25: types of caries saliva and caries

Transcribed by Erica Manion September 3rd, 2014

Diagnosis and Treatment of Oral Diseases-- Lecture #25 – Saliva and Caries by Dr. Wolff

[1] – [Title Slide: Caries, Plaque and Saliva][Dr. Wolff] – Are we there? Ok, so we are going to spend some time together now! [student: sarcastic “yaaaay”] [Dr. Wolff] – I told you the hearing’s not gone yet. The memory is fading quick but the hearing is not. You can hope by the time you’re a senior I forget what you look like! That’s ok ehhh it’s too late, you’re too distinctive! Uh, so this is actually the area I got my, I received my PhD and was studying saliva and its relation to tooth decay. I get really excited about it so I presume that you folks will get excited too. Or not. And that’s ok. Did enough people show up that I post the… [slides]? Yes? We’ll post the slides in a few minutes to the class so you can have the PDF of it. So caries plaque and saliva, as it turns out…

[2] – [What is a Biofim?]…the theory about what caused caries has changed over the years in multiple, multiple ways. At one point it was very clear that the tooth worm was eating the outside of the tooth. Everybody knew it. Then everybody knew that as food rotted, the acids of the food rot would eventually break down the tooth and cause tooth decay. And it was a rich, famous person that actually proved that it was the consumption of carbohydrate that releases the acid that causes bacteria to release acids that dissolve the teeth. It was Miller, 1890. That’s an important step, if I knew anything on an examination, that would be one of the things that I would keep tucked in the back of my head. So Miller showed that it was the release of those acids after exposure to carbohydrates that caused this. Now after that, everybody pursued what bacteria were creating the acids. Miller actually got it wrong, he thought it was lactic acid produced by lactobacillus, and yes, lactobacillus produces lactic acid and it does dissolve the tooth. But it turned out, well actually, some of the best scientists did a really neat experiment. If we take a, if we take a little swab of plaque and throw it on a plate and make it grow, we can go look at what bacteria grows faster. So in that particular plate or that particular environment. And everybody found that people with higher amounts of decay had Strep mutans. Lots and lots of Strep mutans. So for a very long while, typically the entire 80s and 90s, there was a group of researchers that swore that a bacteria, if we could come up with a method of killing that bacteria, we could prevent tooth decay. Now first they looked at injections to kill this bacteria, they looked at immunologic, they forgot that the mouth is almost outside the body, an amount of antibodies, immune system response very different inside the oral cavity then it is even inside the gut which is outside the body as it turns out. It’s not fully inside the body. So that turned out not to be so true. A theory emerged, actually, as I was doing my PhD, my mentor, Israel Kleinberg, actually was proposing, 1994, that it was a mixed ecology almost like the grass. Anybody garden? We’ve done some grass discussions. If I go ahead and I stir up the ground, I tear up this grass – anybody play golf? That’s probably better. No golfers? You ever see a weed in the middle of the 16th green? Almost never happens. These greens are – particularly not in Florida, in Florida, the greens are terrible but no. In a professional golf course you get very tight grass that is grown and cropped extremely short. Every blade of grass on that green is almost identical. And the thing that keeps it that way is actually the health of the grass. Everything that’s there – you don’t get that giant weed with

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that little dandelion growing up the middle. Anyone have a lawn that has dandelions? No never mind. That grows where there is opportunity on the lawn. Very hard to get that weed to grow in the middle of the putting green on the 16th hole. Well it turns out that the mouth is very similar to that. So in the early 1990s Kleinberg and this guy Marsh, one in England, one at Stonybrook, were making a proposal that it was a mixed ecology, it was a balanced existence between good bacteria and bad bacteria that lived inside our plaque at all times. And it was when this balance went off in one direction, what happens if it becomes too anaerobic, too thick, too anaerobic in existence, what disease do we see pop out? What’s that? It’s not caries. It’s periodontal disease. These are facultative – these are anaerobes they actually enjoy living in a shortage of oxygen, they can live deep inside the pockets. As a matter of fact, if you look at the oxygen tension deep inside the pocket, it’s almost totally depleted if not totally depleted. Many of the periodontal pathogens, and we’re not going to speak about it, just the simple stirring and adding of air to the surface disturbs periodontal disease. That’s one of the mechanisms that flossing is so effective. Now caries tends to be a little bit different. Facultative anaerobes or pure aerobes that like being at the surface, like thin surfaces, makes it a little more difficult to brush away. So this plaque - which by the way we call plaque in dentistry but we’re the only group that calls it plaque, it’s biofilm to all others, has this very complex organization both in the molecular structure and actually in the communication between bacteria and the environment. Now you can get plaques, as plaque grows thin what do you think is happening at the surface? Are they aerobe or anaerobe? Aerobe. What do you think it is 10mm into the pocket? [students mumbling, saying “anaerobe”] Yeah, so you can get a plaque that is actually mixed ecology with a very mixed EH (pH? Unclear) and oxygen tension as you go from the surface to the very base of it. It actually becomes more electronegative, it favors spirochetes, it favors the pathogens deep inside the pocket. Well, I’m a cariologist, I’m gonna just cover that upper area, the aerobe and the facultative anaerobe.

