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Welcome to episode nine of the Six Lessons podcast, where we bring you the history and the technique that is changing the world of dentistry.
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My name's Dave Alleman I'm the father of the Six Lessons.
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Today we're going to talk a little bit about 1999, the next year of the big change.
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1998, at the ADA convention, we met Charlie Cox, John Kanca III.
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We spent some time with Ray Bertolotti.
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And my second mentor, Gary Unterbrink.
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The next year, I came in contact through an organization called the World Congress of Minimally Invasive Dentistry, with two great friends and mentors in the world of minimally invasive dentistry.
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And that's Tim Rainey and Graeme Milicich.
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In 1999, the World Congress of Minimally Invasive Dentistry was in Chicago.
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I traveled there to meet Tim Rainey because he was the father of minimally invasive dentist in the United States, and then his partner in teaching and writing articles was Graeme Milicich.
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Is Graeme Milicich.
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They're both still alive.
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And Graeme Milicich came to Chicago from New Zealand and he talked about the concepts of minimally invasive dentistry, particularly with using air abrasion and actually lasers.
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Hard tissue lasers was a popular topic of the conference, but the main thing that he had that he published in the next year 2000, was the concept that manifestation of stress in teeth was a precursor to actual infections into the pulp from cracks that go into the pulp and communicate with the pulp.
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And so the paper that they published in 2000 was called The Manifestation of Stress.
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I better quote it exactly clinical presentations of stress distribution in teeth and the significance in operative dentistry.
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So everyone who's been trained in the six lessons approach has always had that as one of their main articles to study.
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It contains the concepts of a peripheral rim fracture as a manifestation of occlusal forces in restorations that are not connected side to side, and every amalgam restoration ever placed has been not connected side to side because these structures that are key, that are called sub occlusal oblique transverse ridges that were named by Tim Rainey and in 1994 and 1996, these structures that connect to side to side, they are made out of enamel, but you don't see them because they are underneath the pits and the grooves that dentists have always been fixated on because the grooves and the pits on a molar accumulate plaque.
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This is where decay often starts, but the process of removing the decay also.
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Dentist 100 years ago was instructed to prevent future decay by destroying these ridges in these grooves, connecting them into a smooth flowing preparation.
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This was called Extension for Prevention by GV Black, the founder of systematic operative Dentistry.
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But this extension for prevention and his other concepts were retention.
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Former resistance form made preparations that did not need to be adhesive bonded.
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They were just mechanically stuck into the tooth.
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And if you remove decay and you remove parts of the tooth that are fundamental for it's natural ability to withstand occlusal forces, then this is doing some harm to the tooth.
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But again, you have a risk assessment.
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Is the harm of destroying part of the tooth worth the reward of perhaps preventing future decay in parts of the tooth that are susceptible?
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All of these questions should have been discussed more aggressively.
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You know, I have 20/20 hindsight, so it's easy to to know where everybody else made mistakes.
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But in reality, in 1981, a very important paper was published and another paper, the year before, there was no as well known, was published in Brazil by Mondeli But both Mondeli and Larsen under the direction of William Douglas at Minnesota, both of these independent researchers on two different continents came to the conclusion that the fracture resistance of teeth with traditional filling preparations was reduced greatly.
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In other words, they actually measured a 40% or a 60% loss in fracture resistance every time a tooth had a filling because there was decay in the tooth, even if it was very small.
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These ideas of extension for prevention, resistance form retention form required grooves and depths that damaged the tooth.
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But it took 80 years to really measure that and to see that this led to cracks and fractures.
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Well, in 2000, 20 years after the Larsen, Milicich and Rainey, went a step further, they gathered some information that had come out of Australia and it was published in a Ph.D.
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dissertation there that nobody would ever read unless Graeme Milicich didn't discover it.
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But he actually was able to see, and it was later published by a Dr.
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Walker in 1998.
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The effects of a crack that's moving and accumulating or allowing bacteria to enter that crack a naturally occurring crack is called a lamellae and that happens naturally.
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a defect in in the Emilio genesis of the enamel will allow a crack that acts like a crack.
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The tooth now is not connected side to side, but it's opening.
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So this lamellae opening allowed a bacterial biofilm to form, decay to form.
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And that was documented in 1998 by Walker.
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And in 1974 it was part of the dissertation and theorized.
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But to have a 20 year lag between 1974 and 1998 happens all the time.
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in Science.
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Somebody writes a Ph.D.
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Nobody reads it.
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Finally somebody reads it.
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Somebody asks some questions, so many documents and makes some proofs.
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All of a sudden it needs to be taken from the science to the verification.
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And then the next step is the popularization.
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But this idea of cracks into dentin and what they can do as far as allowing decay to develop that was popularized and actually named by Milicich and Rainey in 2000.
