ETYOLOGY AND RISK FACTORS.pdf

And now we will see the additional like risk factors. Because as of now we said we consider the primary theology to be bacterial plaque. Unless we're talking about the non biofilm induced gingival diseases which is a different category. So we will go over mainly the local systemic risk factors that...

And now we will see the additional like risk factors. Because as of now we said we consider the primary theology to be bacterial plaque. Unless we're talking about the non biofilm induced gingival diseases which is a different category. So we will go over mainly the local systemic risk factors that you see in the clinic. And we're going to talk very briefly about the epidemiology what to expect to see. And we're going to see how we can classify that. Obviously a lot of those factors fall under the classification of the disease that we talked. Either it's like smoking diabetes or local factors. So we're going to go over those as well. So a couple of things is as a question what is the main etiology of biofilm induced gingivitis or periodontitis. We said bacterial plaque right. Is plaque sufficient to cause disease. Not where we went before that. No, before, because we can have adequate plaque accumulation, but we can have different forms of the disease. As you see, you can have a lot of plaque and minimal just gingivitis, and you can have minor plaque in those severe forms of the disease, those aggressive forms as we talked about. So things to consider when we talk about that. And we're going to talk like why are risk factors important to disease development and etiology. Because who developed the disease. How severe the disease is. Which side of the dentition will be affected. How fast or slow the disease will progress, and what is the record, the response to the therapy? What is the recurrence rate? Everything you know depends on the patient. And that's why we are also talking about this personalized medicine and eventually dentistry. Because yes, we do have textbook answers. We see something. We want to make it work for our diagnosis for something. And we try to fit that. And sometimes it's beyond this one. We have to have our eyes open and understand what's happening. And I'm going to share towards the end the case that I actually came across last week, which, you know, I'm going to say that I fall under this trap saying, okay, I have to make this fit what we know about this case. Okay. So just to keep your mind open. So remember I told you about this scheme and we already talked about the bacteria. We talked about the host response. All this antigens, the LPs, the neutrophils, the cells that play a role, the macrophages the maps, the cytokines and how eventually we lead into connective tissue and bone destruction, going to the clinical signs of the disease as we saw as we see. And today we're going to talk about those two yellow boxes as we see over here with environmental and genetic factors. So an individual's like susceptibility to personal disease depends on an interplay between several factors, like the nature and virulence of microbial challenge, the oral ecology, the robustness of the host defense genetic factors. And you can have on top of those things. That's like an interplay in a game. With that, you can have a bunch of risk factors, either local or systemic, and we're going to go over those things that can make things work worse, more challenging. Either diagnose to treat and see what you're going to be doing there. Okay, so a couple of definitions before we start. What is a risk factor is like behavior a lifestyle as we see over here, environmental exposure a characteristic that changes the susceptibility to parental disease. It can be local which increase can increase like the infection at a site. And in order to identify like risk factors and their importance to the disease, we need to have studies that confirm those things. Okay. So in dentistry and I'm going to talk about ontology mainly. We have a lot of cross-sectional studies because they're easier to be done. Like looking at one specific point of time. You have your patients. You're looking at them clinically sub clinically trying to exclude confounding things and find risk factors, which you do consider those purely risk factors when you do have these longitudinal studies, like when you start a clinical study looking for the patient, onward. That's how you try to identify true risk factors. You can have evidence for causality in animal and in vitro studies in terms of their mechanism of action. But on the other hand, in order to have a true like the causality and the measurement, you need those randomized clinical trials. If you've ever heard about those are the top of our pyramid in terms of evidence. Because if you design and obviously they have to be very well designed, right. Because you can have bad, poorly designed clinical trials with poor outcomes. So if you have proper randomized clinical trials, you should be able that if you remove the risk factors that you identified from here, you can change and measure the disease outcome. So there were studies that were trying to find smokers let's say versus non smokers. They have to have everything else kind of identical as much as possible. Like you can have other factors, but you're trying to identify those things in order to truly see like the impact of this specific risk factor and the disease outcome. Okay. That's how we get our knowledge with that. So as a backup here, for example, for the studies and the characteristics. So with those cross-sectional studies. You can in your analysis. You can have you can eliminate confounding factors like other factors that may play a role. An example for that would be. Let's say you want to find a specific impact of bacteria and clinical case scenario in paired entities. You exclude, let's say smokers because we know about that. But there could be other things like the age, the ethnicity, other things that may play a role. Because we do know that specific, you know, racial groups may have more prevalence and more the disease may be more prevalent in those. So there are statistical analyzes that you can exclude those and just look for the specific factor you're looking for. When you're having those longitudinal epidemiologic studies, you're trying to see those those response effects in order to find like this causal pathway and something that I need to keep to stress out here is the different difference between causation and association. Okay, there. There's plenty plenty of studies that we try to associate what we see with something else that exists. This may be a connection, but it doesn't mean that it's a true causation of the disease. Right? Makes sense. What I say, it's like I should have had a picture here. There is a funny picture around whatever social that there is, like a metallic trend, if I can say so, which is destroyed and a cat sits on that destroyed part, doesn't mean that the cat destroyed it, right? Could be associated, as we say, but it doesn't mean that the cat actually did that. So having said that, a lot of times when looking at the studies and it's really important for you to draw conclusions, because whatever you read and you say you're saying those things to your patients, like, and it's not only this, patients read those studies. And sometimes to make it easier for the population, they come up in either magazines or newspapers in a way, or websites that it's easy for the