Red & White Lesions PDF

Red & White Lesions May Bilal Assoc. Prof. of Oral Medicine, Periodontology, Oral Diagnosis & Radiology  Aim Recognition the different types of white and red lesions.  Intended Learning Outcomes Ide...

Red & White Lesions May Bilal Assoc. Prof. of Oral Medicine, Periodontology, Oral Diagnosis & Radiology  Aim Recognition the different types of white and red lesions.  Intended Learning Outcomes Identify the etiology, clinical features, principles of diagnosis, treatment and prognosis of different white and red lesions. Distinguish between the different forms these lesions. Choose the different tools and investigations for diagnosis and treatment of white and red lesions.  Content Lichen planus Lupus erythematosus Etiology Clinical and histopathologic features Investigations & differential diagnosis Treatment Lichen Planus ◼ Definition ◼ Lichen planus is a relatively common chronic inflammatory dermatosis involving the oral mucosa and characterized by the development of raised white multiform lesions as well as areas of erosion, ulceration and vesicle formation. ◼ Etiology: ◼ The etiology of lichen planus is not fully understood and can be classified into: ◼ I. Idiopathic lichen planus: ◼ A) Psychological stress ◼ B) Autoimmune cell mediated immune response. ◼ II. Lichenoid reaction: ◼ a. Drug induced ◼ b. Graft versus host disease following bone marrow transplantation. ◼ 1. Idiopathic Lichen Planus: ◼ A) Emotional stress has been implicated in the development of lichen planus since the disease may be incident by: ◼ a. Death of close relative or friend. ◼ b. Adjusting to new environment, job. ◼ c. Presence of disfiguring disease (psoriasis). ◼ d. Persons holding position of responsibility who live and work in an environment of tension. ◼ Diabetes, hypertension and lichen planus which are disorder sharing emotional stress factor were found to be associated together "Grinspan Syndrome". ◼ Correlation with Hepatitis C. ◼ Lichen planus may be related to the pattern of immune dysregulation induced by HCV, probably in a host with an underlying susceptibility for autoimmune disease. ◼ (B) Autoimmune Cell Mediated Immune Response: ◼ Although the etiology of idiopathic lichen planus remains unknown, it is suggested that lichen planus represents a cell mediated immune response associated with lymphocyte - epidermal interaction culminating in degeneration of the basal layer. ◼ The basal cells are destroyed by cytotoxic CD8+ T cells. ◼ The tissue destruction originates from the lymphocytic infiltrate and production of cytokines, characteristic of T‐helper type 1 immune cellular response (IL‐12, TNFα, interferons). ◼ They activate keratinocytes for increased expression of ICAM1 and the class II major histocompatibility complex (MHC) antigens. ◼ Other cells participating are CD4 cells, dendritic cells, natural killer (NK) cells, and mast cells. ◼ B cells and antibodies are not contributory. ◼ Two hypotheses concerning this interaction have been presented: ◼ 1. Alteration of the keratinocytes due to unknown events resulting in antigenic alteration of these cells, thereby stimulating an immunologic reaction. ◼ 2. A primary immunologic reacting leading to alteration and degeneration of the keratinocytes. ◼ Basal cell damage is the primary target in lichen planus and attributed to cell mediated immune process involving Langerhans cells, macrophages and T-Lymphocytes. ◼ Langerhans cells recognize, process and present appropriate antigen (altered keratinocytes), to T-lymphocytes which has been attracted to the area by IL -1 secreted by Langerhans / macrophages. ◼ IL-1 can also stimulate T-cells to produce IL-2 which causes T-cells proliferation. ◼ Activated lymphocytes (autoreactive Tc) become subsequently cytotoxic to the basal cells, inducing basal cell damage. ◼ Tc can damage basal cells through two distinctive pathways: ◼ 1) The first mechanism: Tc synthesize and release cytotoxic protein e.g. perforin onto the basal cells. ◼ The toxic proteins can induce pores in the basal cells and kill the cells by osmotic lysis. ◼ 2) The second mechanism: Tc stimulate some basal cells through mechanism that is not yet understood to undergo apoptosis or programmed cell death (induce suicide). ◼ In apoptosis, the basal cells become shrunken with little eosinophilic cytoplasm and pyknotic nuclear fragments. ◼ In addition to basal cell damage, activated Tc also secrete gamma interferon which induces keratinocytes to increase their rate of differentiation resulting in hyperkeratosis.  