Understanding the Third Most Common Dental Pathology

Cracks are the third most common dental pathology dentists treat, but treating them in a predictable way requires an understanding of principles from engineering, histology and immunology. How do cracks in teeth form? Why do cracks in teeth cause infection? How can we treat cracks predictably and prevent root canal therapy? In this episode Dr. David Alleman discusses his research process for crack treatment and the results he has seen in his practice for over 20 years.

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Transcript

0:33

So we are ready for the second episode of lesson two. Last time we talked about how failures happen, how they're related to stresses and infections underneath restorations, and even in teeth that do not have restorations. But the idea of treating a tooth as a material is kind of new idea, a new idea for dentists, dentists, you know, you don't know anything about teeth. You know, you kind of figure out that teeth are connected to a body. So you kind of know that that dental school, you'll be talking about histology, you'll be talking about the idea that there's health in a body or there's disease in a body, and you'll have a general understanding of medical terms and a general understanding of pathology. But the pathology of dentistry is fairly limited and fairly simple. Pathologies that we have, although there's not 35,000 pathologies, there's basically 3 or 4 that we see regularly. The most common pathology is decay bacterially mediated decay. Then the second most common pathology is a bacterial infection around the teeth themselves into the supporting tissue. And that's called periodontal infection. Again bacterially mediated. The third most common cause of tooth loss is actually fracture of tooth structure. And the fourth word would be neoplasms. Cancers that can obviously cause jaws to be lost and teeth to be lost. And then the fifth is trauma. But you know, five is just something we should be able to wrap our mind around. But as I evaluated my failures in 17 years, I had very few teeth loss from cancer, very fewer teeth loss from trauma, a few teeth loss from periodontal conditions which have been improved the United States over the last 50 years tremendously by brushing and flossing. You know, it's like if you don't brush and floss, then bad things happen.

But the last two: 2:43

decay I was familiar with but cracks. I had no foundation. But when I bought my microscope in the year 2000 January, I started seeing things that I understood were fractures that were not complete. So a partial fracture of a tooth was something that I was seeing and visualizing for the first time is kind of analogous to the first time, five years before or three years before 1997. I could really visualize different areas and different degrees of decay with this caries detecting dye that could stain red or pink, or three shades of red and three shades of pink. That's what the science says. There's six shades of red, but the idea is that we have the ability to classify decay with caries detecting dye. Now, when I started visualizing the cracks, to me it was very obvious that the cracks were going in different directions and a fracture that would go horizontally or vertically might take half of the tooth out, but a crack that went vertically and not obliquely or horizontally, that was the one that could go down a root and you'd lose a tooth out. And I had many teeth that were lost with that kind of fracture and a catastrophic end, that the tooth is lost. I read in textbooks about crack management. It's what I learned in dental school. You should put full coverage on a cracked tooth that had symptoms of pain on biting. So I did that, of course. Yeah, for 17 years. And then I'd have patients who would come in and the crown was in their hand, and part of the tooth was inside the crown. And I would look at it and I would say, wow, you must have really bitten something hard to break that crown off. And now you've lost part of your tooth structure. Sometimes you could rebuild those teeth, sometimes you couldn't. But I had no idea that the endpoint of the crack propagation, which was the fracture of the two structure, had a beginning, probably years, maybe even decades earlier, because I didn't know the cracks started at the molecular level, and then they increased in size to the millimeter level. And finally forces a tooth can be breaking off. And that whole process had an engineering name crack initiation, crack propagation, and a catastrophic failure as I was introduced or ask questions of my friends who were engineers, I would always ask them so tell me what you know about cracks, and they would talk for an hour. Wow, I didn't know you could talk for an hour on a crack. And they said, yeah, you can write a textbook on cracks. And so you have any you have any chapters? And I got a few engineering books, a few material books, and it have a chapter on cracks. And all of a sudden you get into nanometers and even angstroms to understand how atoms hang together until they're forced apart. It takes a lot of stress to force apart a molecule, and those splitting a molecule takes energy. And so these engineers would talk a lot about energy. And then the energy I got to see, you know, a tooth situation is created by muscles. And so you can bite soft or you can bite hard. And if you bite hard it's because your brain is telling their masseter