 Hello everyone welcome back to a new session on dentistry and more so in oral pathology today's session will be dealing with Three syndromes namely stiogram syndrome phrase syndrome and plumber Winston syndrome So we have many syndromes in oral pathology So this session is just highlighting three syndromes and the coming sessions will be dealing with the further syndromes so let's see what is stiogram syndrome phrase syndrome and Plumber Winston syndrome So we'll start with the first one that is chagrin syndrome So it is a autoimmune disease. So we know what is autoimmune disease the immune The immune system is acting against our own body cells Actually, it is supposed to act against the antigens the foreign bodies, but it is by some error It is acting against our own body system So that is autoimmune disease So the most common striking features of chagrin syndrome is Dry eyes and dry mouth So there is lack of Tear and lack of saliva will be present in chagrin syndrome. That is the most striking feature of chagrin syndrome So what happens is The immune system affecting its own cell that is it affects the lacrimal glands and salivary glands So these glands are supposed to produce saliva and tears. So when it affects these gland, there will be Improper production of tears and Salivary gland so there will be dry eyes and dry mouth and it most commonly associated with rheumatoid So risk factors include age that is 40 years or greater than 40 years It usually diagnosed in this age group that is more than 40 years and Women are more prone to have chagrin syndrome compared to men And rheumatic disease is common for people who have chagrin syndrome Also to have a rheumatic disease So rheumatic disease also a risk factor for chagrin syndrome And the most common symptoms we already discussed they are Like skin rashes, dry cough and most commonly stiffness and swelling It can have thyroid problems, kidney, liver, lungs, skin, nerves So most of the organs are affected by this autoimmune diseases And what are the complications? We know it has problem with production of saliva and ear. So there will be dental cavities Why because the saliva is keeping the mouth clean by its fleshing action When saliva is less, there will be more chance of caries And also east infection will be there And since it is dry ice there will be problem with vision So how do we treat this? So treatment is very symptomatic We can provide eye drops medications The eye drops are also known as crocodile tears And pylocarbon which is for salivary gland So it improves the saliva and we can Suggest the patient to sip water frequently and also use Saliva producing Chewing gums and such a symptomatic way we can manage this And diagnosis we can diagnose this by saliva flow test Silogram Schumer tear test So tear test is a special test for counting the tear drops And biopsy is another method for Sjogren syndrome So Sjogren syndrome The basically you should remember the triad that is dry eyes, dry mouth and rheumatoid arthritis It is a autoimmune disease which affects Lackrimal and salivary glands Now let's move on to the second syndrome that is Phrase syndrome Phrase syndrome is also known as auriculotemporal syndrome Also another name is dupai syndrome So what happens is here also it is affecting salivary gland but it is not a autoimmune disease Sjogren syndrome is a autoimmune disease This is Salivary gland is affected due to a surgery or a trauma or a neck dissection In that case the salivary gland and auriculotemporal nerve is affected And what happens there will be fleshing and gestatory sweating And where this happens it is in the pre auricular area when this happens in response to mastication Or salivary stimulus when we think about a very peculiar food like lemon or so type food There will be Saliva production usually but that time there will be sweating in the pre auricular area Because the auriculotemporal nerve is damaged So parotid gland and auriculotemporal nerve is damaged by any of these surgeries So this fleshing and gestatory sweating will be there in this particular area And also they may have erythema anesthesia and parasitia Regarding phrase syndrome So how do we diagnose we can use minor iodine starch test so we can apply starch And iodine and Get this test done for phrase syndrome and treatment we can Uh use botulinum injection And anti-cholinergic ointments like scopalamine and also surgical interventions So shogunin syndrome and phrase syndrome it is both affected The salivary glands are affected but here it is autoimmune disease and here it is a Trauma to the auricular temporal nerve and parotid gland So both the cases there is problem with saliva Here there will be pre auricular area fleshing and sweating when there is a response to mastication Or a salivary stimulus when we think about particular food Or such things there will be sweating in the pre auricular area So that is phrase syndrome or dupai syndrome or auriculotemporal syndrome And the third syndrome to this session we are discussing about plumber winson syndrome It is a very different one not related to these two It is also known as Patterson kelly syndrome. These are the people who reported these uh syndromes first and it is Also known as sidropenic dysphagia. So dysphagia we know it is the difficulty of uh swallowing And why this is happening this is due to the