooth and 5 years later saying we have recurrent caries. Re-occuring caries. Is it because you didn’t remove it Dr. Wolff. No! It’s new caries occurring at the margin. Is it recurrent? Or is it caries around the margin? Now this becomes an important new discussion, because we are starting to talk about not removing all the decay anymore and there will be a difference between recurrent and caries around the margin, caries around the restoration. What we currently call recurrent decay is actually caries around the restoration. Activity, we talked about it. You can either see it in progress, lesion either getting worse and worse, you can see it in the ICDAS classification, you can feel it.

Activity[Dr.Wolff]: Now one of the interesting things, and I was not a full understanding about this, if you probe the gingiva, and it bleeds, what does gingival bleeding have to do with caries? You saw Gregory’s tooth, that canine with caries on it, what does probing that surface, that perio tell you? If it bleeds what does that say? And what caused the inflammation? Not well, it’s not really an infection, an infection yes, that means that there’e plaque accumulation there. So bleeding on probing when doing a perio examination when the patient has caries, the caries is not related other than


it’s a sign that there’s been plaque accumulation the last minute. So you can’t cheat the last minute. The kid brushes his teeth really well right before he comes in and his gums are bright red and you know he hasn’t brushed in 3 months. I see it all the time, their teeth are perfectly clean and their gums are bright red. I know every time, because mom got them to brush before they came to the office. I said, you brushed today? How about yesterday? Really? Because your gums are all red, they bleed when I touch them. You’ll learn a lot about plaque from that. So gingival bleeding indicates in a large extent whether or not the lesion is active, Because it demonstrates the plaque accumulation and remember if you see white spots and there’s no plaque there, it’s probably not from plaque, it’s from another type of acid exposure- what would that be? Erosion. So I’m drinking my citric acid right now, pH 3.2, a little bath around the tooth. What’s happening to that tooth surface right now? I’m dissolving in the same way I’ve taken that sugar and eaten it.

Activity[Dr.Wolff]: As a matter of fact if I left plaque on my teeth, the plaque tends to protect against erosive acids associated with oral consumption which is pretty remarkable. So we use a visual examination, tactile, I like using the perio probe because I can’t put any force or break any enamel, run around the surface you want to see if there’s caries there. Run the perio probe in there feel whether there’s a hole. You can do that you can’t put it into tactile, you can’t do that. We use radiograph al lthe time, radiograph is still the gold standard for aproximal lesions. We still haven’t come up with new technology that beats it. Laser fluorescence, we’re going to teach that to you this year. Have you learned about that yet with Dr. Glotzer yet? Transillumination is interesting. The probe is dead. Stop sticking it in the teeth. Rat them out, I’ll come get them- I’ll stick it right up their…Faculty appointment.

Caries diagnosis[Dr.Wolff]: I don’t need to stick a probe- that’s a terrible picture, I don’t need to stick a probe in there. I can dry that tooth, I can look carefully at the surface and I can determine whether or not there’s dentin exposed in it. What I know about these surfaces is if I take a sharp pointy thing and push it into a deep V wedge it’s going to stick. And unless I see visual image that indicates caries the likelihood of that probe telling you that it’s caries that’s there that I didn’t detect is less than 50/50 and since when do you get to amputate an arm that’s almost gangrenes.

Image of occlusal surface[Dr.Wolff]: Dentists take this attitude ‘well I’d rather drill it before it became carious.’ Well then let’s put restorations on every tooth in the mouth! I know, you guys think that’s a good idea because you have a lot of student debt. But the truth is there’s no rational for ever destroying a tooth with good tooth structure in the hope it’s going to prevent decay from occurring. It’s just faulted logic. So I hear faculty all the time. If we don’t get it now it’ll be carious in a few years. Well in a few years your restoration is going to go bad because we know the average life expectancy of a restoration is 8 years. Ohhh I forgot. You’re Dr. Perfect, everything you put in the mouth lasts forever, unless you visit another dentist and looks at your work and


goes dr. perfect didn’t do such a good job. We can take it out and do it better. And in fact- that’s the number one determinant of the expectancy of a restoration, I’m going to say it over and over again because you’re going to be evaluating someone elses work. And you will be as criminal as they will be of you if you don’t look at it and go Okay, the margin is ratty it doesn’t look, but I don’t see any evidence of caries, the evidence of demineralization, the evidence of breakdown, and the rationale of let’s change it before it goes bad- just bad logic. Talk to the patient, you have a number of old restorations in the mouth that may not last many more years, but we’ll keep an eye on them. Much more valuable. Guiding Principles[Dr.Wolff]: This is an electrical conductance- there’s some faults in this concept this is a meter that’s for sale and available on the market. You actually dry the tooth and take this and you stick this into the groove and if there’s conductivity it means it’s going through dentin and that means that if there’s caries it gives you a red, yellow, green indicator on it to say that there’s caries. But it overdiagnoses areas that have no caries. Because conductivity does not directly relate to whether it’s carious, it relates to whether or not it’s communicating with dentin. So if you have a groove that’s malformed open to the dentin it’s going to read just like caries .You still have to fall back on your visual identification.