patients to understand. And they come like, for example, and we're going to learn about those in our next semester. When a whole hype came with cardiovascular diseases and dental diseases, I had patients that came with a paper and said, these tales that I'm going to get a heart attack because they have peritonitis, and now we need to explain what happens and what the risk factors, indicators, etcetera are. So having said that, we can have the mechanism studies that are studies that are trying to find consistent result among the population, and finally, the intervention studies that you're trying to find the relationship that is biologically plausible, plausible, and see the disease outcome. So let's see some examples we said about for example, smoking. So that's considered a risk factor for disease. There are numerous biologically plausible explanations for these agents. You know, for smoking to have an impact on periodontal disease and have a lot of prospective studies that have shown that clinical trials and shown that smokers are more likely to developers on theories of non smokers. The question now is being raised in terms of other smoking products, from marijuana to these electronic cigarets and vapes and everything like that. We have very preliminary results. They started with in vitro studies in terms of that. So eventually this may have an additional, you know, explanation in the future, but just bring it up because a lot of things are happening when you see patients in the clinic, for example, do you remember from the classification, if a patient is a smoker, we take that into consideration for what the grading. Right. And let's say the patient says, oh, I'm just using a vape or I'm just smoking marijuana or something like this. So it's difficult for you to put the grading over here because you don't have the evidence, because as of now, we know not only the impact of the smoke per se, but we do know the impact of the bless you, the nicotine, you know, the tobacco, the deleterious effects and everything like that. Okay. So a risk indicator is something that is associated with increased probability of the disease based on those cross-sectional studies. So what are those cross-sectional studies. You take a population, you see them at a specific time a specific slot in time. You extract data and based on what your connections and associations you see over there, you draw conclusions about what. So where is it associations, right. You can say, oh, that's what am I doing something. You can't draw conclusions of direct like risk factor from a cross-sectional study, because it's a one time thing that you see the patient for. It could either be a probable or a purely risk factor. And if you confirm it in longitudinal studies and eventually clinical trials, you can eventually call them risk factors. And obviously, you know, the smoking. That's how it started, right. They notice those things and eventually they move to the other side. An example like for risk indicator, the presence of this herpesvirus as we see over here is considered like a risk indicator for period disease. There is a biologically plausible explanation why this can lead and cause can be related actually to disease. But we don't have so far like evidence that actually the evidence is being associated mainly in cross-sectional studies. Okay. And finally, in terms of risk marker, these are like let's say exposures or. That may are increased with an increased probability of the disease. But they are not factors in the causal pathway. They are somehow associated with the true risk factor. And they may be associated with the disease but are not in this causal pathway. And if you change the causal pathway or actually if you change this risk marker, it may not affect the disease. And how does it work? You know that a, you know, has a causation for B, but C is associated with A. So you assume that C may have an association with B. That's how it works in that. So for example A missing teeth, and you may have seen in several studies that people that researchers actually evaluate the number of missing teeth for their grading, for prognosis, for everything. They consider it a risk marker for disease. But it doesn't mean that if you missed it, you definitely has a causation for burden theories. I'm happy that with the new classification, they differentiate the reason for why one is missing teeth, right? Because 1st May be missing teeth, because of trauma, of caries, of anything else other than a disease. And that may have no association with that. Clear with that. Okay. Are risk factors modifiable? Yes or no? Yes. Some of them. Right. Some you can do something. Some you can do something. All right. Like genetic factors. You can't do much over there. It's what it is. So an example of modification. If you're having like smoking you're having your patient have a smoking cessation sequence for diabetes. You're trying to improve the glycemic control and other like risk indicators. As you see here with the calcium the osteoporosis you give specific either medication diet changes, advice anything like that. Stress. Good luck with that. I don't know if we can do this. Like this question. Like have you ever tried to stress less? Yes. I'm trying every single day. Yes. How can you differentiate between. These factors or the indicators. So this goes back to what we said. What is considered a risk factor based on what studies you have the results from, if you're having from longitudinal studies and then clinical trials, you know that it's a risk factor if you're having from cross-sectional studies. So risk indicator clear. That's clear. Good. And eventually. I mean, as of now, that's what we know. Eventually, in the future, you may add things. I mean, in terms of risk indicators, we're adding more and more because now that we have more research, we find more things either subclinical or clinically that may be associated, especially now with inflammation or we talk about. So eventually in the future you will have more information. But that's what we know as of now. So in terms of the risk factors there is a clear dose response. So the more exposure you have to the risk factor the greater the susceptibility to the disease. So that's like examples. The more you smoke for how many packs per year we say like how many cigarets a day for how many years is obviously brings in increase your risk for diet, for attachment loss, deeper probing, bone loss, periodontal disease etcetera. So there are several studies that there is. There are several studies that show that on these at the same time we have like a clinical, as we say, threshold that anything below that may be clinically, you know, negligible. So we don't carry about that. If somebody said, oh, I smoked two cigarets ten years ago, it may have a negligible effect on what you see clinically. So let's go and analyze a little bit those local risk factors. And these are actually all the things that you will see in the clinic coming up. And you should be able to diagnose and find them, because the more you see them and you try to eliminate them, the better outcome you have. Usually those are local factors associated with either a specific tooth or size or something that you see specific destruction. And what are they most mostly associated with plaque retention. Right. So we know about the role of bacterial plaque of biofilms. So these just help bacteria to accumulate and and create more risk for the disease. So