Periodontal Disease Classification PDF

So similar to last time. We need to know about the normal stuff, the development, the classification and know how we diagnose diseases. We talked about the normal appearance of the motor last time where the gingiva is pink is pink and firm and scalloped. The bone levels within 1 to 2mm from the stag...

So similar to last time. We need to know about the normal stuff, the development, the classification and know how we diagnose diseases. We talked about the normal appearance of the motor last time where the gingiva is pink is pink and firm and scalloped. The bone levels within 1 to 2mm from the stage. And we don't expect to have exposed some symptom like either with recession or with deeper pockets. So we will start seeing how things may develop and how we see those clinically. So we talked about the inflammation as well. And remember those three stages, the initial the early in the established. And we're going to move on to the advanced stage today with a little bit more information. So just as a summary, we talked about the pristine gingiva, which is like fastidious oral hygiene, state of health, that you don't see it very frequently. But again, it may exist. You may have some sparse migration of neutrophils, but there is no actual inflammation. The initial one where you start seeing more neutrophils being present, but clinically you can't see anything. So again, you would identify that as healthy gingiva. And then at the early lesion you start seeing some clinical signs with inflammation, edema, some bleeding and probing marginal rhythm, etcetera. The established lesion, as we said, that it's more advanced and established lesion in terms of gingival inflammation with some plasma cells as well in the neutrophils, the redness and the bleeding on probing clinically, you see the redness, the edema and everything. And eventually when this continues to be the advanced lesion. So this is in periodontitis patients. So we talked about that last time. When do we move from the established to the advanced? There is no study that says exactly in so many days. There are people that may stay here for years or forever. They may be people that just transition very easily. And that's our assumption that we have to go through those stages and eventually end up to burden. Titus Right. There is no study that has proven exactly all those things because there's no way to find that out. Okay. So having said that, that's when you start developing pockets, some attachment loss, bone loss. Eventually, you can see here like slightly bone loss. You have a lot of inflammatory response with plasma cells mainly. And depending on how your attachment is being lost, you can see here you may have a deeper pocket. The attachment loss may be 1 or 2mm where you can also have more severe forms, where you can have more attachment loss, more infiltration, bone loss in different patterns. We're going to talk about all those things today as well. So this is how like several different states of advanced lesions may look like. We talked about the classification, how it developed, how you got developed and where we end up for. So we're going to move on where we left it last time. This is everything we talked about last time. That's why I have it here, so that you connect things together. And now we're going to go to the second part of that classification and starting with what we used to call chronic periodontitis. Again, as a reminder, we do use more and more the current classification with the staging and grading. We're going to go over that today again. But as I told you, you're in that transition period. The concept behind the disease hasn't pretty much changed. Like what we know is pretty much the same. It's only how we classify that. And since still if you go to insurances and ads charting and everything, they still use that. Eventually at some point they will change. So you will be discarding that. But that's also the reason we are mentioning those here. So talking about what we used to call chronic periodontitis, which is the most common form of periodontitis. You can see in adults, you may see that in younger population, but not so frequently. Pretty much the things that characterize those is clinical attachment loss, bone loss, pocket formation, recession, friction, all those things. But that's the main thing as we see here, clinical attachment loss. So what differentiates from the gingival disease, gingivitis, everything that you used to have before where you don't have attachment loss, the prevalence, the extent, the severity and all those things may be influenced by several risk factors. And we're going to talk about risk factors in future lectures, either local or systemic risk factors. We do consider microbial plaque that to be the key theological factor, like the main etiology. And then we have those additional risk factors that may predispose a patient to the disease. And it's all about the balance, as I write here between the host and the bacterial challenge. And that's what differentiates the clinical signs that you see in a patient's mouth. There can be people that may have identical bacterial species and completely different host response, okay, it's all about the balance you get there. So we talked about those features. We're having the clinical attachment loss, especially in proximally. Sure, you may have facially, but keep in mind when you're getting, for example, recession, we talked about that last time where the gingival margin migrates apical because you're very excessive, excessively brushing the right. That's not burden type. It's a different form of attachment on that side. So you need to have clinical attachment loss, pocket formation, which is more than four millimeters. We do consider depth 1 to 3mm to be within the normal limits. There is typically, we say, a horizontal pattern or a cratering. So cratering is having small lacuna inter proximally because of the way the disease progresses with exacerbations and remissions. So usually you see that kind of horizontal pattern. It doesn't mean that you can have irregular bone loss pattern in terms of angular or vertical bones. It's exactly the same thing, but that's what you usually see. You may see, as we said, some vertical infra bony angular. This is all the same thing, bone loss on some sites and obviously you can have the etiology plaque is poor plaque control, as we said, the etiological factor and we can have supra sub gingival calculus, you can have tooth mobility. Shifting or drifting. So sometimes with parental diseases, the thing with those diseases is that patients don't feel much again. Usually they may ask for help when it's progressed a lot. Main chief complaint could be, Oh, my gums are bleeding. So this you may differentiate. Gingivitis are present in more severe forms. The chief complaint that the patient may come is my teeth are shifting or my teeth are moving. It's not like I'm in pain. I could be with a fractured, severely carious tooth or whatever. So usually when this happens, the disease has progressed and may have also other contributing factors that it's in such state that it requires way more treatment. So you may see those things. You can have different bacterial flora. We're going to talk about bacteria in a couple of weeks. We have those phases of exacerbations and remission that we said. So there are phases that it just flares up and we have progression of the disease and phases that it kind