[3] – [Why is one biofilm carious and another not]So we keep asking this question about one biofilm being…

[4] – [Image]

...no caries there. Redness, periodontal disease, ugly. I’ve told you, have you guys met this physics professor, doesn’t brush his teeth? Ok, this is my patient, physics professor, brilliant, writes formulas down in the middle, on the bracket table cover, sits back down, comes to the office once a month. Actually, came, he died of cancer, but came to the office

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once a month for us to clean his teeth because he was too lazy to brush. Periodontal disease all over.

[5] – [Image]

But we have this guy over here, pink gingiva, and the teeth are melting away. Absolute clean, has this very thin biofilm. And it was the contention of Kleinberg and Marsh that the mediator, the thing that controlled whether this patient got decay or doesn’t get decay, turns out not so much to be the bacteria, because we all come plus or minus some with our full range of bacteria, but it is the ecologic pressure that pushes us towards caries or pushes us to periodontal disease or sometimes both. What’s the ecologic pressure on this guy? Look at his tissues. [Student: saliva?][Dr. Wolff] - No saliva. So the ecologic pressure on this person was a lack of saliva.

[6] – [The BIOFILM is where it ALL happens]We are going to spend some time right now talking about how saliva controls what is going on in the biofilm and what some of the mechanisms of that actually are.

[7] – [Plaque Accumulation]

Plaque builds up very quickly on the teeth. Dr. Caufield is absolutely correct that it is a niche environment, it builds up quickly, it spreads from defects, it hides in the defects. Bacteria sit there as a reservoir, they grow, they expand.

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[8] – [Role of Dental Plaque in Health and Disease]

Marsh made it very clear that in this healthy environment, it is very hard to take a bacterium and stick it in here. And that is one of the reasons that this idea of giving you a probiotic and expecting it to grow and compete appropriately doesn’t work so easily. Because getting a healthy biofilm to grow there when something is already surviving is not easy to stick another species in. Everything is already functioning. And when we go ahead and look at these ecologic pressures, it can be anything! Increased carbohydrate, suddenly eating lots of sugar, what does that favor? I eat lots of sugar. What does that favor in my biofilm? Are the two of you working that question out over there? No, the ecologic biofilm, we add more sugar, what does it favor and why? You’ve already taken your micro course, what’s the answer? Size 7. We weren’t looking at shoes? Oh no, I’m sorry. Never mind, it was just a different conversation. Oh you were looking at shoes! She’s turning red! If I add lots of sugar to a patient’s diet suddenly, I favor the bacteria that like to eat sugar. So we take our fermentable carbohydrate consuming bacteria, like Strep mutans, lactobacillus, actinomyces, any of the bacteria that like fermentable carbohydrate and they start growing. What does this do to reproduction? How does the ecology change? If I have bacteria that are producing acid and they produce it constantly, what type of bacteria will want to grow in that environment? Base-forming bacteria? No, it is bacteria that don’t mind acid forming environment. Favors acid-producing bacteria as it turns out. So even though I may have a healthy base-forming bacteria in there, it doesn’t get a chance to reproduce. It doesn’t get adequate food, it doesn’t start to grow, it doesn’t reproduce. The colony counts start moving towards acid-formers. So lactobacillus goes up, and Strep mutans being the big two players start rising. It means less carbohydrate produces an even greater drop in pH because there are more bacteria that produce acid. So the minute I start taking this balance, I got some good guys, I got some bad guys in here, I take the good guys and feed them, I take the bad guys and I feed them some sugar, they produce some acid, they prevent the good guys from reproducing, but the bad guys can keep reproducing, they make more of them, now I add a little more sugar, I get more acid, more acid makes more environment, we push this pressure in this direction and there are a number of different ways we can do it! We can stop brushing our teeth. What does this do to the environment? It does two things. It increases not the biofilm, because increased plaque is increased biofilm, that’s just the word. If I stop brushing my teeth, I get a thicker biofilm which means

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I get more biomass, more bacteria, more. So the counts start to rise on the surface of the tooth. If there’s lacto if there’s strep there we are going to get more acid to sugar. What else happens in that plaque? Right it becomes more oxygen consuming. The base of that now starts to be more anaerobic. It means I may be favoring redness of the gingiva, difficulty in the periodontal status, more spirochetes, more anaerobes, more everything will start developing inside the pockets where it is anaerobic. We deplete the oxygen at the surface with rapid oxygen consuming bacteria. So that pushes a stress that changes the flora, decreased saliva changes the flora too.

