مواضيع المحاضرة: white and red lesions

audioplayaudiobaraudiotime

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WHITE AND RED LESIONS

lesions of the oral mucosa, which are white results from a thickened layer of keratin epithelial hyperplasia intracellular epithelial edema reduced vascularity of subjacent connective tissue
White Lesions


white or yellow lesions may also be due to fibrous exudate covering an: ulcer submucosal deposit surface debris fungal colonies
White Lesions


(1) Leukoedema (2) Leukoplakia (3) Lichen Planus (4) Candidiasis (5) White Sponge Nevus (6) Nicotine Stomatitis
White Lesions


(7) Geographic Tongue (8) Hairy Tongue (9) Dental Lamina Cyst (10) Fordyce’s Disease (11) Perleche White Lesions


generalized opacification of buccal mucosa that is regarded as a variation of normal can be identified in majority of population
(1) Leukoedema



Etiology & Pathogenesis to date, cause has not been established smoking chewing tobacco none alcoholo ingestion are bacterial infection proven cause
(1) Leukoedema


Clinical Features usual discovered as incidental finding asymptomatic symmetrically distributed in buccal mucosa
(1) Leukoedema


Clinical Features appear as gray-white, diffuse, filmy or milky surface more exaggerated cases, whitish cast with surface textural changes wrinkling or corrugations
(1) Leukoedema


Clinical Features with stretching of buccal mucosa, opaque changes dissipate more apparent in non-whites, especially African-American
(1) Leukoedema


Treatment NO treatment is necessary since there is no malignant potential if there is any doubt about diagnosis, a biopsy can be performed
(1) Leukoedema



also known as Leukokeratosis; Erythroplakia Leuko= white Plakia = patch defined by World Health Organization (WHO) as a white patch or plaque that cannot be characterized clinically or pathologically as any other disease
(2) Leukoplakia


clinical term indicating a white patch or plaque of oral mucosa cannot be rubbed off cannot be characterized clinically as any other disease biopsy is mandatory to establish a definitive diagnosis
Leukoplakia
(2) Leukoplakia


Mild or Thin Leukoplakia Homogenous or Thick Leukoplakia Granular or Nodular Leukoplakia Verrucous or Verruciform Leukoplakia

(2) Leukoplakia

Proliferative Verrucous Leukoplakia (PVL) Erythroleukoplakia or Speckled Leukoplakia

(2) Leukoplakia

(2) Leukoplakia



Mild or Thin Leukoplakia seldom shows dysplasia on biopsy may disappear or continue unchanged
(2) Leukoplakia


Homogenous or Thick Leukoplakia for tobacco smokers who do not reduce their habit 2/3 of such lesions slowly extend laterally, become thicker + acquire distinctly white appearance
(2) Leukoplakia


Homogenous or Thick Leukoplakia affected mucosa may become leathery to palpation fissures may deepen become more numerous most thick, smooth lesions remain indefinitely at this stage
(2) Leukoplakia

Homogenous or Thick Leukoplakia some, perhaps as many as 1/3, regress or disappear

(2) Leukoplakia


Granular or Nodular Leukoplakia few become even more severe develop increased surface irregularities
(2) Leukoplakia


Verrucous or Verruciform Leukoplakia lesions that demonstrate sharp or blunt projections
(2) Leukoplakia



Proliferative Verrucous Leukoplakia (PVL) high risk form of leukoplakia development of multiple keratotic plaques with roughened surface projections
(2) Leukoplakia


Proliferative Verrucous Leukoplakia (PVL) tend to slowly spread involve additional oral mucosal sites gingiva is frequently involved although other sites may be affected as well
(2) Leukoplakia


Proliferative Verrucous Leukoplakia (PVL) as lesions progress, there may go through a stage indistinguishable transform into full-fledged squamous cell carcinoma (usually within 8 years of initial PVL diagnosis)
(2) Leukoplakia