Etiology & Pathogenesis (Burket, 2022) Diagrammatic representation of possible pathogenic mechanisms in oral lichen planus, a cell‐mediated autoimmune disease where cytotoxic CD8+ T lymphocytes are responsible for apoptosis of the keratinocytes in the basal cell layer. Autologous antigen peptides from basal cells or elsewhere are presented by Langerhans cells (Lc) to autoreactive T cells (Tc), which clonally expand and induce apoptosis in the basal cell layer and lead to the clinical lesions of oral lichen planus. ◼ II. Lichenoid reaction: ◼ (A) Drug Induced: ◼ Lesions like lichen planus (lichenoid lesions) can be due to drug reaction, particularly to gold, penicillin, NSAIDs and anti-malarial. ◼ Resolution of the lesions occurs when the offending drug is withdrawn. ◼ It may also occur due to hypersensitivity reaction to the restorative materials (Hg), tooth pastes and mouth washes. (A) Drug‐induced lichenoid reaction at the dorsum of the tongue following one month of medication with a cholestyramine‐containing drug. (B) Three weeks following withdrawal of the drug. A B ◼ (B) Graft Versus Host Disease (GVHD): ◼ GVHD is an immunologically mediated reaction where T-lymphocytes in the donor graft mount an immunological reaction against the recipient tissue. ◼ A characteristic feature of GVHD of lichenoid reaction that may involve skin and mucous membranes. Oral manifestations of graft‐versus‐host disease. (A) Irregular depapillation of the dorsusm of the tongue with apparently keratotic patches; and (B) nonremovable white patches of the hard and soft palate in the same patient. A B Oral chronic graft versus host disease (all images are from a single patient). (a) Diffuse erythema involving more than 75% of the right buccal mucosa. (b) Diffuse erythema and linear ulceration of the left buccal mucosa A B ◼ GVHD has tow forms: ◼ 1. Acute GVHD; (during 100 days post bone marrow transplantation). ◼ It varies from mild erythema, to ulceration or severe sloughing. ◼ 2. Chronic GVHD, (after 100 days post bone marrow transplantation) ◼ It may be presented clinically in the form of : ◼ a. Lichenoid lesions (purpuric maculopapular rash, violaceous scales, erythema, bullae). ◼ b. Scleroderma like lesion (Scarring and fibrosis leading to trismus). ◼ c. Feature similar to Sjogren's syndrome. This is attributed to the graft induce epithelial cell damage of minor and major salivary gland as well as the lacrimal gland. ◼ d. Superficial mucoceles of the palatal and buccal mucosa which are occasionally symptomatic. ◼ e. The patients are liable to bacterial , viral and fungal infection. ◼ Clinical Features : ◼ Age: ◼ Lichen planus affects up to 2% of the population, mainly those over 40 years of age and it is rare in children. ◼ Sex: ◼ Both sexes are affected but tend to be more in females. ◼ Oral lesions may accompany or precede the skin lesions, and about 50% of patients who have oral lichen planus, also have skin lesions. ◼ A. Skin Manifestations: ◼ The primary lesions are small, flat topped, papules polygonal in outline. ◼ Varying in color from pink to violaceous to brown as the lesions progress. ◼ These pink papules have white streaks on their surface (Wickham's striae). ◼ The common sites of involvement are the flexor surface of the extremities, sacral region, nails and genitalia. ◼ The wrists and palms of the hand may be the only part of the skin surface affected. ◼ The skin lesions are often accompanied by pruritis, and some pigmentation is left on the skin following regression of the disease. ◼ Linear lesions may follow trauma or scratching and called Kobner phenomena. ◼ When a skin lesion alone is present, the condition may be expected to last for two years maximum. Nail involvement: Longitudinal ridges or grooves on the nails Splitting or thinning of the nails ◼ Oral lesions may be classified into the following, often overlapping categories: ◼ Reticular/keratotic (classic) oral LP ◼ Erythematous/erosive oral LP ◼ Ulcerative oral LP ◼ Atrophic oral LP ◼ Bullous