Oral White Lesions Overview PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6473409/ Overview of the Oral Mucosa Normal Mucosa: Hyperkaratosis: Generally, white lesions of the oral mucosa result from: 1. Thickened layer of keratin - induced by local frictional irritation, immunolo...

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6473409/ Overview of the Oral Mucosa Normal Mucosa: Hyperkaratosis: Generally, white lesions of the oral mucosa result from: 1. Thickened layer of keratin - induced by local frictional irritation, immunologic reactions, or more crucial processes such as premalignant or malignant transformation 2. Epithelial hyperplasia 3. Reduced vascularity of underlying tissue 4. intracellular epithelial edema Oral White Lesions These lesions represent a wide spectrum of lesions with different etiology and various prognoses. The diagnosis of white lesions varies from benign reactive lesions to more serious dysplastic and carcinomatous lesions. Although white lesions constitute only 5% of oral pathoses, some of these lesions such as leukoplakia, lichen planus, and proliferative verrucous leukoplakia have malignant potential as high as 0.5–100%. Therefore, white lesions mandate an appropriate clinical diagnostic approach to exclude the possibility of malignancy. Accordingly, when a clinician confronts a white area on the oral mucosa, the first issue to be clarified is whether it can be scraped off by means of a piece of gauze or not. If so, a superficial non-keratotic layer such as pseudomembranes, most commonly caused by fungal infections or caustic chemicals, should be suspected. In the next step, any specific clinical pattern of white lesions such as papular, annular, reticular or erosive-ulcerative patterns, or a combination of them (characteristic for lichenoid lesions) should be inspected in order to differentiate white patterned lesions from non-patterned ones. Clinical steps to approach oral white lesions: 1. Determine whether the lesion is congenital or acquired; 2. Inspect if it can be wiped off or not and if it has a special pattern or not. I. HEREDITARY / CONGENITAL LESIONS 1. Leukoedema - a common normal variation of the oral mucosa. a generalized mild opacification of the buccal mucosa that is common and regarded as a normal variation of the oral mucosa The prevalence has been reported up to 90% among blacks and between 10–50% in whites, with no sex predilection. Higher prevalence among blacks is possibly due to more mucosal pigmentation making this condition more apparent. It is more distinct in smokers; however, after smoking cessation, it becomes less obvious. Clinically it presents as a diffuse, gray to white, non-scrapable and veil-like condition, which can be described as a filmy or milky and opalescent transformation of the oral mucosa. In more prominent cases, leukoedema is characterized by mucosal folds or wrinkled surface with whitish streaks. This condition usually disappears temporarily after gentle stretching of the mucosa, which reappears after quitting the manipulation. Leukoedema often involves the buccal mucosa and sometimes the lateral borders of the tongue bilaterally. Differential Diagnosis White sponge nevus, the response to chronic cheek biting, and lichen planus all may show clinical similarities to leukoedema. 2. White Sponge Nevus - (WSN), also called Cannon disease or familial white folded dysplasia, An inherited autosomal dominant disorder that is defined as dyskeratotic hyperplasia of mucous membranes. Mutations in keratin result in lack of normal keratinization WSN is a rare condition with no sex predilection. The lesions generally present at birth or early in childhood, but sometimes the condition appears during adolescence. Intraoral lesions are symmetrical, thickened, white, corrugated or velvety, diffuse, spongy plaques of variable sizes with an elevated, irregular, and fissural surface. Lesions tend to be thickened and have a spongy consistency. Buccal mucosa is affected bilaterally in most patients. Other areas of the oral cavity such as the ventral surface of the tongue, labial mucosa, soft palate, alveolar mucosa, and floor of the mouth can also be affected. White sponge nevus can cause dysphagia when the esophagus is involved; otherwise, the lesions are asymptomatic. No treatment is necessary for this condition because it is asymptomatic and benign. Wrinkling of the surface does not disappear when the mucosa is stretched. II. REACTIVE LESIONS 1. Nicotine Stomatitis – Pipe Smoker’s Stomatitis Nicotine stomatitis is a common tobacco-related form of keratosis. It is typically associated with pipe and cigar smoking, with a positive correlation between intensity of smoking and severity of the condition. Smoking has direct effect on the oral mucosa. Removable prosthesis, protects the mucosa beneath the appliance from hyperkeratosis. The combination of tobacco carcinogens and heat is markedly intensified in reverse smoking (lit end positioned inside the mouth), adding significant risk for malignant transformation Pathogenesis The palatal mucosa initially responds with an erythematous change followed by keratinization. Subsequent to opacification or keratinization of the palate, red dots surrounded by white keratotic rings appear. The dots represent inflammation surrounding the minor salivary gland excretory ducts. Responds rapidly to abstinence from pipe smoking. Treatment and Prognosis This condition rarely evolves into malignancy, except in individuals who reverse smoke. Although the risk of carcinoma development in the palate is minimal, nicotine stomatitis is a marker or indicator of intense tobacco use and hence may indicate increased risk of epithelial dysplasia and neoplasia. 