long-term iron deficiency anemia. So iron is very much Vital nutrient for our body. So when this iron is deficient And anemia causes and it lasts for a very longer period It might result a from plumber winson syndrome And it has a peculiar triad. So what is that right? The anemia dysphagia and esophageal webs. So why this esophageal webs? There is small and thin growths of tissue partially blocks the foot pipe or esophagus So on the track of esophagus there will be small and thin growths of tissue will be there So this is why the swallowing is difficult or dysphagia is formed The person is not eating properly. So there will be weakness and Person may have burning mouth Glossitis spleenomegaly Coelone Ikea and all these are associated symptoms with plumber winson syndrome And diagnosis is basically by endoscopy, blood test and biopsy treatment. It is mainly nutritional intervention because it is iron deficiency anemia and nowadays iron deficiency anemia and this plumber winson syndrome is quite rare because the nutrients Interventions or the nutrients deficiency Are a little bit not very much heard And it's the complication related to plumber winson commercial carcinoma So today's session was about three syndromes. One is jocline syndrome phrase syndrome and plumber winson syndrome So these two syndromes were associated with salivary glands and lacrimal glands. This is a autoimmune disease This is a disease due to the trauma to the salivary gland and auriculotemporal now And this is a nutritional deficiency Iron deficiency plumber winson syndrome So these three are commonly asked questions. So whatever I put in this spot is asked once or twice in the university exam So try to understand the difference between these three. So I'll come up with more syndromes in My next sessions. Thank you. Hello, everyone. Welcome back to another session on dentistry and more So let's continue our syndrome So last class, we have seen few syndromes. So today's class is about Stevens-Johnson syndrome and papillon-leafer syndrome Stephen Johnson syndrome. It is also known as toxic Epidomolysis Necrosis or Lyal syndrome. So these two should be studied together So let's see what is Stevens-Johnson syndrome and papillon-leafer syndrome So let's begin with Stevens-Johnson syndrome So we should study Stevens-Johnson syndrome along with Lyal syndrome It is also known as toxic epidomolysis Necrosis Because the both having same clinical presentation differs only with the severity of clinical presentation. That is the skin reactions So it is an immune complex mediated hypersensitivity reaction. So this is a hypersensitivity reaction to certain drugs or certain infections And it is a severe expression of erythema multiforme and it is also known as erythema multiforme major So we should know what is erythema multiforme? So erythema multiforme is basically a skin immune reaction Due to an infection or medication Its name combined from erythema Multi-anforma erythema means redness multi is many and form A is shapes So it describes the main symptoms which is a rash on the body So the rash on the body where each mark resembles a bullseye form So it is a severe form of erythema multiforme It is also known as erythema multiforme major So the basic etiology is Infection It could be a herpes simplex virus infection Cytomegalase virus infection It could be due to the AIDS or ebstein bar virus infection And it could be due to drug induced either that is the main reason that is the penicillin Drug induced reaction is a two-third of total cases of stefans johnson syndrome And also it could be due to finitoin NSAIDs or allopurinol so these drugs can Result in this hypersensitivity reaction And also it could be an idiopathic reaction So it is nothing but a immune complex mediated hypersensitivity reaction So we know classifications of hypersensitivity one two three and four So this is immune complex mediated hypersensitivity So there will be always a causal factor that is either infection or a drug or it could be a idiopathic in nature So it is also known as erythema multiforme major because a clinical presentation is all same because it is forming erythematous reaction on the skin surface And the risk factors include The males having more predilection compared to the female almost double because it is two is to one Ratio we can see So in risk factors, uh, the second one is age It is most commonly seen in 20 to 40 years. That is the middle age people are more affected with This stefans johnson syndrome. So what are the clinical features? It is most commonly affecting Uh, the surface that is skin and mucus membranes are involved Uh, most commonly the oral nasal IGI tract respiratory tract urethral Tract so all these surfaces are involved with this muco skin and mucus membrane and also we can, uh See sore throat chills malice and fever associated symptoms with stefans johnson syndrome So it's it's like muco-cutaneous lesions. They develop abruptly and clusters of Outbreaks which last from two to four weeks And the lesions are typically non pruritic And fever will be there in almost 85 percentage of the cases An involvement of oral and mucus membrane may be severe enough that patient may not be able to eat or drink And also there is conjunctivitis And patients with genital urinary involvement may complain of dysuria or an inability to void So these