Demineralization/Remineralization of Orthodontically Treated Teeth – Domenick Zero

as you know we're launching a study on remineralization of white spot lesions resulting from taking brackets off orthodontics patients and so we thought as part of this we should have someone come talk to us about the demineralization remineralization process and what's involved and so we're pleased to have dr. Dominic zero Dom is associate dean for research director of the oral health Research Institute and professor and chair of the department of preventive and community dentistry at Indiana University School of Dentistry he's had been involved in research for a number of years his current research interests include the evaluation of the clinical efficacy of topical fluorides in prevention of of caries and erosion non fluoride remineralisation agents and new early caries diagnostic systems all of which come into play into what we're gonna be doing with this study so we're very pleased to have him here and look forward to it thank you Tom in terms of my background one thing that wasn't mentioned is I am a general dentist I was trained at Eastman Dental Center and to be a sort of a super generalist now I've only practiced off and on over the last number of years because I've gotten very involved with research and administration but one thing I do want to say is that you know part of the reason I've been at research is because what I love dental school I was trained at Georgetown which is a very clinically focused school I have to tell you I did graduate first in my class there was a very good clinician I'm not bragging but I just want to give myself some credibility with this group but one thing I realized when I came to Eastman Dental Center is that I knew nothing about cari ology and I think the number is something like 70 billion with a big B dollars is spent to deal with dental caries and its consequences the sequela of the nickel dental caries so is a huge problem for our society and unfortunately even to this day dental schools do not put that much emphasis on teaching Carey ology and so my career and my efforts of my research have really been trying to understand the disease and ways of improving human health through understanding and prevent Karia so my focus is really on prevention and not that I don't value restorative dentistry and and and and the need for that so just to start off with a little bit of some definitions most of us as dentists really think of dental caries in terms of the caries lesion which is the second of the two bullet items here and really this is really a manifestation of just one stage of caries as a carry ologist I think about caries as a process which involves an interaction between the dental plaque biofilm and the tooth surface and the subsurface enamel so there's actually a lot of interactions a very complicated process I won't go into too much detail about it but basically it's it's a very dynamic interactive process but we do know from the literature and and from and from experimental evidence that the very early stages of caries we can remineralize the tooth mineral especially the enamel and to some extent the dentin and as the caries progresses we can both remineralize and arrest that process and then if it progresses further then we need to use our restorations to to deal with managing the disease process but it's one continuum it's one disease there's not two different approaches prevention on one side and restorations on the other this is one process it's one disease we need to manage it as one disease so in terms of the modern manager of caries we're dealing with early lesion detection and assessment what I mean by assessment is caries activity assessment of the lesion is the is this an early lesion that we see clinically is it active or inactive it's a very important determination risk assessment a number of studies are being done by the year pprn in terms of risk assessment in establishing a diagnosis and a prognosis and then determining the appropriate preventive or restore and restorative interventions depending what's needed and then determining looking at the health outcome of that poll process and one of our problems is that we really don't assess this as a system we sort of look at the individual components but we really don't look at the whole the whole system to really see how effective it really is and in all honesty it's really a black box for us even though we've been at this for a long time if we look at the paper by Bader and sugars this tremendous variation and and and what dentists do and how they decide things we do know from the literature that there's a there's a very high rate of caries why I should say these white spot lesions that form in to some extent carries around orthodontic brackets and there and actually if you look at the range of studies it ranges from something like 17 percent to as high as 80% or even 90% so there's a pretty high incidence of this of the same problem so I ask you is is this a successful web design a case when we see an outcome like this and I'm my thanks to dr.