muscles, and your temporalis muscles and your pterygoid muscles to put more force on because you need them to bite or to crush some kind of food. And most of that is totally subconscious. We just eat our apple or eat our hamburger or donut. Doesn't take much to eat a donut, I know that, but the idea is that you start thinking about this idea of stress and forces and muscles, and all of a sudden the engineers of say you understand the idea of stress. Okay, but now they introduce a new word to you, and that word is strain. In a technical term, if you put force on a material. So this is the force, okay. If you put force on the material and the material doesn't move, then the force is stored up in the area that's trying to move this immovable object. But most objects have, a limit of how stable they can be. So when you put a force in, if the object moves, that's called strain. Now, if you have a connection and the force is going the other way, then when the force is going the other way, if it strains, it's moving in the other direction. But it's the same idea. Forces of pushing or pulling causes movement in the material. And that's called strain. And so the understanding of the relationship of stress and strain was finally standardized in a mathematical, way in the 1800s. And in the 1800s, a doctor Young, had the ability to make a curve. It's called a Young's curve. It can also be called a stress strain. Curve can also be called a elastic curve. And the term is modulus of elasticity. And every material that's ever been studied that would be called a material is elastic. Now this is a book. Everybody knows a book okay. Usually don't consider a book elastic. What does it mean if a material is elastic what it means. So I'm going to put the stress here. You're going to see strain movement. Everybody see the movement of the cover okay. So this is stress being foot by my fingers I'm stressing that lift. And now it's moving. And it's that's called strain. And that can be measured. And when I let go guess what. It goes back to its original shape. And so that's called elasticity. If you push on something and that force causes the strain when you let go of the force, the force is gone and it goes back to the same position. That's called an elastic material. So a steel plate is elastic because if you push on steel hard enough, it will strain. But when you let go it goes back to the same position. Now if you have something that's not elastic, you can have a material that's not elastic like Play-Doh. So if I push, I've got a flat piece of Play-Doh and I push, the Play-Doh is straining, but when I take away the force, it's deformed. So this material is called ductile or plastic. So a plastic material and a ductile material is kind of similar, but Play-Doh has no elastic modulus. The confusing part in engineering is that quite often you have materials that are composite. Composite means something is made of a lot of different elements. In dentistry, we talk about composite that have a resin matrix and have filler particles. Those filler particles can be big and small, made out different materials, the resin matrix and be a little different. So that's the composites that we work with. And restorative dentistry. But once you put the light on the composite, the composite changes from a deformable ductile material into a very stiff material that has a very consistent modulus of elasticity. Now this composite, as the light is cured, you push on it, it can deform, but it always comes back, always comes back until you push. So far then you have a failure of the modulus of elasticity. And that happens at a certain force. It can be measured. And then at that time the deformity now makes that material very different. And that's usually called a brittle material. Then a brittle material could be something like a ceramic dish. Ceramic dish does not deform very much, but it has a little bit of deformity before it breaks. And so it's good for a dish that you drop on the floor. It doesn't hardly ever break. But actually you can have an accumulation of energy just from the jarring. And the molecules in there are never quite back in the same place in that ceramic dish. And then when you drop at the hundredth time or the thousandth time, there's just enough energy to exceed the elastic limit. And then you have a piece of ceramic that breaks or glass or breaks into a thousand pieces, things like that. But there is an overlap between a brittle material and elastic material. An elastic material can have a modulus of elasticity that has a limit that is higher or lower than another material that would be considered brittle like enamel. So enamel, when you push on enamel always goes back. We've measured the amount of strain in two structure under an average biting force of 40 pounds. So this is a cusp. This is a cusp. Here's a central groove. area okay. You're going to bite on something. It's going to move. And what happens is the tooth expands slightly. How much is a tooth expand seven microns. Now a micron as we talked last time is 1/500 the thickness of your fingernail. So if you took 100th of the thickness of your fingernail and you distributed over nine millimeters of a molar, it's not moving very much. But on an atomic level, on the molecular level, you can measure it and then you measure it. When the force of biting goes away and the strain goes away. So teeth are constantly doing this and this and this for 100 years. They can do