Gingival Diseases PDF

So we're going to talk about definitions. As we said in the previous lectures, we need to overview a little bit the normal appearance of the gingiva, how things look, and then variations and clinical signs of gingivitis, classifications, diagnosis, just touching up into treatment because you will ge...

So we're going to talk about definitions. As we said in the previous lectures, we need to overview a little bit the normal appearance of the gingiva, how things look, and then variations and clinical signs of gingivitis, classifications, diagnosis, just touching up into treatment because you will getting you will be getting further lectures on that. So building up on that, if you have seen on Blackboard, there are some additional readings that's going to help you understand what's going on. Okay. I'm not going to say, according to this page of that article, what is happening there, but it's definitely going to help you understand what's happening there. You may have heard that we changed classification came out officially around the 2018. I was actually at the meeting when they presented at and the periodontist were like, Yeah, we got that and the periodontist in the audience. What is that? So you are fortunately or unfortunately you can take it the way you want it in that transition period that we are teaching you both for a couple of reasons. Number one, outside, there's still, you know, then this president is using this classification system from 1999, and there's you need to communicate and understand what they're talking about. Most important importance. Insurances here haven't switched to the new one yet. So when you're submitting claims and everything, if you start saying about wording of the new classification, they have no idea what you're talking about. It's going to happen eventually. But we need to also make your life easier. People like especially specialists, etcetera, they are transitioning, you know, slowly to the nucleus ification. So you need to understand what they're talking about. If you will learn future lectures about staging and grading. And if somebody says about staging and you said, What are you talking about? You need to understand that. And in my opinion, you may agree or disagree. Understanding how things are structured with the 1999 makes it easier to understand small changes that happened a couple of years ago. Okay, you may disagree with that, but I found that understanding that concept makes it easier for you to understand those. So as we know about periodontal disease is the term when you see periodontal disease, it depends. It depends. It refers to a majority of both gingival gingivitis and Berton theories. Together, we're going to focus on the gingivitis. And we talked about the normal appearance of the gingiva, where the color is color pink, the size fits tightly around the tooth, more scalloped architecture in the anterior teeth, more flat architecture in the posterior teeth. Consistency is firm, and the texture we said usually can be stippled in a healthy. Don't see more though. Absence of the stippling doesn't necessarily mean that the downtime is disease or has inflammation. Having said that. All of the following are clinical signs of gingivitis. Except which one? The attachment loss. Okay. So that's something I need you to keep in mind because when you see clinically, you know, work with students and they say, my findings are so and so, I have my probing, I have attachment loss, I have either deeper, shallower pockets, it doesn't matter. And then the moment they present with attachment loss and they do not go to the either reduce production. We're going to talk about operating theories. Makes no relevance with each other. Right? You either didn't diagnose it correctly or your findings are not correctly. So just keeping that in mind regarding gingival diseases, what do they they are actually inflammation of the gingiva, as we say, gingivitis. Everything that ends in it means inflammation. And everywhere in the body they are confined to the gingiva. We do not have attachment loss or we can have stable attachment levels. Thankfully. And luckily the new groups identified there can be patients that had a history of prior disease treatment for that surgical or not surgical, and they are stabilized and they start developing some signs of inflammation. In the past, they were over diagnosing those patients with periodontitis again without having other deeper pockets or further loss of attachment of bone. And they would go again through unnecessary treatment. So they have classified that we're going to learn about this as well. Gingival inflammation can be reversed. Okay. There are several studies and that have proven that with the experimental gingivitis, we can cause it and it can go back to health. If you take good measures of the disease, it's the mildest form. Usually we associate that with inadequate oral hygiene and the presence of dental plaque initiates and exacerbates the severity of the lesion. That's what we believe today, how things work and going back to the signs of inflammation described first by cells during the first century, as you see here. And they're pretty much those with the Latin words. You may understand those as well, but it's pretty much heat, redness, swelling, pain and loss of function. And how do those signs translate to gingivitis? So regarding this one, we have elevated cellular temperature. Obviously, we do not have a temperature, a thermometer or something to measure that. But there have been studies that can measure those things. We have redness, erythema. We have. Uh, edema and fibrosis. We have gingival sensitivity. And obviously when you're having loss of function, as we say, but don't support that happens with Bert and Titus in the more advanced forms. And pretty much that's what you can see in a typical, more severe case of gingival inflammation with gingivitis with red color, sometimes even dark red. I know it's too early for this picture in the morning. It's okay. Size are more enlarged, the tissue is more rolled. Landed ball was cratered depending on how the inflammation has taken place. More than and smooth texture over there. Something that we really pay attention to is the bleeding on probing with increased gingival exudate and what does this actually bleeding on probing mean? So just for you to understand, you see here this instrument, the periodontal probe. When you're examining the gingiva you're taking we said about that last time how the normal anatomy of the production meets the circular area. That's the free gingiva is just resting over there, and you can easily separate it before you reach to the junctional epithelium and connective tissue and measure how deep this number is. And sometimes, especially when you're having inflammation, the moment you put your probe in, either at the same time or the time you remove it, bleeding starts to come out. So that's what we call the bleeding on probing. So the significance of that is, as we said it's called, is caused by swelling of gingiva, gingival, capillaries, ulceration of the epithelium, and you're having some collagen degradation. That's what clinically you are maybe understanding that happens subclinical and also an inflammatory