Recurrent After Stomatitis - PDF

Recurrent after stomatitis. What is the common layman term to describe after lesions? Great food. Canker sores, right? Yeah. Not cold sore. Cold sore represents her particular viral recurrent HSV infection. Herpes labialis. So canker sores. So it is considered to be the most common oral mucosal path...

Recurrent after stomatitis. What is the common layman term to describe after lesions? Great food. Canker sores, right? Yeah. Not cold sore. Cold sore represents her particular viral recurrent HSV infection. Herpes labialis. So canker sores. So it is considered to be the most common oral mucosal pathologies. And the term afters is derived from the Greek word afta which means ulcer. So when we use the term afters it already means it's an ulcer. It's an ulcerated lesion. So what causes after lesions? It could be different things in different people. Different subgroups of patients can have different inciting factor. Could be for one subgroup of patients it could be chocolates. Whenever they eat chocolates they may develop after solutions for another subgroup of patients. It could be tomatoes or it could be strawberries. So it's different things in different people. Although we don't know what is the inciting factor, we haven't identified one triggering factor or inciting factor. Researchers agree that after solutions represent a T cell mediated immunologic reaction with production of TNF alpha, which is an inflammatory cytokine, and this causes destruction of the resulting in the lesions, the resulting in the ulceration. So the pathogenesis is unclear. And different subgroups of patients appear to have different causes. And there could be a genetic component also. So certain patients could be genetically predisposed to developing after solutions. And it is multifactorial. It could be multiple multiple factors that can result in the development of solutions. And it most likely represents an immunologic reaction to an oral antigen. So it could be that is a highly antigenic agent, or it could be a response to and highly presence of a highly antigenic agent. Or there could be a decrease in the mucosal barrier that previously masked the antigen. So patients who smoke are less likely to develop. So smokers are less likely to develop after lesions because when patients smoke the mucosa becomes more thickened, right. It becomes hyperkinetic. It's more keratin ized. It's like a difference reaction of the oral MCUs to protect itself from the harmful chemicals in tobacco smoke. So patients who smoke are less likely to develop after lesions. So. So it could be because of. So when these patients when the smokers when they stop smoking then they are at increased risk for developing after situations. So they are susceptible to developing after situations. So decrease in mucosal barrier that previously masked the antigen. Or it could represent an abnormal immune response to a normally present antigen. So any of these factors can result in development of after lesions. So. So what are the factors that increase the frequency of occurrence or decrease? Mucosal barrier. Trauma. Trauma to the can in some patients can trigger development of associations. Patients can develop after lesions after a dental appointment. Just manipulation of the old soft tissues can trigger development of after solutions in certain subgroup of patients. Accidental biting of the tongue or buckle mucosa or the labial mucosa can trigger development of after lesions. Toothbrush injury can develop can trigger development of after lesions. Nutritional deficiencies. Iron, folate, vitamin B1, B2, B6, B12 deficiencies can trigger development of after solutions. Smoking cessation. So smokers if they stop smoking then they are at increased risk for developing after lesions. Factors that decrease the frequency of occurrence or there's increased mucosal barrier obviously smoking. So smokers are less likely to develop after lesions. But that doesn't mean that we are going to encourage patients to smoke. But but it's a fact. Like smokers are less likely to develop after solutions. Hormonal changes that can trigger, especially in women, the hormonal fluctuations, hormonal changes associated with the menstrual cycle can trigger development of after lesions, and after solutions are less likely to develop in characterized mucosa or attached to mucosa. So after solutions are less likely to develop on the vermilion, the dorsal tongue, gingiva, hard palate so it you don't see after solutions in characterized or bound down mucosa. These are some of the etiological factors for the development of this lesions. It could be an allergic reaction. It could be a hypersensitivity reaction. It could be the food like as I mentioned, it could be, you know, chocolates or tomatoes or strawberries, cold milk. It could be the flavoring agents, it could be preservatives. It can be the oral hygiene products. So in some patients they may develop after lesions when they use certain toothpastes, especially with added chemicals. That could be a genetic predisposition. Hematologic abnormalities like anemia can predispose patients to development of associations. Hormonal fluctuations. Hormonal changes can cause after lesions development. Immunologic factors. Infectious agents could be bacterial infections or viral infections, nutritional deficiencies, smoking cessation. Mental stress. Physical exertion can also trigger after lesions in some patients and trauma. Trauma can also trigger after this lesions