 Hello everyone. Welcome back to another session in dentistry annual. Today we have a new topic in oral medicine and radiology that is red and white lesions. So these are the lesions which is commonly seen in our oral cavity. It could be a white lesion, it could be a red lesion. So there are various categories in both the categories. Some are pre-cancerous lesions, some are non-cancerous lesions. So basically a white lesion is an abnormal area of oral myocosin which is appearing whiter than the surrounding tissue. Okay so it appears a little bit more whiter than the adjacent tissues. So why this white lesion is forming or why it looks like a whiter lesion compared to the surrounding myocosa is because of hypercaratosis that is increased thickness of epidermal covering or it could be due to the imbibation of fluid and coagulation of fluids and formation of pseudomembrane and there will be a decreased blood supply. So all these reasons could ultimately results in a white lesion. Okay so this is the first one, increased thickness of epidermal covering with increased production of keratin. So this is a keratin which is supermost of the top layer. So there is increased production of keratosis which is known as hyperkeratosis which could be a reason for the appearance as white and the second one is benign thickening of stratum spinosum. So we have various layers, stratum bacillus, stratum spinosum, stratum granuline, stratum corneum. So the thickening which is seen in stratum spinosum and there will be accumulation of fluid and intra and extracellular region and there will be formation of pseudomembrane that is a pseudomembrane formation. So all these could result in a clinical appearance of a white lesion. Now red lesion is area of redden myocosa that may be smooth and atrophic looking or may exhibit a granular or availability texture. So this could be due to reduction in number of epithelial cells and also could be due to the increased vascularization. Okay so there will be atrophy that is a reduction in number of epithelial cells. The classification of red and white lesions. So we have red and white lesion with pre-cancerous potential then keratotic lesions with no increased potential for cancer, variations in structure and appearance of normal oral myocosa, non-keratotic white lesions and oral candidiasis. So leucodemophoresis, granules and linear alba there are the normal anatomic structures which is present in the oral cavity which are the variations in structure and in non-keratotic white lesions the habitual cheek and lip biting burns, uremic stomatitis, radiation mucositis, poplix spot, mucospatia and oral candidiasis. Oral candidiasis could be classified as acute and chronic and keratotic lesions with no increased potential for cancer. There stomatitis nicotinability, frictional keratosis, white sponginevus, psoriasis, keratosis follicularis. Whereas red and white lesions with pre-cancerous potential, their leukoplakia, erythroplakia, cosinoma in situ, palatal changes associated with reverse smoking, OSMF, lichen planus and dyskeratosis congenital. So this is a classification of red and white lesions and we should study lichenode reactions. They are a family of lesions with different etiology. So the reason could be different but they appear as that is a clinical and histologic picture is common. So in lichenode reactions we have lichen planus, lichenoid contact reactions, graft versus host disease and lichenoid drug eruptions. The first one is lichen planus. It is a chronic myocutinous disease of unknown cause. This was described by British physician Erasmus Wilson in 1869 because lichen means funky, planus is flat, its appearance is like a flat appearance. It is distributed in oral mucosa and the etiopathogenesis could be it is an autoimmune disease. It could be the changed keratinocyte which is presenting as antigen and it is affecting CD4 and CD8 helper cells which ultimately causes basal cell apoptosis. So this magnitude of underlying sub epithelial inflammation determines the types of clinical appearance. So there is cell apoptosis. So what is happening at the sub epithelial level determines its clinical appearance. So if it is a mild degree of inflammation it could be due to epithelial hyperkaratosis and severe inflammation there will be partial or complete destruction of epithelium that is atrophy erosion and ulceration. So these are the various types of oral lichen planus, reticular type papillar, plaque atrophic erosive or ulcerative and pulous lichen planus. So reticular lichen planus it is fine white lines or striate it is known as wicam striate. It is seen as a network or circular patterns can see the white striate wicam striate here. It is commonly bilaterally on buccal mucosa sometimes on lips and vermilion border. This is plaque like and this is papule like. This is homogenous well demarcated plaque surrounded by striate and may appear as clinically similar to homogenous oral leukoplickia. Atrophic that is homogenous red areas seen in buccal mucosa palate and gingiva and most disabling form is fibrin coated ulcers surrounded by erythematous zones sometimes displaying white striate. This is erosive or ulcerative type this was plaque and papule type. The cutaneous manifestation is not just seen in oral cavity it is seen in hands just thoracic erythematous to valacious papules seen in trunk and flexures