this, this, this, this, this and that. Seven micron is a shifting of the actual material that's in mostly the enamel or the rods slide a little bit apart and then come back to the other slide apart. And it's there's no gaps in the tooth, but there's just a little bit of expansion comes back. And so the outside and that's the brittle material enamel after thousands and millions and millions of chews, then these little rods that have been shifting over and over again, they can fracture and they can separate and there can be a crack in the enamel, and that crack in the enamel is usually going to expand. Maybe double. You're probably going to be now having an opening of about 14 microns, then coming back, opening and closing in the crack. So there's seven in the crack and there's seven in the whole tooth. So you've got about 14 microns, but only seven in the crack of enamel. And guess what? That seven is enough to get some bacteria in there. But usually there's not enough layers of bacteria. There's not enough numbers of bacteria to cause enough acid to be produced to cause a cavity formation and a crack of enamel, but it's wide enough, and there's enough bacteria to get a little staining because stains from food are on a molecular level, not on a level of the size of Omicron. And so they're on the nanometer or even, you know, multiple angstroms when you talk about, a molecule of a stain that would make a food dark like Coca-Cola. And so you can have staining and cracks and have no effect. And then these cracks in enamel, they can stop and usually do stop at a failsafe mechanism that's in a tooth is called the dental enamel junction, or also referred to as a dental enamel complex. And the width of that connection between the enamel, which is a brittle material. Then, then that is about 100 to even 200 microns in thickness. So the invaginations of Dentin and the invaginations of enamel in that DEJ are very visible in the naked eye. The naked eye can see 200 microns. I mean, a piece of hair that's thin, like white is about 100 microns. You got black hair is probably thicker. Around 200 microns are very visible, the thickness of a hair. And so even without a microscope, you can see this dentino-enamel junction very clearly. And you can actually visualize cracks that stop there. But under microscopes and you see exactly the mechanism of the opening and closing of these cracks and the expansion of teeth that has been measured in analysis that are called finite elemental analysis and strain gauge analysis, that are engineering the mechanisms that have been used to measure stress and strain for almost 100 years. So what we have is we have a brittle material that is prone to more catastrophic fractures, but we still have an elastic material that doesn't fracture very often. But once you get that crack past this crack deflector crack stopper called the DEJ., and it gets into dentin, then the modulus of elasticity is lower. If the modulus elasticity to then is lower, that just means that once that crack gets in and then we can have a lot more movement. And we have a potential to have crack propagation, but we don't have much crack stopping ability. And then although we have enough to make it not happen 100% of the time for sure. But this idea of measuring and looking at cracks into dent and how they operate and looking at them in a engineering point of view helps a lot. If we have scanning electron microscopy that gives us views in these areas that are seven or 8 or 10 microns, we really don't need the nano meter evaluation like we do on bonding. And so we don't need what's called transmission in electron microscopy. But with scanning electron microscopy we can see cracks and we can see bacteria and the cracks are 100% infected. Now that 100% infection of the body is recognized by the sensory mechanisms in the body, because the pulp has sensory connections and they are in the odontoblastic tubules. So everybody's learned about odontoblastic tubules. Everybody knows that you have a odontoblast. Maybe it's five microns in the body. Is there large cells. But then they have these processes that can go five six millimeters and so you have a five micron cell that has the ability to put out an arm that is not a hundred times bigger, but a thousand times bigger and even 5000 times longer than the width of the body. But the idea is that having an arm that can stretch, that's called a process on the cellular level, and these processes that give the life to the dentin they give the hydration to the dentin. That's where pulp of fluid hydrates the dentin to 20% of its mass by weight. These processes have little flagella, and the flagella are called nociceptors. Nociception just means pain, feeler of pain. Nociception in Latin, I'm not a Latinist, but Charlie Cox, who taught me about nociceptors, knew more Latin than I did, so I always deferred to his mastery. But Charlie Cox, when he wrote about the nociceptors, I've never met a dentist that I haven't trained that even heard the word nociceptors. Oh, well, you know, how do you learn? You get somebody who has a team and sees them and then communicates with others students and finds the master of all masters, Doctor Brannstrom from Sweden. Martin Brannstrom wrote a book in 1982. Charlie Cox knew him until his death, and Charlie Cox died last year. And so the knowledge of the hydrodynamic source of pain, which 40 years ago was called the hydrodynamic theory of pain, ended on