DD Of White Lesions Of The Oral Mucosa PDF

 The normal colour of the oral mucosa The normal color of the oral mucosa is pink due to the passage of light through the translucent superficial layer of soft tissue. Factors contribute to the color of the oral mucosa: 1- Amount of vascularity 2- Thickness of oral mucosa 3- Presence of...

 The normal colour of the oral mucosa The normal color of the oral mucosa is pink due to the passage of light through the translucent superficial layer of soft tissue. Factors contribute to the color of the oral mucosa: 1- Amount of vascularity 2- Thickness of oral mucosa 3- Presence of melanin pigmentation 4- Degree of keratinization 5- presence of pseudomembrane White colour of the oral mucosa is due to: 1.Keratin or Para keratin (hyperkeratosis or hyper parakeratosis). 2.Hyperplasia and acanthosis= increase thickness of epithelium=  Prickle cell layer. 3. Intracellular edema (spongiosis). 4. Intercellular edema. 5.  Collagen fibers (fibrosis). 6. Necrosis and pseudo membrane formation. 7. Lack of vascularity. 8. Submucosal deposits of ectopic sebaceous glands Complete:  White color of the oral mucosa is due to: 1- ………………………………. 2- ………………………… 3-……………………………… 4- ……………………………..  Four factors contribute to the color of the oral mucosa: 1. ……………………………….. 2. ……………………………… 3. ………………………… 4. ………………………. White lesions of the oral cavity White lesions of the oral mucosa can be divided into two groups: those that cannot be scraped off with a tongue blade (keratotic) and those that can be scraped off with a tongue blade (sloughing, pseudomembranous necrotic types). Keratotic white lesions  Leukodema  Papilloma, verruca vulgaris  Frictional keratosis  Verrucous carcinoma  Leukoplakia  Darrier’s disease  Lichen planus  Nicotine stomatitis  Dyskeratosis congenita  Smoker keratosis  Focal epithelial hyperplasia  Smokeless tobacco  Oral submucous fibrosis  Migratory glossitis  Graft versus host disease  White hairy tongue  Lupus erythematosus  White exophytic SCC  Syphilitic glossitis  White spongy nevus  Hyperplastic candidiasis  Actinic keratosis  Hairy leukoplakia  Hereditary benign intraepithelial dyskeratosis Non keratotic white lesions  Traumatic ulcer  Pyogenic granuloma  Chemical burn  ANUG  Candidiasis  Necrotic ulcer of systemic diseases  Gangerenous stomatitis  Another classification of white lesions 1. Hereditary Infectious Premalignant lesions Leukoplakia Leukoedema Syphilis LP White Sponge Nevus Measles (Koplik spots) Lichenoid reactions— Hereditary Benign Candidiasis drug induced, graft- Intraepithelial Dyskeratosis Bacterial stomatitis versus-host disease Dyskeratosis Congenita Erythroplakia Darier’ s disease Actinic keratoses Discoid lupus erythematosus (DLE) Reactive inflammatory white Chronic hyperplastic lesions Premalignant candidiasis Traumatic keratosis conditions Normal mucosal Frictional keratosis Oral submucous variations Thermal burn fibrosis (OSMF) Leukoedema Chemical burn (aspirin burn, Oral psoriasis Fordyce granule uraemic stomatitis) Dyskeratosis Linea alba buccalis Radiation mucositis congenita Reactive mucosal hyperplasias Syphilitic glossitis (stomatitis nicotina palati) Miscellaneous Lesions KERATOTIC WHITE ENTITIES  LEUKOEDEMA Leukoedema is a common variation that appears to be related causally to mastication and possibly poor oral hygiene.  The incidence and intensity increase with age.  50% of black teenagers (male incidence is more common)  90% of black adults have the condition. bilaterally, Features:  asymptomatic and usually found during routine oral examination.  It is whitish-grey, diffuse, and milky opalescence, with numerous surface folds resulting in wrinkling of the mucosa on the buccal mucosa bilaterally, and it may be seen rarely on the labial mucosa, soft palate, and floor of the mouth.  It cannot be scraped off, and it disappears or fades upon stretching the mucosa. Leukoedema  WHITE SPONGE NEVUS Cannon’s disease folded gingivostomatitis a hereditary condition in which white lesions occur on various mucous membranes of the body= defect in the epithelial cell maturation and desquamation (e.g., oral mucosa, vagina and pharynx). Clinical features: ❑ White sponge nevus presents as bilateral asymptomatic grey white folded or corrugated spongy mucosal lesions that often have symmetrical wavy pattern on the buccal mucosa. They have soft or spongy texture and white opalescent hue. ❑ Other sites may be involved as ventral tongue, floor, labial mucosa, soft palate, and alveolar mucosa. ❑does not exhibit tendencies toward malignant change. ❑The lesions of WSN may be present at birth or may first manifest or become more intense at puberty. White Sponge Nevus  HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS Witkop’s disease Witkop-Von Sallmann syndrome  It is a rare genetic disorder characterized by oral lesions and bilateral conjunctival plaques.  