it's very important to identify them during a periodic comprehensive examination. If you miss it, which you shouldn't, you should be able to find it afterwards. Because if you remove or eliminate or modify during your treatment plan, you will have a more successful treatment outcome. I had seen cases that some local factors were not identified, and because of that, and because of that, we were doing our treatments and everything, and they were not working because a specific local factor was not identified. The moment we identified and removed it, everything changed in the treatment outcome. So as you remember, this comes in these localized tooth related factors that predispose to inflammation periodontal disease. And we're just going to go step by step to see those. We talked about the developmental grooves concavity and CPP. So let's get some more information on those. So the grooves as we said it's usually an anomaly that's found on the maxillary incisors mainly on the laterals I think these are yes in the classification I shared a case where there was a small groove on a lateral, remember. And there was like more destruction. So obviously the presence of that is associated with poorer periodontal health, more plaque accumulation, bleeding and probing deeper, deeper probing, as we said, more prevalent in the lateral incisors. And that's an example for of the case I showed you. You can see if you are lacking the radiograph like a small kind of groove over here. Radiographic. Otherwise clinically when you probe right in the where the groove is, sometimes the probe may get deeper. So what's very common is unless you have a severe distraction already formed there is that you may have a considerable, you know within the normal limits pocket like a three millimeter one, which you would not expect, palatal on a lateral on a healthy or a gingivitis. Okay. So that's what we'll say. Like it's a deep three millimeter pocket which brings obviously more caution to the patient and you to see if you need to do something more. Because if it starts to progress, eventually, the more narrow this groove is, the more challenging it's going to be for treatment or elimination. Sometimes, depending on the distraction or when you see the patient, you may have some vertical bone loss in those areas. But this doesn't mean that every single, you know, incisor tooth with a pilot or gingival groove will show periodontal destruction. That's something. What? I see that and there's nothing there. I stress it out to the patient and say, you know, in this area, make sure you brush more efficiently over there and they will check it more frequently. Make sure there's no destruction over there. In terms of concavity, obviously, you should know that mainly those premolars and molars have those cavities, those maxillary premolars that verification entrance can be very low and very narrow. And these are like the most challenging teeth that can be in. Terms of treatment. I think that's why ortho may decide to just remove those for their ortho purposes. It's easier because obviously if you're having severe perio issues in a premolar, we usually end up taking those teeth out unless we can keep them somehow. So keep in mind that this concavity can be very pronounced, especially on the first maxillary premolars. These are things to consider in terms of deeper pockets of bone loss that you may have there of your restorative options, if you ever. Let's say I want to have a crown, I want to have a restoration there. And I maybe need a crown lengthening or something. Those things have to be considered and taking into account when you decide those. The same thing happens with the mandibular and maxillary molars. You see how frequently those concavity show up in those roots, and what you need to keep in mind. Do you see how narrow this for this concavity is? I mean, good luck getting very accurate or something like I can if you can't, great. But like the entrance can be so narrow, like 0.70.5 and the diameter of the cured is usually larger than that. So it's very, very challenging. And that's a great house housing let's say for bacteria to accumulate and create issues. That's why teeth with vacation involvement. If you do remember from the classification, automatically they move the staging because they're a complexity factor that makes things more challenging, clear. And I think we did go over the vacation classification in a few lectures ago. So keeping that in mind regarding the key piece, the cervical enamel projections, we talked about those briefly. They're being found in molars more frequently. You're going to have this greater one, which shows like a small dip towards the vacation, which could be associated with attachment loss, either in the form of recession or deeper pocket. As you see on that side, the grade two, it extends towards the vacation, but it doesn't reach the vacation. And finally the grade three extends towards the vacation. So one and three are usually the more frequent ones. And obviously teeth with grade three four with a grade three projection are having usually poorer prognosis because you you're losing depending also how deep this goes and how low these vacation entrances as we see here, they're more prevalent in mandibular molars and second molars. We said about the grade one and three, there's obviously a correlation between those caps and deprecation. It's like an anatomic trap. Depending on the case, you can do some plastic there and try to eliminate it and remove it. But if you already have severe distraction in the vacation area, you may have to weigh the pros and cons like, is it actually worth it? Will I gain anything back? So I'm not saying that you have to take the 2000 per se, but that's something that you need to keep in mind when evaluating if it's worth it for the tooth. The other things is sometimes they can be pretty deep, those seeps, and they can go closer to the pulp. They may include, like even some pulp endings, depending on where they are. So you have to be careful how much plaster you do towards the vacation there. Okay then let's see those other three categories. Regarding the enamel pearls. We talked about those. We showed them up a few lectures ago. So these are in the vacation areas mandibular and maxillary usually third molars. But you can see in other molars as well. And you see like there's fusion here with the dentin located apical to the s.j. And mainly third molars are affected. And that's great because if they are third molars we can easily say let's take them out compared to being a first molar obviously radiograph, you see like those round areas around them. They may include like popcorn. So you have to be careful if you decide let's say if it's on a first or second molar and you decide to keep the tooth and you say I'm going to do some plastic there, you have to be careful about that. So you see like radio structure over here. Regarding root proximity, you have several cases we've showed about that. So what's the issue with the root proximity. Super challenging for the patient to clean. The septal bone is super thin sometimes if you know not present. And we've talked about how approximately the disease can go in this non canonized crawlspace. Create inflammation. Remember from this host response what's happening there in terms of bone resorption. You barely have any thick cortical bone here. So it's very easy for these to be resolved and have periodontal destruction on those