in certain subgroup of patients. Potential antigen. Sodium lauryl sulfate in toothpaste can trigger after lesions in some patients. Systemic medications like NSAIDs and beta blockers in bacterial infections, streptococcal infection, or H. Pylori infection. Viral infections like herpes simplex virus. Varicella zoster virus, cytomegalovirus. These are considered to be some of the antigenic agents potential antigens. And we already discussed about food, right food preservatives flavoring agents. All these can trigger after lesions. And in patients with inflammatory bowel disease like Crohn's disease or ulcerative colitis. These patients can develop after slight lesions involving the. Clinical variance of after lesions. Minor after lesions. Major after lesions form after lesions. Minor after lesions. It's the most common clinical presentation. 80% of the cases represent minor after lesions, major after lesions, and her body form lesions, but they are rare. In the examination, we are likely to show just minor after solutions because these are more common and you can make a diagnosis just based on the clinical presentation. So please don't write major after lesions or deformed lesions. And don't confuse the term. Don't confuse after lesions with herpes lesions. Viral help regulations okay. Some researchers believe patient syndrome is also a variant of this lesions. Minecrafters ulceration. So obviously the most common clinical presentation 80% of the cases represent minor after ulcerations, mostly seen in children, teenagers and younger. Alza most patients will tell you that they develop the first after lesions before the age of 30. Among all the three variants of this variant, this clinical type has the fewest recurrences, so most patients may develop after lesions maybe every two months or every six months or once in a year, and it has the shortest duration. The ulcers heal in 7 to 10 days or within two weeks. There is a slight female predominance and the frequency declines with age, so older patients are less likely to develop after solutions, and this is important after solutions develop. Minor after solutions occur exclusively on the non characterized mucosa. Movable mucosa. So after solutions can occur on the labial mucosa, buccal mucosa, ventral tongue, maybe lateral ventral tongue, floor of the mouth, soft palate, oropharynx. But you are unlikely to see after lesions on the vermilion dorsal tongue gingiva hard palate so after lesions. Minor after lesions especially occurs exclusively. On the movable mucosa non characterized mucosa. You have to remember that. So what is the clinical presentation. So before the development of this lesions patients may have prodromal symptoms. They may experience like burning sensation pain tingling sensation in the oral affected oral. And then a red macular develops. What is a macular. It's a flat lesion. Right. So they develop like a circular red flat lesion. And within a day this the center becomes ulcerated. So clinically the after solution will resemble like a central ulcerated area that's covered with yellow, white fibrin or purulent membrane surrounded by a peripheral red change with peripheral erythema and the size of the lesions. They are usually small lesions one millimeter, three millimeter, or five millimeter very. It's less likely to exceed one centimeter. So usually these are small lesions but they are very painful. So the pain is disproportionate to the size of the lesion. It could be just a one millimeter lesion but it can be very painful. The number of lesions usually it's a solitary lesion. So any single episode any single outbreak the patient may have just one after solution. Or they may have like more than one but usually less than five lesions per episode. And these lesions reach full size within a day. And they typically heal in 7 to 10 days or definitely within two weeks. So here's a nice example of and I have this lesion on the uvula. You can see there is a this this area is ulcerated. It's covered with yellow white fibrin membrane and the surrounding erythema. This is a classic presentation of an after lesion. So where is it located? It prefers the movable mucosa. Right. Non characterized mucosa. Labial mucosa. Buccal mucosa. Soft palate. Floor of the mouth. Ventral tongue. Lateral ventral tongue. Those are the common areas. And this is the classic presentation like what is the size of this lesion. It's probably just 3 or 4 millimeter right. 4x4 millimeter ulcerated area covered with this yellow white fibrin membrane and surrounded by an erythema. Right. It's surrounded by this red area. So that's that's the classic presentation. A different example, you can see and have this lesion on the upper labial mucosa buccal mucosa area. Another example of this lesion on the ventral surface of the tongue. A different. This is a closer picture. You can see more than one Elsa. So in a single episode or in a single outbreak, the patients can develop more than one lesion. But usually it's less than five ulcers in a single outbreak. And here's an example where you can see an after solution. But whenever you see after solutions involving the attached mucosa, it's mostly extension of the lesion from the mobile mucosa. So this lesion is mostly in the mobile mucosa in the vestibular mucosa. But that is extension of the ulcer into the attached gingiva. So you. After solutions. They don't develop on the keratinocytes mucosa. So if at all you see involvement of the attached mucosa, it's mostly extension of the