The oral lesions are similar to those of WSN, with thick, corrugated, asymptomatic, white “spongy” plaques involving the buccal and labial mucosa.  Other intraoral sites include the floor of the mouth, the lateral tongue, the gingiva, and the palate.  On stretching the mucosa, the lesion appears as a soft plaque with pinpoint elevation.  The significant feature of this disease is the formation of corneal plaques that may lead to blindness. Hereditary Benign Intraepithelial Dyskeratosis  DYSKERATOSIS CONGENITA  Premalignant lesion  Include: 1. Dystrophic nails 2. hyperpigmentation of the skin of the face, neck, and chest. 3. hematologic changes; pancytopenia, hypersplenism, and an aplastic anemia. 4. The oral lesions commence before the age of 10 years as crops of vesicles with associated patches of white ulcerated necrotic mucosa often infected with Candida( tongue and cheek). Dyskeratosis Congenita  FOCAL EPITHELIAL HYPERPLASIA (Heck’s disease)  is considered among the most contagious of the papillary lesions affecting the oral cavity (caused by HPV) Clinical features  It is usually seen in children and adults.  characterized by multiple soft, circumscribed, sessile nodules of whitish colour  The common sites of involvement are the lips, buccal mucosa and the lateral borders of the tongue  Well-circumscribed, papular lesions on the labial mucosa in Heck disease. Well-circumscribed, sessile nodules mimicking the colour of the adjacent oral mucosa in Heck disease.  FOLLICULAR KERATOSIS (DARIER’S DISEASE )  Darrier disease (DD) characterized by greasy hyperkeratotic papules in skin, the papules crust, ulcerate and become verrucous with foul smell. Affect neck and overshoulder  Palmar and planter keratotic thickening  Fingernail changes: fragility and splintering  The oral lesion appears as small whitish papules, located in the gingiva & hard palate inducing cobblestone appearance. The papules may coalesce to produce a white keratotic patch with rough surface. Enumerate: Hereditary white lesions are: 1-…………………………………………….. 2- ………………………………………………. 3- ………………………………………………. 4- ……………………………………………….. 5- ……………………………………………. Choose:  Which of the following lesion is most likely to present with eye lesions? A. Leukoedema B. White Sponge Nevus C. Hereditary Benign Intraepithelial Dyskeratosis D. Dyskeratosis Congenita  Choose:  A patient presents with a bilateral greyish white lesion on buccal mucosa which disappear when stretched. The most likely diagnosis is: A. Lichen planus B. Leukoplakia C. Leukoedema D. White sponge nevus  FRICTIONAL (TRAUMATIC) KERATOSIS  a white patch with a rough surface which is clearly related to a source of mechanical irritation and that will disappear over a period of time with the removal of the stimuli.  linea alba buccalis, and cheek, lip or tongue biting or chewing can be considered as frictional keratosis.  Frictional keratosis is frequently associated with rough or maladjusted dentures and with sharp cusps and edges of broken teeth.  LINEA ALBA BUCCALIS (White Line) It is a horizontal streak on the buccal mucosa bilaterally at the level of the occlusal plane extending from the commissure to the posterior teeth. It is often scalloped and restricted to dentulous areas. CHEEK CHEWING Cheek chewing is most commonly seen in people who are under stress or in psychological situations in which cheek and lip biting become habitual. The occurrence is twice as prevalent in females and three times more common after the age of 35 years. ❑ Chronic cheek, lip and tongue chewing presents as thickened and shredded whitish areas. ❑ Habitual oral mucosa chewing can sometimes lead to areas of localized erosion and ulceration. ❑ The lesions may present bilaterally or unilaterally. ❑ Individuals with chronic cheek biting (morsicatio buccarum) have a habit of either sucking the cheeks frequently or pushing the cheek in between teeth with their finger. ❑ Similarly, individuals with chronic lip chewing habit (morsicatio labiorum) and chronic tongue nibbling habit (morsicatio linguarum) present with macerated appearance of the labial mucosa and lateral surface of the tongue, respectively. ❑ The lower labial mucosa is usually affected in lip chewers SMOKER’S KERATOSIS  Smoker patch: white keratotic patch on the vermilion border at the site of handling the cigarette  Diffuse white milky bilateral lesion on the buccal mucosa  Stomatitis nicotina= red and white lesion  Reverse smoking habits: hyperkeratosis of anterior hard palate, precancerous, does not reverse after stopping the habit  Nicotine Stomatitis stomatitis nicotina palati smoker’s palate  White lesion that develops on the hard and soft palate in heavy cigarette, pipe, and cigar smokers.  