areas. Regarding open contacts, we talked about those. They're associated mainly with food impaction. And we know that food impaction is associated with increased probing that and increase clinical attachment loss. So if it's a solid tooth with an open contact because of how the tooth is being located there, I always consult an orthodontist to see if we can do something orthodontic and closer contact. If it's because restoration is not well done made and the contact is not adequate, we need to make sure that it's a matter of a restoration only or restoration, because if the space is bigger, sometimes it try to close the contact with a restoration and they make these bulky, weird restorations which can create then other traps underneath her, which is not solving the issue. There's plenty of seats here. Regarding occlusion. So what's the issue with occlusion? Apart from any orthodontic issues that you may encounter? Any questions? No. Okay. That's fine. The other thing is that you may have some tissue trauma. Right. So you see over here this patient was biting and it was actually a huge wound underneath those central incisors because of these deep bite creating issues. The same. This is like another patient the moment the way they were actually I think that's the patient. Yeah. So the way she was biting, you see because of various diseases and other things. So it's a kind of association like teeth migrated forces were in the way. So teeth tried to adapt. So creating issues both auth and barrier. So thinking and keeping those in mind in terms of your treatment plan as well overhanging restorations. We talked about those as well. Obviously if you're having those little or wider peaks in this case we have an additional issue, which is what the open contact. Right. So you have two things that play a role. And obviously the solution to those things would be I mean, I don't know if you can save this tooth. It's such an apical restoration, although the radiograph may be deceiving but obviously evaluating if you can save it. And if you can replace that with a proper restoration and proper contact. We talked about the sub crown margins in the biologic way. Do we remember the biologic width. Yes. No. Know a little bit. They will remember how we call it now. Super progressive attachment. Excellent. So just as a reminder here, we talked about the biologic with which we. On average, we consider it about three millimeters. I talked about that last time. I'm going to say that again. It all depends on the patient the side the tooth. Right. That measurement doesn't qualify like doesn't is not the same for every single side, for every single tooth, for every patient with two. We do take this into consideration when we try to do our planning. But proper biologic width measurement because these may vary. How much junctional epithelium, how much connective tissue attachment you have, how deep your sulcus is. So all those things have to be taken into consideration when you're evaluating for your crowns, because eventually you may either end up with recessions or you may end up with deeper pockets and inflammation. And in those cases, when you know that your crowns will have to end up gingival for whatever reason, for ferrule, for retention, for esthetics, for whatever reason, which is totally acceptable, you need to see what is the that's what you would discuss with the president is okay, can we do a crown lengthening? And if you just ask me, can we do a crown lengthening and said, yes, I can do a crown lengthening even on the root tip, I'm just opening and removing bone. That's not a big deal for me. The amount the rationale is to know how much you need. So my next question will be okay, how much you need and where. And then based on that answer, I identify okay, do. If I do that, will I compromise? My treatment outcome will have like a poorer crown truth ratio will expose vacation will compromise neighboring teeth, will have a concavity in the way. So there's a lot of things to consider. It's not about being able to do it. Yes, we can do we can do a crown in a hopeless tooth. That's not a big deal. The point is to identify what's the right thing to do. And obviously the answer is not okay, I'm just going to put the crown. I'm going to call some inflammation so I will get my crown. Anything like this, naturally that doesn't exist. I'm pointing it out because I've heard it being said, you're not just putting a crown and hoping that whatever inflammation is being caused there will give you the crown lengthening that you want to have, right? It will just give you issues discomfort from the patient. It doesn't mean that every patient will have like bone resorption. On that side. We can have constant bleeding, inflammation pockets, irregular margins. So you have to be very careful with that. So in terms of your restorations and I know I'm a periodontist, but before becoming a periodontist, I was a dentist and I had to deal with the restorations. And that's why I chose to become a periodontist. You have to be careful with the roughness of the restorative materials. I've seen that rough. I couldn't believe it until I saw it. That's a little rough and can be very harmful to the gingiva, the interface between the tooth and the restoration to either be rough or uneven, either having an overhanging material x marginal discrepancies expose segment margins, subject margins, and over contoured crown. So all those things have to be taken into consideration because sometimes it's just a matter of one changing something that's not right here and not needing an actual crown lengthening. Right. I had once, it was once a patient here at school. The student said, we need some crown lengthening. There's inflammation. I said, sure, let me take a look. But the temporary was not very well made. So I talked with restorative faculty as well and said, let's try to fix that first and see what's happening. And the patient didn't need it. The moment they fixed the temp, everything was fine afterwards. Okay. So I would have had the patient go through an unnecessary procedure, maybe reduce more bone and support that was not needed for something that could easily be fixed with newer and well designed. And so when we're doing the restorations, we also have to be mindful about the core, the cords that you're putting over there, how you put them, how long you leave them, take them out, don't leave them there. I've seen this happening. It doesn't look nice, so just keep that in mind as well. You also need to have contact areas that allow for the normal papilla. Yes. What is the time frame that you take to decide either if it was the restoration of the temp that was affecting the area, or you are going to go ahead and and okay. If I understand your question, let's say you say I think it may be the temporary or the restoration. Let me fix that. How long you're waiting before you're deciding for a crown lengthening. So. It depends on the situation. But to be honest, if it was something as a clear fix, we've learned about the healing of the gingiva in terms of that can happen within a couple of weeks or even less. Right? I would usually wait about a month just to be on the safer side, but I wouldn't drag it for longer if I see that there is. Venous inflammation. And obviously I would definitely make sure that the patient is cleaning and brushing, you know, effectively over there because you may eliminate the contacts. But if there is no good oral hygiene then you