Image[Dr.Wolff]: It’s not a great technique. Then we have these laser fluorescence devices. You hold them on the tooth, you shine the light in there and they reflect back and show back the byproducts of caries and give you a physical reading you use as a measure of whether or not you have tooth decay. Once again- very suspect to over-diagnosis because stain in groove also increases measure of whether or not it’s giving that indication- they detect stain and caries byproduct in the same way. So it’s an overestimate. These are great helps, I’m looking, I’m arguing Dr. Wolff is that an ICDAS 3 or should that be sealed or is this an ICDAS 4 that should be surgically treated? Let’s take out the diagnodent and take a look at the caries around the groove not into the groove, around the groove, and if you see elevated numbers- I agree, let’s restore it. These are great adjuncts after you’ve done the clinical diagnosis- not substitutes for it. So you go ahead and shine the light on the surface.

Image[Dr.Wolff]: This is actually a great one that you guys don’t use nearly enough in the clinic. What’s it called? Transillumination. Using energy to go through the tooth and cause a reading that allows you to see differences in density. What’s another product that allows you to use the exact same way? What’s that? X-ray! Radiograph! We’re using photons in this one- and that’s using high energy. This one doesn’t cause any damage to tooth. It doesn’t put you at risk of cancer or anything else. The other one comes with ionizing radiation it puts you at risk for damage to tissue. You can shine a light on this look through any anterior teeth totally and actually for the boards this is an effective method of isolating a tooth that has caries to the dentin. They accept transillumination. Why doesn’t it work in the posterior? It’s too thick- the light won’t penetrate through. It doesn’t transmit all the way through the


aproximal region. We can go ahead and offer a whole load of other methods to manage these in a different fashion. What do you do with this? It’s dry, it’s frosty. What’s that? We first look a radiograph and make sure that there’s no evidence that it’s into the dentin. If there’s evidence that it’s into the dentin, there’s good rationale for surgery. If there’s no evidence that it’s in the dentin- you seal it. It’s frosty- it’s active.

Management of Pre-cavitation[Dr.Wolff]: You know this is a photograph from Dr. Kaim. That little hole in all this demineralization that you see here when it was open up was this giant carious lesion. But it’s still was at minimum an ICDAS 5 this was never a seal this tooth. There’s a hole in it and should have been judged as having a hole. This decay was into dentin this area was kind of suspect and as we opened up the tooth we could see the penetration to dentin in a number of areas but the real question is could this have been sealed.

Image- J. Kaim[Dr.Wolff]: This was an ICDAS 4 that was at that breakpoint and you probably could have sealed this and the person could have done just as well. We tend to surgically treat that at the school, I’m not going to argue this point at this moment. I don’t want you guys surgically treating ICDAS 3s or just touching dentin on the radiograph.

(switches between various images)[Dr.Wolff]: Abfractions are unique items. DO you know that that is, right there? What’s that? Tell me what was inside that tooth. That was the pulp chamber. It’s actually the pulp has receded, disappeared, it’s gone. Pretty incredible. You can have this loss- it’s thought to be from occlusal loading and some sort of activity. Why do I know this isn’t from a toothbrush? The adjacent teeth have nothing going on on them.

ABFRACTION[Dr.Wolff]: Unless you use a very small toothbrush on only 1 tooth, you couldn’t reproduce that. It’s not erosive because what? I’m only putting the acid on that one spot on the tooth. There’s something else functioning there. Erosions tend to be this shaped, they’re an acid event, they cause sensitivity frequently, they’re relatively simple- the acids come from 2 sources- extrinsic being from drinks and things like that- remember sports drinks have lots of acids. Intrinsic is vomiting and internal items. This is probably caused by regurgitation. This erosion is clearly caused by regurgitation- this one is caused by pregnancy and this one by bulimia. Not on facial surface why? Acids coming out.

Chemical Erosion[Dr.Wolff]: Some key items, brushing your teeth in the shower, brushing your teeth frequently, throw up and brush immediately, it’s a common finding. This what is that?


Dentin Exposure[Dr.Wolff]: What is this? And what is this? Ahhhh-hahhh. They’re both caries!