[9] – [Image]Everything exists in the mouth. Good guys, bad guys, we like to see a balance of it

[10] – [Flow Chart]This is a crop out of his textbook, and each of these things, if I put fermentable carbohydrates on the top, it produces acid. If it produces acid, I culture things that like to be low pH, so I get my Strep mutans, my lactobacillus, and in the end product I see demineralization. And on the other hand, if I can produce a food in there, it makes the base-formers grow, that makes the base-formers grow, it results in a neutral or a rising pH. As it turns out that that was the invention that came out of my particular mentor, I don’t get any penny of it, but I am a Colgate consultant so I have to tell you the patent is held by Colgate, it’s the new pro-argine technology that feeds arginine to the plaque, trying to take this environment that is highly acid forming, give the base-forming bacteria some food that they like, and push the pH of the plaque up. In fact studies that Dr Allen and myself, and dr Klachani have run here, have demonstrated that we can take a plaque that is acid forming and by feeding it the pro-argine chemical, which is just and L- uh, a lysine, uhhhh, an L-arginine, containing food, umm um toothpaste with uhh, um, calcium carbonate in it, if we take that and feed the plaque that over a period of two weeks, we make a plaque that has a resting pH of about 6.2, 6.3, 6.4, and push it up to 7.2. We actually change the ecology just by having the patient brush with a different toothpaste. Same patient brushing with Crest winds up with the pH staying the same. Feed it the right food, we push it in a proper direction. [Student question: If you are brushing to get rid of the biofilm, how would you feed… inaudible][Dr. Wolff] – You never get rid of biofilm. It’s a fallacy. My belief, the belief of my mentor from literally 20 years ago now, was that we’re not going to at some point go for total removal of the biofilm. We are going to go for biofilm management. Ecologic management. So, biofilm elimination. That was the idea of having you rinse with a chlorhexidine, a poviodine, taking an antibiotic to kill everything. But what winds up occurring is it doesn’t kill everything – whoop wrong button [screen goes black]. Instead, one or two of these bacteria (back to slide 9) survive, and unfortunately the ones that survive tend to be the most nasty in what we deal with. If we wipe out the healthy portion of the flora, what comes back frequently is a flora that we are not as happy with (back to slide 10). It has the preponderance of the ones that – so if you leave the ecologic pressure that’s going to want to make Strep mutans, you’re going to get more Strep mutans than when you started, and in fact a number of studies that have looked at what kills with products like chlorhexidine, that’s in the outcome. You don’t take all the plaque off. You thin the plaque. You reduce

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the biofilm. You take most of it and you put it into solution inside your mouth, you spit some of it out. It recolonizes coming out of – the dextrans now start to hold it, it sticks to the outer tooth, and it starts to regrow. It populates from defects on the tooth and grows outward like we showed on that ultraviolet photo.

[11] – [Breakdown of Microbial Homeostasis]

So when we kill normal diet or diligent hygiene,

[12] – [Breakdown of Microbial Homeostasis]

we wind up with either demineralization or inflammation depending upon which direction and what food we’re feeding it.

[13] – [The Role of Plaque in Development in Demineralization]

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This is decay. If it is dull and matte it is active caries. If it is not it is arrested caries, but that was or is decay. It is the byproducts of decay. Demineralization. All this is is a cavity, a cavitation waiting to occur. 6 months, a year, 2 years keep feeding it, the surface breaks down, you get caries.

[14] – [Biofilm is Where it All Happens…]Biofilm is where it happens, but not what controls it. Saliva controls what is happening inside the biofilm and we will talk about how that occurs right now.