Jeff Dean who's an orthodontist at our school and our associate dean for faculty affairs who who let me have this case and we can see that it's probably a reasonable aesthetic result and I'm not going to ask the other – in the room to critique this but but from a Kerry's point of view it's a real failure and also from a periodontal health point of view this looks like not necessarily the best outcome in terms of etiology the – vocation and the morphology of teeth is very important and basically carrying the caries generally occurs in areas of stagnation where plaque can grow undisturbed and limit access by saliva and the caries process forms typically in these locations and then of course we need a carry genic biofilm dental plaque what acid said – genic an acid Doric properties acid or properties means the bacteria not only can produce acid but can continue to produce acid as the pH of the plaque drops down to below the critical pH that the mineralization can take place which is generally thought to be around 5.5 but really there's a range of pH is that the mineralization can occur and then of course frequent dietary exposure mental carbohydrates and then salivary flow rate and composition plays a big role in modifying this process and is really our main protective factor in the human mouth so in terms of a site-specific disease process dental caries is highly localized and it's got very complex and incursion areas and stagnation as I mentioned or the biofilm can accumulate undisturbed each tooth site represents a unique environment that influences plaque composition the metabolic status of that plaque the thickness of that plaque and the thickness is very important as well as access by dietary substrates clearance of those substrates saliva and Aunty caries agents so basically when you have undergoing orthodontic treatment you're basically creating what could be referred to in the lingo of this gentleman named Phil Marsh an ecological disaster for that tooth and that you're actually allowing plaque to accumulate undisturbed – it gets very thick around these brackets courses protected normally on the buckle of the smooth surfaces of teeth then even without tooth brushing there's a limitation on how thick a plaque can get it's usually about 500 microns but once we have this Hardware there and keeps them yet the mucosa from rubbing against a tooth you can get millimeter thick plaques and that's part of the problem and it's in this situation so what are the so when I look at caries I think I said a site-specific so I look at what are the the modifying factors that can that can affect the site specificity of caries well the pre erupted and post erupted of Florida exposure oral hygiene practices obviously play a big role in modifying the thickness of plaque and how and how much accumulates on the surface the actual composition and metabolic properties of the biofilm including its thickness is a very important factor that I mentioned and then access by saliva its flow rate in its composition and then there's also pellicle formation this is an organic film that coats the tooth surface and it is in between it's in between that the tooth surface and the dental plaque and it has somewhat of a protective role and then of course oral physiology and then everybody's a little bit different in this regard and how fermentable carbohydrates get cleared from the mouth Florida gets clear from the mouth and it varies in different locations in the mouth and to some extent explains the site district the the difference in distribution of calories throughout the mouth so to sort of look at this in a little bit more of a cartoon way we have the composition of the plaque we have the metabolic state of the plaque we have the thickness and a thicker plaque generally is more cariogenic but not necessarily because of a plaque is really really thick it actually becomes somewhat diffusion limiting and it actually can you know so the carbohydrate has to diffuse through that plaque you know and acid actually has to get from the plaque to the surface so acid production in a really thick plaque at the surface is not going to affect the caries process it's really the acid production going on adjacent to the tooth surface that drives the caries process that holds true for we think about anything that's preventive a fluoride gets stuck in the outer surface of the plaque and doesn't get down to this the surface adjacent to the tooth surface where the action is again that fluoride is not going to be effective it also holds true for many of the antimicrobial agents which tend not to be very effective because they have two problems one they don't get through the plaque and two they don't stay around long enough to do to do any good and then the diffusion properties the plaque would we've been doing some research in this regard and that if you of plaque is formed in the presence of sucrose sucrose tends to produce something called glucan which is like it's an organic and said it's a glucose polymer and it's a very unique thing would dismiss a specifically sucrose in the diet and this creates that actually allows the great rate of diffusion through the plaque so that substrates like dietary substrates can penetrate and go deeper through the plaque and get to the tooth surface and cause cause the problems so that's that's a symbol for carbohydrates acid is produced and then that acid then diffuses and attacks the tooth surface and we'll get into the details about the dividual ization process in a second another important parameter is the degree of saturation of the plaque and the plaque fluid that's the fluid flay phase of the plaque itself that is really that's the fluid that interacts with the tooth surface per se the cells of the bacteria really aren't the problem it's the fluid phase in between this that drives the Carrey's process and so in terms of degree of saturation and calcium phosphate in Florida in that plaque basically has a protective role because through a common ion effect with the calcium and phosphate it basically slows down the mineralization process it actually can shut it down if enough calcium and and and and a phosphate build up in that plaque adjacent to the tooth surface and we did we know well fluoride and is protectable which I'll get into a little more detail later on so in terms of saliva also a site specificity in terms of proximity to the salivary glands we have different salivary film thicknesses in different areas of the mouth and the work of Colin Dawes the Manitoba has been very instructive in that regard we also have something called the salivary film velocity which is the rate of fluid across the tooth surface and that's very important in clearing away the carbohydrate and the acid so the faster the salivary film velocity the faster we can basically neutralize the caries process and then pellicle composition will tend to be which is mainly driven by celebrate components will also be variable throughout the