ulcer from the mobile mucosa to involve the characterized mucosa major after ulcerations. These are less than 10% of the cases represent major afters. Ulcers these are larger ulcers. The size of the ulcers could range from 1cm to 3cm. So these could be pretty large and they take a long time to heal. They take like 2 to 6 weeks to heal. And these are deep ulcers and they heal with scarring. So if patients develop recurrent major after salsas involving the mucosa, since these ulcers heal with scarring, the patients may develop in Christmas because of the scarring of the buckle, and the number of lesions can vary from 1 to 10, and it's present for a longer duration. Because it takes about 2 to 6 weeks to heal, so it's present for weeks. These are deep ulcers. They heal by scarring and mostly prefers the mobile mucosa. So most common locations are labial because the soft palate. Area. So and also involving the lower labial mucosa. And it's it's not easy to make a diagnosis of after major after lesion just by looking at the clinical presentation. It's mostly a diagnosis of exclusion. You have to exclude all of the conditions. Could this represent a tuberculosis lesion. Could this represent a deep fungal infection. Could this represent a cyclic neutropenia ulcer. Oral mucosal ulcer in cyclic neutropenia. So we have to rule out all other conditions before making a diagnosis of major after's ulcer. So. A different example. This is a large ulcer involving the lateral ventral surface of the tongue. On the right side. And could this represent a traumatic lesion? Could this represent a traumatic ulcer. There is a variant of traumatic ulcer. Traumatic ulcerative granuloma with stromal ation Ophelia. It takes a it's a deep ulcer. It takes a long time to heal. So could this represent a traumatic ulcer? Could this represent tuberculosis or cyclic neutropenia or deep fungal infection. So it's a diagnosis of exclusion. So we cannot just look at an ulcer and make a diagnosis that this is a major after lesion okay. Her body from this ulceration is also very rare. Maybe I have seen just one case. Mostly seen in adults. Mostly involves the mobile mucosa. Non characterized mucosa. There's a female predominance. So in this variant the this variant shows the greatest number of ulcers. So one single episode the patient develops a cluster of ulcers that look like manner after ulcers. But they are like a group of ulcers a cluster of ulcers that form in one location. And then they heal. And then patient develops another crop of ulcers in a different location. So the patient feels like they are never free of ulcers. Because they resemble because it's like a cluster of ulcers. They resemble therapeutic lesions. That's why this confusing term, her body form after ulcers. Usually the lesions heal in 7 to 10 days, but a new recurrence there's increased recurrence rate. And so patients develop a new set of ulcers in a different location. As soon as the ulcers heal, they do not. These ulcers do not respond to antibiotic or antiviral treatment because these are not related to bacterial infection or viral infection. So we are looking at the ventral surface of the tongue and you can see small ulcers. They look like each individual ulcer looks like a minor after solution. Right. You can see that there is a central ulcerated area surrounded by erythema. But the there are lots of ulcers involving the right and then a right and left ventral tongue. It's like a group of ulcers involving the right and left ventral tongue. It is pathetic for me. And those. Antiviral help. These are no, these are not related to HSV infection because they clinically mimic hepatic lesions. That's why they have this confusing term. It's very rare. And patients will develop these groups of ulcers a cluster of ulcers that heals mostly involves the mobile mucosa, whereas the recurrent hepatic lesions typically prefers attached mucosa. So we will talk about viral lesions Herbert Iglesias next week. But remember after lesions they prefer the mobile mucosa because of the clinical appearance. This cluster of ulcers that are developing in one area because it resembles a habituation. That's why it has this name. But it has nothing to do with viral infection. It's like any other after solution. We don't know what triggers it. So what is the treatment first? Identifying the triggering factor, if it's possible, if it's something in the diet. Patients can be advised to maintain a food diary, write down everything that they ate. It's very difficult. They have to write down every. Every food that they ate so that they. If there's any relation between a particular food ingredient and development of the solution. Um patients can be referred to physicians to their clinicians to rule out nutritional deficiency. Iron. Folate. Vitamin deficiency. Remember, patients with inflammatory bowel disease can develop Crohn's disease. They can develop after slight lesions. So that needs to be rolled out. And patients can be typically they are managed with topical anesthetics. In symptomatic patients you can prescribe topical corticosteroids. If there are just 1 or 2 lesions, then you can prescribe like a light gel which is a topical corticosteroid gel. But if the patients have multiple lesions like lesions in the mucosa or floor of the mouth soft palate, then it's easier to use a rinse. In those cases, you can prescribe topical corticosteroid runs like dexamethasone. Patients can also be prescribed antimicrobial rinses like tetracyclines or