[15 - 17] – [Venn Diagrams]So we know that when we cut saliva out totally we wind up with a patient that is very hard to resist caries. There is a very high correlation to dry mouth., but dry mouth does not guarantee that you are going to get caries. It just makes you much more likely to get caries. If you reduce the biofilm radically, if you control the tooth’s surface by addition of fluorides and other items, you can control the risk of caries. That poor patient that had radiation therapy actually kept his mouth immaculately clean, was using fluoride, he had a bad floor, he probably would have been a candidate for us to try to go in with a very aggressive eradication of Strep mutans using any of a number of items. Another study we have recently run in the school and will be running again is a targeted peptide that attacks Strep mutans and kills that bacteria alone. Shows a lot of promise because if you can be feeding the right nutrients to the plaque when you kill that one bacteria, you stand the chance of shifting the flora in a totally different direction.

[18] – [Comic]I told you all this. Bacteria in your mouth eat sugar and excrete acid, which harms your enamel. If you eat a candy bar, more bacteria will poop in your mouth and that is all this. Bacteria do a couple of things. They eat, they reproduce, and they poop acids. Not all bacteria, the acidogenic bacteria. And that is all they do. And if you think of it in that sense, and then add the step 2 of the Miller equation which we’ve already shown you, acid in presence of tooth makes dissolution, you now understand the entire decay process and how to manage it.

[19] – [History of Caries: Saliva]We talked about this

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[20] – [Plaque pH]Stephan talked about – have we spoken about the Stephan curve last year with you? Stephan spoke about the fact that when we go ahead and take plaque and add sugar to it, the pH automatically goes down. What makes this pH come back up? It is saliva. If we take the saliva away, it takes about four hours which is about this length of time, it goes from 20 minutes to about four hours before that pH rises above the critical pH. What is the resting pH of a patient that starts out with dry mouth? About 6.2. It means they live very close to dissolving all the time. As a matter of fact, if they have exposed root structure, dentin has a critical pH of 6.2. What would effect this line here? How do I change the position of that line? Below that line, everything dissolves, above that line we get remineralization. What’s that line called? Critical pH. Below the line it dissolves, above the line it remineralizes. How can I move that line? [student: Fluoride.] And which way will it move? Up or down, you can’t choose them both. Well, you can, but one is right and one is wrong. It is going to move it down! What it does is it says the tooth doesn’t start dissolving until I get to a lower pH. And if the tooth doesn’t dissolve until I get to a lower pH, I stand a better chance, instead of it being this long dissolving, it is only this long. So it decreases the amount of time the tooth is dissolving. That is one of the values of fluoride and the tooth structure. That’s the critical pH there.

[21] – [Caries Rates]So, Eskimos and the African Bantus adopted sugar containing foods and went from being a population of no decay to a population with nearly the highest decay.

[22] – [Image]We spoke about these guys already, they made fun of my inability to make fire. But they also don’t get tooth decay.

[23] – [In Vivo Plaque pH Responses]They don’t get tooth decay because they have a saliva that buffers the same amount of acid, the same amount of sugar-causing acid – I’m sorry. The same amount of sugar – the same amount of acid produced by the bacteria in the mouth, they buffer it back quicker than other patients with different saliva. They do that by a number of things. They have slightly higher bicarbonates, they have slightly higher levels of the amino acids associated with remineralization instead of demineralization. Arginine being one of them. So caries-active people have lower pHs to start and have pHs that go down and stay down longer. It is associated with saliva and what causes it.

[24] – [Volume of Saliva Produced]We produce a lot of saliva in our mouth, about a quart and a half a day. Its resorbed by the gut, it is one of the fluids we use it when we speak when I get dry here. A little water helps but saliva is what normally does it.

[25] – [Protective Functions]It does a whole load of protective items. You know we talked a lot when we were children about the digestion with saliva. As it turns out that was just a phony story. You don’t need

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the amylase in saliva to digest your food. It breaks some down but it doesn’t do a whole lot. It does carry a bunch of antibodies that we believe give the tissues some protection.