mouth and its thickness of the salivary pellicle also varies depending upon location and mostly abrasive forces so when we when I think about what the Dyna creat meant of course we don't use bands as much as we used to but one of the models that was introduced by a guard who's a orthodontist who is also a carry ologist was he would induce caries by using these bands the way he did it is he created a little spacer here between the band and the tooth surface and within about four weeks you can get significant and aggressive the mineralization of the tooth surface I don't know if that shows up very well but basically that's a pretty extensive area of the mineralization caused by food packing in there and bacteria producing acid and then being cut off from saliva snore Mille protective effects so one of the points I do want to make today is that all patients with automatic client appliances are high caries risk patients until proven otherwise in other words you know some of your patients that you're treating orthodontically do not develop this problem but I think with the high incidence of this problem you have to treat them at least the start as all high-risk patients and I think they should be given and managed by high-risk protocols so the next feature of the Carrey's process that is a time-dependent disease process that is modified by a protective factors so our historical understanding of caries goes like this fermentable carbohydrates producing acid by that by the biofilm leading to breakdown of the mineral of the tooth leading the caries and the way it worked was dental caries restoration larger restoration and the dynamics extraction prosthodontics you know so basically that's basically the life cycle and that's that's pretty much what dentists do to a large extent I think this is very good for dentists but maybe not the best for patients necessarily because I think some of this cycle of of caries restoration rear ester ation larger restoration can be can be broke by more aggressive prevention so the other point I wanted to make is that our profession is heavily biased towards our successes so when you go to most of your continuing education questions you get to see all these wonderful treatments right and all these perfect results and we we tend not to talk about our failures and I think that's also creates a certain bias in the system we do that definitely in the education of our dental students I can tell you that so the my understanding is again an understanding of the caries process and that that the conditions that the dye creates in the plaque as we understand the fluid phase of the plaque which leads to the mineralization that by removing the dietary challenge or increasing salivary flow and fluoride or perhaps I'd say perhaps introducing more calcium and phosphate we can basically change the carriage Anisa T of that plaque and drive it back to a more super saturated State and lead to love remineralization and we know that fluoride plays a dramatic and role and modifying both the demon realization process the early stages of caries may be prevented or reversed or rested primarily through elimination or modification of the illogical factors and or enhancing the protective factors and fluoride seals and salary' stimulation are the most evidence-based approaches that we do have at hand right now okay in terms of the actual the mineralization process this is a study that was that play doctor and always on my faculty and basically if you expose a tooth before I was the acid that's somewhat artificial because typically we don't well that's not so what official someone's drinking Mountain Dew continuously they're getting exposed to acid almost continuously throughout the day so this is maybe it's so not not so unrealistic after when I think about it so I have to four hours to get this initial surface awfully and these kind of micro channels that sort of extend down or the acid is diffusing from the surface now remember caries occurs from the surface down keep that in mind and eight hours we saw I see a thickening or a deepening of the the mineralization but further mineral dissolution at twelve hours we start seeing in fact a reformation of the surface layer to a certain extent and after 16 hours again we see more de mineralization and again that surface layer seems to build up even a little bit more so that's how we come up with the so called non cavitating white spots basically through this process it's a fairly good demonstration of how this can occur and but i do want to make the point that we a lot of people like that to use the term an intact surface layer that is wrong the surface is not intact it is actually partially the mineralized it's actually very porous and that allows the asset to diffuse through the surface and attack the more soluble subsurface enamel and that's where the lesion so and the reason why this surface layer reforms is because as the body of the lesion as the mineralization is occurring right now the mineral for caries to occur has to go somewhere so it has to go past the surface to get out into the saliva and into the oral environment so what happens actually is it reaper CIPA tastes on that surface and that's one of the reasons the surface stays intact there's other reasons and a lot of it has to do with the with the dynamics that goes on between the biofilm and the buildup of calcium phosphate at the biofilm interface as well as the effect of fluoride for it mainly interacts with the surface layer and I'm going to talk a little bit later on about low 4e concentrations versus hikent flora concentration because that's a topic that seems to be of great interest or that not this and well we'll get into that in a little bit more detail so this is what the surface layer looks like so does that look solid to you after it's been the mineralized it's very porous and basically you have all these little diffusion channels that allow the asset that the fuse down from the surface down if you magnify that it looks like a sinkhole pretty much so that's how the asset gets past the surface down to the deeper enamel so and we then we wind up with this sort of clinical appearance of a white spot and basically the reason it appears white is because when we get this the subsurface the mineralization it changes the optical properties of the tooth so that when light enamel is very translucent normally when it's in when it's sound and intact so when light passes through the enamel it basically scatters when it scatters it basically puts off the full spectrum of light and basically will comes back to your eyes white light that's what you see when it when light an intact enamel normal alike transmits through the enamel and basically it looks translucent you don't see the whiteness so that basically explains why white spots or the subsurface lesions look white and the other again this illustrates the fact that the surface layer for these white spots tends to be it has some areas of intactness