Best Practices to Avoid and Treat Pulp Exposures

Dr. David Alleman’s landmark paper written with Dr. Pascal Magne in 2012 gave practitioners predictable steps for deep caries, and now crack, treatment without exposing the pulp. But why is preventing pulp exposures so important? Dr. Alleman discusses research about the outcomes of pulp exposures and their effect on the tooth long-term in addition to proven treatment for teeth that have had exposed pulps.

Adhesive dentistry offers these teeth a second chance, but only when the seal is bonded at the nanometer level, like with biomimetic dentistry. Just like each step in the Six Lessons Approach to Biomimetic Dentistry, the protocols for treating pulp exposures offer predictable results and protect the tooth’s long-term vitality.

Article referenced in this episode:

• Thompson T., Et al. Treatment of deep carious lesions by complete excavation or partial removal. JADA. 2008;139:705-712.
• Hafez A., Et al. An in vivo evaluation of hemorrhage control using sodium hypochlorite and direct capping with a one- or two-component adhesive system in exposed nonhuman primate pulps. Quintessence Int. 2002 Apr;33(4):261-72. 

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Transcript

0:33

All right. Welcome to episode six of season two of the Six Lessons podcast. Today we're going to talk about pulp exposure. The first two lessons of the six lessons gives you a technique to avoid pulp exposures by only going deep in the peripheral zone, but by stopping at certain levels of five millimeters from your occlusal surface and three millimeters horizontally from the contact of a neighboring tooth. We stop and we create what's called a central stop zone, where we don't go deeper than that to prevent a pulp exposure. Why is it so important to prevent a pulp exposure? A paper by Van Thompson and his team in 2008 was a meta analysis of all direct pulp cap studies and indirect pulp studies that have been carried on long term. So exposing pulps have been happening ever since dentists tried to restore teeth for 200 years. Once a pulp is exposed. It responds with certain biologic responses. But of course, those biologic responses were not known in the days of early dentistry in the 1700s or 1800s. But the end of the 1800s. It was understood that the inflammation, infection and even fatal diseases came from germs. So germ theory of Louis Pasteur and the understanding of diseases by Koch and his postulates understood that infectious disease and these microbe were very related. And then, continuing on in 30 years, we found out that there are things smaller than bacteria, these viruses that were unfiltered, able, in early techniques, trying to find infectious agents. These viruses were so small that completely new technologies need to be developed. And those really came to fruition in the 1950s, 60s. everything rotated around the discovery of DNA. Nobel prizes were given to three men. Rosalind Franklin did not receive it. She died of cancer tragically before she should have received a Nobel Prize. But the ideas of DNA and analysis on this molecular structure of biochemistry, this added to the idea of how do the individuals respond to infections from viruses, from bacteria. And the whole connection of the immune response. It's in our body that we take for granted every day. That keeps us alive by screening for potentially cancerous cells, eliminating the viruses and bacteria. it's a miracle that we're alive. But we need to understand as dentists, we are not in an art guessing about these things anymore. We're actually in a science, and that science can tell us things about how the human tissues respond to these assaults. And in dentistry, the major assault is decay, a fracture or an iatrogenic exposure of the pulp with a birth. And the studies on this showed and Van Thompson and his team out of NYU did this meta analysis when they evaluated all the studies from the 50s and 60s about exposing pulps and how that was followed up into the 2000s. In even some cases, they found out across the board an indirect pulp cap technique where all the K was not removed was always more successful than a complete. caries removal, where the pulp was exposed. The histologic studies show that the exposure to the pulp projected infected bits of dentin into the pulp, and these little projectiles increase the inflammatory response greatly, and that contributed to the death of the pulp mill tissue. And so, as direct pulp caps become less valid based on science, the scientific approach is always now, and it continues to be that direct pulp caps are contraindicated, that direct pulp exposure through complete carries removal is contraindicated. Now, that doesn't mean that the pulp is not infected. The pulp is infected once the bacterial decay process goes one millimeter past the edge. The difference between the DEJ and the pulp is usually 4 to 5mm. Now, if you have to go 4 or 5mm and you're a one millimeter bacteria that doesn't have a flagella, then all of a sudden it's like swimming up the Mississippi River. It's a long ways. But if you have enough energy, you can swim up the Mississippi River. It just takes time. But these initial bacteria that are in the tubules that are going upstream and trying to move towards the pulp, or maybe they're not trying, but they do. They're replicating their way into the pulp. And eventually we get what are called pioneer infections. These pioneer infections are just 1 or 2 or 10 or 100 bacteria that have a massive infection near the deejay, but the pulp is now getting bacteria and having to respond to these individual or groups. Small groups of bacteria. And what do they do? The pulp does what all connective tissue does. If it senses bacteria, it starts a cascading of an immune response. Some of those are called cytokinesis. But mainly it's a phagocytosis mediated neutralization of the bacteria. In other words, white blood cells. Phagocytes are looking for bacteria. They're in the bloodstream all the time. Once they find one and start eating up 5 or 10 bacteria, they release biochemicals that go into the bloodstream that say, hey, we got a problem here, come give us some help. And so they elicit new phagocytes, new white blood cells. They accumulate and try to get into this