The lesion is not considered to be premalignant.  Reverse smoking” produces significantly more pronounced palatal alterations that may be erythroleukoplakic and that are definitely considered premalignant.  Nicotine Stomatitis Typical features:  This condition is most often found in older males with a history of heavy long-term cigar, pipe, or cigarette smoking.  Due to the chronic insult, the palatal mucosa becomes diffusely gray or white. Numerous slightly elevated papules with punctate red centers that represent inflamed altered minor salivary gland ducts are noted. SMOKELESS KERATOSIS  Betal-nut chewer, oral snuff keratosis  Diffuse keratosis of buccal mucosa, tongue and vestibule  Premalignant lesions Smokeless Tobacco–Induced Keratosis ❖Commonly noted is a characteristic area of gingival recession with periodontal-tissue destruction in the immediate area of contact. This recession involves the facial aspect of the tooth or teeth and is related to the amount and duration of tobacco use. ❖The lesion is usually asymptomatic and is discovered on routine examination.  Smokeless Tobacco–Induced Keratosis snuff dipper’s keratosis tobacco pouch keratosis Typical features: ❖Smokeless tobacco are seen in the area contacting the tobacco. ❖The most common area of involvement is the anterior mandibular vestibule, followed by the posterior vestibule. ❖The surface of the mucosa appears white and is granular or wrinkled. ❖These lesions are accepted as precancerous ACTINIC KERATOSIS  Secondary to long term exposure to ultraviolet light in white patients  Appear as wrinkled dry atrophic erythematous keratotic and crusted  Actinic cheilitis: the lower lip become cracked, atrophic and ulcerated with areas of hyperpigmentation and scaling and indistinct mucocutaneous junction. Actinic Keratosis (Cheilitis)  Actinic (or solar) keratosis is a premalignant epithelial lesion that is directly related to long-term sun exposure.  These lesions are classically found on the vermilion border of the lower lip as well as on other sun-exposed areas of the skin (forehead, cheeks, forearms). The surface may be crusted and rough to the touch. Enumerate: Reactive and inflammatory white lesions 1- …………………………………… 2-……………………………………… 3- ……………………………………. 4- …………………………………….. 5- …………………………………….. 6-……………………………………. 7-…………………………………… 8-……………………………………… Case : 40 years-old nervous female came to the clinic complaining of roughness and small tags of tissue in the buccal mucosa. 1- What is the clinical diagnosis?  IDIOPATHIC KERATOSIS “TRUE” LEUKOPLAKIA  Oral leukoplakia (OL) is the most common precancerous lesion of the oral mucosa.  Leukoplakia is a white keratotic patches that cannot be rubbed off and a precancerous lesion with a recognizable risk for malignant transformation.  Precancerous lesion as a “morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart.”  WHO defined Leukoplakia as “a white patch or plaque that cannot be characterized clinically or pathologically as any other disease”.  Etiology  Unknown  Tobacco usage  Alcohol consumption  Sunlight  Candida albicans  Human papilloma virus (HPV)  Electrogalvanic current  Chemical irritation  Systemic predisposing factors: nutritional deficiency (Vit B 12, Iron deficiency) when exposed to various local insults may predispose to both leukoplakia and carcinoma.  Clinical Features  Leukoplakia: adult men older than 50 years of age.  the most common sites: buccal mucosa, alveolar mucosa, floor of the mouth, lateral border of the tongue, lips and palate;  Lesions of the tongue and the floor of the mouth account for more than 90% of cases that show dysplasia or carcinoma.  By far the most affected oral sites are the commissures(60- 90%)  Early lesion appears as a slightly elevated greyish-white plaque that may be well defined or may gradually blend into the surrounding normal mucosa.  As the lesion progresses, it becomes thicker and whiter, sometimes developing a leathery appearance with surface fissures and show evidence of loss of elasticity and flexibility.  