response from cells. We're going to learn about those in the host response lecture. But usually when you're seeing bleeding, unless you literally poke to the patient to the bone, but you're going to know that because the patient will scream will not like that, especially without anesthesia. This indicates the inflammation that takes place, which has all those signs that we've learned about. So what is the significance of that? There has been this landmark study, so just remember the name. If anybody says what did Lung say about bleeding and probing, you know what they're referring to. So it has low sensitivity but high specificity and very, very high negative predictive value. So what do those things mean? It means that seeing bleeding on probing, you can't say, oh, it's bleeding, you're going to lose attachment, you're going to lose the tube. You can't say that to the patient there, actually. So in that study that only 30%, as you see over here, up to 30% sites with presence of bleeding and probing over a period of the observation period, they lost some further attachment. So that's not something that you can say for sure to the patient. On the other hand, the absence of that is an indicator of stability. Okay? It's a predictor. And especially when a patient comes and you do your periodontal charting and you write about your probing and everything, you write about bleeding and probing about plaque, you wanted the re evaluation after treatment, etc., to see those scores to have reduced significantly so that you can say to the patient, look, less bleeding, less inflammation, more stability. We're happy with that. Right? So that's something that you need to keep in mind, the way you're presenting to the patient, because there can be patients that are going to be very scared, like, oh, my gums are bleeding, what does this mean? Am I going to lose the tooth? Or so So being more specific with that. So yeah, just remember that study and the significance of bleeding on probing regarding the histopathology of gingival diseases. You can see here also in slides, histology, slides, vasculitis of the blood vessels, progressive destruction of the of the collagen, you know, infiltration of inflammatory cells. You will see more information when we go to the horse response. Just giving you up some information of how things look like histologically. So let's see those stages of gingivitis that have been described by Paige and Schroeder. And this is. A table. I think it's the easiest way to remember what's happening and questions are coming from that for boards and stuff like that. So keeping that in mind that this is important and I'm putting it over here. So we have the initial phase. I think I have it step by step afterwards, but I'm just going to bring it up together here. So the initial stage that happens like the first 2 to 4 days, you have more like very minimal gingival fluid flow. So clinically you can't see anything there. Okay. You see this one? You're saying that's fine when you go to the early phase when it happens, like after the four within the first week, you're having more lymphocytes getting there, more erythema. You may have some bleeding on probing, more signs of inflammation established. You're going you know, it can vary from 14 to 21 days where you're still continuing seeing like this redness, inflammation, bleeding, etcetera. And eventually the fourth column, we're going to go over that next time, the advanced one where it happened with predators with more infiltrate of plasma cells, connective tissue loss, bone loss, et cetera. So going step by step, I just had the table over there so that you have it. Everything together. We have this pristine gingiva. And you see, histologically in this scheme how things are looking. You can you may rarely see that. Like patients having this, as we call pristine gingiva, there's very sparse like neutrophil migration. You may, if you take a piece of the gingiva and look it in the microscope into the sulcus, but there is no inflammatory response. Okay. So that's pretty rare that you may see clinically, but it may exist. The initial lesion, as I said this again, clinically, when you see that, you don't realize that something is happening there, right. Clinically, I would say that looks healthy. The tissue is pink. It has the shape, the texture, everything that we talked about. But inside you may still have some plaque or biofilm forming. There. We all have it. We know how it forms. You can have some neutrophil migration over there. And it's as we said in the beginning, it's always there in the connective tissue, in the epithelium ready to attack and response and multiply depending on the challenge, the bacterial challenge that may happen in the oral cavity. So having said that, you may have heard I don't know, may or may not have heard some people say, you know, everybody has gingivitis. Sure if you find those signs. But the fact that subclinical, you see that. But clinically, according to our criteria, it's healthy. You wouldn't diagnose them with gingivitis. Is it like a very high percentage of our population that you may diagnose them with that? Fair enough. But it's not like everybody has injuries. Okay. So just keeping that in mind, going further to the early lesion, that's when you start seeing your first clinical signs with some inflammation, with some marginal redness, maybe some bleeding and probing delayed or not, you know, more edema, a little bit more smooth gingiva. Obviously you start having lymphocytes appearing apart from the neutrophils. You may see some collagen degradation, but we're still you know, attachment levels are the way we have them. And finally, the established lesion, that's like the most, if I can say so severe form of gingivitis where you obviously have evidence, signs of the inflammation with bleeding, swelling, edema. Some plasma cells are getting inside that area, too. So that's a whole cascade of immune reaction. We're going to learn about that so a patient can stay here. For days, months, years. It doesn't mean that everybody that goes here, they will jump right away and go to the Advanced Legion, where we call the president. Titus. Right. We do not know when this happens. And our assumption is that you need to go through those three stages first in order to end up to that advanced legions. There's no way for us to figure it out. So that's why we're saying this like that. So that's where this whole staging by Page and Schroeder, as you see here, has been established, understanding how those lesions work, what you're seeing clinically and what you're seeing clinically. So going to the classification to understand things, everything started in 1977 when they started talking about percentages in some categories. And then since then they've been having several classifications, like reviews of the classifications are in categories, as you see over here with pertinent titles, more categories being more informative with that. That's 1999 as we see here in 1999. That's this classification. That's where they had a huge a huge section of gingival diseases which they didn't have before. In description of that, in 2015, they reviewed that classification and finally 20 1718, that's when it kind of came out. That's the most updated neural classification that we have over here. And as you see here, that's where the gingival diseases were added to our diagnosis and be able to find them out. Okay. So going to that system, we're going to go with the first page. Yeah, I know it sounds a lot and it's pretty much going to go over all those things. It's not that chaotic as it looks like. I will try not to make it that chaotic. And that's the whole the other section of periodontitis. We're going to talk about that in the next lecture. So talking about gingival diseases, let's have a question. Our Gingival disease is always induced by bacterial plaque, dental biofilm. Mm. No. Right. Because, you see, there will be a big category of non plaque induced invisible diseases. So we need to recognize that that's the two major categories. Now, in the reality, when a patient comes and you see clinical signs of inflammation, as we said, with redness and bleeding and edema and everything. 