of stabilizes itself. And we have found that the destruction is consistent with the presence of plaque and other modifying local risk and local and systemic risk factors and specific factors like smoking, stress, poorly controlled diabetes have been definitely associated with way more prevalence, way more susceptibility to the disease. So things to keep in mind. So that's a very extreme, extreme example, how things may be looking with deeper pockets, severe bone loss. You can have way less than that, obviously, but just giving you an example of those things and clinically, obviously, as we said, you will, having gingival inflammation in presence of bleeding on probing redness, swelling, erythema, edema, pocket formation, clinical attachment loss, recession, mobility, friction, involvement, bone loss or all those things may be seen in cases like that. And having, for example, like smoking and diabetes as contributing factors, you can see that those patients may be presenting with a little bit more exacerbating and alarming form of the clinical presentation. So if a patient comes like that, my very first question is, okay, what's the medical history, any diabetes, any other systemic factor and medication? Because yes, it's definitely severe inflammation, but there may be something underlying that we need to address to regarding the extent if it's localized or generalized. We talked about that last time with a 30% cut off. They used to say sides, we move to teeth, we're not going to have you count all that size. I don't know why these decided as such back then. And the severity just need to remember that 1 to 2mm of attachment loss is mild, 3 to 4 moderate five and above is a severe. Okay. We still keep the same things even with the current classification. In 2015, they did a little bit of a revision of that classification because of some. Um, over estimations that were being made. First of all, just as I'm writing here, the localize is the 30% cut off is again the same equal and more than 30 is the generalized as we talked last time and we're talking about teeth, it's easier for you to calculate that having what of being affected with clinical attachment loss, inflammation as we said, and bone loss and deeper pockets. Okay. Because saying, for example, gingivitis or it's generalized or localized, it's more or less than 30% of teeth having just gingival inflammation right here. We're talking about all these things that have to be found to diagnose that. So what they added here was, yes, sure, we need to have clinical attachment loss, the same category of 1 to 2, 3 to 4, five and above. But we need to have some other signs of the disease in terms of inflammation, deeper pockets, bonus, why you can have, as we said, clinical attachment loss one, two, three, four, whatever as part of a facial recession without anything else in the mouth. Right. That's not prudent. It's because of a trauma or excessive brushing and all those things. So they had to differentiate what's going on. They had to differentiate. Remember last week we talked about these reduced very long time, right? In the past when you just had recession, reduced periodontal history theories, you would always say it's buried on Titus. Right. We do know that these patients have had the disease, have been treated and controlled. We know that they may be more susceptible having, again, a breakdown. We know about all those things. But when you see them and everything is nice and stabilized, shallow pockets, good hygiene, minimal or slight inflammation or so, the fact that they have already attachment loss and bone loss because they used to have the disease does not mean that they have actively the disease there. Okay. So these are the updates that they did all those these articles are also on Blackboard if you want to read them for your reference to understand more than that. And that's a typical example of chronic periodontitis where you see the edema, the recession, the bone levels more like a horizontal pattern. As you as we said before, you may have some areas with a little bit more irregular angular bone loss, but that's a typical what we used to call chronic periodontitis case. Any questions on that? No. I'm sorry. Is it on every 2 or 2? Non-existent. What do you mean, non-existing? Oh, oh, yeah, yeah, yeah, right. Question Very good. You mean for the percentage? How much? Yes, excellent question. To say if it's generalized or localized, we only count the tea that are in the mouth. Right. If you're having five teeth, if I understand correctly, if I have five teeth in the mouth and four of them have clinical attachment loss and bone loss and pockets that generalized, if you have 28 teeth and four of those, 40 have clinical attachment loss, bone loss, that would be localized. Right? You count it with what you see in the mouth. That's what you asked. Okay. 40. That doesn't mean it has to be or do not exist. Well, then it's gone. Yes. So I have the criteria for percentiles later on because this is with the updates, with the newer classification, I'm going to go over that. I don't want to confuse the audience, but yes, there are specific guidelines of what we consider a periodontitis case. I have this in 30 slides or so. I don't know. I just said a number. Any other question? But I have it. All righty. So let's go over to what we call aggressive. We used to call like aggressive on. You will find a lot of fight on that. There are people that they even knew the previous classification, what they used to call like juvenile and early onset and they used to call it this way. And when I heard that, I said, Oh, come on, that's so old fashioned. We call it aggressive now. Now the newer Come on, aggressive. That's so old fashioned. We have the staging and grading. So they have changed several names in that, because the fact is that when they first started seeing this pattern of disease, they would see it more frequently in younger population and that's why they started calling it this way. But then eventually seeing way more adults as well. They had a different form. That's why they call it aggressive person titles. So what you need to keep in mind and to be honest, we so that's a good thing. I remember now on Friday I was in the clinic with some students working on consultation, diagnosis, treatment, planning. So the students, while we were waiting for the radiographs, rushing to me and say, Doctor, doctor, come and see that what's going on in here? So they show me some of the PA's that had so severe bone loss with calculus like angular bone loss to the molars and stuff. We're going to learn about those things. And I said, Excellent. I say, I need you to think about the diagnosis because that's a textbook case. And one student said, Yes, I know it's a textbook case for referral. I'm not dealing with that. So I said, okay, that's the second step anyway. So what you need to know about those cases is that patients usually are healthy without having any other medical issues. There is rapid attachment loss and bone destruction and the way to see that is usually in comparison with the patient's age, right? If you see, let's say, 80% of attachment loss in a 20, 30, 40 year old is completely different than seeing 80, 80% of attachment loss in a 90 year old. Right. So that's the concept. And usually there is familial aggregation. You may have this information when I'm suspicious of these form of the disease, I always ask the patient, Has any of your parents or