Proliferative Verrucous Leukoplakia (PVL) lesions rarely regress despite therapy strong female predilection minimal association with tobacco use
(2) Leukoplakia


Erythroplakia leukoplakia may become dysplastic even invasive, with no change in its clinical appearance however, some lesions eventually demonstrate scattered patches of redness called erythroplakia
(2) Leukoplakia



Erythroleukoplakia or Speckled Leukoplakia such areas usually represent sites in which epithelial cells are so immature or atrophic that they can no longer produce keratin

(2) Leukoplakia

Erythroleukoplakia or Speckled Leukoplakia intermixed red-and-white lesion pattern of leukoplakia that frequently reveals advanced dysplasia on biopsy
(2) Leukoplakia


Etiology & Prognosis many cases are etiologically related to use of tobacco in smoked or smokeless forms and may regress after discontinuation of tobacco use
(2) Leukoplakia


Etiology & Prognosis other factors, such as alcohol abuse may have trauma a role in C. albicans infection etiology
(2) Leukoplakia


Etiology & Prognosis nutritional factors have been cited as important, especially iron deficiency anemia
(2) Leukoplakia



Clinical Features associated with middle-aged + older population vast majority of cases occur after age of 40 years
(2) Leukoplakia

Site of Occurence Vestibule Buccal Palate Alveolar Ridge Lip Tongue Floor

(2) Leukoplakia


leukoplakia of lips + tongue also exhibits relative high percentage of dysplastic or neoplastic change
(2) Leukoplakia


Treatment & Prognosis absence of dysplastic or atypical epithelial changes periodic examinations + rebiopsy of new suspicious areas are recommended
(2) Leukoplakia


Treatment & Prognosis if diagnosis as moderate to severe dysplasia excision is obligatory for large lesions, grafting procedures may be necessary after surgery may recur after complete removal
(2) Leukoplakia


chronic mucocutaneous disease of unknown cause relatively common typically presents as bilateral white lesions occasionally with associated ulcers
(3) Lichen Planus



Pathogenesis although cause is unknown generally considered to be a immunologically mediated process resembles hypersensitivity reaction
(3) Lichen Planus


Clinical Features disease of middle age affects men + women in nearly equal numbers children rarely affected
(3) Lichen Planus


Clinical Features Types: Reticular Erosive (ulcerative) Plaque Papular Erythematous (atrophic)
(3) Lichen Planus


Clinical Features Reticular Form most common type numerous interlacing white keratotic lines or striae (Wickham’s striae) produces anular or lacy pattern (3) Lichen Planus


Clinical Features Reticular Form buccal mucosa is the site most commonly involved may also be noted on: tongue gingiva – less common lips (3) Lichen Planus


Clinical Features Plaque Form resembles leukoplakia but has multifocal distribution range from slightly elevated to smooth and flat
(3) Lichen Planus

Clinical Features Plaque Form primary sites are dorsum of tongue buccal mucosa

(3) Lichen Planus


Clinical Features Erythematous Form red patches with very fine white striae attached gingiva commonly involved
(3) Lichen Planus


Clinical Features Erythematous Form patchy distribution often in four quadrants patient may complain of burning sensitivity generalized discomfort
(3) Lichen Planus


Clinical Features Erosive Form central area of lesion is ulcerated fibrinous plaque or pseudomembrane covers ulcer changing patterns of involvement from week to week
(3) Lichen Planus


Treatment although it cannot be generally cured some drugs can provide satisfactory control corticosteroids are the single most useful group of drugs in the management of lichen planus
(3) Lichen Planus



Treatment corticosteroid ability to modulate inflammation + immune response
(3) Lichen Planus