are the basic, uh, clinical features And the next thing is If the basal, uh, body surface area involvement is less than 10 percentage. We can say that it is a minor form of Toxic epidermolysis necrosis or you can say that stefans johnson syndrome is now very much wide And the basal surface area is 10 to 30 percentage. It is a combination of Compilation of both stefans johnson syndrome and toxic epidermolysis necrosis and If the basal surface area is greater than 30 percentage it is Toxic epidermolysis necrosis So that is a severe form of stefans johnson syndrome So basically what happens in this is There is a death of keratinocytes. So which causes separation of dermis from epidermis. That is why the Skin changes are seen the keratinocytes which connects the dermis and epidermis Is dying of then there is a separation of dermis from epidermis And what are the complications associated with stefans johnson syndrome? So the complication includes esophageal strictures renal failure respiratory failure And also there might be scarring and deformity of face. So the esophageal strictures renal failure and respiratory failure on extensive cases And also scarring and deformity due to this particular skin lesion And regarding the investigations, there is no laboratory studies other than biopsy exist Which can aid the doctor in establishing the diagnosis Basically the skin biopsy is a definitive diagnosis Because we can see that bullay are sub epidermal and epidermal cell necrosis may be noted So these are the Pathological features and while coming to the treatment and management basically only symptomatic treatment is possible So it is mostly dealt just like How it is in the extensive burns So it is almost like an extensive burn case, but the cause is little different So that's all about stefans johnson syndrome. It is an immune complex mediator disease Which is a extreme form of erythema multiforma. So etiology could be infections and drugs and idiopathic nature And it involves skin and mucus membranes of various organs like oral oral cavity nasal cavity eye gastrointestinal and respiratory tract and it is associated with toxic epidermalysis necrosis if it is greater than 30 percentage And there is a death of keratinocytes. That is why this is separated. That's dermis and epidermis and the complications and treatment So now let's move on to the papillone lefay syndrome. It is also known as pama plantar kerata derma with pyridontitis So as the name suggests it has involvement of keratinization on palms and plantar region and also it associated with severe bone destruction. That is the alveolar bone So we can say that it is a disease with pyridontitis and keratinization in the palms and plantar region So it is a autosomal recessive region recessive disorder. So it is an immune complex hypersensitivity So when you are studying syndromes always study in two or three syndromes together So you never get confused if you are studying one syndrome at a time The high chances of you mixing up the clinical features and the course with another one. So always study the syndromes Two or three at a time. That's why I'm keeping the syndromes in a single board with two or three syndromes. So you always keep Comparing the diseases and studying. So it will be in your memory for a very long time So always compare and study not just one syndrome at a time So two or three syndromes take at a time and study and compare the course the clinical features the Manifestations and the treatment. So it will be very easy and it will be remembering for a very long time So this is a autosomal recessive Uh disorder and it is a disorder of charactinization So what happens is there is a thickening of soles and palms So severe charactinization causing thickening of soles and palms and also severe destruction of Paradontal bone. So severe parodontitis is there So why it is happening? It is due to the mutation in cathabcin C gene So that is a particular gene which is involved with this syndrome. So there is a mutation And causing this syndrome. So what are the clinical features from the name itself? You know that There is charactinization in palmar and plantar region and also parodontitis. So Gintraeva, stomatitis, parodontitis and swollen Gintraeva extreme Resorption of bone and deep pockets. So these are the parodontal manifestation So thickening of soles of palm and plantar region So the patient has premature loss of deciduous teeth and permanent teeth. So deciduous teeth it is uh Exfoliated completely by the age of 10 to 12 years that is a Molas deciduous molas replaced by primolars around 10 to 12 years But in this case what happens is by age of 4 to 5 years Complete tooth is lost that is deciduous tooth is completely lost by age of 4 to 5 years And if it is permanent teeth it could be completely Gone by the age of 14 or 15 years that is supposed to be for a lifetime It is completely lost because of severe parodontitis that is the extreme resorption of bone and Deep pockets. So the teeth will be completely lost and the Gintraeva will back to its normal shape So it's a very weird condition the loss of deciduous teeth And skin lesions will be there white brown red or Scaly in nature. So what happens is these types of lesions undergo Crestation cracking and deep fishing So the hand and foot region will undergo the crustacean cracking and deep fishing