but it also tends to break down and you actually the other point I want to make here using this as an example is that you actually see surface erosion so part of the caries process is actually loss of some of the surface and you can see this when you study the early phases of caries on surfaces you actually get like a little indentation in the enamel so it's so that surface has not intact this actually is being eroded to a certain extent as well as this area is where you actually have very thin and once this breaks through then you're into a cavitation and then caries process accelerates greatly and I sort of illustrate what's going on is if you look at sort of the normal eating habit of the average American here where they constantly graze all day long you basically have the mineralization remineralization demineralization realization so every time the pH of flat goes down you get the mineralization the pH thoughts rise and get some remineralization so at the end of the day you're going to get some net loss of mineral now if this continues over many many many days eventually you going to get a cavitation and in patients that have decreased salivary flow or continually you know expose themselves to fermentable carbohydrates like Mountain Dew then you're going to get more the mineralization and then and that carries rate is going to be greatly accelerated if we project this out over the years when teeth first erupted in the mouth teeth the most susceptible caries when they first erupted in the mouth they go through a poster of the maturation process this is a great time to get forward on teeth and matter of fact one thing that sort of troubles me about how we we use them preventive services we sort of do it every six months we should really concentrate our preventive services at a time when it's most needed and that's in children when their teeth are going through active eruption and then you know then then there's other periods where things are more quiescent and we don't need to be as intense that's a smart system approach but we're not really doing that right now in dental practice so teeth go through a little bit of a maturation process they actually acquire mineral and then they can start the mineralizing over time and with a metabolically active biofilm and then we can get to the point we can actually see these clinically as white spots and and then they can cross on and become cavitations of the time or we can actually arrest the lesions at this product at this time so the question is can we ever bring teeth back to here it's at a point where they started no we can't there's no evidence that we can remineralize teeth back to where they started once they've been to mineralized so let's just make that very clear up front we can do it in the lab and the nice clean systems where you know everything's perfect but in the human mouth for lots of reasons I'll explain later on we can't do that so again looking at this whole process again look taking the this this diagram this that silverstone published years ago and made popular we have the different zones of caries that's the so called relatively intact surface layer and then the body of the lesion under the dogs no in translucent zone but I'm going to use this to Silla Strait what's going on here we have the acquired pellicle coating that surface which is actually somewhat diffuse in limiting its limits both acid from penetrating the surface but it also limits calcium and phosphate from limit from penetrating the surface so it has a dual role one positive one negative so as we accumulate plaque on the surface that's producing the acid once it comes in contact with fermentable carbohydrates and the acid then diffuses through the surface into the body of the lesion where it causes that the mineralization and if we can get me mineralization going we have to again diffuse through the pellicle and then and then remineralize down in the body of the lesion it's very hard to do that most of what happens what we see clinically is happening at the surface layer the remineralization is mostly happening at the surface layer and that is the reason why most white spots don't necessarily disappear once they're formed they can get a little smaller they can be abraded away but they rarely remineralize completely and I'd like to talk to you folks a little bit later on about your clinical experiences in this regard because I need to learn more about that so let's move now from the mineralization to remineralization first of all I mentioned that teeth are the greatest risk when they first erupt and they will go undergo a match poster off the maturation process which is sort of a remineralisation process they acquire more fluoride once they RuPt in the mouth they actually acquire more get inorganic material they also acquire some organic material which is somewhat protective and the form the acquired pellicle we mentioned how this process of is dynamic and it can reverse and be arrested at various stages along the way I mentioned that that we can remineralize teeth in vitro almost completely but in vivo it's a much slower process and we can never achieve complete remineralisation let me qualify that at at the clinical level when we see a we see a white spot that is too advanced to expect everything get complete remineralisation what what's going on every day in our mouth at a subclinical level as well partially demineralized enamel crystals we can remineralize them almost completely on a daily basis that's before it gets too advanced as we as it does you know for a carry ologist a white spot as a relatively advanced lesion just want to make that clear does a lot going on before we get to a white spot stage and the very very early stages of caries can actually be reminiscing and basically prevents lesions from ever getting started it shuts them down at a subclinical level but it also slows down and lesions from progressing that's why we see some white spots in the mouth and probably see a higher instance of white spots in the mouth since the introduction of fluoride but we're also shutting down the actual clinical incidence of caries as well though in terms of actually actually seeing it in the mouth yes okay for uh for a a white spot to be clinically evident it has to be about 200 microns deep that's pretty deep well he's you know from my perspective because I'm usually studying things and they in the very very surface so I you know to remineralize all that 200 microns is very difficult so is that is that the perspective you needed no more than five five microns basically you can surface soften about up to about ten microns so when I I also do research with our dental erosion dental erosion is this is just a surface initially a surface softening that occurs and then only penetrates down ten twelve microns once you get beyond that then you're you get into a whole different kinetic and that actually leads to the subsurface lesion information but you need a plaque for that