Perry dex. It's an antimicrobial rinse antibacterial antifungal, so it's an antimicrobial rinse that can be prescribed. Laser ablation can be used for treating after solutions. It can reduce the duration of the ulcer. Chemical cautery should be used with caution. If it's used incorrectly, then it can result in necrosis of the mix in severe cases. Immunosuppressive medications. Immunomodulatory medications can be prescribed, but these are serious side effects. Borchardt syndrome initially. Traditionally, Borchardt syndrome was thought to affect just the oral skin, genital, and ocular regions. But now we know that it's a multisystem disorder. It's caused by systemic vasculitis. So it involves multiple organ systems like CVS, cardiovascular system, central nervous system, respiratory system, renal system. All those can also be involved. Bassett syndrome. We don't know the exact triggering factor, but it can. It can represent an abnormal immune response. And it can be triggered by either an infection could be a bacterial infection or a viral infection, or it could be an environmental antigen, like a pesticide or heavy metal in a genetically predisposed individual. So there is a distinct racial predilection. It tends to affect patients from Turkey, Japan, eastern Mediterranean countries along the ancient Silk Road. So the and the Turks, when they traveled along the ancient Silk Road, when they had children with the locals, those people became genetically predisposed to developing Bassett syndrome. But when these patients who are genetically predisposed to developing Bassett syndrome when they moved from endemic areas to a non endemic area, the the chance of developing Bassett syndrome decreased. So which means apart from a genetic component, there's also an environmental component that causes Bassett syndrome. Mostly seen in anger. It's very rare in children, very rare to see Beckett syndrome in patients older than 50, so mostly seen in young adults, uncommon in black patients. And that is a male predominance. So ulcers the oral manifestations of Bassett syndrome. The oral ulcers they resemble minor or major after lesions. And they tend to involve the posterior parts of the volume. So the soft palate, oropharynx area, the genital ulcers, they resemble oral ulcers, but these are deep ulcers. They heal with scarring. Patients can have ocular involvement. Uveitis. Conjunctivitis, corneal ulceration. Patients can develop skin lesions. They can develop papules, pustules. Bulla arthritis is considered to be a minor manifestation of this condition, and we know that this is a multi system disorder because patients have systemic vasculitis. So it can affect multiple organ systems like cardiovascular system, central nervous system, respiratory system, renal system. So patients with Bassett syndrome can develop oral lesions. And these lesions will resemble minor or major after lesions and usually involves the posterior part of the oral MCA. They can also develop genital lesions which are deep ulcers, and they heal with scarring. Erythema multiforme. You guys are familiar with this condition, right? Erythema multiforme. So we'll just review some of the major features. So this is a blistering ulcerative micro cutaneous disease uncertain pathogenesis. And we believe that it is a immunologically mediated process. The major initiating factor the major triggering factor for majority of the patients is herpes simplex virus infection. Just quick, quick question. So in order to. Friends. Also the one that we just thought with. Minor Arthur of mayor will be the critical condition. Because they look. The same. You mean how to make a diagnosis of minor after solutions? No. For the. Oh, the. Oh, yeah. Patient syndrome. Remember, it's not just the oral lesions, right? The oral lesions, they mimic the minor after solutions and they tend to involve the posterior oral markers. But they have additional. Yeah. Signs and symptoms. Yeah. We have to give that history. Yeah. Okay, so the initiating factor for erythema multiforme is the habituation. Patients will give you a history of recurrent herpes lesions. It's either recurrent labialis or recurrent intraoral herpes lesions. And in some patients it can be. Other less likely causes could be mycoplasma pneumonia or medications. And usually it's an acute onset typically affects young adults and there's a slight female predominance. Patients can develop prodromal symptoms one week before the development of the lesions so patients can develop headache malaise. So throat cough one week before the development of the lesions, the patient then one week later patients can develop the skin lesions and the skin lesions. They are described as targeted lesions or bullseye lesions because of the classic target like lesions. So they can develop these concentric circular erythematosus rings on the extremities or on the face. And oral lesions are usually they involve the labial mucosa. They involve the vermilion. The oral lesions can be erosive or ulcerative changes. Irregular large ulcers involving the vermilion. Labial mucosa. Tongue. Buccal mucosa. Soft palate. Usually the gingiva. Gingiva is spared in erythema multiforme, and the classic presentation with erythema multiforme is the hemorrhagic crusting of the lips, so patients will have erosive ulcerative lesions on the vermilion of the lip that's covered with dried blood. That's a classic presentation for. So it's acute onset typically affects young patients. Patients can have skin lesions. They