oral LP ◼ B. Oral Features: ◼ The clinical manifestations of oral lichen planus are extremely variable and depend essentially on three basic types of tissue changes; papular, bullous erosive and atrophic type. ◼ 1. The Papular Type: ◼ The development of pinhead sized white keratotic lesions referred to as papules. ◼ The papules may be discrete or arranged in various clinical patterns such as linear, reticular, annular or plaque like configurations. Papular OLP on the buccal mucosa A. Reticular OLP occurring on the vermilion border of the lip. B. Classic reticular OLP on the buccal mucosa. C. Annular form of papular OLP. A B C ◼ The plaque pattern manifest itself as white patches, raised, thick and dense. ◼ This form may be easily mistaken for leukoplakia. ◼ In lichen planus there is no change in the elasticity or the flexibility of the involved tissue. ◼ Plaque pattern tends to be multifocal and affects cheek mucosa and dorsal surface of the tongue. ◼ A fine network of bluish white Plaque form of papular OLP. lines called Wickham's lines or striae are seen radiating from the periphery of the lesion. ◼ Chief complaint: ◼ In the papular type, patients either have no complains or they may complain form roughness of the cheek or change of the color of the lip. ◼ Prognosis: ◼ Poor as clearing of the lesion or remission is not excpected. ◼ 2. The Bullous Erosive/Ulcerative Type: ◼ The lesions start by the development of vesicles or bullae as a result of severe degenerative changes in the basal layer of the epithelium with separation of the epithelium from the underlying connective tissue. ◼ The bullae and the vesicles soon rupture, and give rise to chronic, multiple, shallow, irregular, well defined ulcers. ◼ It also may appear as ulcerated oral mucosa with a yellow fibrin pseudomembrane and are surrounded by erythematous haloes around which radially arranged bluish white dendritic extensions can be seen (Wickham's striae- peripheral reticulations.). ◼ Chief complaint: pain is an initial symptom which interfere with eating and even with speaking. ◼ Prognosis: Very poor. Erosive OLP of the tongue and palate. ◼ 3. The Atrophic/Erythematous Type: ◼ The highly differentiated epithelial structures may undergo atrophy, as a result of epithelial degeneration and dense inflammatory infiltration in the underlying corium. ◼ The epithelium may become very thin so that it appears as erythematous red, smooth, poorly defined area with peripheral fine Atrophic LP in the lacy white net work of Wickham' s posterior mandibular striae. buccogingival reflex ◼ The thin epithelium is also more subjected to trauma and erosive areas may occur. ◼ Atrophic oral LP is best seen on the tongue dorsum where there is loss of the filiform and fungiform papillae and there is diffuse keratosis or white papules. ◼ Erythematous oral LP frequently involves the gingiva and presents as red, erythematous areas of mostly buccal (and less commonly palatal and lingual) gingiva which is commonly referred to as desquamative gingivitis. ◼ It should be remembered that desquamative gingivitis is not a diagnosis itself, these lesions must be biopsied to rule out the possibility of pemphigus vulgaris, mucous membrane pemphigoid, bullous pemphigoid and lichen planus. ◼ Early lesion of atrophic or erosive type lichen planus may appear in the form of desquamative gingivitis, in which the full width of the attached gingiva appears bright, red with marked edema and the gingival epithelium can be easily detached. Chief Complaint: The patient usually complains of soreness or burning sensation. ◼ The papular lesions are observed more commonly than the other varieties, but the bullous erosive and the atrophic types are not uncommon. ◼ While any region of the mouth may be involved, the common sites are the buccal mucosa near the occlusal line and the tongue. ◼ The lesions are most commonly of bilateral distribution and characterized by frequent remission and exacerbation and persist for years (8-15 years). ◼ Exacerbation may be associated with emotional upset or menstrual cycle in females. ◼ Malignant transformation: ◼ Lichen planus is considered as a premalignant disease. ◼ The malignant transformation is more commonly noted in the erosive and the atrophic forms of the