Early Diagnosis of Caries and Cracks

Early diagnosis and treatment of dental pathologies allows for more conservative treatments while saving patients time and money. When developing the Six Lessons Approach to Biomimetic Dentistry, Dr. David Alleman created a risk assessment for determining if teeth were at risk of caries or cracks based on pathologies and treatment history.

Drawing on research from how teeth experience pain, the pulp’s immune response and how dental histology affects restoration, the risk assessment has been proven to be an effective tool over the last 20 years, especially where x-rays do not identify a cause of symptoms. Now that we understand how gaps and cracks cause pain and sensitivity, identifying them early is the next step for more conservative treatment.

Article referenced in this episode:

• Brannstrom M. The hydrodynamic theory of dentinal pain: sensation in preparations, caries, and the dentinal crack syndrome. Journal of Endodontics. 1986;12(10):453-457
• Galler K., Et al. Inflammatory response mechanisms of the dentine–pulp complex and the periapical tissues. Int J Mol Sci. 2021 Feb; 22(3):1480
• Milicich G, Rainey J T. Clinical presentations of stress distribution in teeth and the significance in operative dentistry. Pract Periodont Aesthet Dent. 2000;12(7):695-700.
• Larson TD, Douglas WH, Geistfeld RE. Effect of prepared cavities on the strength of teeth. Oper Dent. 1981(6)2-5. 