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So that's almost 25 years ago.
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How many dental schools teach the peripheral rim fracture, PRF, and then how that leads to occlusal effect carries.
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I mean, when I read that paper in 2000 for the first time, it changed my life forever.
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It taught me something that I needed to know when I'd graduated from dental school 22 years earlier because a class to lesion is taught to dental school as a manifestation of a patient not flossing every class two lesion.
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Pretty much you can guarantee the patient not flossing.
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So the classic effect, it's not proven, but you can just say you've got a class two cavity is because you're not flossing.
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So you need to floss and then you fix the class two cavity and then you look at the patient's teeth and there actually isn't a lot of plaque.
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They're brushing really well, but maybe they've been flossing a little bit.
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But all of these things, you know, I accepted the dogma forever and but then I would have patients that I knew were brushing and floss, but they had amalgams in their teeth.
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And then after two years, three years of seeing them every year regularly, no decay, all of a sudden this class one amalgam would have a class two lesion.
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And I'd go into my spiel or tell the hygienist, You know, I got a class two, you got to, you know, get some more flossing on.
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And but in the back of my mind, subconsciously, there's a cognitive dissonance.
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In other words, the facts are meeting the narrative that I'm giving to the patient.
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So I've got to, for several years deal with this.
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As soon as I read the 2000 article, I go, That's the answer.
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We have a there is lesion developing from inside the tooth, working its way out instead of plaque induced demineralization working its self into the tooth.
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I mean, once that happened, then my new diagnosis was this due to structurally compromised.
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I see a sign of this structural compromise on the marginal ridge.
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And that marginal ridge fracture leads me to say this tooth is at risk of decay and fracture.
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That's just the truth.
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And when I had these discussions with Graeme Milicich and Tim Rainey in Chicago before the published paper, obviously I expected as soon as the paper to be published that it would be worldwide accepted, everybody would be wining and dining Milicich and Raney and blah, blah, blah.
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And, you know, I was just glad that I got to know them early before they became famous.
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When this article came out and I started to use it in my private practice, I, in my mind said, Every dentist needs to read this.
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They're in.
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And I would talk to dentists.
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I would you know, I was a member of a dental golf league, and I knew 70 dentists that I knew well, and I'd talk to them and, you know, none of them were reading the literature, but a few things that I would say made sense.
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And some of them had questions.
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And if they had questions about this new kind of dentistry, adhesive dentistry that I had been studying for five years, they would ask me, But that's not the way a dental profession is going to change.
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You just can't have a few dentists talking about something.
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It's got to be a wake up call.
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In other words, a dentist needs to say there's science, there's an applicable way to use this science.
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And I've been doing it for three years.
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I've been doing it for five years.
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That's the position that I was getting to in 2000.
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And then as we get to 2003 and I start teaching and I start reconnecting with leaders like Graeme Milicich and Tim Rainey, then we start arranging lectures in our groups, Rainey invited to lecture in Texas for a couple of days, and Graeme Milicich brought us to New Zealand.
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The lecture for a week actually been to New Zealand twice.
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But these leaders in their areas, if they don't connect with other leaders in other parts of the world, then it just becomes a very small influence area.
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There's a perfect example again from Australia.
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Australia doesn't get the respect it deserves in Australia.
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There were some ended on us that I didn't know about independently for five years from 1995 to 2000.
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The next problem that I had after decay was cracks.
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And so this period of 1999, 2000, 2001, this connection with Milicich and Rainey really helped the solidify.
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But when I got a microscope in the beginning of the year 2000, then everything was like, Man, we are neglecting something that's huge.
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So many of these teeth had cracks in the dentin and they were symptomatic.
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They hurt patients, had a symptom, they had a problem.
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They came to you to solve their problem.
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The dental school treatment for that was full coverage crowns.
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In other words, you're cutting off all the important enamel into the structure surgically.
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We call the biofilm now and then you're covering it, trying to stabilize these micro movements.
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It worked a little bit, but not enough to keep all the teeth from having to have root canals.
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So this became more apparent to the engineers who are treating these severe crack and these severe symptomatic teeth more than anyone.
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And in Australia, 2009, some Australian dentists who had some connection with Walker understood that these cracks not only been a path for infection, but a fact path for a pulp that gets infected and then dies.
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And so these endodontists Their name was Abbott, and Lowe published a paper based on their research and their treatment in their office in 2009.
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This is nine years after Milicich and Rainey.
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But what they do is they say we dissected the crack, we remove the crack, and then the symptoms went away.
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Everybody else in Europe was just bonding over these cracks and the symptoms modified a little bit, but a lot of the teeth died.
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A lot of the bulbs were dead from the infection, from the crack.
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So we have two groups European ended on as European adhesive dentists saying just bond over them.