100%. Our assumption is it's a dental plaque in use unless there is a textbook, you know, pathology or, you know, the patient has a systemic disease that has this specific representation clinically in the gingiva and you can diagnose it. But usually 100%, we think that everything is like dental plaque or biofilm induced gingivitis. You do your treatment. And what did we talk before that? It's a reversible disease, right? So if you do your proper treatment and you teach oral hygiene to the patient, I think Dr. Ann talked about the experimental gingivitis study. No, some shake knows some. Okay, I'll review that. If not, I'll bring it up next time as well. Anyway, they had the experimental gingivitis, so you know that it's a reversible disease. Okay. Having said that, you're expecting, whether it's proper treatment and proper oral hygiene, you would see the signs, the clinical signs to be eliminated if those signs persist, especially specific clinical textures and redness that do not go away, that's when you're suspicious that there can be a non plaque induced gingival disease that may need further investigation, further lab work or test treatment, etcetera. So and that's why usually in those cases when we're suspicious of maybe something else, we do our treatment and we say to the patient, Let's have you come back in a couple of weeks, months, because I'm expecting that I if everything is plugged and use you, it will be fine. And if not, that's when you proceed with other things. So going with the plaque induced gingival diseases, we can have the ones that are associated only with the dental plaque modified by systemic factors, medications and malnutrition. So dental plaque again, this picture, you will never forget it. Today I should maybe put different cases so you can. That's like a very typical case. No other contributing factors. You have the gingival inflammation, no attachment loss, no bone loss, and you have presence of plaque. Obviously, there can be there can be times, like we say here, like a puberty when kids at some age say, you know, I'm going to be like a rebel here. I'm not going to brush among everything. So having said that, you can see those peaks throughout the life. The change we said from health to disease histologically clinically is not detectable from that. Like pristine, you know, to that initial stage when you're going to the early stage that when you start seeing clinical signs and obviously these includes all everything that we talked about, about color, contour, shape, consistency, et cetera. Apart from that, you can have other contributing factors. You can have dental appliances, restorations, you can have tooth related factors like a groove, like a root anomaly or something that can contribute to further plaque accumulation. So why do we say that? Because obviously in Imagine like this groove plaque can stay there comfortably, rest no instruments, toothbrush or anything, can get there to disrupt it and break that biofilm so it can accumulate way easier and colonize that area. Those diseases can also be modified by systemic factors like the puberty associated gene devices, as we said, with the menstrual cycle, pregnancy or diabetes for women, especially depending on the where they are in their cycle, they can have more inflammation. You can see that in your patients. They may bleed more easily and it can just be part of the cycle that you have over there. And why does it happen? It's all about changes in the hormones level, increased level of specific hormones or either progesterone or estrogen, depending on the phase. It can happen more intense before ovulation and obviously inflammation can develop in the presence of very small amounts of plaque. So it's all about that balance. And all those hormonal changes can cause changes in alterations in the response, in the oral cavity. So we need to have, as we said, the bacterial plaque, the biofilm in conjunction with those hormones. And depending on the plaque, whatever plaque you have, it's not like it has to be specific. It can be the presence of specific bacteria to cause the reaction, but it doesn't have to be specific. And again, you know, estrogen is responsible for alterations in the blood vessels and progesterone in the inflammatory response so that how you see those changes regarding the pregnancy associated gingivitis, something that I wanted to bring up. Apart from the gingivitis, is what we call the fire genic granuloma. You may see that in pregnant women usually they may say, I suddenly saw a swelling which is present over there. It can bleed easily, it can be uncomfortable. And when they deliver the baby, usually that swelling shrinks. Sometimes it may disappear depending on the size and where it's found. It doesn't cause any pain or discomfort unless somebody injures that, but it can bleed easily. So depending on the case, you may decide to do something to remove that over there. But obviously that's because of accumulation of plaque. It just swells significantly on that side. You can have gingival diseases that are modified with specific blood is contagious, like the leukemia one. This is very I mean, if you see a patient like that, you know right away that there's something systemic happening there, that this cannot be happened only because of dental plaque. Right. And usually those patients, they bleed very easily. You can see that more common in acute leukemias. They can be also the gingiva can be painful and sensitive. So you know that you need to refer your patient to the doctor, do a blood work. And especially in case they don't, they are not aware of that and find out what's happening. The immune response is very suppressed. So you have to be very careful in terms of treating those patients. There can be gingival diseases that are modified by medication. This comes very, very frequently like drug induced or influenced gingival diseases like especially enlargement. That's what you may see more frequently. You can have gingivitis influenced by specific medications like the oral contraceptives, but usually we're talking about Gingival enlargements. In case you have heard about it, which of the following? No, it does not cause gingival enlargement. I forgot that. Hey. Hey. Okay, I'll give you the answer. You don't have to know