may still have inflammation. And again, do you do a procedure when somebody is not good with their oral hygiene, knowing that this may have a negative impact on the healing, you know, on in terms of how long the healing will take, how predictable and everything like that. So it depends on what you're expecting to heal. If we're talking about soft tissue, you know that the turnover of the epithelial cells are way fast technically, sometimes even within a couple of weeks. You can see that just to make sure everything is stable. And we wait a month. Now, do you need to wait longer for whatever reasons shouldn't harm as long as your restoration you temporary is fine. Okay, any other question? Nope. So we said about the contact areas we need to allow the popular to grow. Do not like suffocate or strangle the poor papilla over there. Obviously we prefer super gingival margins when possible and if we have to go sub gingival for esthetic purposes, usually we place them really, really shallow. So you have to be very careful with your preparation and your design of your crowns, which means that you are invading, if I can say so, towards this biologic width space, because you're getting in the circular area, but you're not violating that. Right. So there's a difference in terms of that in the gingival crevice. So you need to have sufficient tooth reduction to avoid to overbuild crowns. Obviously a good impression with a good cord excess cement should be removed. That's very very important. And obviously if you're doing fixed procedures, having hygienic contacts have shown that it has a better outcome in terms of the hygiene over there. So yes, that's not what I will be doing. But if a patient comes and has any of those that are not this way in term, instead of just rushing doing procedures, the first thing I would say is, you know what, let's try to fix those and see what we can get over there. Okay. We got the same thing applies for your removable prosthesis. The partial dentures or poorly designed acrylic dentures can have issues on the gingiva with inflammation, trauma sometimes either in the papilla or the attached gingiva, depending on how the denture is sitting. So obviously if you remove the partial denture, the procedures and you see some redness, you know that something is not working properly either from the denture, the hygiene or anything like that. And regarding the design here, like what is the problem here on this one? Like you have the metal sitting all over blocking everything, right. So these eventually will create issues. So obviously try to have a design that supports the appropriate here that supports the appropriate like use of the rest seats. You have clearance of the gingiva. You know a similar thing on the other side. Utilize it. The design should be kept simple. The less the better, the more simple the better and maintained adequately long term. In terms of having like a whole bar closing everything here. Okay. And again, I don't take credit on that. On the denture. You know I don't do those. I'm just saying as an advice, like if you see that the first thing we're expecting is the gingiva to be inflamed underneath. Regarding orthodontic appliances, yes, we could have injury. So it's important how those are being placed. The most challenging with those orthodontic appliances is not their place per se, because sometimes you may not have the space to do things, but it's the plaque retention. So it's very, very important to be able to maintain that. Usually patients with during ortho treatment, I see them way more frequently than other patients because sometimes they try their best. They may not have the best oral hygiene outcome. Sometimes they don't try their best, so things are even worse. So having said that, I it's very important to know how those are being designed. Sometimes those bands can be placed very sub gingival creating issues. So keeping that in mind as well. Regarding root fractures obviously we said about the root fractures what is a possible differential clinical finding for a root fracture. Huh. Isolated deep pocket right. It doesn't mean that any tooth with a deep isolated pocket is has a fracture on the one hand, but on the other hand it can because it could be associated with an endo issue with combined endo and other things. But when everything is probing fine and suddenly you're probing deep in one side, you're suspicious of a root fracture. And unless you see that clinically, obviously you want to do an exploratory flap and see if the tooth is fractured like it was. In that case, we have talked about cervical resorption that can create perio issues like in this young patient. Sometimes those are challenging to be diagnosed because if they're early at an early stage we may think, oh, it's a burnout in the radiograph as you see over here. But it's very important to diagnose that. We talked I think we talked about resorption in our diagnosis part where using Sid scan and everything is helping to find how how much it extends. If it goes closer to the pulp the circumferential like spread and everything. So these can cause problems because when the patient came in they said everything is fine, he just has something there. And this was like a 16 or so year old patient. And the parents were afraid, oh, my kid may have cancer there. So that's the thing that they're thinking of, right? Because everything else seems to be fine. So keeping in mind those local factors that can show up their segmental tears, we have talked about them. These are like, you see those thin lines as you see on those sides, which may look like a fracture, but it's actually the cement that has been removed. And this was actually a case that was referred to me. These two had trauma years ago, obviously. You see, like it's obliterated like calcified canal. The patient had a crown again some years ago because the tooth got discolored and eventually was symptomatic. They said, you know what, we won't be able to find a canal. We can try, but chances are we won't be able to find that. And eventually they tried with the endo Dantes, who's very good, apparently because he was able to find the canal and go all the way down, do the medication. I said, great, so we can give some time on these tooth. But then a few months afterwards, the patient showed up with even more delusions and swelling and pain and severe mobility on that tooth. And if you see a little bit over here, that little thing, that was that little thing. So what happens with those things? They show up as some foreign bodies. And that's why you have a reaction of possible abscess or anything like that. Calculus. Yeah I know we talk about calculus. It's calcified plaque but it's obviously a rough irregular surface. It can collect more plaque. It can accumulate like plaque and seed over there cannot be removed. You know, the moment you have the toothbrush cannot remove the calculus. It acts as a reservoir for periodontal pathogens and endotoxins. Shelter from the host defense. Whatever is happening, it's like a perfect bed for plac to sit on top of that. And as we all know, as of today, the majority of our period treatment is targeting on removing all this calculus or this reservoir of plaque and calcified plaque that we have over there, keeping and actually knowing the difference between supra and sub gingival calculus. Obviously, you can see the difference in the color for the supra gingival one. Keep in mind that depending on the extrinsic