Subtypes  “Homogeneous leukoplakia”= defined as a predominantly white lesion of uniform flat and thin appearance that may exhibit shallow cracks and that has a smooth, wrinkled or corrugated surface with a consistent texture throughout  Nodular (speckled) leukoplakia= white patches on erythematous base, high malignant transformation, 60 % superimposed candidal infection (Candida leukoplakia)  Verrucous leukoplakia or “verruciform leukoplakia” red and white but the white is much more thicker and covered by multiple papillary projections and heavily keratinized  Viadent hyperkeratosis “Sanguinaria- induced leukoplakia ” associated with use of oral rinse contains extract from blood root plant (sanguinaria), localized sharply demarcated white velvety wrinkled or corrugated patch involving attached gingiva and vestibule.  In general, nonhomogenous leukoplakia has a higher malignant transformation risk, but oral carcinoma can develop from any leukoplakia. Homogenous leukoplakia on the alveolar ridge and buccal mucosa. Keratotic white patch in the labial vestibule Commissural leukoplakia. Homogenous leukoplakia on the buccal mucosa  Investigations  Toluidine blue staining: Toluidine blue clinically stains malignant lesions, but not normal mucosa. Toluidine blue staining uses a 1% aqueous solution of the dye that is decolourized with 1% acetic acid. The dye binds to dysplastic and malignant epithelial cells with a high degree of accuracy Toluidine blue and  Cytobrush technique: This technique is more accurate than any other cytological technique used in the oral cavity. The cytobrush technique uses a brush with firm bristles that obtains individual cells from the full thickness of the epithelium.  Biopsy: Incisional/excisional Histopathologic Features 1. Benign form: there may be various combinations of hyperkeratosis, hyperparakeratosis and acanthosis and the basal cell layer is always intact. There is diffused chronic inflammatory cell infiltration into the underlying connective tissue.  Histopathologic Features  2. Epithelial dysplasia: the diagnosis is made when less than the complete thickness of the epithelium demonstrates the characteristic features of dysplasia, this includes the presence of:  Mitosis is increased and abnormal  Individual cell keratinization  Alteration in the nuclear cytoplamic ratio  Loss of polarity and disorientation of the cells  Hyperchromatism  Large prominent nucleoli  Basiar hyperplasia  Division of nucleus without division of cytoplasm Carcinoma in situ & Carcinoma  Carcinoma in situ: the epithelium demonstrates dyplasia throughout its full thickness (from top to bottom), but the basement membrane is intact,  Carcinoma: a loss of basement membrane and invasion of the underlying tissue.  Markers of proliferation in leukoplakia:  These are markers for determining future cancer development in oral premalignant lesions.  genomic markers: include DNA aneuploidy, loss of heterozygosity and changes in the expression of oncogenes and tumour suppressor genes (p53)  proliferative markers: include keratins and carbohydrate antigens. leukoplakia  Case: This patient presents with white patches on the buccal mucosa with loss of flexibility in a heavy smoker 1. What is the clinical diagnosis? 2. How to manage this case? Case Patient discovered lesion in front of a long standing broken down tooth in a heavy smoker. 1) What is your diagnosis ? 2) what are types of this lesions? exam I  ORAL LICHEN PLANUS  The word lichen planus is derived from the Greek literature; lichen means ‘tree moss’ and planus refers to ‘flat’.  Wickham (1895) described the characteristic appearance of whitish striae and punctuations that develop atop the flat-surfaced papules.  Oral lichen planus (OLP) is a common chronic immunologic inflammatory mucocutaneous disorder that varies in appearance from keratotic (reticular or plaquelike) to erythematous and ulcerative. The exact aetiology is still unknown. ❑ The most accepted and current data suggest that OLP is a T-cell-mediated disorder in which there is production of cytokines which leads to apoptosis. Autocytotoxic CD8 and T cells trigger apoptosis of oral epithelial cells (basal cell damage). The immune system is triggered because of the interactions among genetic, environmental and lifestyle factors. ❑ Another possible theory includes the genetic background, there is weak association between HLA antigen and LP. ❑ There is strong association of psychological factors such as higher level of anxiety, greater depression and psychic disorders in patients suffering from erosive LP.rapid appearance of the lesions 7-10 days after an incident of intense emotional stress. ❑ Lichnoid reaction: drug induced( Gold therapy, nonsteroidal anti- inflammatory drugs (NSAIDs), diuretics other anti-hypertensives, and oral hypoglycemic agents of the sulfonylurea type) or graft versus host disease (It is an immunologically mediated reaction where lymphocytes in the donor graft mount an immunological response against the recipient keratinocytes).  