2. White Hairy Tongue Etiology and Pathogenesis Represents an opportunistic infection that is related to the presence of Epstein-Barr virus (EBV) and is found mainly in human immunodeficiency virus (HIV)–infected individuals. In a small percentage of cases, hairy leukoplakia may be seen in patients with other forms of immunosuppression, particularly those associated with organ transplantation (medically-induced immunosuppression), hematologic malignancy, and long-term use of systemic or topical corticosteroids. The prevalence of hairy leukoplakia in HIV-infected patients has been declining as a result of new chemotherapeutic regimens for HIV. An overgrowth of the filliform papilla results from retardation of the normal rate of desquamation. Clinical Features § An overgrowth of the filliform papilla results from retardation of the normal rate of desquamation. § Hairy leukoplakia presents as a well-demarcated white lesion that varies in architecture from a flat and plaquelike to a papillary/filiform, or a corrugated lesion. It causes white patches on the tongue. § It may be unilateral or bilateral. Commonly located along the lateral margins of the tongue, with occasional extension onto the dorsal surface. § Tongue has matted surface that serves to trap bacteria and foreign material. § When extensive elongation of the papilla occurs, gagging or a tingling sensation may be felt. § Color may range from white to tan to deep brown or black depending on the diet, oral hygiene and the composition of the bacteria. III. OTHER WHITE LESIONS 1. Geographic Tongue - Erythema Migrans and Benign Migratory Glossitis A condition of unknown cause. Geographic tongue is more prevalent among whites and blacks and is strongly associated with fissured tongue. In a few patients, emotional stress may enhance the process. Clinical Features Characterized initially by the presence of atrophic patches surrounded by elevated keratotic margins. Multiple, well-demarcated, erythematous, depapillated patches, typically surrounded by a slightly elevated whitish border. The desquamated areas appear red and may be slightly tender. Usually restricted to the dorsum of the tongue. After a few days or weeks, the pattern changes, appearing to move across the dorsum of the tongue. Lesions periodically disappear and recur for no apparent reason. Lesions persist for a short time in one area, then disappear completely and reappear in another area. Although most patients with geographic tongue are asymptomatic, patients occasionally report irritation or tenderness, especially in relation to the consumption of spicy foods and alcoholic beverages. It often coexists with fissured tongue. 2. Oral Lichen Planus (OLP) A common chronic mucocutaneous disease of the skin and mucosa with unknown etiology. Oral lichen planus commonly arises after middle age with a mean age of 55 years. Women are affected more frequently than men. Although the etiology is multifactorial, imbalanced immune system plays a principal role in the evolution of this disease. Other factors such as stress have also been noticed in the development of this inflammatory process. Oral lichen planus has various clinical manifestations: § Papular form - found in the primary phase of the disease § Reticular form – most common form - small white papules are usually combined together to form the reticular pattern; - has interlacing fine white keratotic lines or striae known as Wickham’s striae, which may form a lace-like or annular (circular) pattern § Plaque-like form - tends to resemble leukoplakia clinically but has a multifocal distribution. - slightly elevated to smooth and flat plaque - appears as a homogeneous well-demarcated white plaque with peripheral striae § Ulcerative-Erosive form - the central area of the lesion is ulcerated and covered with a fibrinous plaque or pseudomembrane - changing patterns of involvement is noted from week to week. - careful examination usually demonstrates keratotic striae peripheral to the site of erosion, along with erythema. § Erythematous or atrophic form - appears as red patches with very fine white striae. - The attached gingiva is commonly involved in this form of lichen planus - exhibits a patchy distribution, often in four quadrants - Patients may complain of burning, sensitivity, and generalized discomfort. § Bullous form - a rarely