And also you can see follicular keratosis hyperhidrosis calcification of foc cerebrae and Choroid plexus So these are the another features which is seen with this syndrome that is follicular keratosis hyperhidrosis calcification of foc cerebrae and choroid plexus So what are the histopathological features is hyper keratosis hypergrandolosis and acanthosis So basically we treat this disease mainly we Treat the parodontitis that is a infectious in nature that is scaling and root planning we can perform with antibiotics and retinoids and a good oral hygiene by providing him continuous chloraxidine mouthwash In case of non-savable tooth we can go for extraction and provide him a Rehabilitation with Removable dentures or complete dentures or even with implants So that is about papillone leafy syndrome. It is also known as parmo plantar keratoderma with pyridontitis So it is a autosomal recessive disorder of keratinization which causing tooth loss and Palmer and plantar keratinization that is papillone leafy syndrome stevens Stevens johnson syndrome is a different one. It is also known as Toxic epidermolysis necrosis or loyal stasis in its severe form Stevens johnson syndrome is itself a severe expression of erythema multiform So it starts with erythema multiform then stevens johnson syndrome and toxic epidermolysis necrosis The severity is increasing So that's all about stevens johnson syndrome and papillone leafy syndrome So we have more syndromes coming up in the further sessions. So so far we have covered phrase syndrome, gorlin got syndrome, plumber Winston syndrome And down syndrome Stevens johnson and papillone leafy syndrome. So a few more syndromes are left So i'll come up with those syndromes in my next sessions. Thank you. Hello everyone Welcome back to a new session on dentistry and more. So today we have two syndromes It is myofascial pain dysfunction syndrome or MPDS or burning mouth syndrome or BMS So it's the continuation of our various syndromes last three sessions. We have covered various syndromes So today's session also we'll be covering these two syndromes There are actually various syndromes present in our oral pathology Subject but we are focusing only on the syndromes the main syndromes which have been asked for university exam So the idea is to give you some tips about each syndrome So you can easily memorize this and write it for the exam So let's see what is MPDS and what is BMS So we'll begin with burning mouth syndrome. It is a burning sensation without any detectable cause So it is nothing but burning Painful or itching sensation located in oral mucosa And the tongue is the most affected part followed by lips and palate So it is a problem seen in oral cavity, especially the tongue Lips and palate without any detectable cause that is burning mouth syndrome So usually we know ulcers and other lesions which causes burning sensation But this is without any particular cause So the clinically no apparent alterations are present in patient's mouth So what are the epidemiological features of this disease? This is most commonly seen among women That is it is increased with age and it is like sixies to one prediction Compared to males that is female prediction is almost six times compared to the males And it is seen among women after menopause that is 3 to 12 years after menopause it is commonly seen And it is very rare before 30 years So that is something related to the epidemiology of BMS. Now, let's see The classification so it is classified into three type one type two and type three It is based on the symptoms present when person awake Or or upon waking that is type one There is no symptom upon waking but it increases throughout the day type two is The symptoms present when upon aching and it is throughout the day It is present and this is the most common type that is type two type three There is no regular pattern and it is the least Common one and let's see what are the etiological factors Actually, it is not confined to any particular factor. We cannot say that This course is born burning mouth syndrome. There are many factors which can cause The burning sensation in mouth. So those are We can classify that into local and systemic factors. The local factors involves oral candidiasis, lichen planus, allergy Allergy, lichen planus, oral candidiasis and systemic factors involves hormonal changes vitamin, betrothal, folic acid or iron deficiency Diabetes, malitis, maybe the side effect of few medications Few autoimmune diseases and salivary gland disorders and some medications like ac inhibitors And even trauma and psychiatric problems So local factors like danger problems also could be there like ill-fitting Interincisal space and vertical dimension problems And maybe the median rhomboid glossitis hypersensitivity to certain food materials lichen planus I mentioned already And also oral habits like tongue thrusting and even carcinoma And maybe the prolonged use of chlorxidine mouthwash also could be a etiological factor Some disorders like chagrin's syndrome also could be a factor because it is associated with dry mouth and dry eyes. So burning can be seen in these patients So these are the etiological factors associated with burning mouth syndrome And what are the clinical features? Most common clinical feature is burning sensation Especially the anterior part of tongue And dyscusia