Treatment topical application + local injection of steroids have been used successfully in controlling but not curing this disease
(3) Lichen Planus


common oppurtunistic oral mycotic infection develops in the presence of one of several predisposing factors immunodeficiency endocrine disturbances hypoparathyroidism diabetes mellitus poor oral hygiene xerostomia
(4) Candidiasis


caused by Candida albicans infection with this organism is usually superficial, affecting the outer aspects of involved oral mucosa or skin
(4) Candidiasis

in severely debilitated + immunocompromised patients such as patients with AIDS infection may extend into alimentary tract (candidal esophagitis bronchopulmonary tract and other organ system
(4) Candidiasis

Clinical Features most common form is acute pseudomembranous also known, as thrush young infants + elderly are commonly affected
(4) Candidiasis


Clinical Features oral lesion of acute candidiasis (thrush) white soft plaques that sometime grow centrifugally + merge wiping plaques with gauze sponge leaves a painful, eroded, eryhtematous or ulcerated surface
(4) Candidiasis

Clinical Features Chronic Erythematous Candidiasis commonly seen on geriatric individuals who wear complete maxillary denture
(4) Candidiasis

Clinical Features Chronic Erythematous Candidiasis distinct predilection for palatal mucosa as compared with mandibular alveolar arch
(4) Candidiasis

Clinical Features Chronic Erythematous Candidiasis chronic low-grade resulting from poor prosthesis fit failure to remove appliance at night
(4) Candidiasis

Clinical Features Chronic Erythematous Candidiasis bright red relative little keratinization
(4) Candidiasis

Treatment majority of infections may be simply treated with topical applications of nystatin suspension nystatin cream or ointment often effective when applied directly to denture-bearing surface itself
(4) Candidiasis

Treatment topical applications of either nystatin or clotrimazole should be continued for at least 1 week beyond disappearance of clinical manifestations of disease
(4) Candidiasis


Treatment Hyperplastic Candidiasis topical + systemic antifungal agents may not be effective at completely removing lesions surgical management may be necessary
(4) Candidiasis

Treatment Chronic Mucocutaneous Candidiasis associated with immunosuppression topical agents may not be effective
(4) Candidiasis

Treatment Chronic Mucocutaneous Candidiasis associated with immunosuppression systemic administration of medications: Ketoconazole Fluconazole Itraconazole
(4) Candidiasis

autosomal-dominant condition due to point mutations for genes coding for keratin . affects oral mucosa bilaterally NO treatment is required
(5) White Sponge Nevus

Clinical Features asymptomatic folded white lesions may affect several mucosal sites lesions tend to be thickened + spongy consitency
(5) White Sponge Nevus

Clinical Features presentation intraorally is almost always bilateral + symmetric usually appears early in life, typically before puberty
(5) White Sponge Nevus

Clinical Features usually observed in buccal mucosa tongue + vestibular mucosa may be involved

(5) White Sponge Nevus


Treatment NO treatment necessary since it is asymptomatic + benign

(5) White Sponge Nevus

common tobacco-related form of keratosis typically associated with pipe + cigar smoking with positive correlation between intensity of smoking + severity of condition
(6) Nicotine Stomatitis

combination of tobacco carcinogens + heat is markedly intensified in reverse smoking (lit end positioned inside the mouth) adding a significant risk for malignant conversion
(6) Nicotine Stomatitis

Clinical Features palatal mucosa initially responds with an erythematous change follwed by keratinization

(6) Nicotine Stomatitis

Clinical Features subsequent to opacification or keratinization of palate red dots surrounded by white keratotic rings appear dot represent inflammation of salivary gland excretory duct

(6) Nicotine Stomatitis

Treatment condition rarely evolves into malignancy except in individuals who reverse smoke discontinuation of tobacco habit
(6) Nicotine Stomatitis


also known as erythema migrans, benign migratory glossitis prevalent among whites + blacks strongly associated with fissure tongue inversely associated with cigarette smoking
(7) Geographic Tongue

emotional stress may enhance the process

(7) Geographic Tongue

Clinical Features affects women slightly more than men children occasionally may be affected characterized initially by presence of atrophic patches surrounded by elevated keratotic margins