stains, diet habits like smoking or whatever, it may also change color, but usually it's more whitish compared to the sub gingival one which is brown brownish black base. Also on the pigments it's get over there and obviously the volume is derived from the saliva while sub gingival we have from the GCF. So on the calculus sometimes you see it more pronounced in areas where you have these major salivary ducts, like the sublingual ones, and the buckle maxillary molars where you have the parotid gland. So where you will have you will see those clinically regarding local trauma. You know, this can be with excessive brushing, with any habit, with local factors. One of the things like if I see very isolated destruction on mandibular incisors, either buckle or lingual, I always ask, did you ever had a tongue, lip, whatever, piercing or so. Usually those they hit more these areas they continue trauma I was told by. Uh, how do you call them? Like. I don't know. Piercer. The two artists who does piercing, I don't know what's the name that eventually those. I don't know if it's true, because I haven't done the research that eventually they have to change to smaller size of buttons or like something that goes over the piercing. That wouldn't create those issues. I don't know if it's true. He said that he did a lecture for that on Harvard. I don't know, I'm just telling you out, but obviously I've seen that the longer and the more traumatic those piercings are, the more challenges you have. Um, you can have issues in terms of recession, bone loss and periodontal issues. So here you can you have this recession. So when you see that what do you think it could be. Why do we have this one over here. Brushing. Brushing. Sure. What else. Huh? I'm sorry. Asked for the first one. No, no, no. Here. This is the piercing. We know we talked about it. I'm talking about this one. That's great. Okay. Yeah. I don't see much of a freedom. Brushing is fine because the first thing is like, you know, show me how you brush. Brushing was fine. Trauma. What kind of trauma? Occlusal trauma. And what did we learn about occlusal trauma? We learned can occlusal trauma caused periodontal disease and attachment loss? Both. No occlusal trauma. Let's clarify that cannot cause periodontal disease, right? Only if you're having severe forms of periodontal disease can exacerbate the progress. But it doesn't cause that, right? The restoration. Maybe it's a virgin tooth toothbrush. Nope. Huh I like what? I said. Yeah, you're getting close. So actually it was she's talking about oral habit. So when you take those things out, you're taking out restoration. You're taking out any issues, any restorative issues, anything like that. Then the next thing I'm saying is, okay, tell me what you're chewing. Because usually they have habits. So this specific patient was actually scratching his gums with pens. You know, there's this habit. Everybody does those things. I mean there's worse because this can be fixed easily compared to this one. Who lost the temporary. No, it wasn't a temporary. It was like a fixed prosthesis. She lost it and she went and took superglue to put it on. And now you don't see the exact you don't see like the beauty of that. She even realized that this is way wider than the other one. This is pink. So she was taking nail polish to make it pink as well. So yeah, this one. I don't have a solution. You just need to take the teeth out. Okay. We talked about three nail attachments. Yes. Obviously they can be a contributing factor because of the pull that you can have usually could be associated with some recession areas. It doesn't mean that whoever has a free nail attachment, which is more pronounced, they will get that. But you will see that frequently in those areas. Some more plaque retention, because the access on hygiene may not be easy or may not be comfortable for the patient. Usually patients like these, they would say, I can't brush there. It's sensitive. Obviously there's things that we can do to fix that, but keeping that in mind and then mouth breathing and adequate lip seal, obviously you see in those patients they have more edema to smooth gingiva, mainly on the maxillary interiors with the surface is dehydrated. The environment the microenvironment here changes and you have higher levels of dental plaque and inflammation. So obviously finishing those local factors section the oral hygiene we know that it can, you know, has a clear causal relationship between poor hygiene and gingivitis, gingival inflammation. It has a minimal, you know, very little effect on sub gingival microflora because you can there go there deep on the one hand. But obviously meticulous oral hygiene is a key thing for our patients for maintenance of our treatment outcome. And we stress it out because we can't clean our patients teeth every single day. And we reinforce it again. I know people may say it's just an oral hygiene, but a proper session can take at least 20 minutes for people to understand what they need to do and why. Because if you tell them, yeah, I do brush and then you ask them like, okay, show me how you brush. Well, I do this thing and I'm done. And it's nice. So it takes time to change habit. And obviously the more. You need to change this, the more changes you need to do for this habit, the more challenging it may be for your patient. So going to the systemic risk factors, you do see here that you have a bunch of those that may play a role. Those that I have it in a red box that are considered risk indicators. We mentioned those in the beginning. So a few things regarding smoking. This will be coming again and again and again because we need to know the impact of that. We have in the exaggeration of the inflammatory responses, the suppression of the immune response. We have the direct toxic effects of the cells, the thermal effects that we have of the smoking. It can contribute to increased stain staining and calculus. It can change the oral flora. Obviously, it suppresses the hemorrhagic response as we measure by bleeding and probing. That's why a lot of time smokers, you may probe and you don't see bleeding. That doesn't mean that they do not have disease or inflammation. Smoking does mask the inflammation as we see over here inhibits, like the growth and attachment of fibroblasts in the PDL and enhances production of cytokines like the TNF alpha that causes the release of other cytokines. It has been confirmed by numerous studies as a true risk factor. That's why we have it in our classification in many longitudinal studies. And obviously heavy smokers have higher chances like more than two times. And let's. In terms of losing attachment and bone. And obviously smokers have increased risk for tooth loss even sometimes following periodontal treatment. They may not respond very well to treatment. They have delayed wound healing. So there are things to keep in mind when treating a smoker and why smoking cessation is very important. The majority of the patients that have refractory periodontitis are usually smokers. The healing is slower, as we said, and that's why sometimes if you're considering doing surgeries from implants to whatever in a smoker, you know that your healing outcome may not be the ideal. And obviously the smoking changes that microenvironment in the oral cavity promotes the habitation for periodontal pathogens and even in shallow pockets. So there is a true clear evidence that smoking is a major risk factor for prolonged