Associated with systemic diseases (Grinspan’s syndrome= LP+HYPERTENTION+DM+HCV)  Clinical Features  Age of onset: 40-70  There is definite female predilection with ratio of 2:1.  40% occur on both oral and cutaneous surfaces, 35% occur on cutaneous surfaces alone and 25% occur on oral mucosa alone.  The characteristic manifestation is the appearance of white papules that usually coalesce forming a network of lines that may intersect or crisscross each other forming various patterns.  Louis Frederic Wickham described the presence of fine, white or grey lines or dots seen on the top of the pruritic papular rash on the skin in LP (Wickham’s striae).  Skin lesions are characteristically itchy and violaceous to brown flat-topped polygonal macules or papules, very frequently distributed over the flexor aspect of the wrist or ankles, extensor aspect of the lower legs, genitals  Wrists and palms of the hands may be the only sites involved.  Nail changes.  Koebner’s phenomenon  Koebner’s phenomena  Linear lesions result from trauma or scratching “Koebner phenomenon”. Heinrich Köbner  Oral manifestations  The basic lesion of OLP is papule arranged in the linear or annular forms and crisscrossing each other forming various patterns such as annular and reticular forms.  OLP may occur at any oral mucosal site but the buccal mucosa is the most common site followed by tongue and gingiva.  OLP may be associated with pain or discomfort, which interferes with function and with quality of life.  Lesions are bilateral and characterized by remission and exacerbation. Lesions do not disappear on stretching, cannot be rubbed off, do not cause loss of flexibility of the oral mucosa.  Lesions are surrounded by a network of bluish white lines called Wickham’s striae radiating from the periphery of the lesion. louis frédéric wickham  Types of lichen planus  OLP is classified as reticular, papular, hypertrophic (plaque like), atrophic, erosive, bulous  Oral Lichen Planus Histopathological findings: Epithelium: **Liquefaction degeneration of the basal cells.  Hyper-keratosis, acanthosis, and elongated retepegs showing “saw teeth” appearance (Papular type).  Sub-epithelial cleft of epithelium from the C.T (Bullous-erosive type).  Thin epithelium with little surface keratinization and absence of retepegs (atrophic type). Histopathological findings of Oral Lichen Planus Connective tissue:  Dense sub-epithelial band of T-lymphocytes.  Isolated degenerated epithelial cells (Civatte bodies), are often scattered within the epithelium and superficial C.T.  Civatte bodies will be phagocytosed by macrophages or coated with IgM (Colloid bodies). Direct immuno-fluorescent studies  Characteristic but not diagnostic  Shaggy band of fibrin deposits along the basement membrane zone in 90-100 % of cases.  IgM stained cytoid bodies in dermis along the dermo- epidermal junction 97% of cases. CASE A 50 year old female patient presented to the clinic with severe pain , a white and red lesion was observed related to buccal mucosa bilaterally. Patient complains of itching skin lesions. 1) What is the diagnosis?  A 50 year old female patient presented to the clinic with severe pain , a white and red lesion was observed related to buccal mucosa bilaterally. Patient complains of itching skin lesions. 1) What is the diagnosis? 2) What is the name of gingiva?  ORAL HAIRY LEUKOPLAKIA  Oral hairy leukoplakia is a corrugated white lesion that usually occurs on the lateral or ventral surfaces of the tongue in patients with severe immunodeficiency.  The most common disease associated with oral hairy leukoplakia is HIV infection.  Epstein-Barr virus (EBV) is implicated as the causative agent in oral hairy leukoplakia.  Oral hairy leukoplakia may present as a plaque-like lesion and is often bilateral.  Diagnosis  The definitive diagnosis can be established by demonstrating the presence of EBV electron microscopy, or polymerase chain reaction (PCR). Choose:  In AIDS, hairy Leukoplakia is found in which location A. Hard palate B. Buccal mucosa C. Lateral border of tongue D. Soft palate Choose:  Which one of the following diseases has been associated with Epstein-Barr virus: A. Lichen planus B. Angular chilitis C. Oral hairy leukoplakia D. Leukoedema