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Transcript

0:33

Hello. This is episode five of season two. Of course, the topic is the six lessons approach to Biomimetic Dentistry. The last two episodes we talked about cracks and we talked about decay and how they were confounding to myself and are confounding to other dentists that are dealing with these two major pathologies in dental practice. But after cracks and decay are understood as the problem. The approach that these six lessons takes is to try to make an early diagnosis of the teeth that are at risk of decay and of cracks. And as we talked about last time, that is always related to gaps underneath restorations or cracks into teeth. And so what are the symptoms that we look for in a tooth that has a risk or is developing cracks or gaps under restoration? I wanted to use the information that I gleaned from studying the actual anatomy of teeth. There's many, many outstanding books that have given great detailed descriptions of brittle enamel and how tough dentin is connected to enamel through a miraculous interface called the dentino-enamel junction. We also call that the dentino-enamel complex. But once you understand this incredible creation of a tooth, to try to mimic it, we have to understand certain things and the basic foundation that a tooth is not acting like a tooth. If it has sensitivity to cold, sweet, or biting. Now, when we say that we have to be a little more sophisticated. If a tooth is sensitive to cold, when you eat a very cold ice cream or any type of cold refrigerated dish that's normal and that normal reaction to higher cold or lower cold temperatures is something that we use to evaluate the health of the pulp. And so cold testing is something that needs to be done on every tooth to determine if the pulp is vital or it has some level of inflammation. So that's the first thing we want to test with cold. And if we have a normal response it may be high normal or low normal. There is a bell curve and different people have different sensitivities in their teeth. Some people all teeth are highly sensitive to cold. Other people, they don't have any sensitivity in any of their teeth. So that's a very confounding variable the bell curve of sensitivity. But it's the best we have. But to extreme sensitivity to cold we usually associate a tooth that has a crack or a gap underneath the restoration or the crack into dentin. So this is founded on the research from Martin Brannstrom that was published in the early and mid 80s. He was a very, very prolific researcher on pulp histology, a very good friend of Charlie Cox, who passed away last year, and Martin Brannstrom was able to with some pretty sophisticated testing on vital teeth, understand exactly how the movement of purple fluid was a response to these thermal stimulus. And then he was able to show also that a cracked tooth also had an exaggerated response, and that crack in the teeth indicated that the pulp was being irritated by an opening and closing of that crack, and that opening and closing pulled ondontoblasts in and out of the tubule, and it also caused circulation of pulpal fluid. And as was later discovered and documented, actually 25 years later by Charlie Cox, that there were actually flagella off of the odontoblastic processes and these little flagella. Charlie called those nociceptors. And so the movement of the nociceptors stimulated actual nerves that were in the pulp. And then that purple fluid was the means by which the nociceptors and the nerves were communicating with each other. The next thing the Brannstrom showed was that if you have a crack, not only do you have a movement from opening and closing the gap under mask to a function, but you also would have a possibility of having a sensitivity to sweets. How does that work? Again, the theory that has been validated is that we actually have an osmotic gradient, and most of us have studied osmosis a long time ago. We have an idea that certain molecules can get through certain permeable or semi-permeable membranes, and then that can cause a different gradient of certain molecules on each side of the membrane. I mean, all that stuff that cell biologist study a lot. Here's a good example of a paper that was published that is kind of way over my head, but that's the only way you can learn things. Pulp biology, basically to master that takes four years at a PhD level, 13 pages with, about 196 references. could be a start. But again, when I talked to actual cell and pulp biologists as they understand inflammation and they understand in this, complex movement, some of it is osmotic, some of it is just a pressure, and some of it is just a mechanical movement of fluid. If there is a infection in the pulp, meaning bacteria are now being parasitized in the pulp, then that starts a cascading of certain cytokinases and the cytokinases communicate with the general immune system. That is all of our bodies 24 7 365 for as many years as we live. We're not really aware of those, but the immunologic response and having a prime or a an improved immune system, these are really hot topics for all people interested in nutrition and health. But in the teeth, we have a pretty good idea that if we don't have pain on biting, there's no crack or gap. If we don't have cold sensitivity, there's no movement, exaggerated movement of the pulp of fluid. But once we get into the infection, then that cold sensitivity and the sweet sensitivity, which is that osmotic, gradient that becomes exaggerated and all of a sudden we have a pretty good idea that we have an actual infection in the pulp from either decay or cracks. Cracks are infected. A very nice article from Doctor Ricucci from Italy was published a few years ago, showing the infected cracks and how they open about 200 microns, 200 microns or 200 thicker than bacteria. The bacteria making acids in these infected cracks do cause a decay process. It's been termed occlusal effect caries by Graeme Milicich and Tim Rainey. But these ideas of if we have what I call an easy prediction device, what we call a risk assessment for cracks and a risk assessment for decay, the inter related symptoms of cold sensitivity or exaggerated cold sensitivity, pain on biting, and then a sensitivity to sweets which is indicative of this exaggerated, response in the pulp when there's actual infection in the pulp. This 1234 system that I developed for myself, became very, very useful to evaluating these teeth that before I would just say, well, the X-ray doesn't show anything, but the first breakthrough is that question about cold sensitivity. And that was for Martin Brannstrom. And so when I read Brannstrom’s book in 1995 96, it was already 14 years old. It was published in 1982. And, I was actually introduced to brand some research from Fusayama that was introduced to Fusayama by Ray Bertolotti in 1995, and the 1993 book that Ray had at one of his seminars. I purchased it, and then, as I would always do, because I have a historical background, when I quit dentistry, I became a historian full time for six months. After seven years of getting a second major in history. But if you're a historian, you always read the footnotes first. Because if there's any ambiguity to a document's conclusions in history is always revealed in the footnotes. In other words, this is what I said, but maybe I'm not quite sure. So you have to read this and this and this and these footnotes, these references that historical documents in professional historical circles really live and die on. You know, my dad was a physicist and not a historian, but there's certain things in common with getting a PhD in physics or getting a PhD in history, and that is that you have to understand that it's an evolutionary process that builds on the shoulders of former physicist or former historians, in our case, former dentist. And whenever new information comes out, it always has to answer questions that previous publications didn't answer. And the questions usually come in the footnotes. And this is the case in Fusayama’s book. He had a question. And the question is how long is the ondontoblastic process? And, there were two schools of thought. He felt like it went five millimeters. So you got a cell body that's, eight microns in