are the skin lesions are described as targeted lesions or bullseye lesions because of the clinical appearance. And patients can develop oral ulcers erosion erosive and ulcerative changes. But hemorrhagic crusting of the of the lips. Vermilion of the lips is considered to be very classic presentation of erythema multiforme. This is a self-limiting condition heals within 2 to 6 weeks. Patients are usually managed with either topical or systemic corticosteroids. Because they have ulcers in travel ulcers, they may be unable to eat or they are dehydrated, so intravenous rehydration, topical and systemic corticosteroids, and identifying an initiating factor. If the initiating factor is a herpes lesion. If the patient says that they develop recurrent orthopedic lesions often and then develop erythema multiforme as a result of the medications, then they can be put on continuous antiviral therapy so that they don't develop a piece lesions, and it doesn't trigger erythema multiforme. Yep. You guys must have seen these pictures, right? Yeah. Classic target lesions involving the skin usually involves the extremities. These are concentric circular erythematosus rings. And then the classic presentation hemorrhagic crusting of the vermilion of the lip. These are arrows. What is the difference between erosion and ulceration? Erosion is superficial. Loss of epithelium. Ulceration means complete loss of epithelium. So patients will have erosive and ulcerative lesions involving the vermilion. And it's covered with dry bladder. And introverted lesions can be large ulcers that can involve the tongue but typically spares the gingiva. A different example patient with hemorrhaging, hemorrhaging, crusting of the vermilion, and ulcers involving the tongue and the target like lesions involving the skin. Classic targeted lesions involving the skin. Different patients. Kind of an irregular, large ulcer involving their tongue. Labial mucosa. Steven Johnson syndrome and toxic epidermal necrosis. Initially, these were thought to be like a severe form of erythema multiforme, but now we believe that the pathogenesis for these conditions. Is different from erythema multiforme. In erythema multiforme, the main triggering factor is the herpes infection, whereas for these two conditions it's the medication. Several different drugs, more than 200 drugs have been implicated that could cause Stephen Johnson syndrome and toxic epidermal necrosis. These represent hypersensitivity reactions, and Stephen Johnson syndrome is considered to be less severe. Variant of toxic epidermal necrosis Stephen Johnson syndrome tends to affect younger patients, and typically patients who develop toxic epidermal necrosis or older patients. Patients are older than 60, and less than 10% of body surface is involved in Stephen Johnson syndrome, and more than 30% of the body surface can be involved in toxic epidermal electrolysis. So this is like more severe compared to Stephen Johnson syndrome. Patients will develop flu like symptoms fever, headache, malaise, cough, sore throat, and then they develop skin lesions. The skin lesions tend to involve the trunk, and it can appear as papules or pustules or bicycles. Bullough and oral lesions can can be nonspecific ulcers and erosions. Patients can also develop ocular and genital lesions. Treatment is these patients because they develop like sloughing of the skin. They are typically managed in the burn unit. Because these can be life threatening, the first step will be to identify the drug and discontinue the drug, and lesions typically heal in about 3 to 5 weeks. So this is like toxic epidermal electrolysis. Okay. Transient lingual politesse. Transient lingual politesse. It's a very common condition. I'm sure you guys have experienced this where one or more fungi form papilla or papillae, they become inflamed and enlarged, and as a result of an hypersensitivity reaction, it could be an hypersensitivity reaction to something in the food. Or it could be a flavoring agent, or it could be a preservative, or it could be even a dental hygiene product, so it's unknown. Pathogenesis. Typically involves the anterior dorsal tongue so the involved fungi form papilla or papillae. If more than one papilla gets involved it becomes enlarged. It's inflamed. It appears as red papules with an ulcerated surface, like with an ulcerated cap. No treatment is necessary because the lesion will resolve on its own within a few days, or a few hours or few days. So this is an example of. Geographic term, but I just use this example because you can see the white structures of the fully formed papillae. Right. And these red dots, those are the fungi from papillae. So in transient lingual colitis the fungi form papillae can become enlarged and inflamed and the surface can get ulcerated. So it can be painful and it can cause discomfort. But it's an hypersensitivity reaction. It could be to anything in the food, or it could be even the oral hygiene product can, like toothpaste, can trigger transient lingual abilities. It's transient. So it heals within a few hours or a few days. No treatment is necessary, but if the patient is symptomatic, you can prescribe like a topical corticosteroid gel. This one is a popular variant which is very rare. These patients are asymptomatic, but multiple spongiform papillae can develop. It's not ulcerated. In this case, it's enlarged, but it's covered with a hyper characteristic surface. So it's it's called papilloma Karadzic variant, which is very rare. Erythema