to occur it will not occur it doesn't occur with dental erosion it's just purely a surface phenomena okay we also know that individuals vary greatly in their remineralisation capacity so not every patient is gonna be mineralize the same and III do a lot of work with these cold I'll show you one of them later on insight to models where we actually put pieces of enamel in the mouth and we see tremendous variation in our subjects with some remineralized very strongly summary mineralized holiday at all some a very responsive to fluoride some are not very spot responsive at all in terms of mineralization and you know when I think of dental calories and I think that the main mechanism of action afford I think a remineralization when I think a dental erosion I think of demon inhibition and that's something that I've come to very recently because I as I said I continue to be a student of all this another very important point is once we repair enamel and reharden it or remineralize it it's actually more resistant to subsequent acid challenges than that intact sound enamel so one of the things that some dentists like to do is when they see a stained tooth surface that has had caries it's sort of a scar they don't like the way it looks they and they sorta they sort of question whether it can can progress and they get out the little burr and they remove it well you're actually removing something that is actually more resistant to calories you're replacing with a filling material that's going to break down over years they have to be replaced and it also has margins which makes the tooth more susceptible to caries so in fact when we take out arrested lesions unless we're doing it purely for cosmetic reasons we're really doing the patient a major disservice yes um could you clarify that two statements that I'm having trouble putting together here there's no evidence that animal can be Rieman early lesions resistance of caries that's correct and yes I know and yeah remineralizing the lesion makes it less susceptible to carries than it was originally yes how do those two statements coexist well you're thinking in terms of this beautifully formed enamel that is perfectly formed that's gonna prevent s at the solution it doesn't exist or even enamel which is pure floor apatite as much for it as you can put it into it into the tooth structure which is forty forty thousand parts per million which is basically shock enamel it's a pure floor apatite that you put that in the mouth you put a plaque over it at the minerals I didn't realize there's no such thing as a perfectly formed enamel so I don't care how much biotechnology we're going to talk about right now if you put it in the mouth it's going to diminish and other right conditions now you can make it less soluble so what's really going on it's and I'm going to talk about this in a few seconds is this like an adaption process that takes place when you de mineralize enamel and then remineralize it the the crystals that form are no longer prismatic the more disorganized there is really called a prismatic enamel that's one thing they tend to be larger which means they have less surface area relatively speaking which makes them less reactive to an acid dissolution they acquire more fluoride which makes them less soluble and they also acquire more organic material which actually protects them from the mineralization so those are the main things that happen with the adaptation process that occurs in the mouth over time thank you you're welcome good question so most of the evidence that we have about remineralisation comes from a heavily quoted study by back of Dirk's in 1966 this was a very interesting study where they examined the upper first molar of eight-year-olds and then re-examined that surface when they were 15 year old and you can see the transitions that can take place between sound enamel some of the sound becomes a white spot some of the sound actually becomes cavitating and white spots can can sort of become sound they can stay the same or they can become cavitation so that's basically most of the evidence that people cite to to to justify this whole concept the remineralization because 37 almost half the white spots disappeared if you read the article and and and don't just accept the data for what you know just the data there's a clear statement in an article that the author's do not know whether that was really remineralisation or these white spots which actually brushed away okay so that once you soften enamel it's susceptibility to toothbrush abrasion or any of the abrasive forces was the mastication which is food abrasion or to pressure abrasion or even the mucosa rubbing against the tooth the enamel is the hardest substance in the body once you soften it it becomes very susceptible to wear so you basically can brush you away your calories literally so what happens when a tooth erupting it you know the plaque accumulates at the free gingival margin and then the tooth erupts a little more and now that area where you had that the act of the mineralization is no longer in a carry genic area because you know you're now the free ginger has moved further down the tooth or further up to – towards the root and now it's no longer subjected to that same carriage in a plaque and so then it basically is soft you have better access to it you can brush it away so this is this is what we have pretty much and this is this study is constantly quoted but again if you read the article it's not very clear whether this is true remineralization if you look in the literature there's all sorts of terms for remineralization this remineralisation in terms of research terms mineral deposition mineral repo CIPA tation decreased lesion depth mineral gain rehaan ding decreased porosity these are sort of terms we use in research mainly clinically you have arrested carries carries reversal reharden lesions lesion repair vision consolidation lesion healing so I in my mind there's a lot of confusion around what what remineralization really is and what we should expect so I actually believe a good outcome for a white spot is arrested keep it from progressing that that's a good outcome of course if it's if it's a patient who's been treated automatically and they have these white spots on their prominent anterior teeth that's not a good aesthetic result and I understand that but from a carry ologist perspective it's a good outcome to arrest these lesions keep them from progressing so just to illustrate how you know remineralisation I work with these and cite two models where we basically cover enamel specimens or gauze and then we study them with study their hardness using a surface micro hardness tester we do studies where we measure the baseline hardness we de mineralized them in the laboratory and then we remineralized them in sight to in the human mouth for usually for a two-week period could be three weeks four weeks whatever but just to illustrate that over a two-week period you actually