siblings, if you have any, lost their teeth at a young age or issues with their gums and teeth? And usually they say, Oh yeah, my parents lost all the teeth when they were 30 or 40. They're wearing dentures and stuff like that. So they used to have some they are having this familial aggregation, so they have some secondary features and obviously some of those are subclinical, which you can't evaluate unless you do a test. But something that I need you to keep in mind here is the elevated proportions of a that's a bacterial species. We're going to learn about that in two lectures. The aggregate doctor acting on competence. Yes. I'm not talking something weird. I have it in two lectures. So that's a bacterial species that it's very, very frequent and pronounced, especially the serotype B in this form of the disease. And some people may take population for bacterial culture and this comes up very frequently. Obviously other bacteria are present, but something to keep in mind. So with those we have the localized and the generalized. But this is a different way of identifying what is localized and what is generalized. This is what they used to call even before that is juvenile or early onset, mainly on a younger population. So that's they say it's around puberty. When you may see that coming up, you're having this AA, the bacterial species being responsible and they have this first molar incisor pattern. I'm saying this word because this is how we call it now. Okay? First molar incisor pattern. So where you're having more attachment loss and bone loss on the first molar incisors and the localized presentation does not include more than two other permanent teeth and those first molars and incisors. That's how they develop. They mention about this localized. So let me ask you why molars and incisors? Mm. First to erupt. Right. That's why those teeth are being affected either in and that's why there's this pattern and that's why they started saying something is happening here because yes, they're first to erupt maybe more in the mouth prevalent with bacteria, but it's exactly a very typical pattern with those. So with a localized, you don't have more than other two teeth other than those first molars and incisors. And that's, for example, a case where you see patients are not having like such a bad hygiene per se, but usually the anterior teeth may have more severe attachment loss and bone loss. The first molars as well. That's a way younger patient, obviously, that you may find that the generalized form is pretty much the same. They they say here less younger than 30 years. But if a 35, 40 year old patient comes to your office and hasn't been to the dentist for 20 years and has the disease, which was actually the case, I talked to you about before, that I saw with the students. That's definitely a case like that, right? It was just undiagnosed. And the generalized it affects obviously more three teeth and more three permanent teeth and more other than those first molars and incisors. So they have considered a poor serum antibody response in those infecting agents, the bacteria. It all has to do with this balance with the host response and the bacteria. And they do have this episodic nature in the destruction of periodontal attachment. So it may happen at some point very aggressively and severe. And then at some point it may just self arrest and depending on when you see the patient. To be honest, until now, in my clinical experience, I've only had one patient that I was running next to the disease was going to be faster, me or periodontitis. There were times I'm not a good runner. I'm saying that. But there were times that I, I said, okay, that's a typical localized, aggressive, younger patient in the early 20s and all the bullets, things that I have to do with treating the disease. But little did I know that the disease was just exacerbating the time. And although I had the patient on a three month recall, to seeing all those things was continuing to keep breaking down. And we were doing everything according to what we knew. You know, the patient was great, the cure from the dentist, the highest periodontist and everything. So that was a really interesting thing that it was just a battle between the disease and what we can manage to stop the progression of that. But I've only had this once and I hope I never have it again. It was exhausted at the end. So that's a generalized pattern. You can see here with the first molars having like this severe bone loss while the neighboring teeth I'm sorry, first molar here, severe bone loss. Why some neighboring teeth may not have as much the incisors. Same here. You see how much more bone loss and severe bone loss the first molars have and the second ones may have a little bit less. So obviously, these are way more than three teeth affected. That's a generalized form. Something to keep in mind because of the rapid progression of the disease that is happening. In those cases, you usually find very frequently what we call these angular vertical in bony, whatever you want to call it, bone loss. Okay, So because the way the teeth are disrupting the destruction is happening too fast. And that's why it's very common, like what we call a textbook case, that everything is like a wave. That's how I can say that. So you have the bone levels being fine, dropping significantly around the first molar second, and if it's affected, then up on the pre molars dropping again in the in the incisors, then up in the premolars and then dropping again in the molars. So even if it's like a severe form of the disease, this kind of wavy pattern exists because you have this first molar incisor pattern. Okay? And that's why you may see more angular bone loss around those teeth. Any questions? Nope. And I just have here as a reference, this is again from the same classifications. You can read those verses all on Blackboard about the differences between chronic and aggressive. Just keeping in mind those three main characteristics of the aggressive with a rapid attachment loss, the familial aggregation, and that usually patients are healthy apart from having that severe form of periodontal disease. So moving forward, we're having what we call here the Titus as manifestation of systemic diseases. Nobody knows like this classification, this part of the classification, because these are usually more extreme diseases. So just to have it in your mind, usually those forms are associated with systemic issues, either hematological or genetic disorders that have other characteristics, other features. The patients may know those things so they inform you. So you're expecting that you will see specific periodontal issues as well. So regarding the hematological disorders, we talked about some leukemias in the gingival diseases, but you can have also forms with affecting more the predominant, not just the gingiva. First one is the acquired neutropenia where you're having ulceration, necrosis of the gingiva bleeding. You can have deep pockets, you know, bone loss affecting the permanent dentition and similar to the leukemia, either it's acute or chronic, you can have gingival enlargement bleeding, swelling, bone loss attachment. So obviously, if a patient knows those diseases and has also this exacerbated picture, it's something to know about that the immune system is compromised. So it's something that we're expecting that clinically, even with not as much bacterial plaque being present, we can see a more