times. Okay. Going to our second through major risk factor, which is diabetes, we do know that we have a bidirectional relationship. The we have those two types the type one diabetes and type two diabetes. Oh my god why did it change? I'm sorry about that. I think it goes by itself. Okay now. So where we have the type one the insulin dependent and the non insulin dependent where the onset is on in childhood. Here usually the type two we see that in adults which we can associate with other medical issues from obesity with high cholesterol other cardiovascular issues. So keeping that in mind because there is an association and we're going to see about those connections in future lectures second semester, keeping in mind that how the range is in terms of the A1 and the glucose are. But we usually ask for the A1 C, because that shows us a matter of measurement for at least three months. Usually patients do it every three months. And remember how what's the the threshold we have for a1 c to make sure it's controlled seven. Remember they used to say 6.5. Yes. But remember for the cutoff for the diagnosis anything below seven they consider that like control diabetes okay. So yes 6.5 is how you do the diagnosis. But in terms of controlling it it's anything below seven. Clear okay. The complication complications. You need to know those those five complications that are for diabetes which is retinopathy in the property neuropathy vascular disease and altered wound healing. And the sixth one is disease. It has been established it's considered like a sixth complication for diabetes. So keeping those in mind is everything okay. Now, is something bothering you? Because suddenly the class is a little bit hyper. You were talking about that race and we had a test yesterday. Oh, okay. So did you answer correctly? I was a 6.5 thing. Yeah, okay. I don't know how. The question was asked, so don't take me. Wrong. But I'm saying based on the newer findings and how we have it in the classification. Okay, okay, okay. So suddenly they are so hyper about diabetes. I remember with a grading like how can diabetes modify things if the a if patient is not diabetic, obviously it falls under the low the grade if patient is diabetic but controlled which is ANC below seven okay. That's considered grade B and everything. If diabetes is not controlled which is ANC above seven. Yes. To be diagnosed you need to have the ANC over like the 6.5. They used to have that in before because they have the range of pre-diabetic. Whereas my thing. Yep. So they have the pre-diabetic range here. Anything between this range is considered pre-diabetes and obviously after 6.5 is diabetes, but control is 6.5 to 7. So I'm not saying you answered wrong, but I'm just saying I don't know how the question was. Okay. Are you talking with weird names? Okay. Is it clear? And that's how you ask your patients. The first question is like, how has your A1 said to know how you're going to classify them? So both type one and two diabetes are thought to lead to increased infections. Obviously non controlled diabetes I had seen one patient who came in with I don't think I've ever seen more abscesses in the patient's mouth and young patients in his late 20s or early 30, something like that. And he had at least 15 abscesses in the mouth everywhere. So initially I thought there is something else going on, but apparently he was uncontrolled diabetic because his agency was like 15 or so. I don't know. So obviously things to keep in mind. Impaired immune response like the protective one impaired wound healing, this hyper inflammatory state. We've been talking about this hyper inflammatory state. And now a little bit besides that, because of all these things that have we have explored and found with, with a with Covid, they had because the whole thing is about inflammation. Right. And there are studies that show that patients that were pre-diabetic after getting Covid, they shifted to a diabetic stage and patients that had like family history of diabetes and were more prone to get diabetes. Eventually, after getting Covid, they became more pre-diabetic. So obviously this is something to consider. Not sure how long it stays, because the last time I checked there's been discrepancies. Sometimes they say it can eventually, after some time, go back to where they were, but sometimes it persists. But obviously this hyper inflammatory state, that's what I need you to keep in mind is what affects everything. And periodontitis, it has to do with inflammation. Obviously, you can have increased tissue destruction and greater levels of infection, and poor diabetic controlling the presence of calculus is associated with an increased frequency of probing depths like more than four millimeters in this case. So a lot of studies have shown that trying to control diabetes and periodontal disease has very good and positive outcomes for both diabetes and disease. There have been several studies, like almost there in the 90s, were done in Pima Indians with type two diabetes, and they found that they had the ones that had diabetes had greater incidence of burden tears compared to the ones that did not like even like three fold increase. So a lot of studies confirm that these poor glycemic control leads to both increased risk for alveolar bone loss and severe progression of disease. So studies that were done in this population. And funny story like one of the investigators, I think it was in this study, one of the investigators sister is my patient now like out of the blue he said, you know, my brother did this study. I said, oh my God, now I have and everything I say. She reports to the brother to make sure it's right. And they said, yes, my brother agreed with you. We can move ahead. I said, okay, as long as we agree. So. And that's why those two things remember with a great modifiers smoking and diabetes, they they may change the grading in your diagnosis for your patients. Clear. No. Okay. It's almost done. Don't worry. Regarding genetic factors. I love this era of genetics and genes and everything like that. I love it. If I wasn't here, I would have been a molecular biologist or something. So there have been several studies, especially twin studies, that have tried to find contribution to periodontal disease. They have found many single nucleotide polymorphisms. They call them SNPs or SNPs, depending on where you hear those things described their candidates for periodontal disease. They can change, you know, they can they can have a lot of variation. They can. They have found a lot of polymorphisms, especially in the interleukin one gene, one beta in terms of many tests to assess dental risk. And they investigated other biomarkers for interleukins and and things like that. So in the late 90s, this is like a landmark study considered by Kauffman, 1997, where the conclusion was the combined presence of a polymorphism in both the interleukin one gene and interleukin beta gene is associated with increased risk for developing severe Titus in nonsmoking Caucasian patients, making people like having a change in the gene of interleukin one, which is one alpha and one beta in patients. In Caucasian patients like white patients that are non smoking y, non smoking. Because we know the impact of smoking this would have been a confounding factor. Has an increased associated not doesn't cause it's associated with increased risk for developing severe periodontitis. So that was the first thing. That's