migrants or geographic channel. Benign migratory velocities. It's a common benign condition, predominantly involves the tongue. Patients are typically asymptomatic. So it's the dentist who notices these lesions. Sometimes the patient's notice may notice these changes and may be worried whether it's a fungal infection or if it's like cancer. They and occasionally patients can be symptomatic. They may complain of mild burning sensation. Etiology is unknown. Could it be more common in atopic individuals, individuals who are at increased risk for developing hypersensitivity reaction? Allergic reaction. It's possible. Clinical presentation. Multifocal erythema patches on the tongue that's surrounded by scalloped or irregular Hippocratic border. These erythematosus patches they represent areas where there's atrophy of the fully formed papillae. And these lesions they develop in one area, they heal, and then they reappear in a different location. So they migrate. And that's why this term erythema migrants or migratory gloss itis often seen in association with fisher tongue. One one third of the patients with fisher tongue can also show geographic tongue can occur in other mucosal sites. That's very rare, but it can occur not just on the tongue, dorsal or ventral surface of the tongue, or lateral tongue. They can also involve other areas like the buccal mucosa, soft palate, buckle vestibule. Then we use the term geographic stomatitis. Treatment is rarely indicated. Most patients are asymptomatic. For symptomatic patients, you can prescribe topical corticosteroid. So here's a classic example. Classic presentation of geographic tongue multifocal erythematosus patches devoid of fully formed papillae, surrounded partially or completely by this white Hippocratic border. Different examples. Right. You can see that this Apache multifocal Apache erythema that is surrounded partially by these white border. Here's another example. This involves the lateral surface of the tongue. This is like a lateral ventral tongue but it's a resolving geographic tongue. So you just see that linear white change and a subtle erythema. So that's a resolving lesion. Sometimes lesions that look like geographic tongue can involve the buckle mucosa, palate, buckle, vestibule, and we use the term geographic stomatitis to describe these lesions. So today we will finish yearly. So I'm just going to continue okay. Allergic mucosal reaction to systemic medications so patients can develop oral mucosal lesions as a result of an allergic reaction to the systemic medications that they take. And most patients are middle aged or older patients. They are on multiple medications, so patients will take more than one medication. The more number of medications a patient takes, they are at increased risk for developing oral mucosal lesions. And these are nonspecific erosive and ulcerative changes. You cannot look at these lesions like geographic tongue. You can look at the lesions and make a diagnosis. But with regards to these lesions these are nonspecific presentation. They present as erosions and ulcerations. Unless you ask the patient, unless you think about whether this could be systemic medication that's causing the oral lesions, it's not easy to diagnose. So various clinical presentations anaphylactic stomatitis. So in addition to all mucosal lesions these patients may have other signs and symptoms. They may present with vomiting skin itching cutaneous lesions respiratory distress intra world fixed drug eruptions. These patients they develop erosions and ulcerative changes in the recurrent erosive and ulcerative changes involving the same area of the volume. It goes up like an A drug reaction. So it looks like like an planner's or like an eye, like an mucositis. The lesions may resemble lupus or pain figures or pain guide. So it's very nonspecific erosive ulcerative lesions. So when patients present with these gingivitis erosive erosive lesions ulcerative lesions you will consider configures and configured in your differential. You have to recommend a biopsy. Submit the tissue for both histopathological examination as well as immunofluorescence study, in order to make the diagnosis, so they can mimic a lot of these conditions internally. So no consistent clinical features. It's very nonspecific. Yeah. In this first one, you see a patient. A characteristic. And how long you should wait until perform biopsy. Is okay if patients present with squamous gingivitis and erosive and ulcerative lesions. I would recommend a biopsy because if Benfica's and figure is in my differential, I would recommend a biopsy right away because I don't want to wait to make the diagnosis. So unless you have unless you suspect that it could be the systemic medication that's causing these oral lesions, it's difficult to make that diagnosis. It may take, even if the patient discontinue the medication. So many of these medications could be high blood pressure medication. Or they could be taking medications for the heart condition. It could be high you know, for hyperlipidemia, hypothyroidism. Those are very common medications that can trigger oral mucosal lesions. You cannot just ask the patient to discontinue the medication. You can work with the patient's clinician to maybe switch to a different class of medication with the same therapeutic results, or the patients can do like a drug holiday. They can discontinue the medication just for a brief period to see if the lesions improve. Most patients are treated with symptomatic