it. I said in case it does not. Right. I didn't change in the first. Okay. So phenytoin the calcium that comes very, very frequent in the clinic. Like calcium channel blockers for high blood pressure. They come very frequently and obviously specific immunosuppressants like cyclosporine. So something because I know we have tons of meds and you don't have to remember everything. I get it. And if you don't know anything, there's no shame to look for it and open and say, you know, let me see what kind of medication it is. But usually those calcium channel blocker and example is like the Philippines, as you may see. Sometimes it can cause those fibrotic gingiva. Usually the meds that end in I'd pin. There are these categories. So if you hear that even you've never seen that before, say, could it be these categories or look it up and like I'm ripping these kind of medications. That's how it happens over there. So usually they have an impact on the fibroblast and in presence of plaque inflammation, you know, the tissue swells as part of the response, the inflammatory response. And in conjunction with some of those medications, you can have more fibrotic tissue as you see clinically. And this one, this can be I mean, in developed countries, I'm not expecting you to see that frequently unless there's a specific malnutrition problem like the Azubuike acid deficiency, the scurvy, as we say. But obviously this is not a very comfortable situation for the patient. They have weakness, anemia, bruising, bleeding, enlargement. So again, you know that something is going on in those cases. So that's pretty much what you're going to see the majority of your cases pretty straightforward, associated with dental plaque, more or less. It doesn't have a specific impact because we're going to learn on the stages of actually Dr. and talked about that the presence of specific like of the presence of plaque does not necessarily mean that it's going to cause the specific kind of the disease. It's a combination of specific bacteria response, the ecological changes that are happening, creating like the Keystone pathogen hypothesis, everything that you talked about a couple of weeks ago. So that's pretty much what you will see. And the majority of those, unless the patient has no teeth without any restorations or deformities, you may have some additional local factors or systemic factors that may influence the presence of inflammation there. And now there is a list of non plaque induced gingival diseases, as you see over here, that you may come across across. So there could be specific gingival diseases of bacterial origin. How do we say that sometimes again, if you don't see any response, some dentists may say, okay, you know, let me do a bacterial culture and see what kind of bacteria I have, because sometimes you may develop a specific bacterial species that may need specific antibiotic or other treatment. So you can have specific bacterial origin that can cause that inflammation. You can have viral some viruses that can have gingival manifestations, as you see, not only on the gingiva, but also in the oral cavity like the herpes stomatitis oral herpes. This is dead again, oral herpes or the varicella zoster. So those usually can have manifestations on the lips or the cheeks or the throat or the palate, etc.. So this rings a bell that something else is happening there as well. And you see like there's more like red spots or vesicles or that you can see over there and be species of a virus that may be present and fungal origin. You may have seen that in other classes as well, are patients that are immunocompromised, maybe are wearing, you know, specific appliances like removable dentures not being maintained properly or sitting properly. They can have like the candida albicans histo plasma C So this linear gingival erythema as you see here, you see this redness in the marginal tissue. So when I see that clinically, yes, it's red, red, it's enlarge, it's smooth, it's a diameter. So it has all the signs of plaque inducing devices. But I'm 99% sure that there's something else there. Right. And in these cases, even if you clean those areas, these redness won't necessarily disappear. And that's where you're suspicious that something else is happening. And that's, for example, this linear gingival erythema that's more frequently seen in HIV patients, where the immune system is also compromised. It's like this erythematosus lesion because it had this pattern, people just mentioned it and said, That's how it looks like. It's more like a pronounced redness. And obviously patients, you know, about their HIV that is not controlled. You may see that. And if you don't know that, that's a very good time that you're going to tell them, You know what, I would advise you to do some blood work to make sure that everything is fine. There was once a patient actually in my first couple of years when I was here, a very young patient that came to the clinic to get a tooth cleaning, saying that your gums are hurting. And she was not diagnosed with HIV, unfortunately. And when we sent her for that, because the moment she opened her mouth, there was such an alarming picture. She was very sensitive, like she had a lot of fungal infections, a lot of erythema edema. I was like, I haven't seen a clinical picture like that. And that's when you say, you know what, I'm not going to do a tooth cleaning because that's what you came from. I need you to check what's happening. And glad that she came because she was so severely compromised. She barely had any t cells in your body, so she needed to go into treatment like right away. And she was maybe 17, 18 years old. So yeah, that was super, super sad. But this is something that they may come, they may not know. And you see that and you need to direct them correctly going forward. You can have specific genetic origin cases like the hereditary fibro mitosis where the tissue is more enlarged. It may look more inflamed because it's swollen and enlarged. And it can have obviously more extreme cases like here where the tissue is covering the teeth. They're perfectly covered over here. These are cases that you need to do sometimes multiple treatments of gingiva, ectomy to expose the teeth depending on the severity. And it doesn't mean that you do it once and it doesn't happen again. But something to keep in mind with that. Now, regarding the systemic conditions, this is something that may come. More frequently than we're thinking of. I've been seeing way more cases of all those disorders. And I used to. I don't know why, but that's my experience so far. So going with the first category, you need to know those things, what they come with clinically. You may have heard I don't know if you've taken Oral Path yet or not. You may have get you may get more information from them. I'm not going to go into that big detail over there, but that's something that I've seen many patients like that I've treated many patients. I needed to do biopsies for those patients. So that's something that's coming way more frequently than I actually thought of. Like in planners, you think, Oh, it's only 1%, but you can see several cases like that. You can see lesions on the skin and the mucous membranes in conjunction with immune