us, learned about a general dentist usually did not, but the idea is that we actually know how the pulp, which is connective tissue, and in histology we learn the connective tissue always has blood vessels and always has nerves and has some fibroblasts, and it has some moisture and it has some ability to receive chemical signals that would correspond to an excitement of the immune system response to infection. You know, the whole idea of studying connective tissue, it takes a PhD to learn all of the different elements of what's called cytokine cascade. I mean, it sounds pretty impressive when I say cytokines cascade, and I'm not reading it off a teleprompter. Right. But the people that taught me about cytokines cascade, they they knew stuff, you know, I mean, I'm just trying to pass an immunology class that BYU in microbiology, but it gives you a start of an appreciation for the complexity of any part of the human body and connective tissue. Is it every part? As it says, it connects bones to muscles. It connects organs to the framework that is supporting the organs in the musculoskeletal network. But this connective tissue stuff is really good if you have a trauma, even an amputation or infection, because these bodies have the ability to swell up. They're not constricted by a hard exoskeleton. So they have the ability to have inflammation without causing much tissue necrosis. But the connective tissue in a pulp has a problem. It's constrained by a hard shell. It can't swell. So swelling was identified by Galen Way before the birth of Christ, as part of the inflammatory process that sicknesses or injuries, the part. And so this idea of rubor tumor these are again Latin words two more means it gets big a tumor. But the swelling part of inflammation can't happen inside a pulp. And so these different chemicals that are used to heal actually if they're too great of concentration concentrations start to degrade other tissues. And the response causes tissue necrosis. And that would be called pulp death or a dead pulp. But the question that I had when I was trying to make my better dentistry better was how much of the inflammatory response, which I had a pretty basic knowledge of, can be used in the pulp to heal instead of heal itself? When you get these massive infections of bacteria into the pulp through cracks or through decay. And I found out that nobody had the answer. Nobody knew if one bacteria is going to kill a pulp, or 10 or 100 or 1000 or 10,000, the idea is the more infection, the worse, because a greater inflammatory response. But that's a theory and theories are great. But you have to kind of figure out is that theory good or does it have any use or, you know, what does it mean? And so as I investigate and read all the endodontic literature that I had at University Pacific, it was considered the leading dental school in endodontic treatment in the 1975 1978 period. When I went to dental school, my endodontic teacher, Steve Cohen, and his associate of the faculty, William Burns, now wrote the book called pathways to the pulp, and the best and brightest in our class became ended honest like Steve Buchanan. But I was average. I was in the middle of the class, so I didn't have to worry about specializing or reforming the treatment of endodontic procedures like Steve Buchanan had to do, because there were problems with the protocols that ended. I'm sad, but under Steve understood infection. Steve understood what was going on, and I invented and started teaching the six lessons. I had lunch with him. He came to give an ended on a lecture training in Salt Lake. We had lunch. I explain the, the philosophy of advanced adhesive dentistry and allowing pulps to heal by sealing them early as possible in the infective process, which began as soon as you have a lesion that's a half millimeter acid. There are bacteria in the pulp. The pulp might be sensitive and have a little inflammation, but not enough to kill the pulp. And so these pioneer bacteria that every ended on as new were in the pulp. They had the idea that it could heal. Just nobody knew how to make a diagnosis of a reversible pulpitis versus an irreversible pulpitis. But even to this day, there is not a reproducible diagnosis like there is and caries with outer caries, is highly infected and has collagen in that has been denatured through the process of MMP activation and inner caries, which has the collagen totally in place, but de mineralization, which makes it a little more difficult to treat with advanced adhesive dentistry. I mean, these are I'm getting off the subject. There will be for the next the lecture that we will record for the season two. But as I explain these things to Steve Buchanan and I had been introduced to the microscopes two years earlier in an endo course that I'd taken from Steve at the Ohio State University. And then when I had lunch with him, 2003, then had been teaching the six lessons since that time. His conclusion was, gee, Dave, you're going to prevent a lot of endo it’s like, he's an endodontist. He makes his living, you know, doing root canals, but he said with this technique. You're going to prevent a lot of root canals. And he just said, that's great. I mean, he's over worked. There's not they're not going to be a shortage of dead pulps from traditional dental treatments in anybody's lifetime. Who's ever going to listen to this lecture? But the idea of prevention is so appealing to a patient because nobody lines