exacerbated host response because of that. And then we're having these manifestation of systemic disease in terms of genetic disorders. It's like 11 different diseases. They're not very common. You will definitely see I've seen of those maybe like eight of those so far. So they can come along. Usually when patients come, they know that they have this kind of disorder. So you're expecting that you will see something respectively clinically. And obviously those patients, because their teeth are being affected at a very young age, they're starting they start having issues, periodontal issues at a very young age, and they need a specific treatment. So starting with the neutropenia, the familial neutropenia, it all has to do with how the immune response works. You can have, again, ulcerations, severe form of gingivitis and on Titus you can affect both primary and permanent dentition. And what I need you to keep in mind for all those genetic disorders, they have a common thing. The immune system is compromised. Clinical features are pretty much the same with severe attachment loss, bone loss, inflammation, bleeding, swelling, First molars and incisors are affected because again, they start when somebody has a disorder. As a kid, these are the first teeth to erupt. So they start being affected earlier and that's why those teeth may be lost way earlier compared to other teeth. And the the distinction usually needs to be made between what we talked about and aggressive personalities versus those. Although when you know that there is an underlying genetic disorder, you know that there's an association with that going to the Down syndrome. So this you may see that way more frequently than you thought about, because the approach with patients with Down's syndrome has changed dramatically. The life expectancy has changed, the cure has changed. Their understanding for those things has changed. But what you usually see in those patients and their teeth, especially lower anterior, may be missing prematurely because of being affected. Again, same incisor, molar pattern, high prevalence of parental disease. Those patients need frequent care and even their primary teeth may be affected without waiting to the permanent one. So knowing about those things, the Leukocyte Adhesion Deficiency syndrome. Now, whatever we're starting talking about, most of those genetically, they're autosomal recessive. So the previous one was the Trisomy 21. The rest of the disease I'm going to having over here, the genetic disorders are autosomal recessive. That's why you don't see them very often. A lot of those on. Honestly, they can be very fatal at a very young age. And the pattern is, again, the same with inflammatory periodontal disease and severe periodontal infections. Papillon, Lefevre. You may have heard about this. This is the keratosis, the plant or keratosis, a very common thing. If you see the feet or the palms of the patients, they have those characteristic lesions over their periodontal. The teeth can be super alarming, like even floating sometimes in the mouth. Again, same thing you see first molars or floating incisors are pretty much lost with some exceptions, while the other teeth are trying to wrap with less issues. And that's what you would be expecting to see clinically. The Chetak Hegazi. I hope I say that correctly. Again, autosomal recessive. It's all about the immune response with abnormal neutrophil chemotaxis and functions if we're on Titus form. Same thing you see here first molar and incisor pattern that's being affected. So usually those patients come at a young age at the office and they may be a pediatric dentist like a patient or something that you may need to refer if they come to your office. But at least to understand how those diseases work. He still psychoses syndromes. I've seen those as well. These are actually from some patients I've seen as well. You're having some necrotic ulcers? Yes. It doesn't look good. It's very painful. And initially we think that it's like a necrotizing form of the disease because of how they look. But obviously, if you're getting a bloodwork with a Langerhans cells, he still say ptosis. We can establish what the underlying cause may be over there. The patient I told you about with this rash I had with the aggressive form of the disease, Initially I thought it was something like this because the molars, when he first came to the office were like floating. Right. So in those cases, especially if you don't have any background, you ask, go and do all this blood. I mean, I literally wrote to the doctor, I need complete bloodwork. I need you to check for that. I need you to check for that to eliminate any other contributing factor. So that's what you would see in those Langerhans cells. Ptosis in those patients with severe destruction. The glycogen storage disease again, autosomal recessive again low neutrophil numbers, impaired neutrophil function. It's about the host response. You're having periodontal issues. Also, keep in mind a lot of those patients, younger patients, they have to deal with so, so many things. The oral hygiene may not be the best. Obviously it's not helping. So also education is very, very important for the patients and the parents as well. Infantile genetic granulocytes. This is so rare. I couldn't even find a picture. I don't know how it looks like I searched a lot to find something to show you, but it's so rare as a disease. And the other thing is, because it's so rare, it's also very fatal. So you may not see patients. They have it in the classification. So I'm bringing it up for you over here. And again, similar concept with severe neutropenia and early onset periodontitis, as we said and talked before, coin syndrome and autosomal recessive form again of genetic disorder. Patients may also have other issues with non progressive mental and motor retardation or obesity and other neutropenia issues. They're having more bone loss, severe attachment loss and severe form or presentation of periodontal disease. The error loss that's I've seen a couple of patients with their Danlos syndrome, which is a group of connective tissue disorders where they're having a defective collagen synthesis. Usually the types of four and eight have more susceptibility to personalities. They can have resemblance of this aggressive form of presents with this smaller incisor pattern. And these syndrome has different types and types, and they can affect also the joints, the skin. And those patients also have other systemic issues as well. Hypo phosphatase here. I've only seen one patient like this in my life, which was so weird. I we actually figure it out during extractions because the way the bone was there was like so fragile. It was becoming like chalk. I have never seen that before. Was very, very interesting how it looked like. So obviously you're having decreased serum alkaline phosphatase, you're having severe bone loss in those patients. Similar thing with first molar incisor pattern. Deciduous teeth are being can be affected, especially in the interiors and being lost prematurely. So these are the 11 things so that you're not getting confused. You know, the first couple months with the neutropenia and the Down syndrome, they're specific ones. The rest of those diseases are autosomal recessive, resembling those aggressive forms of first molar incisor pattern, severe neutropenia, immune response like impairment and early loss of teeth, especially interior, sometimes molars