[26] – [Factors Affecting Saliva Flow Rates]Things that effect how much saliva we have. You know time of day, circadian rhythm, turns out to be a very interesting item. Anybody drool on their pillow at night? You don’t need to confess, it is ok. Some people are droolers, some people are not. Most people decrease the amount of saliva flow at night, and that’s totally normal. And that prevents us from drowning, choking on our own saliva and things like that. That’s good news, not bad news. But the question actually goes a step further than just – what happens if I give you a cookie before you go to bed? And what does that Stephan curve look like when you’re salivary flow is naturally slowing down? It’s combining the concept of cookie, the concept of saliva and the concept of circadian rhythm. What’s going to happen? We haven’t gotten to caries. The pH will drop, that is because of the cookie, and it will stay down long, it doesn’t affect the critical pH, it just stays down below the critical pH for a longer period of time because you don’t have the natural saliva production. Where do we see this as a tremendous problem? Early childhood caries with patients that are using nursing bottles. You provide the sugar during the night, there is no saliva at all to buffer that back to neutrality, it makes the matter worse. And don’t get me wrong I don’t say that all childhood caries is from the nursing bottle, I’m saying that nursing bottle can increase the likelihood of childhood caries. Standing up keeps you dry, drinking makes you dehydrat – dehydration makes your mouth dry. Light, daytime actually makes you salivate more. Smell has an effect on salivation. Picture does not. I show you this lovely warm cinnamon cookie, and nothing happens in your saliva. I bring a tray of cinnamon cookies into this room, and everybody salivates for the next hour. Many medications reduce our saliva. Several thousand at this point.

[27] – [Stimulation of Saliva]We can stimulate saliva a number of different ways. We can do it with drugs like pilocarpine. These are stimulants for saliva but they are hard to live with because they cause palpitations. We can ask patients to chew on things, chew on gum, whether it is flavored or not, most chewing gums loose their flavor after a few minutes. Now that chewing gum, does it still stimulate saliva? Actually it does, but not for the entire time you’re chewing, after a while it actually causes you to dry out a little bit. We can give you citric acid, which actually is a chemical stimulant to saliva.

[28] – [Flow rate vs. Concentration]We know that when salivary flows go up, we get one really great effect and that is increased bicarbonate flow. Bicarbonate neutralizes acid. So that’s where we get this chew gum after eating meals, to reduce the likelihood of getting decay. It neutralizes the acid, it helps wash away the byproducts during that time.

[29] – [No Title]This is a Kleinberg graph, and it’s typical of what we used to get examined on. If you go ahead and add urea, you actually cause base-formers to grow. If you add short chain carboxylic acids and serine, we see the pH come back to neutrality. Sugar, we go ahead and

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see the pH drop, below neutrality, but we won’t see it drop below neutrality in serine. Ok, we see arginine, it rises just slightly above neutrality, and then it tops out in its ability to control the bacteria base or base-form in the environment. So our saliva supplies a myriad of things that help balance out what the pH remains in our mouth.

[31] – [Graph, Mean Whole Saliva Flow Rate]This is stuff that was actually from my thesis, but what I need you to pick up out of this is patients that have very high saliva flow are very near neutrality in the acidity. When salivary flow drops, ok, when whole saliva flow drops below 0.1, which is where we call people dry mouth, we see pH drops near 6.2. And we did this on several hundred patients, looking at their salivary flows, and then measuring what their pHs were. Their wetness is different and their wetness is different and their pHs were different in each case. So pH drops as we get dry, and our wetness so we get that sense of dryness. As it turns out, patients don’t complain about dryness until they start getting below 0.2 ml/min at rest. So 0.1 turns out to be that critical number.

[32] – [pH of Saliva, Brawley]Brawley in the 1930s sampled thousands and thousands of patients for flow and pH, and what he found was that the pH of patients, the highest population of patients had a flow of nearly 6 – I’m sorry. The pH of patients with the highest flows of saliva were up near 500 of these people had a pH near neutrality. Out in the wings we get people with very high and very low pHs. So the population tends to be centered around that neutrality, and that is why the population tends to be balanced as far as decay.

[33] – [Hyposalivation]In the general population hyposalivation is about 15, 20, 30% at most. Elderly are slightly more, anyone want to tell me why? What’s that? Polypharmacy exactly. It’s not that the acini got old.

[34] – [Hyposalivation]Resting flow rates, you need to know these. Resting flow rate of less than 0.1 or stimulated flow rate of less than 1.0 ml/min are generally signs of patient dryness. We flip the lip open, we can go ahead and look at it, it looks dry. Dr. Glotzer, did you do salivary collection in his laboratory yet? You actually can physically measure it. Stimulated is easier to collect than resting. Resting you have to actually rest when you do it otherwise you get a higher flow rate.

[35] – [Medication Categories Associate With Dry Mouth]Lots of drugs cause dry mouth. We’re not going to spend much time on it. But what we are seeing is that if we don’t deliver the amino acids, if we can’t put the bicarbonate there, we see patients that actually wind up with higher caries rates, lower pHs in the mouth at rest and longer term functioning.

[36] – [Buffering Capacity of Saliva]Uh, the ability to neutralize acid…

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[37] – [Saliva Eliminates Acids in Several Ways]…we dilute, we neutralize, and we make base-forming bacteria.