get some remineralization of these partially the mineralized enamel just putting up them back in the mouth to get about ten percent recovery and hardness if you increase the floyd concentration of the dentifrice you get about about a forty percent recovery i've also done studies with much higher flora concentrations up to twenty seven hundred parts per million fluoride and I can remineralize up about fifty sixty percent but that's as far as I can go in the human mouth with these partially de mineralized enamel so I'm never able to remineralize the teeth even under these carefully controlled experimental conditions using these appliance systems yes know what hardness testing we can't DeMint always very deep so the lesions are only about at the very most 25 microns in terms of salt and this surface often they're not white spot lesions you just surface often so they're usually about 25 microns the softening that occurs so they're very superficial these would be subclinical the mineralization it's it's well it's recovery in hardness I can recover back of forty percent of the original hardness that the tooth had at baseline okay so clinically we can arrest remineralize but notice that it's not white it's it's blood brown these are called brown brown spots and in this clinical situation what occurred here is the first bicuspid was extracted when's the first because it was extracted we've changed the oral environment we have better access to the toothbrush and to enter saliva we've arrested the lesion but that is not a pearly white tooth it's it's actually acquired a lot of organic material the reason it's organic and I know it so again because you can't stain pure hydroxyapatite you can only it's organic material that it acquires the stain so that's what we're seeing there it's actually a consolidated lesion it's arrested if you took this tooth and you put it in acid the the sound enamel around that will dissolve and that one area where its arrest it'll stay intact it's the most resistant part of the two so when you go in and you may want to do it for aesthetic reasons but if you're doing it for disease prevention you're not doing the patient any good and I can tell you that right now no teeth can arrest even at very advanced stages I'm not saying this is a good clinical outcome but after an extensive caries process to the point where the the cusps were completely undermined and they broke away once the dentin was exposed to saliva it basically becomes it consolidates it remineralize azide get acquires organic material becomes very leathery not soft at all and this is the patient I saw clinically so I know it was hard there was no calories there at all again it's not a good clinical outcome now this is a patient that had orthodontic treatment I happened to her father on the pizzeria and she drank Mountain Dew continuously all day long while she was working and this is how she presented and how to be de bandit and the clinician dr.

Giudice who's on our Faculty's pediatric dentist she provided this case for me and and she actually used in some of the areas glass ionomer to repair the defects but she was able to reserve observe in certain areas maybe remineralization maybe brushing away the caries it's hard to say it's really hard to say but basically it's a much better clinical presentation than when the patient first and and in this case what she did is she put the patient on initially on Provident rinse because the patient's teeth was so sensitive she couldn't even brush and then switch their over to private then gel to brush yeah to paste I'm not a big fan of Mountain Dew did you get you get that the drift that's a good question it's two things it's just it's it has a high level of sugar in it it has a high level of caffeine that combination in my mind is addictive the kids and then the advertising that's behind all this the kids don't stand a chance unfortunately you know I can tell you in Indiana we got legislation going on right now before the the ID a the board to make come out with very strong statements about soft drinks I mean I sometimes think our society is you know you never see the the movie plan of the apes you know it's you know they pick up the Coca Cola bottle that's it that's that's what did us in any way all right oh let me finish I'm sorry I guess so there's sugar if you have for old hygiene and sugar you drive yeah but a thick plaque you drive the sugar through the plaque so it's close to the tooth surface the s it gets produced down there once that acids produced it it doesn't come back out it just attacks the tooth surface so the concentration of the sugar is important and the frequency of exposure is important because saliva can't wash it away and remineralization can take place so you're constantly getting the mineralization all day long the acid in Mountain Dew because it's also acidic in a citric acid if you have a plaque of a tooth surface the citric acid is not a factor however if someone's drinking Diet Mountain Dew or regular Mountain Dew and they have clean teeth with no plaque on it then you have to worry about dental erosion so it's a double whammy but but it's not both at the same time to see the caries or erosion the sugar carries the asset erosion okay and we're seeing acid erosion and kids that's a whole nother topic that I could talk about it another time so what is someone that excuse me just for say it's not particularly the citric acid or the phosphoric acid that's in those those soft drinks it's the carbonic acid is what rips those things apart I don't I'm sorry I don't have to disagree with you I the studies that have looked at carbonic acid carbonic acid is very weakly buffered and so carbonic acid is in salsa water it's not erosive the studies have looked at it's not erosive it's too weakly buffered it just you know it has a low pH but then the minute it hits the mouth it gets neutralized by saliva it's the stronger asses the the things that have a higher total acidity that are buffered at a lower pH that drive the equation the additional thing would citric acid it also is a key later so not only does it attack the tooth service with the asset it also complexes the calcium and so the calcium doesn't build up to sort of prevent further the mineralization it's so it just keeps on producing the vernalization that's a whole nother presentation it is and Utah ranks number one in the United States in the amount of soda ingested on a per capita basis and we literally destroy our teeth in Utah and doesn't make any difference if it's diet or regular soda I grew up here it is and it's that proton that comes off of that carbonic acid that just rips teeth apart I'm not sure about that but I'd love to see the data so the number of factors then modified rate that can modify the remineralisation process I mentioned the tooth itself and in terms of its fluoride whether it's enamel dentin the acquired pellicle the biofilm itself saliva diet so the dye can affect two ways by