diseases. So actually I lied. I do not know why they come or often. That's the secret word. Okay. With everything that people are going through and the stress and all those things, we have a complete peak of autoimmune diseases that are showing up and obviously those can have some oral manifestations as well, or conjunction or exacerbating other autoimmune diseases and disorders. So what you can see clinically, that's the most frequent that we can strike over here. Those white lines on the cheek, usually bilateral, you can have the bullet form or the erosive form. So this one, if you see the erosive form, that's the most alarming one because these can go undergo malignant transformation. So you need to keep an eye on those. But that's how you would see clinical pictures and manifestations of lichen plants. Again, as you will see with the majority of these diseases in this section, there is not like actual cure. Whatever we do is more to palliative treatment to reduce the effects, the symptoms and whatever discomfort the patients may be feeling, usually giving topical steroids, sometimes systemic. It's very if it's very exacerbated some retinoids immunosuppressive medications. So depending on the case, it can. And all those diseases can have flare ups depending on the patient's state, not only orally, but also medically, emotionally, everything like that. And as we said, specific and severe cases, especially the erosive ones, may increase risk for oral cancer. So you should be able to identify those regarding figured. Again, it's a chronic you will see the pattern is pretty much the same rare autoimmune blistering skin disease it says rarely involves the mucous membranes. But you may see patients having that. And what you see over here in the histology is that the full thickness of the epithelium, like a blister here, is separated from the underlying connecting connective tissue. And what happens over here is that you can see also with direct fluorescence that there is a separation where the hemi desman. So where were the hemi desmos forms? Remember from last time the basement membrane with the epithelium and connective tissue, while what did we have between the cells, there is Muslims, right? So in this one on the go, that's where it's being targeted. And you can see with the direct or direct immunofluorescence the staining with those antibodies, the IgG localized to the basement membrane. And that's pretty much how you differentiate between the Benfica's and the Penfold. We're going to talk about the scenario a little bit. And just as a reminder here that where the Hemi desmos forms are with a connection, as we said, with the basement membrane regarding the void, you know, you have blister disk promoters. This is actually these are pictures from a patient of mine. She didn't have anything on her skin. She came complaining that my gingiva is hurting and I've been doing cleanings and it's not working and it keeps bleeding and it's sensitive. So that was her chief complaint. And seeing that obviously there is inflammation, I again, as I told you before, I'm suspicious that something else is going on because the tissue was so fragile. The moment I would touch it, like the whole skin would peel off right there is because of the separation. So that's when you will need to do some additional test, a biopsy to confirm diagnosis. And it's exactly what's happening. Like the epithelium like unzips from the underlying. Connective tissue. Regarding the pamphlet, again, the treatment is directed mainly to reduce the inflammatory response and the antibody autoantibody production. And again, we usually use corticosteroids and immunosuppressants. Going to a different one and only. We have no like fantasy with the names. So we can use Pam Figo just to confuse each other. Again, similar thing, autoimmune disease of the skin and mucous membranes, pretty much similar clinical representation. So obviously the histology is the one that's going to differentiate and give you your final diagnosis and that's where the Desmos homes are being targeted. As we see over here, the one that I said glue or connect the cells together. Remember from that slide when the cells are being connected together. So what you're going to see Histologically is, yes, over here a separation within the epithelium. Okay. Compared to the Pam figure where you see the whole epithelium being separated from the connective tissue here you see like a widening. So that's the separation within the epithelium. And if you remember basically how the layers epithelium layers look, those four layers we talked about, it's easy to identify where the connective tissue is and when the epithelium starts and where the separation is. Again, that's where the auto antibodies attack. And what you see is what we call the acanthus slices. So the lysis, like the separation of the acanthus like layer, the biggest layer, as we said in the in the epithelium, that's where it's being targeted, where the desmos forms are connecting the cells together. And that's where you will be seeing that both in Histologically and Immunofluorescence evaluations. The source may originate in the mouth compared to the Penfold, where you may have sores and lesions on the skin first and then they may appear in the mouth. So that's when the patient may complain about discomfort, pain, bleeding. ET cetera. And that's where you need to investigate it further. And treatment as usually pretty much the same concept of reducing inflammatory response in the autoantibody production with the corticosteroids and immunosuppressants. So because questions come always about those two things and I have no. Nothing to play with the words and make it easy for you. So you figure it out how it works for you. But pretty much these are the main differences that you need to know where in the world you have a separation of the full layer, where it's within the epithelium. So that's why you're having these anthologies where you don't have it here, less common in the oral cavity, more common in the oral cavity, and vice versa with the skin, the ages. That's where some reports have been found. But obviously it can vary. Female population may be affected more. Again, these are specific epidemiologic studies. Nothing to say de facto. And obviously the treatment is the same with reducing the system with symptoms, with corticosteroids, immunosuppressants if needed. And you always need to be in communication with the dermatologist and oral pathologist to see what's the best for your patient. So when those patients come and they have those clinical signs and you see them, remember we talk about diagnosis now, right? And obviously Oral Pathe has talked to you about that, that you always have a differential diagnosis. And why? Because in oral path you see something, you can see a blister and it can be many, many things. Right. And that's why you're having this differential diagnosis. And you usually start with the one that you think that's most probably what it is, and then going to the least possible option. And obviously the only way for you to confirm the diagnosis is when you take a biopsy. They check it in the microscope. They do immunofluorescence depending if you're suspicious of those like disorders. I