of arms and legs. Trauma may aggravate the disease which is known as copna phenomena which is a short note what is copna phenomena which is the trauma which aggravate the oral lichen planus which is commonest extra oral mucosal site involved genital mucosa. Diagnosis is presence of papules or reticular components which is striking feature of oral p. It may exist along with plaque like erythematous or ulcerative lesions and biopsy and histologic examination is required for final diagnosis. So investigation in histopathologic we can see the sawtooth retipics and liltifaction degeneration of or necrosis of basal cell layer isonophilic band which is just beneath the basal membrane and dense infiltrate of inflammatory cells such as lymphocytes and macrophages in immunofluorescence it looks like this. Now move on to the management treatment strategies are limiting the progression of disease reduce the exacerbation and relieving the symptoms. In diagnosis we have history taking examination biopsy and elimination of other contributing factors alcohols, tobacco, poor processes for oral hygiene, amalgam restoration, medications. So if it is non-erosive or asymptomatic we need to just follow up. If it is erosive or systematic non-erosive we need to start the topical steroids. If they have the full response we just keep the steroids in regimen and we need to follow up. If there is no response we need to think of systemic steroids and to follow up. If provided that there is no contraindication to use steroids. If contraindication to steroids we need to think of topical cyclosporin or tracholimus. So this is a treatment region for oral lichen planus. So corticosteroids we need to topically use as a gel or mouth rinse two to three times a day for three weeks. Then taper during next nine weeks till a maintenance dose. So we need to reduce the doses and two to three times a week is reached. So maintenance dose of two to three times a week is reached. We need to taper the dose. Systemically used as one milligram per body weight kilogram body weight once a day for one week followed by a reduction of 10 mg in each subsequent day. So topical steroids we have on 0.5% flucinonide gel which is two times a day for two weeks. Then clavetazol gel and triamcinolone dexamethazone elixir then topical anti fungal therapy. Other topical agents are calcineurin inhibitors such as cyclosporin and tracholimus, retinoids and uv phototherapy. So differential diagnosis it could be lichenoid contact reactions, drug induced oral lichenoid reaction, GVHD that is graft versus host reaction, biscoid, lupus, erythematosis or bullis membrane, femfiboid. Now we have drug induced lichenoid reactions. They are skin eruptions which occur after ingestion or inhalation of certain chemicals. So they represent a delayed type of hypersensitivity which is a type 4 hypersensitivity. So pathogenesis we consume the drugs. So protein is a haptans which act as antigens and perceived as foreign objects by the t-cells and there will be immune reaction okay. So drugs could be penciline, gold or sulfonamides. So clinical features it resemble as lichen planus but this drug induced lichenoid reactions are predominantly unilateral. Okay the other one is bilateral and present with an ulcerative reaction pattern. Management the first thing is discontinuing the drug and then symptomatic treatment with topical steroids. Lichenoid contact reactions they are considered as a delayed hypersensitivity reaction to constants derived from dental materials. So all the etiopathogenesis is almost same as previous lichenoid drug reaction and it is also resemble oral lichen planus. The clinical difference between oral lichen planus and lichenoid contact reaction is the extension of lesion okay. And management is replacing the dental material which will result in cure or improvement in most of the cases and most lesions should be expected to heal within one or two months. And we have GVHD that is graft versus host disease is a common complication of allogeneic bone marrow transplantation. So here what is happening the immune cells in the transplanted marrow recognize the recipient as foreign and mount an immunological attack. It is like auto immune so the transplanted marrow will be considered or gnazed as a foreign material and immunological attack will be there. Clinical features they are indistinguishable from oral lichen planus but are more wide-spirited in nature. Skin lesions are present. Management is topical steroids, flucenonide and clovectazol gel treatment of opportunistic infections like candidiasis and development of secondary malignancy as we recognized as a complication of this. So that is all about um red and white lesion. It is just addressing the lichen planus and its lichenoid reactions. We have various lesions and red and white lesions so we have seen the classification. So they are they are we have leukoplakia erythroplakia um osmf. Now leukoplakia osmf you can find the videos which were uploaded previously and osmf lichen planus and leukodemaphoresis granules linialba are the normal anatomic appearance and oral candidiasis also another session is uploaded in the channel so you can go through it. So this all comprises red and white lesions not just lichen planus so i just covered lichen planus and lichenoid reactions. So i'll come up with a new topic in understand mode. Thank you.