treatment treated with topical or systemic corticosteroids. So this is like a screen you know, picture of the. The oral pathology textbook. So you can see the list of medications. Right. It's a big list of medications that can trigger oral lesions. And here's a patient. This patient was taking high blood pressure medication for medication for hypertension. And develop these erosive changes involving the gingiva erosive ulcerative lesions involving the anterior flow of the mouth. You can see that the this is an ulcer. And in this area it's covered with this yellow white fibrin membrane. A different patient. So it's kind of a erosive ulcerative change involving the labial mucosa. This is an ulcerated change involving the left buckle mucosa. You can see that there is this peripheral radiating white stripe. Kind of resembles like an planner's, but it's not like an L.A.. Diffuse erosive ulcerative changes involving the palate and buckle mucosa in a patient taking medication for arthritis. The next example, 72 year old female. She was taking three different medications for hypertension for high blood pressure and erosive ulcerative changes. Large erosive ulcerative changes involving the buccal mucosa, the palate, the dorsal surface of the tongue. You can only imagine how painful this these lesions will be. And this is the patient. After treatment with systemic corticosteroids there's a dramatic improvement. And you can see that most of these ulcers have healed even the ulcers on the tongue. They are showing signs of healing and there's regeneration of the fully formed papillae. Allergic contact stomatitis from dental restorative materials like like an eye contact reaction to dental restorative materials. So this one it's more localized. It's involves the oil makers are that comes in contact with the dental restorative material. And it could present as a erythematosus lesion or a mixed red and white lesion. And if you suspect that it's it's probably an allergic reaction to the dental material. Patients can be referred to a dermatologist who can do patch testing to identify which material the patient is allergic to, so that you can avoid using that dental material in future restorations. We have used this example before. You have seen this, right? Yeah. This is a nice example. You can see the class by amalgam restoration. And in the oral mucosa that's. That comes in contact with this amalgam restoration shows this red and white change. It's like a red patch that is surrounded by peripheral, radiating white straight. So it's like an eye contact reaction to dental restorative material. So in this case the patient may be symptomatic or asymptomatic. If you have any question, especially if you suspect it's like not reaction. But if it involves the lateral surface of the tongue that can be tricky. You don't want to miss dysplasia. You can always recommend a biopsy. In this particular case, you can try polishing the amalgam restoration or replace the restoration to see if the lesions heal. And if they don't heal of the or the patient is symptomatic. You can always recommend a biopsy to confirm the diagnosis. Allergic contact stomatitis to oral hygiene products, either to toothpaste so patients can develop allergic contact reaction to toothpaste or mouthwash. And this is a very common presentation with strips of epithelium that peels away. This is a very common presentation as a result of contact reaction to toothpaste. So toothpaste with whitening agents or tartar control flavoring agents like mint flavored or cinnamon flavored toothpaste. Patients can present with these superficial sloughing of the oral. This is a nice demonstration of that. So patients will be able to pull the strips of superficial oral mucosa. This is like a contact reaction to toothpaste. And usually it's to the extra chemicals that are being added to the toothpaste. So not all patients will present with this. But some patients may be sensitive. And they can have this allergic reaction to the chemicals in the toothpaste. And. White. I've seen it. With whitening agents. Yes. Correct. And patients are worried when they are able to, you know, peel off mucosal tissue like that. They are usually worried. They are worried whether this is a fungal infection, whether this is cancer. So you should you know, you should be able to educate the patient, reassure the patient that this is this is just a contact reaction to the toothpaste. And it's a benign finding. So it's a classic. You know this is a nice demonstration of superficial sloughing of the volume. So if you look at those strips of epithelium under the microscope, they are just the static layer strips of layer. Patients are usually asymptomatic because it's so, so superficial that superficial sloughing of the epithelium. So patients are typically asymptomatic. So this is like an oral mucosal change as a result of using mouthwash containing alcohol. So there's thus this whitish mucosal change involving the mucosa. It's like a superficial coagulation of the oral mucosa as a result of contact with alcohol in the mouthwash. And this is two weeks after discontinuing use of that mouthwash. So this is also. Contact reaction to oral hygiene products. So the next time you go to the, you know, like the drugstore or your local grocery store to pick up the toothpaste, you can see that at eye level, it's all toothpaste containing whitening agents, flavoring agents. And if you have to look for a basic toothpaste, then you have it's usually at the bottom