encountered form of lichen planus - bullae range from a few millimeters to centimeters in diameter that are generally short lived and, on rupturing, leave a painful ulcer. Papular form Reticular form Plaque-like form Ulcerative-Erosive form Erythematous/Atrophic Bullous form IV. NON-EPITHELIAL WHITE-YELLOW LESIONS 1. Candidiasis Candidiasis is a common opportunistic oral mycotic infection that develops in the presence of one of several predisposing conditions. Clinical presentation is variable and is dependent on whether the condition is acute or chronic. Etiology and Pathogenesis Candidiasis is caused by C. albicans and much less commonly by other species of Candida. Infection with this organism is usually superficial, affecting the outer aspects of the involved oral mucosa or skin. Clinical Features The most common clinical type of candidiasis is the acute pseudomembranous form, also known as thrush. Young infants and the elderly are commonly affected. This infection is common in patients being treated with radiation or chemotherapy for leukemia and solid tumors. § Oral lesions are characteristically white, soft plaques that sometimes grow centrifugally and merge. It presents as creamy white plaques, patches, or papules that can be wiped off with an erythematous and sometimes bleeding area leaving behind. The classic appearance of pseudomembranous candidiasis is called “curdled milk”. § Plaques are composed of fungal organisms, keratotic debris, inflammatory cells, desquamated epithelial cells, bacteria, and fibrin. § Wiping away the plaques or pseudomembranes with a gauze sponge leaves a painful erythematous, eroded, or ulcerated surface. § Although lesions of thrush may develop at any location, favored sites include the buccal mucosa and mucobuccal folds, the oropharynx, and the lateral aspects of the tongue. § In most instances in which the pseudomembrane has not been disturbed, associated symptoms are minimal. In severe cases, patients may complain of tenderness, burning, and dysphagia. Chronic erythematous candidiasis is a commonly seen form, occurring in as many as 65% of geriatric individuals who wear complete maxillary dentures (denture sore mouth). Differential Diagnosis Candidal white lesions should be differentiated from slough associated with chemical burns, traumatic ulcerations, mucous patches of syphilis, and white keratotic lesions. Red lesions of candidiasis should be differentiated from drug reactions, and erosive lichen planus. Treatment and Prognosis Elimination of predisposing factors, if possible, is the cornerstone of treatment along with antifungal regimen. The majority of infections may be treated simply with topical applications of nystatin suspension 2. Fordyce Granules Fordyce’s granules represent ectopic sebaceous glands or sebaceous choristomas (normal tissue in an abnormal location). This condition is regarded as developmental and can be considered a variation of normal. Fordyce’s granules are multiple and often are seen in aggregates or in confluent arrangements Sites of predilection include the buccal mucosa and the vermilion of the upper lip. Lesions generally are symmetrically distributed and tend to become obvious after puberty, with maximal expression occurring between 20 and 30 years of age. Lesions are asymptomatic and often are discovered incidentally by the patient or by the practitioner during a routine oral examination. Microscopically, lobules of sebaceous glands are aggregated around or adjacent to excretory ducts. No treatment is indicated for this particular condition because the glands are normal in character and do not cause any untoward effects. 3. Gingival Cysts Gingival cysts of odontogenic origin occur in adults, as well as in infants (Bohn’s nodules). In infants, relative frequency is greatest in the neonatal phase. They occur along the alveolar ridges and involute spontaneously or rupture and exfoliate. Another eponym, Epstein’s pearls, has been commonly used to designate nonodontogenic neonatal cysts that occur along the palatal midline (fusion of palatine shelves) Etiology and Pathogenesis Neonatal gingival cysts are thought to arise from dental lamina remnants. Fetal tissues between 10 and 12 weeks of age show small amounts of keratin within elements of the dental lamina. Toward the end of the 12th week of gestation, disruption of the dental lamina is evident, with many fragments exhibiting central cystification and keratin accumulation. Midline palatal cysts, or Epstein’s pearls, are thought to result from epithelial entrapment within the midline of palatal fusion. Small epithelial inclusions within the line of fusion produce microcysts that contain keratin and rupture early in life. Clinical Features Gingival cysts in a neonate appear as off-white colored nodules approximately 2 mm in diameter. Cysts ranging in number from one to many are evident along the alveolar crests. Midline palatal cysts, on the other hand, present along the midpalatal raphe toward the junction of the hard palate and the soft palate.