if you have constant acid production in the plaque you're not gonna get any remineralization but also food itself has some protective factors and that milk is a great thing a great you know kids don't drink milk anymore milk is protective to teeth I just want to say that milk is protective the teeth that's calcium and phosphate in it it has casing and phosphor phosphoproteins it's very very good for teeth except when you put chocolate in it and then it's less kerogen I mean it's a little more tart like my kids drink chocolate so so what are the remineralization strategies fluoride I can almost stop there right now but I'll continue salivate stimulation possibly diet modification possibly if we neutralize the acid production we we should be able to switch the balance towards remineralization then we have the other remineralizing agents which are the subject of the study that's under consideration with this group which i think is an excellent study by the way and it really needs to be done and turns it no it can't help but just it's just that the pellicle modifies the effect this is the mouth and the pellicle is going to be there it just modifies the benefit to some extent it also protects this the tooth surface as well from erosion as well as to some acid from caries so it's a little bit of a trade-off I'm not saying we move to pellicle by the way so floyd has to be at the top of this list but if we look at the level of interest by a lot of clinicians the more interest in these remineralizing agents they are in fluoride to a certain extent not completely so I think we have to get the let the data speak here is that's the way I like to approach it we don't have a lot of evidence that's I'm going to summarize this slide we do not have a lot of evidence about remineralization we have a lot of evidence on demineralization we have very little evidence on remineralization even for fluoride at least according to Jim Bader but we know that Jim doesn't like anything he doesn't anything say nothing works okay there's a tremendous amount of variant in in terms of topical fluoride but I'm gonna try to just make this really simple for high-risk patients concentration is extremely important and I'm a big fan for high concentration of products based on the literature review I think the moment the best evidence right now is for fluoride varnishes although there's also reasonable support for the APF gels as well one thing I do have to mention is that anybody who's applying gel cam which has the same flora concentration as toothpaste is really ripping off dead patients okay it has the same concentration the the stannous iron has somewhat of a protective effect but if you look at this just from a pure concentration point of view you know send them home with a Foley to paste don't don't don't put it on their teeth in practice give them high concentration because we know this greater efficacy with that again I'm going to move quickly there's a lot of good evidence supporting the efficacy of for admonishes I was part of this evidence-based clinical recommendation it was a great process the a DA is doing a fantastic job I have the old version of this Julie showed you the new version which is great this is like you know who could who can read that and then what you show who is really good I'm really I'm very impressed by that that's it that's great you know she showed that one short version which is color-coded and all that to sort of summarizes all this stuff it's fantastic in terms of studies and now focusing on orthodontic patients again we're seeing that with in this case we're talking about floor protector which is actually has the one of the lowest concentrations of any of the four advantages which is only 0.1% which is again just the concentration found the toothpaste but it has this added benefit and it's the polyurethane varnish which actually offers some protection just from the varnish itself unlike some of the other four admonishes what we can see a definite benefit and in both the reducing the incidence I'm sorry the prevalence as well as the incidence of orthodontic induced caries in terms of the home products again concentration is important I think although I have to say from an evidence point of view there's not a lot of evidence to support president and the other Hika higher concentration products but based on our understanding of Forres mechanisms of action I'm still comfortable making a recommendation that we do need to prescribe for concentrations at higher concentrations than regular toothpaste and what we're doing now in our schools you recommend for our high-risk patients that they brush with a regular toothpaste in the morning and they brush with a high concentration gel before going to bed don't rinse don't spit oh I'm sorry spit don't rinse and then go to bed Floyd works for Jennifer's work for it dennah versus very we do at the Oral Health Research Institute we test pretty much every toothpaste on the planet not all four toothpastes are not created equal many of the newer products that have all these claims for marketing purposes or whitening brightening some of these get in the way of fluoride efficacy I just want to make that very clear to you not all of them but but some of them do and so for high-risk patients they really need the cleanest floor and delivery possible because most of the other stuff is just marketing as I said had to choose I usually I use I typically choose things that are simple you know that I know have can release fluoride in my mouth it's the Florida lion that works getting the fluoride in my in my mouth áfourá diet is the best thing we can do in terms of understanding you know how to pace work this is an application phase which is the concentration of fluoride that you can get in your mouth as you're brushing and then the retention phase which is keeping the fluoride in your mouth over a protracted period of time and so a lot of behavioral things come into play and modifying the retention phase just to show you how complicated we're doing a lot of research right now looking at the kinetics of Floyd in the mouth and and what modifies forward efficacy and so obviously the concentration of free fluoride ion is the biggest thing brushing frequency is obviously very important and is good literature to support that brushing effectiveness this is probably an interaction that goes on between brushing effectiveness and flora defectiveness in the sense that if you have a really thick plaque Floyd's gonna have some trouble getting through it so if you can fin out the plaque a little bit it's gonna work better keep in mind that fluoride when you brush the teeth with a fluoride toothpaste and it works on the plaque that stays in your mouth it doesn't work on the plaque you remove because if you're removing the plaque appropriately every day with your brush you don't need the fluoride you're not gonna get caries it's the plaque that remains and so it's a it's the Floyd's ability to