most shelf. You have to really search for it. So most of the toothpaste currently sold in the market, they have all these extra chemicals like whitening agents and flavoring agents, cinnamon flavor, mint flavor, tartar control toothpaste and all these extra chemicals can trigger hypersensitivity reaction in certain patients. Allergic contact stomatitis from artificial cinnamon flavoring. So cinnamon oil, which is used as the flavoring agent in toothpaste, mouthwash, hot candies. Chewing gum. The cinnamon oil is 100 times more concentrated compared to the natural spice natural cinnamon, so patients can develop contact reaction as a result of using these cinnamon flavored toothpaste as cinnamon flavored chewing gum and. Usually if it is the toothpaste, the entire world mucosa is exposed, right? If it is a toothpaste containing cinnamon flavored toothpaste or mouthwash, the entire oral mucosa is exposed can appear. Erythematosus patients can be symptomatic and they can complain of burning sensation. But if it is as a result of using chewing gum or hard candies, that area where the patient habitually places the chewing gum or hard candy that that oral make that comes in contact with the chewing gum can show oral mucosal changes. So this is a nice example of contact reaction to cinnamon flavored chewing gum. So this patient developed these oblong kind of patchy red and white change on the buckle mucosa as well as lesions on the lateral surface of the tongue. Right. You can see kind of a shaggy white changes involving the lateral right lateral tongue. And the right buccal mucosa shows these kind of white shaggy changes as well as with surrounding erythema. So patient is not going to tell you. Oh, I started using the cinnamon flavored chewing gum. And that's why I developed these lesions. So patients will present to you with a complaint that they have this burning sensation in the mouth. They are not able to eat. And you should ask the patient. You should inquire whether the patient uses chewing gum, whether they habitually place if it is a focal area, then you should think of what could cost us what's coming in contact with the makers to cause these lesions. So you should inquire the patient whether they use chewing gum or hard candies. Once they discontinue the using the chewing gum or hard candy, the lesions will resolve within a few weeks. Within a couple of weeks, the lesions will show signs of resolution. Patients using cinnamon flavored toothpaste or mouthwash can. In addition to the oral mucosal changes, they can also develop these exfoliated colitis or pre oral dermatitis, or even the. The vermilion on the skin surrounding the lips can also be involved. You can see these scaly, ulcerated erosive changes involving the pre oral skin as a result of using cinnamon flavored mouthwash or toothpaste. So the last topic for today is Andrew Edema. So this represents a diffuse edema swelling of the connective tissue inside the sub mucosal connective tissue or subcutaneous connective tissue. But sometimes it can involve the respiratory mucosa or gastrointestinal mucosa. It involves the respiratory mucosa. It can be life threatening. And patients should be managed in the hospital. So angioedema the most common causes mast cell de granulation with histamine release. And this represents an Ige mediated hypersensitivity reaction. It could be an hypersensitivity reaction to drugs or plant or dust or food. So it's an allergic contact reaction to an ingredient in food. It could be a topical medication. It could be cosmetics. It could be even dental materials. Some patients may develop angioedema as a result of rubber dam. If the dentist used a rubber dam, they may develop angioedema. So it can be dental materials. It can be food. It's something in the food or drink, or it can be cosmetics that the patient is using. It can be topical medications, physical stimuli. So exposure to heat or cold physical exertion, mental stress can trigger angioedema in some patients. Patients could be an allergic like an abnormal allergic reaction to a drug. Like patients taking Ace inhibitors can develop angioedema. It can occur as a result of activation of the complement pathway, which can be hereditary, or it can be acquired. Angioedema can occur when there is high levels of antigen antibody complexes, like because of a bacterial infection, or in patients with lupus, or because of a viral infection. Patients can develop anxiety and can also develop in patients with elevated peripheral blood level. So here's a patient with edema swelling of the lower lip. You can see that the lower lip is abnormally enlarged right. It's usually acute. And patients will just wake up with swollen face or swollen lips swelling tongue. And it's usually soft. And if you palpate it it's soft and matters. And it's you shouldn't confuse this with oral facial granulomatous. In oral facial granulomatous it's persistent. Whereas in in angioedema it's it's not persistent. Usually this swelling will resolve within a few hours a few days. Whereas in oral facial granulomatous is it's the granulomatous inflammation. Right. So patients will have persistent enlargement of the lips. Whereas in angioedema it's acute onset and it resolves within a few days. Here's a different example. Here. It's enlargement of the upper lip. That's it. Thank you so much. Have a good weekend. If you have any questions, you can always send me an email. But it's a dry topic. But hopefully yeah we covered the major, major lesions. Yeah. Bye.