really graphically. You may see those things like floating in the x rays, as we say. So obviously when you see those super alarming and aggressive forms, you are suspicious of something else being underlying over there. Questions. All righty. So we I mentioned somewhere about those necrotizing diseases that you may like the history of cytology. It looked like necrotizing. So let's see what those things are. So we have two sub forms, the necrotizing gingivitis and necrotizing fasciitis. And the concept behind it is pretty much most probably different stages of the same infection. It all has to do with diminished resistance. Host response to bacterial infection and the tissues are being affected. So I have here like a diagram that you can have some preexisting inflammation with gingivitis and then you can have a lot of other factors, contributing factors, especially stress, anxiety, immune response suppression, some increased corticosteroid production of any viral infection on top of that. So this balance between the bacteria, the presence, the multiplication of bacteria is being changed with the host response and immunosuppression. So the first thing you may have, like with ulcerative gingivitis, obviously if you're having additional risk factors, for example, the HIV infection can lead to further necrosis in those areas. Immune response is being affected. So the whole balance of bacteria. Host And whatever is happening is being impaired. And that's why you can see this developing to necrotizing fasciitis or Stomatitis, which is very, very uncomfortable, painful for the patient. Regarding necrotizing gingivitis, I I'm writing the name ulcerative. I'm not saying it because it's being eliminated. So I thought that if I don't say it, maybe it doesn't stick in your mind. But I write it because that's how they they write it officially. So this you may see that way more frequently than you think of there. Usually patients come because they are in pain on their gingiva. They cannot even touch them. You cannot brush them. They have a bad breath. You can see these like pseudo membranes being formed, like punched out papilla, like those ulcerations if you see them and you're having bleeding and and pain. And obviously you can have a lot of factors, predisposing factors depending on diet, smoking, HIV infection. But the first one stress. My last patient with that was about 6 or 7 months ago, a medical student from BNC. So I said, okay, don't worry, you're having exams. We're going to deal with that. Take it easy. So it's very uncomfortable for the patient, right? And people that are in stress can exhibit that very they can exhibit that easier than you think of because immune system changes, bacterial culture and everything changes. So something to keep in mind, obviously, if this progresses, you can have these more alarming forms of necrotizing periodontitis. I'm not going to show you. Stomatitis What are you having? Also, bone loss, attachment loss, necrosis. Papilla This is a super severe form. You don't see that very frequently. This has to be a very, very immunocompromised patient. In the past, when HIV patients were not having the care that they're having today and they're not controlled, you may you could see that way more frequently. But now when things are being controlled, you may not see that as well. But obviously you're having this infection. We're having necrosis of tissue. It's a painful situation. You're having a lot of underlying systemic issues, especially, as we said, the HIV, severe malnutrition, immunosuppression. So patients that may suffer with other diseases may have this form of disease. And that's why it's very important if we know that a patient will go under any immunosuppression treatment for whatever reason, to see them and make sure they're having a healthier mouth as possible, because that's the last thing they want to have on top of everything else. Okay. And we're going to stop today to the abscesses, the rest of the things we're going to talk about next time regarding the abscesses of the periodontal. So we're having gingival lapses, periodontal lapses and coroner lapses. So where do you see those? More frequently in untreated, untreated patients? Commonly like incomplete calculus removal, foreign body reactions, infections. Why? It's difficult to get in there and clean that and remove calculus or maybe can get stuck there. If somebody is on systemic antibiotics in untreated burden on Titus background like like a super infection, uncontrolled diabetes tooth related factors in trauma. So let's see that because these are very frequent situations that are that can happen clinically. And when you're having them, you need to understand what you do in each specific category. For example, if you are having incomplete calculus removal, you need to go and do a specific to go and take that out. If you're having patients that are having periodontitis, it's wrong to just give antibiotics, right? Because you're changing that. If you're having patients with uncontrolled diabetes, they may show they may present with a lot of abscesses. There was once a patient in his early 30s, I think that came and said my gums are bleeding and are aching and I have never seen so many periodontal abscesses in my life before. In one month it was like eight, seven of those I don't remember. And obviously I said, okay, let's go and do some blood work. And diabetes was so uncontrolled because the patient had not been to the doctor for years, like they was like 14 or so. And I said, okay, let's deal with that first. So and obviously if you're having local factors, tooth related factors that may have some like a trap that, you know, calculus can get trapped over there, anything like a foreign body can get trapped in there. So that's where you would see that those happening clinically, you see swelling, separation, redness, you know, pain. Sometimes it's loosening of the tooth like mobility of the tooth, tenderness to percussion. So extrusion of the tooth. So depending on where it's happening, you may see those things. If we're talking about a gingival abscess, it's like a localized purulent infection involved involves mainly the marginal gingiva or the inter dental papilla. Those can easily be associated with foreign bodies. Anything getting stuck in there, it's usually painful. It's expanding lesion when it is a foreign body reaction. The day the foreign body gets stuck within the next two days, it's like a severe swelling and pain. And that's when the patient may call something. I got a severe like instance swelling out of nowhere. And then unless hopefully nobody has forgotten anything inside their dental related, you're going to check about anything else being stuck in there. You're having this acute inflammation. And obviously when you take it, whatever is happening there, you remove the theological factor. Everything goes back to normal very easily and relieves the patient. And regarding periodontal abscess, again, it's a localized infection. This is on a patient that already has attachment loss, bone loss over here, destruction of the PDL and the alveolar bone. That's a very typical case. On that case, on that situation, you see you having the abscesses here. And if you're putting like a good operation to trace it, it just ends at the crest of the bone. If it was an end related thing, it would go to the apex or maybe for occasion, depending on the teeth. So this is usually associated with deeper pockets or