always send two specimens, one in the formalin for the basic histopathology and one in like a medium as they call for immunofluorescence to be able to identify and have the final diagnosis clear with those. Okay. Erythema multiforme. So this is very specific. Obviously you've learned about you may have heard about that as well. The exact cause is unknown. It's more common in the Stevens Johnson syndrome. And I know those things. There is an overlap with what you may be taught in other science, but these are things that you may see clinically and. When I was a student, I was thinking, Oh my God, unless I become an oral pathologist, I would never see those things, right? Like, I'm going to be a dentist and I'm going to be gnawing my regular teeth, my regular gingiva, and I'm going to be fine. And you just need one case that you don't want to miss and that's it. And among all those things, the majority have just seen them once because they're they're some of those things. And I said, oh, I remember somebody somewhere told me about this thing. It doesn't mean that I'm the one that's going to treat them and do it, but I recognize what's happening and I refer where people need to see these patients and deal with them respectively. So that's why it's important to identify those. So the other thing that you need to know about that they have this positive sign where you take the epithelium and you see this redness so you can have multiple skin lesions with sudden onset. You can see those target know they're symmetrical and they can be in the upper body, the legs, they can be on the face, the lips. That's where you may see them very clinically. And they look like a target or bull's eye, depending on how people think see things. So that should ring a bell on those areas. Again, you will try as a treatment to control underlying the underlying causes with giving specific medications. In mild cases, you want to reduce the symptoms for the patient with specific anesthetic over the counter, medications on the histamine, etcetera. In more severe cases, you may need systemic corticosteroids, immunosuppressants or antibiotic vision infection. So keeping that in mind, and I think that's the last one, the lupus, a similar chronic autoimmune disease. Again, I've seen several patients here in the clinic that have been diagnosed with lupus. They can affect any part of the body. It can harm like even joints, skin, heart, lungs, etcetera. So it can be very severe if not control. The course of the disease is unpredictable so we can have flare ups. That's why the patient needs to be monitored by their doctor very frequently and give this specific medication and it can occur at any age. It may be seen more frequently in women and. You can see try to treat it as we say that with addressing the symptoms with corticosteroids and immunosuppressants. So that's a pretty frequent flare up that you may see in lupus patients like this. They call it, I think, like the butterfly redness on the face. So that's pretty much the whole category of those mucositis disorder wasn't that bad. So was they like plants We know about that. The gold figures, you know, know the basic differences. What you see clinically histologically what's happening with what separation, which one like 3 or 4 bullet things, erythema, multiforme and lupus. So like it's the most common ones that may be associated with a gingiva. And then we go with other conditions like allergic reactions. There can be allergic reactions to dental materials. You may see patients that get a new restoration and suddenly they may develop that reaction to specific toothpaste. So if a patient complains about complains about the weird sensation on the gingiva and you can't see anything that is happening, ask what are you using to brush your teeth or everything? Or did you change any product? And sometimes they may say, Oh, I took this new mouthwash this friend of mine told me about, or this new toothpaste or whatever, and this can have a substance that may cause a reaction. Usually that happens with more caustic like ingredients or the ones that may have cinnamon inside some of those ingredients that can cause more reactions. And then you can have those traumatic lesions, which can be a chemical injury. I haven't seen that like too frequently nowadays, but in the past you would see that more often because patients used to put like aspirin or something next to a tooth that was hurting, thinking that this will calm down the pain and obviously that was destroying the epithelium over there. You can have physical injury. You can see that very common. These, for example, can be from even a dental procedure. Something happened and can cause that. It can be a habit of the patient. So especially if it's not like dental related or so and you see something like that, you need to investigate and find out if the patient has any weird habits. Their patients that are using toothpicks or pencils or whatever they may imagine as a habit and they may injure themselves. So you need to find that out and you can have some thermal injury over here. That's pretty common when I see those things. My first question is, did you have like something hot yesterday? 99%. The answer, I guess I got a delicious pizza. I couldn't wait, so I ate it. And obviously there's a thermal burn. Sometimes there can be with hot tea and beverages. So in those cases, when you see those things, you obviously need to stop whatever happened that caused that. And then I evaluate the patient a couple of weeks and usually those symptoms have disappeared. Foreign body reactions. That's very common as we see over here. I know we associated with the poor popcorn. It's okay. I can get it. Why? But it can happen with even our procedures. Forgetting chords. Yes, somebody said it. The cord. I've seen that. It's very painful. Patient calls usually after the next day and says, I'm swollen and painful and everything. I've seen a wedge being forgotten over there from my restoration. So doctors count how many glasses they use in their surgeries. So we should count what we put in the patient's mouth, making sure that we take it out. And obviously, because we can't know anything in this world, there can be other non specified issues that we don't know and we may find out, but that's pretty much any questions so far. Clear. So that's pretty much what you need to know. I mean, how further down I can break it, you need to know about the gingival diseases. The major categories, the plaque induced associated, as we said, could be associated with other contributing factors local or systemic nutrition drugs. ET. The other category is the non plaque and use the big categories, those mucositis diseases. We talked about those five diseases that I need you to know with like and planus Pam Pam figures, lupus and erythema multiforme and then all those other things with foreign body reactions and injuries and stuff. Obviously there are gingival manifestations that they're not typical of a gingivitis case. And in these areas you definitely investigate habits. Something that has happened, you know, either a patient did something or they had a procedure or anything like that in order to to identify what's the correct diagnosis for those cases. Okay. And now I