[38] – [Graph]The stuff, if we were to go ahead and look at a culture of bacteria, if we were to provide that plaque with sugar, we see the classic Stephan curve. If we just put the hard particles from the saliva into the patient’s mouth, or into the culture, the pH drops, stays down and is very slow to come back if at all. The moment we place in the mixed environment the salivary supernatant, the clear liquid of saliva, we see this pH start to return back to normal. It was one of the sentinel experiments that actually showed that it was the saliva that helped neutralize the acids from the Stephan curve.

[40] – [Dental Embryology]Very quickly, a quick discussion about why we see decay forming in the breakdown of enamel. Enamel crystals are laid down in a very specific format by the Tomes’ process they are arranged in rods. These rods come out from the DEJ to the surface, multiple rods together. They rotate just slightly as we come back up. They are C shaped in format, they fill with an amorphous hydroxyapatite in the middle. This precipitation of hydroxyapatite both in the Tomes process and in the amorphous center of the C shape gives it its color and its shape. When we see demineralization, we start to lose some of that preformed. When we remineralize, after the tooth is erupted, we don’t have to Tomes process to reassemble these crystals. At best we can reharden the surface, but we may not be able to return the surface to its natural color. And that is because of the complex method in which the initial tooth was actually formed. [42] – [Enamel]Enamel is a real crystal. There is very little proteinaceous matter inside it. Its somewhat interesting. Decay in enamel is a pure dissolution process. Whereas decay in dentin, dentin contains a significant amount of protein, it also involves denaturing of the protein to get the dentin to fall apart as it dissolves. So there’s actually collagenases, elastase, in the caries process. It’s actually mammalian, it comes from us. It is activated by acids, it helps dissolve the dentin proteins that are holding the tooth, collagens that holds it together. These organized crystals have tremendous potential for remineralization. Where do we see remineralization all the time? There’s an oral process that remineralizes, it’s the other thing that saliva brings to the table. It was actually in the graph, I didn’t concentrate on it. It’s not calculus it’s calcium. Calculus is what we see. Saliva brings calculus and phosphate to the table. If we make it high pH, it precipitates on its own. It does not form – I don’t think it’s the next slide… (flips through slides).

[44] – [Enamel: Calcium hydroxyapatite]So, hydroxyapatite is a very complicated crystal and you’ll need to know this formula for the examination. You’re writing it down? What can I tell you. If we substitute a fluoride for one of the hydroxide ions, what do you get? What’s that? You don’t get fluoride, you get fluorapatite, which tends to be less soluble. It’s also a slightly larger crystal, doesn’t pack quite as nicely as the hydroxide calcium hydroxyapatite. If I go ahead and substitute a

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magnesium in for the calcium, do I have a more or less soluble crystal? It is a more soluble crystal. So as we see teeth dissolve and get remineralized, they don’t always remineralize in this format. They remineralize in a less mature format that is more likely to dissolve. And that is a slight problem. It may be more likely to dissolve but its harder than the dissolved form.

[45] – [Image]So as we get this remineralization, we get these pulses of demineralization, remineralization, demineralization, remineralization. Calciums are added and eventually the calcium content grows enough that we wind up with hardness that doesn’t let the tooth fall apart.

[46] – [Graph]We see immature calciums. They come out as a calcium and phosphate ion at very low pH, at these acid pHs. At the basic pHs, we get very mature calciums and phosphates. When we go ahead and look at calculus, calculus sits somewhere around here, it its maturity. It is a very immature calcium based product. That immaturity in the product means that it will dissolve easier than natural tooth. Let’s talk about that basic chemistry in that solution. If I add acid to a solution, will it hold more or less calcium? Any of you take freshmen chemistry? None of you did. You’re all getting expelled immediately, how terrible. It was a prerequisite for getting here. If we add acid to the tooth, we get calcium coming out of the tooth into solution. Which calcium is going to come out first? The most mature crystal or the least mature crystal? Because it is more soluble to acids. That becomes an interesting item. We don’t see caries where we see calculus. And that is for two reasons. First saliva is precipitating lots of calcium and phosphates. Second, if I have to put calcium in solution, and if I add acid and it’s below 5.5 in pH, I have to be putting calcium into solution. If I do it in the presence of calculus, it comes from the calculus. It doesn’t come from the hydroxyapatite of the tooth. So we wind up with this being a surrogate source of calcium, protecting the tooth from dissolving in tooth decay. And that is a very mature thought. And that means if we can get calcium species on the outside of the tooth, even if they are less mature species, we can protect the tooth from dissolution. That’s the principle behind MI paste, the new tricalcium phosphate paste from 3M. The Sensodyne with novamin paste. There are a bunch of these pastes that are designed to put an immature calcium at the surface of the tooth that when placed, when acid is placed on the surface, instead of the hydroxyapatite dissolving, these less mature crystals come out of the tooth and wind up filling up the acid contained solution and prevent the tooth from dissolving. It is a surrogate. Now if you brush it away, rinse it away, and put more acid there, eventually you will still make a cavity. So you can overwhelm that environment. But you can also balance that environment such that by putting calcium on there, like wearing an MI paste at night, you can add the calcium at night, in the daytime you have your acid challenges, balance this off, and that is part of this balance between remineralization and demineralization.