disease, this may be due to exposure of the deep oral epithelium to oral environmental carcinogens. ◼ Periodic recall is mandatory for the risk of malignant transformation, especially in patients with erosive or atrophic lichen planus and also for patients with history of tobacco or alcohol abuse. ◼ Histopathological features: ◼ Papular, bullous erosive and atrophic lichen planus share the following common histopathological features: ◼ 1. Damage of the basal cell layer and this include: ◼ a. Liquifaction degeneration (vacuolar changes) ◼ The basal cells are presented with intracellular edema, intracellular vacuoles and separation of basal cells from each other and from lamina propria. ◼ Tc release specific toxins on the basal cells (perforin , granzyme and others) where a transmembrane pore is induced in the basal cells and absorb extracellular fluid and swell, cell death may soon occur with dilution of the cytoplasmic content. ◼ b. Epidermal cell death: ◼ Basal cell death also induced by Tc through a process called apoptosis. ◼ In this process the basal cells separate from its neighbor, and both the nucleus and the cytoplasm become condensed. ◼ The single basal cells become shrunken with little eosinophilic cytoplasm and pyknotic nuclear fragments. ◼ These dead cells are called Civatte bodies. ◼ The latter will be phagocytosed by adjacent basal cells or by macrophages. ◼ Cells which are not phagocytosed are extruded into the underlying connective tissue and become coated with IgM and referred to as Colloid bodies. ◼ 2. Well defined band of intense infiltration of lymphocytes in the superficial lamina propria (mainly T. lymphocytes). ◼ 3. Increase numbers of Langerhans cells within the epithelium, presumably to recognize, process and present the antigen (exogenous or endogenous) to the adjacent T- lymphocytes. ◼ In addition to the above-mentioned basic tissue changes, there is other histopathologic features which can differentiate the three clinical types of lichen planus and these include. ◼ 1. Papular Lichen Planus: ◼ 1. Hyperkeratosis or hyperparakeratosis may be extensive ◼ 2. Hyperparakeratosis is found more commonly than hyperkeratosis. ◼ 3. Stratum corneum may show considerable increase in width. ◼ 4. The extension of rete pegs into saw tooth like configuration is observed in oral lesion, although it is common finding on skin lesions. ◼ 2. Bullous-Erosive Lichen Planus: ◼ There is separation of the epithelium from the lamina propria at the level of basement membrane, as a result of extensive edema collecting at epithelial-connective tissue junction, following the hydropic degeneration of the basal cell layer. ◼ The vesicles and bullae (sub-epithelium type) contain clear fluid and occasionally blood. ◼ The broad band of lymphocytic cells in the upper corium is usually seen prior to rupture of the vesicle. ◼ Once vesicle has ruptured the inflammatory pattern becomes less characteristic in appearance, with lymphocytic infiltrate becoming diffuse into the deep corium. ◼ Histopathologic feature will not be pathognomonic if biopsy is taken from the ulcer, but it should include the normal looking tissue in order to detect all histopathologic features of the lesions at the margin of the ruptured vesicle. ◼ 3. Atrophic Lichen Planus: ◼ In atrophic lichen planus the epithelium is thin and there is absence of rete pegs. ◼ There is little keratinization at the surface and the stratum corneum tend to blend into the stratum spinosum. ◼ Histopathological features of lichenoid lesion are the same as in lichen planus with minor difference, particularly the presence of: ◼ a) Prominent eosinophilic perivascular infiltrate in the dermis. ◼ b) There are lymphocytes as well as eosinophils, neutrophils and plasma cells in the deep and superficial connective tissues. ◼ Immunofluorescent Test: ◼ Direct Immunofluorescent technique is performed by incubating a biopsy specimen of the lesion with a fluorescein conjugated antiglobulin, and the slide examined by the ultraviolet microscope, and this will reveal: ◼ 1. With IgM antisera: ◼ Aggregates of globular structure in deeper layer of epidermis and superficial layer of the dermis, (the same aggregate is seen also in LE, EM) ◼ 2. With Anti-fibrinogen Antisera: ◼ Positive reaction at