up to get root canals. Intrinsically, people are born to hate the idea. You need a root canal. That's my theory. But that being said, how far could you go in preventing root canals in these different degrees of infection? Nobody knew. Even to this day, nobody knows. But in my practice, I've been able to basically have success and well over 90% of the teeth that traditionally would have been diagnosed with an irreversible papyrus. Meaning when you put cold on a tooth, you feel it for maybe 30s. I mean, that's a bad response, and that's why the patient came to the dentist every time you. I'm cold, this tooth hurts. And then the dentist would maybe do a filling and then still have sensitivity cold. Or now it's even worse is pain on biting. And then it's like, oh, what's the next step? And then quite often it went to root canal treatment which would take away the pain short term, but now create a whole new level of structural compromises in the tooth, with or without cracks that, if not diagnose, could be fatal to the tooth or at least require a retreatment. And so, as I came to these conclusions, discuss them with the best people I knew, like Steve Buchanan, is like I would give the patients the truth that I had. We believe that these techniques of sealing out bacteria allow the pulp to heal, but on a tooth, most patients will say, you know, I'm going to give this to the chance to heal. Let's give this connective tissue inside the tooth that really has an important, vital purpose of keeping the tooth flexible and keeping the tooth in a situation where it won't break. And so I feel like I want to try to save this tooth. So when I started to do this 25 years ago, based on using carries, detecting dye and adhesive, dentistry and basic stress reduction protocols, I started to have immediate improvement of symptoms no matter what the cold response was. But I found over the years, the five years that I was beta testing, that the less the cold response, the more chance that that tooth had of probably going to die because probably part of the pulp was dead. And that's why the response wasn't great. If we had more pulp tissue that was healthy, the chances are you would have a greater response to cold if you had low sensitivity cold, which sometimes you can test all the teeth in a patient's mouth and they won't feel cold on any of the teeth. But you're not going to recommend doing root canals on all the teeth, but you have percussion symptoms and signs of periapical lesions. But if you have no spontaneous pain, then you have no period lesions. Then all of a sudden you're saying, from what I can see, the pulp is still alive because I put cold on it, it's responding. We're going to give it a chance to heal. And on that basis, basically I have never in 27 years had a patient say, just do the root canal. But the idea is that there is a reason to avoid root canals and it's healthier for a patient. They have feedback mechanism with teeth that have pulse, whereas if you take the pulp out, all of a sudden the patient will not know if there's recurring decay. It will take them longer to know if they have a crack because the pulp could not respond and tell the patient that they have this hydrodynamic source of pain. They will have to wait until the crack goes into the PDL, which is another three millimeters away, and by that time it's into the root and the chances of catastrophic failure are greatly increased. So the, you know, clarion call, the early diagnosis is in treatment of cracks that I've been trying to put out to the profession for over 20 years. And, there are other people who have written important papers on cracks. And two of the papers that we found, I actually had a one, a clinical trial of cracked dissection, which is our preferred mode. And it's the only predictable mode that I've ever come across or treated. And another paper who suggested that that was the preferred and that came out of a private practice, interestingly enough. But we just found out about that paper last year, that of a private practitioner in new Jersey. But as we're putting the pieces together and just saying this is what we've been doing, what have you been doing? This has been the best collection of data we have. And if you don't agree with us, well, what can I say? You know, sometimes science comes from outside of a university. Actually, quite often it does. But the universities have what's called the standard science and then innovative science that causes what's called a paradigm shift, which was Thomas Kuhn's suggestion years ago. Now, these paradigm shifts, once they're made, then people who understand them don't go back where people who partially understand them and partially believe them, they're on the fence, and they can't benefit humanity by going in the right direction with new science such as immunology or new science, such as bacteriology. I mean, you know, in 1880, GV Black was going out on a limb to say that we need to worry about these microscopic bugs that only, you know, three years ago were proven by Koch’s postulates to be the source of infectious diseases. I mean, the whole history of microbiology immunology is very, very interesting. I hope you all enjoy reading it as much as I have, but even more as a dentist, we have a responsibility to keep the connective tissue free of bacteria and allow the pulse to heal. And that's the message of the episode. Two of season two. Till next time, get bonded. Stay bonded.