don't want to confuse you, but I'm going to tell you how things blend together so you're not confused. So we had this world workshop, both Europe and us, they sat together. They spend their times, their nights, their days, they discussed and they came up with that. I am not here to tell you if I like it or not. If I agree or disagree, I'm here to tell you that what we will be following. Okay. And I know that you may hear people saying, oh, I don't like that. It could be because they're used to how things were and they don't want to change. There are people that may disagree with other aspects, but it's not me to teach you otherwise it's me to tell you that's what you will be seeing. So you need to be familiar with that. As you see over here, they have like the categories. It's pretty much the same. You have also these articles in the in the on blackboard. I have posted them for your reference if you want to read it on the Saturday or Sunday, you don't have anything better to do best you can. Enjoy your morning coffee with that. It's you can digest it better. That's why they added also the very important diseases. So obviously they did some valuable additions that we didn't have before, but you will see that the majority of the others are pretty much the same. Some minor changes that we're going to go over here and that's pretty much the first category. So the other thing that's really important for them is that they added these don't have health and gingival health because, yes, it may not be that common, but you still see patients that have healthy periodontal, right? And especially if somebody has gingivitis, imagine that patient comes, Oh, my gingiva is bleeding, whatever you do your examination and say, okay, excellent. Your gingiva is only affected, so you're having gingivitis. But listen, we have a treatment. I'm going to do the treatment. I'm going to give you instructions. And one, go to cure this thing. And we then I can see you after a week or so or two weeks or whatever, and it should be cured. And the patient comes back and you say, Yeah, because I don't have anything to say about clinical health. You have, again, gingivitis. So this obviously wouldn't make any sense to them. Obviously, this can happen, right? There are patients that may not respond to the treatment or may not do their home care properly, but seeing people that are periodontal healthy and have healthy tissue, it's, you know, it's exists. It's nothing like super rare or anything like that. And this can happen obviously on an intact periodontal or a reduced periodontal. And we're going to go over more details in those things as well in future lectures and reduce periodontal. You know, it can be stable in a previously person Titus patient or non burden type this patient and here it's whatever we've talked about the gingivitis, the biofilm induced. Alone with a biofilm. So dental plaque, systemic or local factors, drug induced. It's exactly the same thing. Right. And here it's the non biofilm induced. And you have all these other like the inflammatory immune responses, the genetic like endocrine traumatic lesions. Everything that we talked about is on that category. And I made it a little bit easier for you. So this is the 1999. So I have put those colored squares or rectangles, whatever you want to call them, to represent which areas are exactly the same. Okay. So the first here with a biofilm induces here, non biofilm induces here. And that's a dental health that you see over here. Okay. Nothing weird. It's different sequence. Okay. It shouldn't confuse you. So going back a little bit on this information regarding the health and the gingival health, we can have it on an intact periodontal or a reduced periodontal. So what is a reduced periodontal? You obviously patients that have a history of dental disease, you can see clinical attachment loss in forms of recession, not like actually the pockets. The pockets are shallow. You can see or you may see radiographic bone loss. So that's a typical case. This patient at some point, the gingiva, first of all, used to be over here, not over there. At some point they had some form of dental disease with inflammation pockets did a treatment, surgical and surgical. It doesn't matter at this point. And that's what you end up and that's what you want to see as a successful treatment of this patient. To maintain that have shallow pockets, the bone levels are stabilized where they are. You can't grow them back in this specific case, and tissue is not inflamed. So that's what's considered reduced periodontal you in. To sum this up, no active periodontal disease present on Titus history presented is reduced attachment levels and bone levels reduced in stable periodontal. Obviously those patients may be at more increased risk of developing the disease again. That's why they need more frequent recalls. We're going to learn about those, but that's something that you can see clinically and with proper care, proper maintenance, proper vehicle frequency. You can see those patients maintaining their health burden, tumor, the reduced levels for many, many years. And what can it be a reduced periodontal mean and non burden? Titus Patient Let's say you need to do a crown lengthening procedure because you want to do a crown you don't have the adequate. Fairly. In order for you to do that, you need to go in the biologic with this super crystal attachment as we talked the other time. And if you do that, the patient will have constant inflammation. So we do a procedure we call crown lengthening where you lengthen the crown. That's what it is. It's a shorter crown. You make it longer. And obviously if you see that afterwards even radiograph, you will see that the bone levels are not where they were supposed to be. Does this mean that this patient is a high risk patient? No. Right. It can have a super independent. You did that because you needed that for your treatment. And sometimes also the patients that have recessions. But what do we mean with recessions? These are the patients. Um, that have intact attachment levels into approximately intact bone levels and having severe not severe illness or they have recession. So i.e. attachment loss in the facial area and their mouth is usually sparkling clean because a lot of those recessions can be induced with aggressive brushing, other factors as well. So in the past, before having these categories, we used to say, Oh, we have attachment loss. That's periodontitis that's not present. Titus Right. That's a completely different category. And you need to identify because with Titus, we're talking about susceptibility of the periodontal to the bacterial challenge and anything else. And the inflammatory response. Is this sensitive to that? No, that's like the patient, very aggressive. It's like a completely different category. So this is something that you need to keep in mind as well. And I have this this is from the article. I'm not going to go into more details here, but it's pretty much the categories of attachment loss, probing pockets. So bleeding on probing and bone loss, what you have in health versus gingivitis in a reduced periodontal human and non permanent site is patient and independent and a periodontitis patient. So the different