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And then these two mavericks in Australia say, well, let's just remove the cracks.
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And they had results that were favorable.
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The Europeans did not.
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That's just a summary of 20 years of dentistry on cracks.
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Well, at the turn of the century.
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During the turn of the century, yeah, 2000, I bought my microscope.
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I made the same conclusion that Abbott and Lowe, I didn't know them.
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I'm not an endodontist, but I’m a general practitioner seeing cracks and associating those cracks with these symptoms and these symptoms go back to a book that was published in 1982.
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I don't know the exact year that I got Branch forms book.
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The branch are analyzed.
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This crack tooth syndrome that had first been written about by Cameron in the middle and late sixties, and I was taught it in dental school practice syndromes symptoms are pain on biting cold sensitivity and if you had that, then the diagnosis of a crack tooth required the treatment of full coverage crowns.
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That's what it was in 1975 through 78 at University of Pacific.
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Well, now we're making this evolutionary change in my mind.
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And in 2003 I start teaching it to other dentists when I teach new concepts, other dentists like hierarchy, band ability or decoupling with time or by replacement, or a semi direct restoration, resin coating, deep margin elevation.
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All these new concepts that we've been using for 25 years.
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These are the new principles.
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But the idea of crack dissection, that was really a new principle.
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It was hard for dentists to keep their mind focused on the idea that these cracks under micro movements move.
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The reason I decided to start dissecting cracks is because I actually talked to crack experts, experts that had PhDs in engineering, that had actually studied cracks in every material, how they start, how they get bigger, and how they can lead to catastrophic failures in buildings and airplanes and bridges, all these kind of things.
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So one of my best friends, Dennis Groh, has a master's degree in engineering, is a crack specialist, fixes cracks on $2 billion stealth fighters.
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But this idea of taking these cracks seriously and training Dennis to dissect cracks.
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We were the first six lessons graduates and quite often six lessons graduate four years later would call me up because they each have my cell phone number.
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They have any problem, they're supposed to call me, we find out what's going on.
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So I get these calls from some of my best students after about four years.
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Well, I've got a tooth that's symptomatic.
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And then I'd say, you know, do you have a picture of it?
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25 years ago, photography was not that common.
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Usually I would say no.
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And then I'd say, What magnification do you have when you treated the tooth?
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And they usually say, Well, three or four to see cracks really well, you really need like six and a half to eight anyway.
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So I would just tell the, the dentist, I'd say if the symptoms are, are consistent and you've got now pain on bleeding, then you need to go in and look, look at the crack because you've got something going on inside, underneath the restoration, you've probably had a deep bond on the side that's connected with the, with the crack into that and all this.
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We do it.
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But, you know, we trouble shot two of my best students are now note and their problem solve pressing or had that problem it always happened about four years out and then they would retreat the tooth actually see the crack with better magnification photograph it and then they would treat it with the protocol of dissecting it without exposing the pulp.
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All of these concepts that we've been teaching and the clinical results and improvement that we've seen lead to great confidence that this is the way to treat that pathology.
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But it all begins with seeing things that you never saw before.
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Let me give you an example.
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Biometric dentistry starts getting taught under the name biomimetic dentistry and well, I didn't call it biomimetic dentistry in 2003.
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I called it Advanced Adhesive Dentistry.
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Later on Pascal Magne, Ray Bertolotti and I in an office at USC, decided that instead of calling it tooth conserving dentistry or advanced adhesive dentistry, we are going to call it biomimetic dentistry because nobody uses that word.
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And it would create some questions and some interest.
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And so that was the decision that Pascal Magne, Ray Bertolotti and I made to call it biomimetic dentistry.
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The idea of a tooth not having a crack into them.
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That's what we were trying to mimic.
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If a tooth has a crack in enamel, a natural tooth, So the biology, the biomimicry of a crack into enamel would be have your enamel replacement fracture.
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That's what a natural tooth does.
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And so this Academy of Biomimetic Dentistry, the first, has a meeting that we organized in Marina del Rey in 2011, and it continues in their academy meetings in 2012 and 13 and Reno and then 2014.
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There's the Academy of Biomimetic Dentistry in Philadelphia.
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I'm an invited speaker.
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Ray Bertolotti was an invited speaker.
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And then from overseas we brought in Graeme Milicich from New Zealand.
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And upon the recommendation of Charlie Cox, one of the other speakers at a previous conference, said you should bring in Inokoshi And I said, That's a great idea because of Inokoshi’s connection with Sema Belli and Tagami and TMDU.
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He was Fusayama’s first Ph.D. student.
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I said, Inokoshi’s great.
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If you can get them, you know, tell them we'll pay them and bring them over and, you know, he came well, the day before this two day conference of the Academy of Biomimetic Dentistry 2014 in Philadelphia, I gave a literature review for doctors who want to pay an extra thousand dollars and spent a day with myself to review 50 articles of the literature.