Erosion[Dr.Wolff]: What’s the distinction between the 2? Stage, activity, this is soft, brown looking. It’s not black or showing signs of remineralized. We get a sense of frostiness when it’s dried- it’s active, it shows signs of an active lesion, do you surgically treat that? In the US yes you do- we would actually consider that relatively moderate to extensive caries and should be treated. If you were speaking with Edwina Kid she would tell you to arrest it and remineralize the caries and leave it alone. That may work in England but doesn’t work in US court.

Image- NYU|Dentistry[Dr.Wolff]: But surgically treating this tooth would be a real real mistake. The American dental association held a conference that’s come up with an absolutely wild, so on tooth 19 it has a site 1 initial lesion that would be rated 19.1.1. Yes? Oh I hate that question, it’s a really good question. Why don’t you seal that surface? There actually is a product recently, it’s still illegal, it’s still not approved in the US, the truth is it’s a viable product and I’m sure you’ll using it before graduation- it’s called ICON

Further Simplified Format of ICCS[Dr.Wolff]: Okay It uses hydrochloric acid to etch the surface and it has a plastic just like our sealant to cover the surface- it’s a new technology that’s out there- the problem is once you put that in place- He didn’t take that bag of chocolate with him did he? If he took that chocolate we’d have a discussion. Is the chocolate over here? No, I don’t really care.

Image [Dr.Wolff]: If we go ahead an seal that we can’t get fluoride or calcium back into the surface so it’s a real problem. This is the ADAs method of defining a lesion and it’s crazy. So you’ve got cervical facial lesion on tooth number 6 it will be a 6F3.3. Cervical, facial surface, 3.3 means it’s extensive. Cervical is 3- extensive- crazy system I don’t think it’s going to get any traction.

Further Simplified Format of ICCS [Dr.Wolff]: But where we are seeing traction is a method of classifying that’s associated with sound, demineralized cavitated severe and moderate cavitation. And we- this system is almost a variation, but so where we have gone on this at NYU and we were here actually before the world has actually followed it, it’s the same classification taught here for almost 9 years. It talks about looking at the surfaces as being in tact radiographically, particularly, just penetrating the enamel. Anything that’s less than hitting the dentin is an E2, if it’s hit in the outer 1/3 it’s hit the DEJ but not progressed passed the outer 1/3 that’s a D1. If it’s progressed beyond the D1 to the inner 1/3 that’s a D2 and a D3 is the deepest and that’s a radiographic distinction.


Caries Score Legend[Dr.Wolff]: It also fits the intial caries, looking at the E1 and E2. The moderate caries being D1 and D2 or the extensive caries being a D3 lesion. WE have now gone on to what is now known as the international caries monitoring system and it’s the ICCMS. Class 2 lesion is not a description of the lesion- you have to go further. You know, I sent out the police looking for the candy. Did you just stuff it outside in your locker or something? That’s what it was. Sugar addicts- that’s terrible. Radiographs are still considered a new standard. This is the new computer system that you’ll be using to help classify caries um when you hit the clinic in January. You’ll actually take the measures and say you know that it’s cavitated moderately and it’s active and you’ll actually chart that on the surface that it’s located. So we’ll be able to measure severity and progression of lesions as you go do it. It’ll be quite simple you’ll hit all of the extensive caries- bing bing bing bing bing. All those surface- you hit add- moderate- ding ding ding ding ding-Demineralized but inactive ding ding ding ding ding and you’ll chart it that way. You’ll have initial lesions, moderate lesions, um and caries into the pulp.

-C0000, Caries[Dr.Wolff]: This would be classified as an initial, this comes from the ICCMS document- this would be considered and initial lesion, early- it’s ugly, but it’s an early lesion with no evidence radiographically or examination as penetrating. When we go ahead and look at these we look at the radiograph to determine whether or not there’s been penetration in here. There’s been some penetration. I’m sorry this came out of their monograph it did not um copy over well.

Radiographic[Dr.Wolff]: These are the extensive lesions and you can see the extensive lesion on all of these. So we will categorize these as mild, moderate or extensive. Anybody have any doubt? This is actually an extensive lesion it’s at the junction of the D2 and D3- I would call this a D3 lesion- looking at the distance from here to here this lesion is in the middle third.

Clinically moderate caries lesions[Dr.Wolff]: And that raises the very end of our presentation- you were a wonderful audience, I appreciated you coming, I promise to reward each and every one of you somewhere in the future- I can’t promise you the location but you’ll be happy you were here- just say August 12, 2014 and it’s golden. They already know the little code they have to flash me with their fingers so it won’t work for those of you that aren’t present. I wish all of you a wonderful day- good luck on that DOD exam- I hear it’s terribly difficult- no I’m just kidding. Any questions? Thank you!


Documents

23/24: Diagnosis of Caries