and dysesthesia So dyscusia is the altered taste and dysesthesia is etching or pain sensation And it is especially present on the anterior one third of the tongue And what are the treatment options? There is no particular treatment options If it is a milder case we can go for psychological counseling and the moderate to severe cases should go for drug therapy like amitripolyne and alpha lipoic acid So burning mouth syndrome is very peculiar because we have many diseases, many conditions, many lesions which can result in burning mouth But without any specific course, without any clinical manifestation The presence of burning is actually known as burning mouth syndrome And it is most commonly seen with women especially post menopausal period And we have three classification and n number of etiological factors So now let's move on to myofascial pain dispension syndrome or MPDS So it is a pain disorder which starts from trigger points in myofascial structures So what are these trigger points? These trigger points are within the skeletal muscle Which is triggered by macro or micro trauma happening to these skeletal structures So it is a pain disorder As the name suggests it is a pain disorder Which is starting from few or many trigger points Which is present in the myofascial structures So these trigger points are elicited or responded by the macro or micro trauma happening to these structures So it is 30% of the total population is affected And the females are most affected 3 is to 1 predilection And it is most commonly seen in middle age group that is 15 to 40 years So we have a cycle of events in this etiology So this is a cycle of events That is stress is causing muscular hyperactivity Again the dental irritation is also causing muscular hyperactivity So what happens when there is hyperactivity of muscle? The muscle fatigue So muscular fatigue which leads to myofascial pain dispension syndrome At the same time, muscular over contraction can also leads to MPDS Muscular over extension can also leads to MPDS So what happens? Due to MPDS, there is contracture There is degenerative arthritis There is internal derangement and there is occlusal disharmony So due to occlusal disharmony and internal derangement The chewing pattern is changed And also due to the degenerative arthritis and contracture Again the chewing pattern will be changed So chewing pattern is changed due to all these reasons That is MPDS affect the degenerative arthritis It causes contracture It causes occlusal disharmony And it changes the internal structure that internal derangement So all these results in chewing pattern So what happens once the chewing pattern is changed It will again cause MPDS So it is a vicious cycle Okay, so it starts with stress, mycular, muscular hyperactivity and dental irritation goes to muscle fatigue And muscular over contraction and muscular over extension MPDS goes to arthritis, internal derangement, occlusal disharmony It results in chewing pattern It itself goes back to MPDS So in pathophysiology, what happens? When the etiological factors So all the etiological factors Which leads to micro or macro trauma to the musculoskeletal system to muscle spasm So all these etiological factors which causes trauma that is micro or macro trauma On the musculoskeletal system which leads to muscle spasm So what happens? So this hyper tonicity May lead to muscle fatigue So this is what I was explaining Hyper tonicity There will be muscle fatigue And accumulation of lots of metabolic Biproducts such as lactic acid Prostaglantin Radicanin And histamines So due to this hyper tonicity and muscle fatigue There will be Biproducts That is metabolic bi-products Such as lactic acid, Prostaglantin, Radicanin and histamine So what happens? The accumulation of these pain mediators Lovers the pain threshold to Mechanical and chemical stimuli Which leads to MPDS So it is a cycle Etiological factors Micro or macro trauma Muscles spasm What happens? Then there is Biproducts Metabolic bi-products Such as Prostaglantin, Radicanin, Histamine, Lactic acid Which goes Pain threshold Lowering the pain threshold to mechanical and chemical stimuli Which leads to MPDS So the classification Spasm of lateral teregoid Either Or it is spasm of elevator muscles Or it is spasm of lateral teregoid And elevator muscles So clinical features includes Pain, discomfort, limited jaw movements The clicking and other jaw noises and who are tendon So in clinical features So there are basically Four categories So we can express these clinical features in four categories that is Neurologic, Autologic, Gastrointestinal tract and Musculoskeletal In Neurological There is Tingling, Numbness, Blood Vision And Lacrimation In Autologic, Tinnitus, Ear pain, Dizziness and Vertigo In GI tract Nausea, Vomiting, Diarrhea or Constipation Musculoskeletal There is Fatigue, Tension, Diagnose, Weakness and Joint pains So how do we diagnose MPDS? The most common four criteria The unilateral pain, muscle tenderness The clicking and limited jaw movements So these are the four criteria for diagnosing MPDS Unilateral pain, muscle tenderness, clicking and limited jaw movements And how do we treat this? The treatment is basically We go for 7 hours occlusion rehabilitation So it starts with 7 hours So that is the first one is remove extraction of teeth Second one is reshape, granting of