for occasions with calculus being present there involvement of infra bony like defect, it could be acute or chronic depending on where you see that swelling, you know, red, smooth, shiny surface, the separation. And patients usually feel like a pressure on the gingiva and the tooth may be more mobile, not only because of the abscess, but also because of the existing bone loss that may be present there. Okay. And you can have in the newer classification, they also mentioned that you can have in abscesses in non permanent patients. And usually these are, as we said, foreign bodies from dental floss or elastic toothpicks, you know, even, I mean, popcorn. And we talked the other time harmful habits, any orthodontic appliances gingival enlargement and alterations of the root surface. You can have variations of the root surface. We talked about a couple of things 2 or 3 weeks ago about those anomalies with the cement and. Projections, the enamel pearls. So all these things like even fractures, as we see over here, all these things are like local factors that allow bacteria to form calculus, to form, to get trapped, to close the environment and eventually create an abscess. And in these patients, you can see that in forms where you're having exacerbations in untreated forms of the disease or refractory, which means that it just goes back. You try to treat it and then just continues to having exacerbations sometimes after scaling and route planning. That's very common to thing when you're having a lot of calculus. If you don't remove all the calculus efficiently, what happens? You remove part of it. For example, when you're doing this treatment, the gingiva tries to heal and attach again on the tooth. And if you're having a piece of calculus that's still over there, it kind of closes the area and that's why it creates these apps. Some of those patients after surgeries, again, similar concepts, especially with foreign bodies, membranes, anything on that side. I'm saying that, again, hopefully we're not I mean, thankfully, we're not doing this anymore that frequently. We don't see that never give antibiotics without treating a patient. That's not I mean and I'm talking about periodontitis patient, right. Obviously, if there is any infection happening on and you need to give an antibiotic, you should. But if you're having a burden to this patient that you need to do your deep cleanings, you're scaling and route planning and everything. The treatment is not to give just antibiotics. You may supplement your treatment if you judge and we're going to talk about antibiotics. But in the past, because they said, are you having proton tides, that's an infection. Get an antibiotic. Right. That's not the treatment of the disease. And obviously, if you're having other medications like the therapy that can cause enlargement, it can trap things inside. So you may get abscesses. I have this here for you for your reference regarding differentiation between periodontal and apical options mainly and the related versus perio related. But something you need to keep in mind is that with the endo infected teeth, usually a patient comes with a lot of pain. You're having other radiographic findings of Lucentis signs of possible necrotic pulp with caries, fractures, whatever. Usually if we try to drain it, drains, it drains through the sinus tract while in the paleo abscesses it drains through the pocket. If you press it, whatever drainage can come through the pocket. And just as clinical differentiation in terms of palpation, percussion, pulp, vitality, et cetera. For your reference, when you see your patients clinically and finally, you have this very coronal abscess, which is a localized infection with a tissue that surrounds a crown of partially eruptive tooth, you see that more frequently in the erupting third molars because of the limited space you're having. This particular food can get trapped and this can have swellings, patients present, complaints about pain and swelling and redness and difficulty in swallowing or opening or closing the mouth, depending on the severity. And obviously it all has to do you have in a super nice area as it trapped there for everything to form and create that abscess on that side. Usually those areas you need to clean. Sometimes you may also need to give an antibiotic depending on how infected it is, and eventually you may need to remove the third molar if it doesn't erupt in a very optimal position. Questions in that? Yes. Yes. Virtual natives. Yep. We have a case like that. You mentioned about doing some writing. Yep. How how much the Brighton is just to make sure there's nothing inside causing that. And or can we start some antibiotic therapy before sanitation to travel to? Okay. Very good question. So I don't have like a black and white answer because it all depends on the clinical case scenario, the swelling. I mean, if the patient cannot even open the mouth and there's a lot of swelling, I'm not going to try to find it there. I'm just going to give an antibiotic for this to shrink so that I can go ahead and do whatever I need to do. If it's if I'm lucky. Let's say I see that way in the beginning, because patients usually have those things coming and going, coming and going. So they're familiar with that and usually they don't wait until it's too severe and painful. Let me say, you know, I start feeling it's happening right now. So in that case, if there's not severe swelling or, you know, a more systemic involvement or something, I can easily go and just debride it. And usually that solves the issue temporarily until we address that, there are times that the tooth may be erupting fine. It doesn't need extraction. It just has like a this gingival part of the gingiva an open column there. And you may just do a victime of that and call it a day. Right. You don't even necessarily need to do an extraction. That's why I don't have a black and white answer. It all depends on the symptoms and the clinical signs. And if you can do something over there. Okay. Hmm. Hmm hmm, hmm. I think. Right. What's with. Very good question. So in case you haven't heard it, it's about the acute and chronic. Again, it's it depends if when the patient comes, it's in just acute form. You're very right. Usually because the pain comes later, they may already be in the more chronic form over there. But depending on where you when you see the patient, you may just see that in an acute phase. It doesn't stay there for a long time. Right. So it's true. And usually when patients see that the if you drain it, then you calm me down and then it can swell again unless you know, unless you treat the patient. But there's phases that, well, while it develops, it can become, you know, it goes through the acute phase and then becomes chronic. So even chronic like abscesses, as we said, they can have acute I'm going to say that acute phases, depending on what's happening over there, you can have a period elapses that has been there because of a necrotic tooth for years. Oh yes, I have this. It drains and it swells and goes. There can be an acute phase in that depending on what's happening in that microenvironment over there. And. Yeah. Yeah. I killed necrotizing. Okay. They don't have bone loss? No. The. Yes. So those patients want you debride them, they're going to be okay. The thing is, because it's so, so painful, you can't just address them the way you would address a regular gingivitis case so they don't have bone loss. I