the level of basement membrane zone in 90-100% of cases. ◼ This appears intensely positive fluorescence that outline the basement membrane zone, with numerous extensions into the superficial lamina propria, (the same pattern is characteristic of LE). Direct immunofluorescence revealed positive staining of fibrinogen at basement membrane zone ◼ 3. With Immunoglobin Antisera (IgG, IgM & IgA antisera) and Anticomplement C3: ◼ There is no reaction at the level of basement membrane zone. (LE show fluorescent band). ◼ DIF helps in differentiating OLP from MMP or PV in cases of desquamative gingivitis, or it can help differentiate OLP from lupus. ◼ Treatment: ◼ The current treatment is aimed at controlling rather than curing the disease. ◼ Patient Education: The first component of disease management is patient education, to be aware of the nature of the disease, the unpredictable clinical course and the rationale of current therapeutic recommendations. ◼ The patient must be advised that lichen planus is characterized by unpredictable exacerbation that may in some cases require treatment for many years. ◼ In addition, the hyperkeratotic striae of lichen planus will most often persist through periods of symptomatic remission. ◼ Medical History: ◼ History of drug administration relevant to the development of the disease should be obtained. ◼ The lesion may regress following withdrawal of the drug. ◼ The following drugs are generally prescribed: ◼ Asymptomatic lesion (papular LP) requires no treatment. ◼ [I] Corticosteroids ◼ Corticosteroids are the drugs of choice in treatment of symptomatic LP. ◼ Although most of the positive effect of corticosteroids used for the management of LP are attributed to the local anti-inflammatory effect, some benefit may be the result of anti- immunologic properties of suppressing T-cell function. ◼ The decision to use topical steroid, systemic steroid or combination is based on professional judgement. ◼ a) Topical Corticosteroids: ◼ Start with the weakest preparation, progressing to stronger preparation. ◼ More potent steroid should be reserved for the most severe cases. ◼ Start by using hydrocortisone hemisuccinate lozenges 2.5 mg q.d.s., allow it to dissolve on the lesion. ◼ Progression can be made to 0.1% triamcinolone ointment in orabase q.d.s. ◼ 0.1%-0.2% triamcinolone acetonide mouth rinse, the concentration is determined on the basis of the clinical severity of the disease. ◼ The suspension can be prepared by the pharmacologist from injectable triamcinolone acetonide and distilled water. ◼ The patient is advised to have 5 ml q.d.s. as mouth bath. ◼ The advantages or rational for the aqueous rinse is its ease of use and provides a wide spread and effective application of topical medication when compared with applied cream or ointments or lozenges. ◼ If this fails or the initial lesions are particularly severe, the management can be started on betamethasone 0.1 mg lozenges, allowed to dissolve on the lesions q.d.s. ◼ Betamethasone valerate aerosol (used for treatment of bronchial asthma), is effective in mild cases. ◼ All topical corticosteroids should be applied four times per day after meal time and at the bed time and to take nothing by mouth for at least one hour after using topical steroids. ◼ b) Systemic Corticosteroids ◼ In cases showing significant clinical ulceration, it is wise to supplement the topical steroid with short course of systemic steroid. ◼ Prednisone, 0.5–1 mg/kg prednisolone, 40 mg given 1.5 hour after arising as single dose for 7 consecutive days seldom result in appreciable pituitary-adrenal suppression. ◼ This is followed by 10-20 mg dose 1.5 hour after arising every other morning for additional 2 weeks. ◼ Reduction of 5 mg each subsequent day. ◼ Once the ulcers resolved, continued control of the oral lesion is usually accomplished through the use of topical steroids alone. ◼ It is advisable to use steroid mouthwash three times a day for one week, then twice per day for one week, then once per day for one week and even every other day if the oral mucosa is retained free from symptoms. ◼ c) Low dose Systemic steroid combined with non-steroidal anti-inflammatory drugs: ◼ This is of value in some patients where there is contraindication for the use of systemic