(7) Geographic Tongue

Clinical Features desquamated areas appear red + may be slightly tender. appearing to move across dorsum of tongue
(7) Geographic Tongue

Clinical Features most patients are asymptomatic occasionally patients complain of irritation or tenderness especially in relation to consumption of spicy foods + alcoholic beverages
(7) Geographic Tongue

Clinical Features lesions periodically disappear recur for no apparent reason

(7) Geographic Tongue

Treatment NO treatment is required because of self-limiting + usually asymptomatic nature of this condition
(7) Geographic Tongue


Treatment when symptoms occur, topical steroids especially ones containing antifungal agent helpful in reducing symptoms
(7) Geographic Tongue

Treatment mouth clean using mouthrinse composed of sodium bicarbonate in water reassure patients that condition is totally benign

(7) Geographic Tongue

clinical term referring to a condition of filiform papillae overgrowth on dorsal surface of tongue there are numerous initiating or predisposing factors for hairy tongue
(8) Hairy Tongue

broad spectrum antibiotics such as penicillin + systemic cortiocosteroids are often identified in clinical history of patients with this condition
(8) Hairy Tongue

oxygenating mouthrinses containing: hydrogen peroxide sodium perborate carbamide peroxide have been cited as possible etiologic agents
(8) Hairy Tongue

Clinical Features clinical alteration translates to hyperplasia of filiform papillae; result is thick serves to trap matted surface bacteria, fungi, foreign materials
(8) Hairy Tongue

Clinical Features extensive elongation of papillae occurs, gagging may be tickiling sensation felt
(8) Hairy Tongue


Clinical Features color may range from white to tan to deep brown depending on: diet oral hygiene composition of bacteria inhabiting papillary surface
(8) Hairy Tongue

Treatment brush/scrape tongue with baking soda maintain good oral hygiene emphasize to patients that this process is entirely benign
(8) Hairy Tongue

Treatment self-limiting tongue should return to normal after institution of physical debridement + proper oral hygiene
(8) Hairy Tongue


also known as Gingival Cyst of New Born or Bohn’s nodules appear as multiple nodules along alveolar ridge in neonates (9) Dental Lamina Cyst


similar epithelial inclusion cysts may occur along midline of palate (palatine cyst of new born or Epstein’s pearls) developmental origin derived from epithelium included in fusion line between palatal shelves + nasal processes no treatment; resolve spontaneously (9) Dental Lamina Cyst

Treatment not necessary because nearly all spontaneously rupture before patient is 3 months of age
(9) Dental Lamina Cyst

represents ectopic sebaceous glands or sebaceous choristomas normal tissue in abnormal location regarded as developmental considered a variation of normal
(10) Fordyce’s Granules


multiple often seen in aggregates sites of predilection include buccal mucosa vermillion of upper lip
(10) Fordyce’s Granules

lesions generally are symmetrical distributed tend to become obvious after puberty maximal expression occurring between 20-30 years of age
(10) Fordyce’s Granules

lesions are asymptomatic discovered during routine oral examination

(10) Fordyce’s Granules

Treatment No treatment is indicated glands are normal in character do not cause any untoward effects
(10) Fordyce’s Granules

also known as Angular Cheilitis inflammation + atrophy of skin of folds at angles of mouth
(11) Perleche

may be due to: excessive lip licking sagging of facial skin in edentulous or elderly persons
(11) Perleche

may be due to: prolonged contact with saliva results in maceration

with possible secondary infection by Candida or staphylococci
(11) Perleche


Clinical Features skin at angles of mouth has erythematous fissures often with exudate + crust further licking to moisten inflamed area exacerbates the problem
(11) Perleche

Treatment applying antimicrobial creams followed by low-potency steroid creams until symptoms resolve protective lip balm may help prevent recurrence
(11) Perleche





رفعت المحاضرة من قبل: Sayf Asaad Saeed
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