area where the infection is on the skin. It's very easy because you would have the ability to swell up and have a lot of white blood cells that sometimes that's called an abscess or skin abscess. But in a pulp these connective tissues are constricted, they cannot swell, they can't accommodate more white blood cells coming in. They can't accommodate the increased the plasma that carries the messenger chemicals and carries actual chemicals to fight the infection and fight the inflammatory response. And so the pulp is at a disadvantage because it cannot swell. One of the classic characteristics of an infection documented by Galen 400 BC was that you have heat and swelling, and it turns red. That's how he described the first infective processes. He knew nothing about cells. He knew nothing about this immune system in any type of detail. But it is an observation that has been having, whenever a human being comes in contact with bacteria, which has been forever, because bacteria have been here longer than us. But anyway, the conclusion the Van Thompson, highly respected researcher ahead of a group that was given$7 million by the United States government in the Pearl network to get some advances in clinical practice in actual dentists. Van Thompson, I'm in his office. I'm talking about this article of 2008 in detail, and we agreed the conclusion of the science is complete. caries removal is contraindicated. Why is that? Because complete removal will increase the number of pulp exposures by 300%, and that directly relates to the number of pulp deaths that we result after. An indirect or indirect pulp cap happens. And the take home message is that if you do expose pulps, you are 300% more likely to do harm to the pulp to have the pulp die. The basic principle of the Hippocratic Oath is do no harm. Well, if you don't know that it's harmful, it's hard not to do it. But once you know what harms something, you shouldn't do it. And we know that direct pulp caps harm. And we also know that exposing Odontoblasts close to the pulp requires a healing process of the DNA blasts that generates a secondary dentin, and that's part of the immune response to fight decay and fracture in teeth. And it delays the problem. But it usually has some infections that are too strong and the pulps die. Some cracks that are too severe that lead to infection in the pulp die. And once that happens, the teeth usually are lost with or without the aid of a dentist. An infected tooth will eventually abscess and then have to be relieved. Usually the dentist can make the process go faster. And so when we talk about this exposure and the science, it says don't expose pulps. But what if you do. So we've been training dentists clinically for over 20 years. We teach them a measuring technique, but they are clinicians. They're not perfect. The measurement technique relies on visualization. Visualization is often altered by the angle that you're looking at a probe. For example, to decide how deep you are into a cavity, which was the innovation that I made on how to prevent pulp exposures by measuring how deep you are and stopping a millimeter before you would hit the pulp. Well, when I train 500 dentist, each of those dentists have a learning curve and each of them will expose some pulps So the question is, what do you do when you expose a pulp? There are two philosophies, and one philosophy is that you bond to the pulp and let that pulp heal. And that philosophy was pioneered by Charlie Cox, and his team and other researchers around the world that did direct pulp caps with adhesive systems on non-human primates. And we had mammalian studies on beagles. We had non-human primate studies on monkeys, but they all showed that a pulp has the ability to repair without a liner or without a base. Every line or every base responded the same as a layer of adhesive. Layer of adhesive has chemicals. Every liner has chemicals, every base has chemicals. But how we respond and what, the pulp is doing, there are some ended honest that say a pulp bottom of removing the most infected areas of tissue, is desirable, but that still requires then a step to stop the bleeding after the surgical incision. And then we have the problem of stain bonded. If we don't keep the seal, then the reinfection into this area of the pulp bottom is the determining factor, whether the pulp bottom is effective or not. doctor Ricucci in Italy, Arthur Duncan at Trinity University in Ireland have long term cases of successful pulp barmy, but it takes time, and the amount of cost and the amount of time it takes means that it's a different procedure. Our procedure of an indirect pulp cap, which has been the most tested, way to deal with these partially infected pulps, has the advantages of not having to stop the bleeding. But if you have a small area of bleeding with a small exposure, then that small area of pulp exposure is infected. But the treatment that's most important is to stop any of those bacteria from continuing to have, a food source. And so there needs to be a seal established. And this is where adhesive dentistry makes the difference between mechanical approaches of direct and indirect pulp caps. If we have great success with an indirect pulp cap with mechanical restorations, now we see that adhesive restorations can give us almost 100% success in allowing those pulp to heal, because now we're sealing and we're decreasing the micro movements of the restoration, which decreases the chance of bacteria coming underneath a gap in a restoration. And so what we recommend is based on a paper that was published by Charlie Cox and his team at UCLA, and this paper that was published in 2002 summarizes many, many, many principles. But the basic principle is stop the bleeding first. If you have bleeding going into your bonding field. And that will, decrease your bond strength. So you have to stop the bleeding. How do you stop the bleeding? The recommendation is using an epinephrine solution from lighter cane. Lidocaine comes in two standard dilutions, But the stronger epinephrine of 1 to 50,000 will have the ability to stop these capillary bleeds that have come from the the pulp exposure. So a 1 to 50,000 epinephrine in light cane on a cotton pellet placed on the exposure will stop the bleeding almost