steroids particularly in high doses. ◼ 10-20 mg prednisone is given 1.5 hour after arising and 1000 mg NSAD/day in divided doses (e.g. Ibuprofen), for a period of two weeks. ◼ NSAD have anti-inflammatory properties which augment the anti-inflammatory action of systemic steroids. ◼ This may give considerable relief in symptomatic lichen planus, in addition to using topical steroids. ◼ d) Intra-lesional injection of steroid: ◼ It may be required weekly or biweekly (2-3 injections) to promote healing of ulcers resistant to healing 2-6 weeks after topical and systemic steroid therapy. ◼ 0.5 ml (40 mg/ml) methyl prednisolone or triamcinolone suspension of injectable triamcinolone acetonide. ◼ It is diluted to 0.5-1ml with Lidocaine 2% since steroid injection is very painful. Erosive OLP lesion on left buccal mucosa before the treatment (a). The lesion perimeter was outlined (b) Left side was treated with TA (c). Appearance of lesion on left buccal mucosa after the treatment (d) (Bennardo et al., 2021). ◼ Antifungal drug: ◼ It is important to manage the superimposed candidiasis. ◼ The clinical appearance is often inadequate to suspect candidiasis when present in association with lichen planus. ◼ Topical or systemic anti-fungal drugs should be administered for at least one week out of every four weeks of steroid therapy. ◼ Tranquilizers: ◼ If the patient shows signs of anxiety, tranquilizer can be prescribed e.g. valium or librium (diazepam or chlorodiazepoxide, respectively) 5-10 mg b.d.s. or t.d.s. ◼ Benzydamine hydrochloride: ◼ Relief of pain and discomfort can be obtained by using analgesic mouth bath (0.15% benzydamine hydrochloride). ◼ Since no specific local or systemic treatment is uniformly successful in the treatment of lichen planus, the following drugs may be prescribed. ◼ i) Vit A analogus-retenoid, have been used for their antikeratin, and immunomodulating effect. ◼ White keratotic lesion can be reversed by topical retenoid only temporarily. ◼ Systemic retenoid have some side effects; e.g. cheilitis, elevation of serum liver enzymes and triglycerides and also it has teratogenic property. ◼ ii) Cyclosporin: ◼ Topical and systemic therapy offer remission for several months because it suppresses mainly T- lymphocytes. ◼ The cost of the drug is high and it can promote viral reproduction and malignant changes in epithelial cells. ◼ iii) Dapsone (sulfone antibiotic used in severe infections and autoimmune disorders has an anti- inflammatory effect as steroids) may be tried in severe bullous- erosive lesions. ◼ It may help to control the lymphocyte mediated process by modulating the release of inflammatory chemotactic factors from mast cells or neutrophils. ◼ iv) Other treatment as phototherapy and PRP, or systemic steroid therapy in conjunction with azathioprine, hydroxychloroquine, mycophenolate mofetil, or tumor necrosis factor inhibitors. Lesion was treated with i-PRF (Bennardo et al., 2021). ◼ Other alternative plant and herbal topically-based preparations such as curcumin, aloe vera, hyaluronic acid, propolis….. ◼ In gingival lesions, achieve good oral hygiene with application of topical steroid gels in a prefabricated plastic tray. ◼ The patients are advised for periodic recall, and the oral lesions may fade, become asymptomatic or may show malignant transformation. Lupus Erythematosus ◼ Definition: ◼ LE is a connective tissue disease of unknown etiology and exist in different clinical forms and types. ◼ It is an autoimmune disease, and a combination of genetic, hormonal, and environmental factors (e.g., smoking and exposure to ultraviolet light) may contribute to its development or progression  Clinical types Chronic cutaneous Neonatal L.E. L.E. and subacute cutaneous A transient Discoid Systemic L.E. self-limiting L.E. L.E. disease Restricted to usually skin (face and disappears at scalp) and the age of six oral mucosa. month. Drug induced L.E. Discoid L.E.  