categories in that to be able to distinguish them. So as a summary of what we said, obviously the majority of those things are the same, right? You have you may have plaque. It starts at the Gingival margin. You're seeing signs of inflammation. You can see bleeding on probing. You can see histologic changes. If you see that, obviously it can still be reversible if you remove the plaque and anything that contributes to that. But the difference here is that you're having a preexisting attachment loss either because of history of theories or, as we said, because of recession in a non periodontitis patient or a crown lengthening or a procedure like that. The main change is that I need you to keep in mind is that we added this gingival health, which I like. Okay? It's something that you see, so you should be able to diagnose that. And it's nice also to say to your patient, you're doing a great job, your tissues look healthy, right? So something to keep in mind. We change the dental plaque and we said it, dental biofilm. Okay. The biologic width. We talked about that briefly in our previous lecture with anatomy. Remember how anatomically the structures are around the tooth? You have the the root, the PDL, the bone, and then between the bone and the CG, you have some space where you're having the connective tissue, the junctional helium and then the cell, the sulcus, right? So these part of this connective tissue attachment and the junctional epithelium that attaches over there, C.J. as well, we used to call it biologic weight. A lot of people would also add a cellular area, but that's another discussion, another topic, and not for now to talk about it if it's right or wrong, but that's what we consider biologic with. And why did I say all these two things? The connective tissue and the junctional epithelium is above the bone right where it touches. That's why we call it supra crystal above the bone. That's what it is. Okay. And remember that linear gingival erythema we talked about the non biofilm induced cases, especially with the HIV patients that you see this pronounced redness. They eliminated that because they said it's not a disease entity to have it like this. It's reddish. Obviously if you see it clinically, that's what your mind says. But they just eliminate as a word regarding the extent the the we have the 30% cutoff for localized versus generalized. And we will learn in a future lecture. But I'm bringing it up here with these new periodontal health. They said that if you're having less than 10% of bleeding and probing, they consider that in a healthy pair, don't you? Again, I'm not here to tell you if we agree or disagree with that, because we can be very specific. But they came up with this information based on epidemiologic studies and what the significance is of having like less than 10% of sites bleeding and actually having an impact orally don't gingival etcetera. But I need you to know, like localized versus generalized the cutoff is 30%. And regarding the severity with your classification, you don't write like mild, moderate, severe gingivitis as they used to write in the past, but to describe how much inflammation you have. I know we're still using the and even the classification says you know you may use that index from the 60s as we said which kind of describes how severe the inflammation is. Obviously if you see everything fine, it's the normal gingiva, remember, pristine or initial lesion. That's what you see clinically when you're starting seeing mild inflammation, slight change in the color edema with no bleeding and probing. You start having these mild inflammation when you're starting having more edema, redness, bleeding on probing, delayed or not, it's more moderate and severe. These are those cases that you touch. They start to bleed instantly. They're very swollen, inflamed. They may be painful. So this is a severe inflammation. So in your findings, when you see a patient, when you see a patient, you can obviously describe like I see severe inflammation or moderate inflammation. And that's a good thing because it gives you a reference of how you started and how you end. And if you need to talk with a colleague dentist, it doesn't matter. That's what we're not expecting that you read us the barrier chart by heart. If you say I have a patient, that the diagnosis that and the inflammation is moderate and we know what you're talking about and we know that what we will be expecting to see clinically. That's why it's important to be able to identify and distinguish those things for our better communication as well. Any questions? The press? Yes. The post is signed. Yeah, of course. Yeah. Can you find that also interesting? Because it was brought to us because we signed on afterwards. Yes. You can see that in the majority of those negotiations, there's a little bit of debate because I've talked with oral pathologists as well about this sign. It's not very, very objective. The way they identify that. But in the majority of those new disorders, because the skin just peels off the way this works, you see the redness and you call it that way. But yeah, I'm not going to like go into oral path details and questions and stuff, but that's something that you see. But the Benfica's and Benfica and everything, Yeah, it's just blisters. Everything like that. Yeah. Any other question? Yeah. It was precisely. Ah, that's. I love this question. If it's 30% what it is. Yeah. And sometimes. You. Know, the question was, if it's right 30%, is it localized or generalized? And I usually argue with the students and I'm just getting 30% and above. We call it generalized. Okay. Yeah, just the 30% I've only found once occasion in my life that was exactly 30%, not 31 that made my decision. Yeah. So they say 30% and more is generalized and less is localized. Okay, that's great. That's my favorite argument with students. Any other question? No. Okay. Thank you so much. I don't think I have anything else. Do I know? Let's take the attendance and I'll see you next week to continue with the periodontitis stuff. One second. Love it. Okay. Now I don't have to do anything with Zoom in and zoom out. Are we all set with that? Yeah. Okay. Yeah. Oh. One second. One second. One second. I'll be with you. Okay. Come. Yours too. Yes. Okay. Yes. Thanks very much for coming together. Yeah, I will. Actually. That's a great way to have this discussion today. We'll be sending soon to your class for you for books so you can be in the same group. That's fine. There. There will be. Maybe. Community service for the community minus like did not work. You just have. In the same way. But you will do that, right? Like if you tell me, like a stale request. What happened? They work, you know, like I got me. A stale request for. I don't know what that means. Sorry. I'm sorry. Did you do that? Yeah. I'm trying to. I think never works. Yeah. That was. Thank you. You're welcome. I'm sorry. You. Okay. Said. I. Oh, no, I did not. I got it. That's why. And then. Getting. Great. If you're. That's a great. I. I think. I. Dad. Dad. I think it. You know. Right. I. I'm the. I. And. I. Oh, no, no, no. I know you like. I knew. Yeah. I'm. I know. And. I. Make. They put in the of. 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