when we started. And since then. So I need you to keep that in mind because that's how a lot of genetic information started. Because right now we're in those genome wide association studies where they study the whole genetics and everything, because since then there have been many, many studies in vitro, in vivo, cross-sectional mainly. And then at some point they started doing some systematic reviews of whatever they had over here. And right now we have those, you know, genome wide association studies. So the impact of that, because of a lot of those studies has changed over the time, because obviously we have many, many genes that play a role. Right? We're still very vague in that aspect. And keeping in mind that a lot of those studies have outcomes in terms of tooth loss, clinical radiographic measures, severity of periodontitis and very few have subclinical outcomes. So it's very yes, there are studies that show that specific ethnic groups or, you know, populations may be more prone because they may have specific polymorphisms. And that's why you may see, let's say, whatever we used to call aggressive is more frequently there compared to others. But you can't draw a conclusion saying whoever is that they're going to get that they may be at higher risk. My input on that, and after talking with people that know way more than I do, is that this whole changes in the gene alters the production of specific proteins, which may have and play a role in the immune system and the host response and the inflammation. And that's why those patients, in presence of other factors that obviously play a role with prior disease, may show more pronounced outcomes, but obviously these are only associations. There was a hype around that time when the 2000 or so with 2010, that they were doing genetic tests for every single patient to find out polymorphism and saying, oh, you have that, so you have a higher risk. Is this actually true? There could be an association, but, you know, charging the patient to do this thing with minimal impact to what you're going to be doing as a treatment afterwards may make no sense at this very moment. Okay. Now regarding gender, there is the hypothesis that the females, especially before menopause, are less susceptible to disease, mainly because of the protective effects of the estrogen. Again, this is a hypothesis. A lot of studies, some studies actually have shown, depending on syndromes that are gender related, that may have specific conditions. But you know, what you would be seeing is in when hormonal changes are happening. We talked about those in previous lectures as well in diagnosis that you can have specific clinical features from those puberty gingivitis, the hormonal changes, the pregnancy associated gingivitis and everything that can affect, you know, depending on the status of the hormones in the patient regarding socioeconomic status. Obviously, low educational levels with lower income levels are associated with increased risk. Why? Because people unfortunately do not have access to care. And. That's something which is unfair. And but that's something that we see over here because we have increased stress, decreased reduced access, reduced educacion. So obviously not proper hygiene. So it's really important with those populations to reinforce that. It's not that whoever has a lower and lower income will get the disease because of that. It's mainly because of the outcomes, like why of the lower education or the lower income, reduced access and stress in this situation. Regarding abnormalities in the neutrophils. So you can have those neutropenia either the congenital or acquired with severe periodontal disease in childhood. We said about those in our classification in some lectures ago. And those cases usually have this first molar incisor pattern which could be associated with that this neutrophil impairment. And remember, even with this aggressive burden Titus, the neutrophil impairment is one of the subclinical findings, the secondary features that you find there. And regarding the HIV infection again under similar category with immune deficiencies, people are more susceptible to periodontal disease. This linear gingival erythema that we don't say that anymore because it's not a different disease entity. But obviously now that, you know, the disease is very well maintained and controlled. The disease, you won't see too many clinical pictures in terms of those patients with infection. They're more a chronic disease. So as I said in the beginning last week before I almost finish up, this is a patient that came who said I have ulcers in my mouth. You can't see it very well, I guess, right. Can you see the wider areas here? A little bit, no. A little bit. So young patient about 20, I think years old I have ulcers. It started about three weeks ago. It's painful. It's bleeding in my mouth so it doesn't go away. So what is this? So. You see the patient? What are you? What are you? What do you think? Huh? Who said that? I did. You did great. We fall into the same thought process. Yes. Why do you see thing lag? So this is necrotizing necrotizing gingivitis okay. Cause the. Pain. The pain. The short term that it happened for three weeks. Okay. And somebody else would ask it was the patient was going under stress or some. Excellent. I asked that as well. And he said well I had my midterm in the CSO, which is computer science, right. Yeah, I'm saying correctly. So I said, oh great, I'm going towards my thing and it's super painful. That's why that's the only picture I could get there because I could at the moment. I would touch them. He would jump. Um, some in the beginning I would think about actually. No, because before I say that. So then I lift his lip and I see that. And now my log is saying I want to fix it. That's what I said in the beginning. I want to make it fit there because that's what I have. But like this is not happening with NUG, right? So somebody didn't ask anybody. Did we miss a question that we should have asked the patient. A. Medical history? Right. Because he's 20 years old, it doesn't mean that the patient is 20 years old. It doesn't mean that the patient is healthy. So patient is healthy. It doesn't report anything. Had a lab work like in. To July or so something like this. And everything was fine. And then I move forward. And I see that as well. Okay. So there's definitely a more systemic thing. There's definitely a necrotizing thing. And the moment I see that I said it's not necrotizing gingivitis, it's necrotizing stomatitis. So when you're thinking about that what are you thinking about. How do you. Autoimmune Crohn's. And then any viral, especially HIV. Remember this? I think I had it in the lecture with, I don't know, one of the classification lectures where you start with necrotizing gingivitis, periodontitis and stomatitis. And this is with and that's why I said to the patient, okay, you need to go back and check for HIV, for Crohn's, for all those things. But the reason I bring it up is like the moment you say it, it's easy to say, okay, that's what it is. That's my diagnosis. It's a necrotizing gingivitis. I see the punched out papilla. It's bleeding. It's oral hygiene is poor stress. So it fits my check boxes. And eventually you have other things that you need to evaluate before you decide what's the right treatment. In the beginning, I when I saw that, I said, oh, maybe it's something hepatic, but it's been there like those gingival stomatitis,