agree. They just have inflammation of the gingiva. But the inflammation, because of this combination with immunosuppression for various reasons, it's like the gingiva is not only inflamed, it's necrotic, it has those punched out papilla, the pseudo membranes and stuff like that. You can't even touch them. Like they scream. They literally scream of the pain. So. So again, giving an antibiotic for necrotizing gingivitis. It's a call that one has to make depending on what they see clinically. There are times that you can do a way super gingival debridement without even approaching the gingiva to start eliminating the bacterial load and giving other chemotherapeutic like a specific antiseptic mouthwash to start because the patients cannot even brush right. And they may have to come to you three, four or whatever times for you to finish a regular debridement. Scaling and frothy. Okay. Any other question? Around. Mhm. Our business is like, when do we start? In one word. Excellent. So when we see these smaller in size or pattern, the question is when we see these smaller in size or pattern, how do we know it's just the prudent thing and nothing else systemic underlying. Usually when there is a super young patient with kids, puberty or anything like that, I would always go and ask for something. And usually they know that if they have, let's say, an underlying genetic disorder, so they would know about that. Now if there is an adult patient, as I told you with this patient I saw in the early 20s, 23, whatever he when he came to the clinic, it was so alarming that my mind said, yeah, most probably it's an aggressive form, but just to be on the safe side, because if it's an aggressive form, because of an underlying disease, sometimes let's say patient is immunosuppressed and I go to do these deep scalings I may even do bad for the patient, right? If he's immunosuppressed, I may cause infection, I may goes in another opportunistic infection. I don't want to do this thing right. And that's why I usually ask when they saw the doctor to show me the lab work. If not, I send them again just to make sure there's nothing underlying. And the way you say that, it's because sometimes you say you need to see your doctor, they may freak out, right? So you say, no, we need to make sure there's not anything else that may contribute to that. So and usually doctors, if you write a form, they know that what kind of bloodwork they do. But obviously if you're having other signs based on the history or clinical picture, that doesn't look so textbook like, okay, I see that, but I also see this one happening. There's no harm of having a patient go and do a bloodwork and say everything is normal. You say, Great, so I know what I'm doing now. Okay, Anything else? Okay, so let me finish up with a couple of things similar to what I did last time. This is the newer classification and I just highlighted whatever we are talking about to do the matching with the older and newer, which is pretty much the same, apart from a couple of things with Titus, which we're going to see right now going back, see maybe it was more than 30 slides. To your question, how do we define a case of Titus? We need to have inter dental attachment loss on at least two non adjacent teeth. Okay. And you see, the word here is inter dental because yes, you may have buccal attachment loss with pocketing on at least two teeth, but those these facial attachment loss cannot be attributed to any other factor. Okay. This is to differentiate what's actually the concept behind dental disappeared entities compared to anything else that can cause a localized issue on the surface of a canine, for example. Right. So that's this. Answer your question. Yeah. Okay. So that's how we define a burden on Titus case and which are the three different forms of pardon tiles that are being recognized. It's necrotizing periodontitis as a direct manifestation manifestation of systemic diseases and periodontitis. So this includes now, they say, and the reason they eliminated the aggressive one is. Because they can't identify it as a. Complete like separate disease entity, Right? They say there's nothing like that. I'm not going to say if it's right or wrong and what's the background because they say the pathophysiology is the same. Now, does it mean that those patients have a specific pattern? Sure. But this is not like a disease that has a completely different pathophysiology, let's say the aggressive compared to the chronic. For you to say that's a different disease. Okay? And that's why they classify everything as one. Periodontitis the necrotizing that we talked about you say you see no ulcerative and the manifestation of systemic disease that you know that you're having an underlying systemic disease. So having said that, those this table and this table, you need to print it out and put it somewhere so that you can read it so that you remember what's going on. So when we classify now the present is we classify it with staging and grading. So the periodontist from all over the world that we're doing this for, I don't know how many years trying to develop those things. They wanted to have a system, that classification system that mimics this cancer classification system. They have the staging grading. So that's what they wanted to do for the updated one. So to make it easier because I know it looks chaotic first thing with the severity it has to do, if it's mild, remember we had mild, moderate and severe. Now we have stage one, two, three, four. Let's make it easy. Stage one. What do you see? The common things. You have 1 to 2mm of attachments, right? This used to be the mild stage two, 3 to 4. This used to be the moderate. Stage three and four have more than five. These used to be the severe same thing. Nothing has changed. The same thing with bone loss. The bone loss, they said it's less than 15% for the mild. They had exactly the same thing with the updated 2015 classification 15 to 30 for the moderate and more than 30% for the severe. That's something that I totally agree with, counting the percentage of the root length because you can have 3 or 4mm of bone loss in an eight millimeter root versus in a 20 millimeter root, right? So this change is completely prognosis and what you may be doing and hoping for these two. And so mild, moderate and severe, it's exactly the same. We just call it stage one, two, three and four. Okay. And the same thing. You're having some complexity factors in terms of probing bone loss, vacations, mobility, et cetera. So a couple of things. What differentiates stage three and four? Number one is the number of teeth missing or need to be extracted because of perio. If the if the patient misses ten teeth because of caries, we don't care about that. That doesn't change the periodontal thing. Right. So if the patient is already missing, let's say more five teeth or more or we are planning to extract, extract hopeless. We don't tell hopeless teeth five or more. This is going to be a stage four case. Severity is the same in terms of attachment loss. All right. In terms of bone loss and everything. And obviously what differentiates those two can also be some complexity factors in terms of rehabilitation. So usually those patients are those that are having a lot of drifting, shifting, moving of teeth, loss of video. Sometimes you need a complete rehabilitation. So these are the more complex cases. Now regarding those complexity factors, what they say in the classification