DISCOID LUPUS ERYTHEMATOSUS ◼ Site: It is relatively common disease confined only to skin and oral mucosa (mucocutaneous disease). ◼ Age: Predominantly in the third and fourth decades. ◼ Sex: More common in females than in males. ◼ Skin Manifestation: ◼ Site: ◼ a) It usually presents on the face, where it involves malar regions and cross the ridge of the nose which assumes butterfly distribution. ◼The butterfly rash is not pathognomonic for DLE as it is seen in other dermatological disorders. like seborrheic dermatitis. ◼ b) Skin lesions may also occur on the scalp, ears, chest, back and extremities. ◼ Character: ◼ a) The cutaneous lesions are slightly elevated red or purple macules which are often covered with grey or yellow adherent scales. ◼ When the latter is removed it reveals numerous extensions "carpet tack" which has dipped into enlarged pilosebaceous canals (follicular plugging) or excessive keratin in active hair follicle. ◼ b) The lesion has sharp borders which slowly expand and increase in size by peripheral growth. ◼ The periphery of the lesion appears white, pink or red. ◼ c) The center exhibits atrophic depigmented Lesion on temple scarred appearance, shows elevated indicative of the chronicity of hyperkeratotic the lesion, with characteristic periphery central healing.  "Initial" LE lesion ◼ Oral Manifestation: ◼ Oral lesions has been reported in 25% to 50% of cases of DLE. ◼ The early lesions begin as irregular erythematous macules which may be elevated or depressed and Typical LE lesion without keratosis. ◼ Later, the atrophic red area may be surrounded by keratotic margin or covered by white keratotic spots. ◼ Other lesions may appear as keratotic lesion surrounded by red (telangiectatic) halo. ◼ A classical lesion has been described as alternating red (atrophic), white (keratotic) and red (telangiectatic) zones, provide characteristic appearance. Typical lesion on the buccal mucosa and palate. Radiating white patches with erythema in the buccal sulcus, which is characteristic of the oral lesions of lupus erythematosus. ◼ Tongue lesion: is usually associated with atrophy of tongue coating. ◼ Lip lesion: The lip may reveal atrophic plaques and surrounded by keratotic border which may involve the entire vermilion border and extend to circumoral skin. Atrophic plaques of Lupus  Discoid lupus erythematosus, and scaling lesions on the lip Discoid lupus lesions on the lower lip Malignant transformation of lip lesion has been reported.  ◼ The margins of many of these DLE keratotic lesions reveal a fine lacy white network or striae like Wickham striae of lichen planus. ◼ The differentiation of both lesions can sometimes be extremely difficult on clinical examination alone. ◼ However, in the DLE, ◼ 1. The lesions are less often symmetrically distributed. LP ◼ 2. The pattern of striae is less defined or conspicuous. ◼ Prognosis: DLE is a slowly progressive disease over a period of many years. ◼ Occasionally spontaneous remission occurs or in rare instances it develops into SLE. ◼ Patients with oral DLE alone should be seen at least yearly to: ◼ 1. Secure an early diagnosis of eventually developing sign of cutaneous DLE. ◼ Early skin lesion responds better to local treatment than older lesions. ◼ 2. The occurrence of oral ulceration is of clinical significance; it may indicate the presence of or signal of latter developments of SLE. Subacute L.E. ◼ S.C.L.E. lies between S.L.E. and D.L.E. and is characterized by: ◼ 1. Skin lesion of mild to moderate severity may appear as: ◼ Patches of thickened skin. ◼ Patches of purpura. ◼ Patches of vitiligo ◼ Urticaria, angioedema or bullae formation. ◼ Skin lesion persist for weeks to months and heal without scar. ◼ 2. Oral lesions are similar to DLE ◼ 3. Mild systemic symptoms in the form of musculoskeletal pain. ◼ 4. Serologic abnormalities: ◼ a. circulating antibodies to cytoplasmic component may be found. ◼ b. Some ANA may be found. ◼ 5. Long term prognosis is good; it is unlikely that this type will progress to SLE.a  References Glick M, Greenberg MS, Lockhart PB, CallacombeSJ, Burket’s Oral Medicine, 13thedition, John Wiley & Sons, Inc. Hoboken USA; 2021. Farah C S, Balasubramaniam R, Mc Cullough M J, Contemporary Oral Medicine, Springer, Switzerland, 2019. Ongole R: Textbook of Oral Medicine, Oral Diagnosis and Oral Radiology, 2nd edition, Elsvier, 2014. Laskaris G, Color Atlas of Oral Diseases in Children and Adolescents, Library of Congress, 2017. THANK YOU For any questions feel free to contact me by mail [email protected] Assoc. Prof. May Bilal Oral Medicine, Periodontology, Oral Diagnosis & Radiology