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So we were getting ready to start a class.
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Right before we started.
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We had 19 doctors in the room.
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In comes Graeme Milicich Great.
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You know, he's coming in for the comp, he's going to speak the next day.
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But he came a day early.
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And you know, Graeme, great to have you here.
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You know, I had spoken and basically lived in New Zealand for three days and we taught together.
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So I know Graeme very well.
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Charlie Cox came after Graeme and I go, Charlie, I didn't expect you to come either.
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But then after Charlie in comes Inokoshi.
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I didn't expect Inokoshi to come in, but he's going to be a speaker the next day.
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And he found out we're doing the literature reviews.
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They just came to hang out.
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I expected him to kind of come and, you know, sign autographs, say hi to everybody and then go do their whatever they going to do.
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Graeme had of the things to do.
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He didn't stay the whole day, but Inokoshi stayed the whole day.
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Charlie Cox stayed the whole day.
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Inokoshi’s expertise is caries detecting dye and adhesive dentistry adhesive bonding systems.
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So that was his talk.
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But the first day Graeme gives his talk on peripheral fractures, occlusal effect caries, shows them, demonstrates them, blah, blah, blah.
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This is how you diagnose the tooth.
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It's a risk of cracks and decay.
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And talked about how black preparations led the way for this to happen the next day.
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And of course, he's on the stage and he's going through his lecture on bonding systems and using caries, detecting dye in conjunction with the bonding systems.
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And he looks up at the screen and he sees occlusal effect caries stain by caries detecting dye very clear red, but it's right in the middle of the contact, right above there's a peripheral fracture.
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And then, of course, he in is very humble way.
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He just said, you know, until yesterday, I never saw that crack.
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Now I'm on the front row, I'm listening to this and I'm going.
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Now, here's an example of somebody who's learning something important and he's giving credit for having learned it at this conference.
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And then after I had finished my lecture, the two day conference is over Inokoshi comes up to me, Graeme was talking over in the side and he says, Can I have a picture with you?
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It is Inokoshi Is like the second PhD in adhesive dentistry.
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You know, Fusayama would be considered the first, Inokoshi is the second.
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Tagami is the third.
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And he was to have a picture with me and he's published, you know, that his name probably on two dozen important articles and I have had a couple but anyway he grabs Graeme Milicich He says, can I have a picture with you.
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So the three of us had a picture me on one side and Milicich the other.
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And Inokoshi in the middle.
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Probably one of the most important pictures is that I have treasure it because you have an example of three different continents, three different cultures.
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We're all dentists.
00:22:22.457 --> 00:22:25.461
We're all trying to do the right thing for our patients.
00:22:25.961 --> 00:22:34.869
We've all been in private practice a lot and all of a sudden we have a transfer of knowledge that can continue to bless the lives of anywhere that we teach.
00:22:35.336 --> 00:22:42.110
How to use caries, detecting dye, how to use a bonding system, you know, how to use a microscope to see what you're looking at.
00:22:42.510 --> 00:22:50.652
But this idea of classification of cracks and treating them, we're still in the process of spreading that knowledge around the world.
00:22:50.652 --> 00:22:52.086
It hasn't been easy.
00:22:52.086 --> 00:22:58.461
There's a lot of resistance because human beings, particularly men, don't want to learn new things, right?
00:22:58.461 --> 00:23:00.762
We like we like the way we do things.
00:23:00.762 --> 00:23:02.497
Let's not change anything.
00:23:02.497 --> 00:23:08.770
So, you know, but the idea is that we do have this network, we do have these connections.
00:23:09.237 --> 00:23:15.610
And if somebody learn something new and want to think there's a other way to do it, I mean, it's a free world.
00:23:15.610 --> 00:23:19.180
You can, you know, make your best cases and you can write your articles.
00:23:19.180 --> 00:23:29.357
And this has happened obviously, the best long term evidence in a scientific sense is a well documented, defined protocol.
00:23:29.625 --> 00:23:31.894
In other words, this is what we see.
00:23:31.894 --> 00:23:33.761
These are the questions we ask.
00:23:33.761 --> 00:23:36.264
This is our diagnosis, This is our treatment.
00:23:36.264 --> 00:23:44.138
And our treatment has five or six or seven or 12 steps, depending on how difficult the case the case is.
00:23:44.439 --> 00:23:52.847
So that's kind of the story of Tim Rainey, Graeme Milicich, and Inokoshi in a nutshell.
00:23:52.847 --> 00:23:56.150
So until next time, get bonded.
00:23:52.847 --> 00:23:56.150
Stay bonded.
00:23:56.417 --> 00:23:57.719
Always fun talking to you.