any occlusion, hypo and such things And reposition That is doing using orthodontic treatment And restore any conservative filling or constitutive treatment Replace that is using processes Reconstruct that is TMJ surgery And the last one is regulate That is regulating the habits and symptoms So remove reshape, reposition, restore Replace, reconstruct and regulate Extraction, granting, orthodontic treatment, conservative treatment, processes TMJ surgery and control of habits That is 7 hours So 7 hours involved with It is 7 hours involved with management of myofascial pain dysfunction So that's all about MPDS So this isn't a complete details of any long assay This might be asked for a long assay But it is to give a very brief idea And a pilot view So I would say a pilot view That is what are the basic features What are the striking features of any syndrome So you can easily build up the content while writing the exam So syndromes We have completed syndromes Which are being asked mainly for university papers So I will come up with a different topic in oral pathology So hope you understood all the syndromes we covered so far We finished it in 4 sessions So anyway, I will come up with new topics in oral pathology Thank you Hello everyone Welcome back to a new session on dentistry and more Today we have two genetic disorders That is Down syndrome and Gorlin God syndrome Down syndrome is also known as trisomy 21 And Gorlin God syndrome It is an autosomal dominant syndrome Which is having a triad of classic symptoms Now let's see what are these two disorders So Down syndrome, it is a chromosomal abnormality Where the problem lies with the chromosome number 21 So it is known as trisomy 21 An extra chromosome is present on 21 So it is clinically presented as Flattened face There will be small head Short neck Protruding tongue And upward palpibril fissure With small ear And there will be poor muscle tone And broad and short hands Short fingers and excessive flexibility There are lots of clinical presentation But I have mentioned very few So the problem with the chromosome number 21 With flattened face, small head, short neck, protruding tongue Upward palpibril fissure Small ear, poor muscle tone Broad and short hands Short fingers and excessive flexibility So what are the risk factors? The most common risk factor One is anyway it is a genetical involvement So there is genetic problems And the familial tendency might be there And another one is the advanced maternal age As the age of mother increases The chances of Down syndrome also increases And these Down syndrome kids or persons Will be having problems with heart And gastrointestinal defect will be there There will be immune disorders They might be facing sleep apnea Obesity and spinal Problems So these are kind of multi-system involvement And on a treatment side There is not much treatment Only just to improve the quality of life And provide a good social support But when we think about the dental aspect Since the patient is having high production of saliva The chances of caries is very less But the patient or the person might not be able to Do a proper oral hygiene measures So in turn the gingivitis and periodontal problems Will be very high And there will be increased bruxism And hypertonic tongue And mouth breathing will be there That persons will be with narrow palate And class 3 prognetic profile Down syndrome is a multi-system involvement Due to the Trisomy 21 So now let's move on to the Gorlin-Gott syndrome Gorlin-Gott syndrome is also known as Nevoid-Pacel-Cel-Casinoma syndrome As the name suggests it was explained by two people That is Gorlin-Gott It is also a genetical problem That is autosomal dominant genetical disorders And the involved gene is P-T-C-H1 gene So that is a gene involved in this particular syndrome And it is expressed as a classical triad That is multiple basal cellular epithelioma That is a malignant condition And the keratosis There will be many keratosis Oral keratosis and bipedrips So this is a classical triad Symptoms of Gorlin-Gott syndrome Basal-Cel-Casinoma, O-K-C's and bipedrips So there are many other problems Other clinical problems Involved with this Gorlin-Gott syndrome And the first one is The calcification of foc cerebri The palmar, plantar, epidermal pits The spine, rib, abnormalities Macrocephaly, frontal buzzing And ocular malformation So this will be most commonly diagnosed By major criteria and minor criteria Major criteria are the presence of More than 2 basal-Cel-Casinoma Under 20 years And O-K-C's that is Ordentogenic keratosis presence And palmar pits If more than 3 And also the bipedrips These are the major criteria Whereas the minor criteria is Microcephaly Sorry the Macrocephaly Then the hypertylarism And frontal buzzing So these are the minor criteria To diagnose the Gorlin-Gott syndrome Or just known as the Gott syndrome So treatment is basically The inoculation of all these cysts O-K-C's and Genetic counseling also can be done As a preventative measure So these are two genetic disorders That is Down syndrome and Gorlin-Gott syndrome These are commonly asked question So you can write all the clinical features The course And some of the risk factors And the diagnosis criteria And relate it to the dental problem In case of Down syndrome I will come up with new syndromes And then just to end more Thank you