length, and all of a sudden it has a process that basically at least a thousand times longer than the cell body. So the odontoblast is in the pulp, and it's got this arm sticking off in the pulp. Fluid in the tubule. That's almost a thousand times longer than the cell body. You know, it's just like you understand these things and you go, oh my goodness, each my teeth. The reason why they're sensitive in a normal way or an abnormal way is because there's actual cells that perceive pain, just like the cells in my skin or different parts of my body, but they're structured in a very, very different way. You know, you just have to shake your head. But Fusayama is taking the scanning electron microscopy records, and he's documenting near the siege the day, I should say, the day that there are remnants of these processes that are being shut down. They get smaller and smaller as they get closer to the enamel. But, his theory was they go all the way to the deejay based on the idea that the actual mineralization of the tooth starts at that DEJ area and we got amino acid go all the way to the top of the enamel, and that's about 2 to 3mm in thickness. And then we got odontoblasts that go the opposite direction of the ameloblast. And they go down farther. They go down about 5 or 6mm. And so the processes that start growing off the cell bodies, as the cell bodies migrate, as they're producing dentin, the Donald blast process is there. Or at least a remnant of it for the whole length? Brannstrom on the other hand, when he looked at the seams, he didn't see those in the same way. And in his book in 1982, which was two years after fusion, his first book, 1980, had a different opinion. He felt like the dinosaurs thought process has got shorter and shorter, and we're only in maybe the first couple of millimeters, not the full 5 or 6mm. Well, these discussions that Fusayama mentioned in his book, and then I would read Brannstrom’s because Fusayama said this was the discussion. But Brandt's room in his book solved the problem of where dental sensitivity came from. Cracks and gaps. These are the things that give pain, just like decay, which is Fusayama’s expertise. created a response, an immune system. So we have these two experts in the 80s, one in Japan and one in Sweden, who disagree on some things. And a person like me is just like, I don't know anything. Let me, you know, let's see what they got. You read both. Then you go back and forth, back and forth. But this is how science works. And so people that don't understand the healing capability of the Pope probably won't be interested in pop biology. But every patient that you have, ones that have teeth that aren't sensitive to the sweet goal or by especially if that's a symptom that could lead to an early treatment. So the six lessons approach is early diagnosis using the 1234 method of risk assessment, look for crack into enamel. Ask about symptoms. Is the cold sensitivity present? Is the biting sensitivity present? is a sweet sensitivity present that would indicate that this crack that you're visualizing in the enamel is now past the DEJ, and is into the sensitive part of the tooth the dentin. That crack in the marginal ridge usually is always a manifestation of some kind of micro movements that has allowed the rods in the crack to separate. They can separate and stop the day. Most of them do. But there is a symptom that is shown, I should say, a sign that can be observed that, particularly in conjunction with the symptom of sweet tooth, cold or biting sensitivity, can very easily be related. And this was done again in that period when Fukuyama in 1980 and brands from 1982. Right between those two years, Larson and Douglas and guides filled the University of Minnesota published a landmark paper in 1981. They got 1980 Fusayama you got last in 1981. You got Brannstrom 82. They're all trying to figure out how much strength does a tooth need to prevent cracks and infection, and it related to the isthmus width. And the isthmus with on intact by customers could withstand 500 pounds of force before they would fracture. But if you did a GV black preparation which removed the interconnection between the cusps which are now termed sub occlusal oblique transverse ridges or Rainey ridges, after the discoverer of this anatomical structure, then those curves move in an exaggerated manner and that leads to initiation of fractures and cracks. So the fracture resistance of a tooth that had a conservative GV black preparation taught in dental school of 1.5mm, that was taught by GV black as a way to prevent decay by eliminating these groups that were prone to decay, called extension for prevention. One of GV Black's original principles. Only one problem it harmed the tooth. And so Hippocratic Oath. Hippocratic says, well, if you don't know what you're doing as a physician, at least don't do any harm. If you've hurt somebody before, don't do it again. It's like do no harm becomes pretty common sense approach to trying to fix a body if it's having problems, which many do. But as we get to this isthmus width of two millimeters. So we got one look for cracking it, and we'll ask for symptoms to look for isthmus width. Once we get past two millimeters we've lost 60% of the fracture resistance of the tooth. According to the Larsen and Mondeli’s experiments on the extracted bicuspid. The third idea of number three of measuring the cusp width, because that predicts if a cusp is at risk of fracture, a thin crust becomes dehydrated because now you have a restoration in between the cusp and the pulp. So the pulp can't hydrate the end of the cusp tip. If that happens, that person is three times as likely to fracture. And that was proved in 2007 by Vedantam and Kishen out of Singapore. And number four is the box depth. And the box depth. Probably let me know all of these ideas in the science of dental anatomy and what it's like to have a functioning tooth without symptoms. Number four is huge because once I started to investigate this area, all kinds of things became manifest that the deeper you get into shoes, the more ology and the more water you have. That gives it flexibility. That's a good thing, except if you're trying to do restorative cohesively. The more college in the more water, the less bond able that two structure is. So as soon as you get four millimeters deep towards the siege, you have all kinds of problems that have to be addressed as far as the sophistication of your restoration, these sub gingival areas. If he's silly, I wish it was simpler, but this works if you understand that the 1234 risk assessment for fracture and decay gives you the ability to make an early diagnosis of a tooth and treat it early and early treatments are easier, less time consuming. They'll cost the patient less. But if the patient is in a proactive first and just says, well, I don't get my tires changed in my car until I have one blowout, you know, that's one philosophy on driving a car, but it's a little risky. Most people will go and have their tires checked, and when they get low and Fred, then they'll say, okay, time to get a new set of tires. I would like to be under control. And I'm driving my car in water or snow anyway. So the 123, four risk assessment, these are the the foundations of the six lessons approach, early diagnosis and early treatment of teeth that are at risk for fracture and decay. Usually, once you start treating a tooth that is at risk, you'll see the vast majority of time there. The processes are already in progress and so early crack removal much easier than late crack removal. Early decay removal, much easier than late removal. And the exciting thing that we didn't know 20 years ago is that if you get trained in the lesson for stress reduction, you have a permanent bond. They don't break down ever. In other words, Bob Paxton, my neighbor, lives two blocks away. I trained them 18 years ago. He's done 10,000 by all bases, never has had recurrent decay underneath a bio base because the tooth doesn't have a gap, there's no cracks, and all of a sudden you have a hybrid layer that's acting like a natural tooth, which is what biomimetics means. Mimic the natural tooth. All right. Thanks for letting me talk with you. And until next time, get bonded, stay bonded.