[47] – [Enamel]Talked about fluoride substitute, carbonate substitute…

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[48] – [Enamel images]...that’s hydroxyapatite.

[49] – [Enamel calcium phosphate- hydroxyapatite]Plaque calcium phosphate we talked about, it is amorphous, saliva calcium and phosphate ions are amorphous, they kind of sit, they dissolve more easily than the hydroxyapatite. Their precipitation on the surface has the affect of protecting the tooth from caries.

[50] – [Salivary calcium and phosphate ions…]Why don’t we leave on the sides of teeth? Are there any hygienists in the room? What’s that? Well calculus is hardened on the sides of the tooth, what else does it do? It is a site for bacteria that secrete exotoxins and irritants that cause other reactions of the tissue and wind up breaking down the tissue, so that’s not a good thing. And that is why we take calculus off. From a caries perspective, leaving calculus isn’t a bad thing. It’s terrible from a gum disease, from a perio standpoint.

[51] – [Salivary Precipitin]I gave you the more soluble, it’s a surrogate calcium source.

[52] – [The balance between cycling demineralization…]The balance between, this cycling between demineralization and remineralization determines whether the tooth falls apart. And its this ragged balance that anything that upsets this ecologic pressure can suddenly result in tooth decay. Is there anything else that I wanted to cover?

[53] – [Enamel Caries]We gave you critical pH

[54] – [Caries Attack on Enamel]Ion, caries, oh yes we do need to go over this

[55] – [Image, same as slide 13]So initially, when this area is exposed, so what caused the acid to be there? What’s that? Tell me. [student: Fermentable carbohydrates, bacteria, and environment?] You pretty much got it right, that’s pretty good. You can go graduate now, you’re done. So the presence of fermentable carbohydrates meant that plaque was accumulating there. The presence of bacteria, and then fermentable carbohydrate provided this environment that caused the tooth to dissolve. So what happened inside this plaque? Tooth dissolved, where did the calcium go? I made acid. Where does the calcium go when I have plaque on that outer surface? Does it get to the tissue? Or does it go into the plaque? It does go into the plaque. What happens if I neutralize the acid? It precipitates. So we take some calcium out of the tooth, it precipitates. Does all of it go back into the tooth? Or precipitate? No. A certain amount of it stays inside the plaque. When we brush it away, eat an apple, do something, it leaves the surface. And that is forever lost, and that is what we are looking at. Somebody who has lost calcium from the surface that was not replaced, but the reason why we don’t have a giant hole is we were replacing the calcium.

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[56] – [Enamel Lesions]And what’s happening on a subsurface level, this is a drawing that came from, his name stars with a C if I remember… It doesn’t matter. It came out of a textbook from somebody, it’s not my drawing I’m crediting it to somebody that I didn’t put down on the bottom of the slide, I’m sorry. This surface stays intact because we dissolved, take the material away, and re-precipitate on the surface.

[57] – [Image]We can actually look at a real ground glass, this is from Silverstone, it’s cut off at the bottom. This is actually what the surface looks like. When we look inside the center of this, we get this microscopic picture, it’s not what we actually see. When we go ahead and look at it we see the inside of the tooth having lost a lot of its enamel. We see a dark zone. What is this dark zone around the outside? Precipitation, demineralization, precipitation, demineralization. Two areas get to neutrality before the rest, what is it? The very deepest part of the lesion gets precipitation, they very outer part of the lesion gets precipitation as we go through the process. We have high concentrations of calcium right next to tooth structure, so we get this precipitation right at the depth of the lesion and we get precipitation at the surface of the lesion. We can see it here also…

[58] – [Enamel/Biofilm/Saliva]…this is just a diagram. Calcium and phosphates come out of the tooth in the presence of acids. They go into the plaque. We can either get it to go out into the surface if we leave it there long enough, leave the sugars, make the acid. It comes out of the tooth and goes into the mouth. The moment it goes into the mouth there is a net loss of calcium from the tooth. If we have a method of forcing calcium and phosphate into the plaque, we get precipitation, we get calcium, we get remineralization.