is that a complexity factor may shift the staging because it just makes the case more complex, right? So if you're having, let's say, 3 to 4 attachment loss and friction three, you're already going to go to stage three. Okay. Now, is it very common that you're having mild attachment, mild attachment loss in class three? No. So usually there is a people things are made coincide, but complexity factors can shift the stage from something lower to something greater. Not the opposite, right? If you're having attachment loss more than five millimeters, but let's say no vacation involvement, it doesn't mean that you're going to go to stage 1 or 2 clear. Okay. I know If we will do, we will see that in example. So this will make more sense. And I know, I know I'll do my best for that. But yeah, when you start seeing that what's happening, it makes more sense. Yes. Yes. I has like 4 or 5. Do you think that is time to. What? 4 or 5mm of pocket. I wish and I hope you could treat it if you want to send it. I'm fine. But again, because I don't want to make things more complicated now, having a 4 to 5 millimeter pocket doesn't mean necessarily that you're having periodontitis because you're going to have a pseudo pocket. Right. So we're not going to go into that detail now, but you will see in action like what you're referring or not, it depends on your ability to treat a patient. So I'm not going to be there telling you, Oh, you should or you should not. I hope you can do a lot of things and only, you know, maybe challenging things as a thing. But it's not like, again, a black and white thing. So is there a question here? Yes. Let's say I would have a patient say Chuan. Yeah, in general, but the patient has an enamel for. The mourners. Pocket of six millimeters. Because of that, it still makes the patient to go. This is great. Unfortunately, that's these are the things that are some downsides, in my opinion, in this classification, because this is a specific tooth related factor. Okay. And the thing is that you may say it over there. Now, I can't prove that if this thing wasn't there, this tooth wouldn't have that form of destruction. Right? But in order to also compliment that extra thing that you're having, we will learn next week that there is also another thing that says localized tooth related factor that predisposes to the disease, and that's the enamel pearl, for example. Okay. We say the pocket, no. So we are not including third molars here. And there is a different thing. The other thing that I like in this one is that destruction on second molars because of third molars is a different thing. Okay. Okay. All right. You're welcome. And regarding the extent nothing has changed, again, you're having the localized generalized with a 30% cut off over here. And the only thing they have added here is the molar incisor pattern, the one we've been talking all day. Right. Because we are not using aggressive form as a disease. So if a patient has this aggressive, what we used to call aggressive theories, let's say generalized aggressive proton tidies, you would say generalized stage 3 or 4, depending on teeth missing and other factors. Molar incisor pattern. Okay. Now, on top of that, we're having the grading. So the staging is a matter of severity. The extent when I'm in extent, I mean, how many teeth are being affected is the generalized localized. And now we're having the grading, which is a way to to measure progression or kind of estimate progression if it's a slow progressing disease or a fast or moderate progression or very rapid rate of progression. So in order for you to do that, the very first and direct thing to say is I need to compare how much more bone loss and attachment loss I've had over the course of five years. And for you to do that, you need to have past records, right? So if you do have the past records and I always ask my patients, Do you have x rays? Yes, bring them. There are 20 years old. I don't care. Bring them. They will always give you some information. Right? So if you're having no loss over five years, it's a slow rate. If you're having up to two millimeters over five years, even 3 or 4 until you reach the five years, it's moderate. And if you have more than two, that's a severe. Now, there is very many cases that you don't have this luxury to. You don't have the luxury to compare the radiographs or having the records. So in that case, you're going with the indirect evidence where you're taking the percentage of the most severe bone loss divided by age, and you come up with a ratio, you see these numbers, I know how it looks weird or anything like that. But I need you to keep in mind of what I said before. If you're having 80% of bone loss on a 30 year old, it's completely different of 80% bonus in a 90 year old. Right. And this division will bring you to these numbers. So something to give you as a clue. The majority of the patients, what we use to say the chronic rhythm is patients. They fall under these category grade B, okay, That's the most common form. Grade A There are very few cases that despite having a lot of plaque and biofilm, you see very, very slow destruction. You know, sometimes you may see a patient in their 70s and they barely have a millimeter of attachment loss or something like that. So that's a super slow rate and the rapid rate usually falls into these aggressive forms, right, because they go too fast. So again, summing up from what I said before, a generalized aggressive entities would be classified as generalized stage 3 or 4 grade C burden theories with molar incisor pattern make sense. Okay, now these are the primary criteria. So when the patient comes and you establish that you will end up with a grade A, B, or C on top of that, because the research has shown as such, we have some great modifiers and the two established one is smoking and diabetes. We can have other factors, but those two smoking and diabetes, we have plenty of evidence that they directly affect the disease. So if a patient is a no smoker, no diabetes, nothing affects the grade. If the patient smokes less than ten cigarets a day or is diabetic but is controlled, which means the A1C is less than 7%. It's on grade B and if it's more than ten cigarets a day with non or non controlled diabetes, it's great. C What do I mean with that? If a patient comes and you're saying, okay, it's great. A But they smoke a pack a day or they or you don't have to have both or they're diabetic and it's not controlled, they automatically will go to grade C. If they come and you're right away, you're saying it's a rabbit, Progression is great, see, But they don't smoke and they don't have diabetes. They're not going to go back to a right because the grading first you have your primary criteria make sense. So. The the the thing that I always ask in the clinic and say, why is it great B or C in the clinic, although I say it here, everybody says because they are not smoking or because they are not diabetic. This is a modifier. The first thing is to know what's happening with attachment loss or bone loss. Establish your grading and then if you have those, it can only make things worse. It cannot make it better because, okay, we have severe attachment loss in a 30 year old everywhere. And but because they're not smoking or not diabetic, it's great. They know that's not going to happen. Clear. All right. So putting those two things together, let's diagnose that. So that's a patient, 50 years old. She's smoking one