to actually get into that plaque get through that plaque and get to the tooth surface that's how for it works in terms of for identify sirs we know that rinsing behaviors this was a poster out there saying that not rinsing after brushing is that was associated with an improved benefit that's that fits the literature and it's an actually a good recommendation for patients not to rinse out to spit and then go from there we know that flow rate oral Architecture modifies florid retention I talked about post brushing behaviors and timing the brush before after meals I think that will be a brush after meals and the reason I say that is because we know that fluoride mainly its benefit in terms of preventing dental caries is in terms of remineralization so I want to get the fluoride in after I have a carrier genic challenge we're also doing some research showing that the amount of Floyd you put on the brush is very important so this piece size recommendation I think is ok but for high caries risk risk patients even children I'd much rather they have less calories than less fluorosis I think we've oversold this fluorosis thing tremendously and I think the main thing is preventing caries so it has to be risk-based of course kids that are at high risk of caries need to get more more for it on the tooth brush because as I said a row the downfall of the downside chlorosis is much less a problem than the downside of caries in terms of aesthetics or anything else also the length of the brushing time we're doing research solving the longer you brush the better the fluoride efficacy which makes sense ok I just want to summarize that if you look at the recommendations that out there and the reviews that have been done which I don't think are all that good we have very weak evidence right now for any of these recommendations and the whole concept of the low the Floyd mouth rinse versus the high concentrations I think is actually wrong and my review of the literature and I'm just going to run through this if we think about a loaf a low flora concentration versus a high fluoride concentration low concentrations basically can do the things we wanted to do decrease the mineralization and increase the rate of remineralization those are the main but an increased rate of enamel remineralization is the main when I focus on but what a high concentration is doing most important thing and I got a bolded here is the high concentration provides the driving force to get the fluoride through the plaque so the plaque that the kids missing or the adults missing or the orthodontic patient is missing high concentration allows the Ford to get through the plaque to the tooth surface where it needs to work makes sense right solder so this whole concept of using a low concentration because we want to remineralize the whole lesion it's bogus it's just totally bogus it's I don't know how that snuck into people's minds but it's wrong and so we have John Featherstone study showing that a fluoride mounts Mountain rinse can be effective but this study doesn't have you know it really you know it's the model is a model and it's not really a clinical outcome so I'm not gonna I think this is all case study but I think I want more I want with data closer to what's happening clinically I don't not rather than I deal with extracted teeth as he did in that study I want to look at some clinical evidence and here's another study that was done by Alexander and Ripper which really looked at which which compared the rinse and the high concentration and showed the high concentration was more effective so I go with this study right here I just trumped the other study with this data in terms of studies done again when insight to models again looking at this concept low concentration versus high constant concentration both low and high concentration was able to remineralize through the depths of the lesion and again these are laboratory induced lesions and they concluded that a high concentration did not block the in the in with the diffusion of floyd into the lesion and they got better efficacy better remineralization with the higher concentration so again that tells me high concentration as well we need to go with these dissipation population again here's another study looking at does low concentration work better it didn't work any better than control so it really didn't do any good so a takeaway point here and a very important point is when we D banned the patient those teeth are going to tend to remineralize anyway do nothing just just changing the oral environment by taking the the the stagnation areas of those teeth are gonna be mineralized naturally to a certain extent we got to keep that in mind so when you see data that's generated by a company they don't have a proper control and they showed you getting a benefit from whatever product this would this disregard that data because it's not you know without a proper control and proper randomization you can't believe that stuff all right I'm going to skip first of all rinsing is the problem with compliance I'm just gonna run through this the the cart you know I look I really want something other than forward because it'll be great to have other other tools out there but right now the data isn't strong enough for me to accept this new tool reviews looking at the evidence the problem with the recalde end data is that it's it's it's all all the positive evidence comes from one group and all the and then everybody else out there is not finding it including me so we have to be very careful I know you're running a study this study really needs to be done it really needs to be done and it has you know and it's a well it's a well-designed study I I just want to commend investigators and the study dentists for really doing this study and then I want to if it's not fully enrolled I want to you know get other people excited about enrolling for this study cuz it's an important study that needs to be done first of all it's much better to prevent demineralization than they try to repair remineralize the damage because you can't fully remineralize all patients on the going orthodontic treatment must be considered at high risk until proven otherwise all patients should be carefully examined at each visit for early signs of the mineralization in other words I think that it should be a standard protocol that every patients teeth are examined at every whether it's at eight weeks or ten weeks or six weeks it doesn't matter they should be have the teeth cleaned and and the stand and the two surfaces should be examined very carefully for science at the mineralization and that all patients again should be put on a high-risk preventive regime except for the patients in your study of course because that has to be controlled I'm going to stop there and I apologize for going over you've been a great audience I really enjoyed the questions and the interaction thank you very much you

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