every time. If the exposure is larger and the inflammation of the pulp is greater, the bleeding will be very aggressive. And to stop that, you'll need a stronger shutting down or coagulation of the capillaries. And this will come by putting bleach diluted. If you put straight bleach, it will destroy the proteins in the capillaries and will bleed more. But if you have a little bit of coagulation of the capillaries or bleeding, then it will shut those down. And so you have a 50% mixture of bleach and water. We use distilled water, but regular water would be fine I'm sure. But that mixture will stop the bleeding. In a situation where it's even more infected and more bleeding. There is a technique that I learned from Ray a lot of years ago, and that's putting super so on a very inflamed pulp. I haven't taught that, but I have done that. And in these situations where I had large pulp exposures, the bleeding stops immediately. But the superoxide is a concentrated oxygen solution. And so that decreases your bond because it inhibits the polymerization. So you have to actually use super oxygen and then rinse that very well. The pulp will turn white and you will see that but I have many successful direct pulp gaps like that. Before I figured out how to not expose the pulp through measurement. Anyway, those through techniques that I've used over the years, a fourth technique is just waiting. if a capillary is injured and bleeding occurs, there are platelets that are released, platelets are very sticky and platelets tend to accumulate in the area where the bleeding has happened and they eventually become a plug. It just takes time. The body doesn't want to have these platelets active too much, too fast, for too long, or else you can create clots. And so if you just wait, you also will get a stopping of bleeding. But it takes patience. Sometimes it takes ten 20 minutes to have that happen. But if you have this exposure and now you've got the bleeding stopped, now this is the critical step in the six lessons approach we always feel and based on science, know that a self etching system will be the strongest bond in these areas that are hydro filling, or these areas that are high percentage of water. The deeper you get to the pulp, the more water there is, in a total etch approach. If you totally etch, then you remove all the hydroxyapatite and all of a sudden you have an increase of purple fluid. So not only you're dealing with bleeding, but now you're dealing with too much pulp fluid. And so the self etch approach is this cover. The bleeding was something that will not be removed where air abrasion doesn't have to be sophisticated. A little drop of glass eye on there, a little drop of unwanted composite that's cured. You could put MTA that's the most expensive approach. You could make your own mBTA with Portland cement. That was Ray Bertolotti’s way to save money on MTA Many entertainers use MTA in these situations. It's a highly basic solution. It kills bacteria because bacteria hate high. They love low. pH is bacteria love acid. Remember, the causes of stomach ulcer are bacteria because the acid in the stomach doesn't bother them at all. But the idea of MTA being basic, that's a that's a good piece of principles of science that many entertainers recommend. But but we recommend just cover that exposure for long enough to er abrade that er abrasion will compact your smear layer, stop the, the tubule from leakage so much because you have smeared layer plugs in each orifice of each tubule, and those orifices are three times as big near the pulp as they are, near the edge. They get smaller as they go towards the DEJ more mineralization. And so when you have this cell filter approach, you cover the exposure. You get er abrade to reduce the smear layer and to put the plugs into the tubules. And then you rinse that and quite often at that rinsing the glass ionomer or the unbonded flow will just, be sucked up and you'll see that the bleeding has stopped, the bleeding hasn't stopped. Do it again, or go to the more aggressive forms to shut down the the capillaries. But once you have that er abraded area now your steps are just the same as the standard protocols where you would prime. But also in that primer you would have something to deactivate the MMPs which is available in SE protect probably will be available in other body systems soon because the patent has expired on SE protect. But if you don't have SE protect with MDPB monomer then you deactivate the MP. Just a 32nd application of chlorhexidine in ethanol. consensus by ultra then is the product we've used the longest. Bisco makes a product many products around the world. Just straight chlorhexidine with ethanol. You don't want to use a chlorhexidine that has any soap in it, or any flavoring or any, abrasive particles like concepts of scrub. You wouldn't want to use that. You just want to use straight can substance from ultra dent. But once you've deactivated DMPs, now you're ready to start your hybrid later development with your primer 20s evaporate your solution. Your solvent, which is water in the SE protect bonding system. And then after that, then you place your adhesive light, cure your adhesive, and then after, like your adhesive, then you would place your half millimeter of resin coating like cure that. And now you're in a situation where the bleeding has stopped. Now the healing of the pulp is going to be mediated by the immune response. And way over 90% of the time you'll have total success. And this is the approach of the six lessons. If you do expose the pulp. But like Davey always says, if you expose the pulp, don't tell your dad. I mean, that's a joke. But in private practice, when I was in private practice, in developing these systems, for the first seven years and then teaching those for another, four years, I monitored and in my practice, it was about one tooth a year would go to endo from teeth that had deep decay or an exposure. And so, you know, if I was treating 3 or 400 teeth a year, one twice a year, it's very, very much less than 1% in these deep areas of decay or exposures, from iatrogenic, treatment. So with that, episode six is in the can. We will see you next time for episode seven season two. Get bonded. Stay bonded. Always great talking to you.