[59] – [Image]

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This is from Don Zero, it’s just a graphic. We see this loss of mineral in the deepest portion, in the more surface portion, if we add calcium phosphate from here we actually work to remineralize.

[60] – [Image]This is once again from Silverstone, that we actually see this occurring in the enamel rods where we’ve lost it, you can see this histologically. So we see areas of less density inside here.

[61] – [Enamel Lesions]And if you go touch it with an explorer, you break open that outer surface, and now you have an area that will retain plaque and actually cause caries. Well, cause deeper caries, this is caries. Because now you can’t brush it and keep it clean, the surface is no longer intact.

[62] – [Image]

And we see this in lots of areas, we can see it in the aproximal region on these teeth.

[63] – [Image]

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Why is it disk shaped? If I put a drop of acid on the surface, it doesn’t bore straight down, it bores in a round shape, almost a funnel, because we are dissolving from the periphery. As we dissolve from the periphery, we loose mineral, and that is exactly what we see here. When it gets inside dentin, dentin has a higher solubility – a lower solubility, it dissolves more rapidly. So we see a quick spread and once again that same V shape as it gets deeper. So it comes in, it hits the dentin, at this very narrow V when it breaks into the dentin it spreads out and engulfs a larger area because it dissolves more rapidly.

[65] – [The zones seen before complete disintegration of enamel are:]We talked about this

[66] – [Image]We talked about this

[67] – [Bitewing Radiograph Image]This is the real type of picture of it

[68] – [Blank slide]And I think we are all done. Any questions? Yes?[student: The crystal structure, like hydroxyapatite, the alkylinity, is that correlated to the number of calciums or is it associated with the structure itself?][Dr. Wolff] – Well, calcium phosphates, the solubility of calcium phosphates is related to the number of calciums in the crystal, and its organization. So the lesser organized the crystal, the looser the crystal, the more soluble that crystal is. [student: On one of the slides it had octocalcium phosphate? Inaudible, …more acidic than tricalcium phosphate][Dr. Wolff] – It dissolves, yeah I know where it is. [Goes back to slide 46] This is showing solubility in the presence of acid. Highly soluble in here. Octocalcium phosphate is more soluble than hydroxy, which is Ca-10.[student: What about tri vs octo? 8 vs 3 calciums?][Dr. Wolff] – It’s not the pure crystal arrangement that determines the ability. The tighter the crystal, the more difficult it is to dissolve. That order is correct. Yes?

[student: You said when calcium goes into the plaque then not all of it goes back into the tooth?][Dr. Wolff] – Right.[student: So where does it go?][Dr. Wolff] – So all items have a solubility for calcium. Even at neutrality a certain amount of calcium stays in our saliva, doesn’t precipitate. It only precipitates when the pH rises and the solution becomes hypercalcium, and you get crystal formation and spontaneous precipitation. SO I can put 2 tablespoons of sugar in my coffee, it dissolves in the coffee. When I put 20 tablespoons in there, eventually it will no longer dissolve in the solution.[student: But so if you have a net loss of calcium from the tooth it has to go back in eventually?][Dr. Wolff] – It doesn’t have to go back in. It can get swept up into the saliva. [student: But to prevent caries..]

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[Dr. Wolff] – It has to get back into the tooth.[student: So where does the extra calcium come from?][Dr. Wolff] – It comes from either us forcing calcification by using acid fluorides that dissolve and then get a spontaneous precipitation using the calciums that are in the mouth. It comes back from us adding calciums in toothpaste, or it comes back naturally from our saliva putting precipitate in, which contains calciums and amino acids into the plaque.[student: Dietary calcium doesn’t have an effect?][Dr. Wolff] – Dietary calcium has almost no effect on tooth decay.[student: And then one more question… How does drinking water after eating effect..][Dr. Wolff] – Drinking water after eating dilutes the acids in the plaque more rapidly.[student: So, in terms of coming back to neutral pH?][Dr. Wolff] – It’s much quicker. It speeds that process along. Come on in! It’s all yours. Thank you. We were just in our question and answer period, Dr. Moghadam.

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25: types of caries saliva and caries

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lactic acid

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higher amounts of decay

particular plate

strep mutans