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Home , Erythroplakia, Leukoedema, Pemphigus, White sponge nevus

Dr. Prerana OROPHARYNGEAL NON SCRAPABLE WHITE LESIONS- A DIAGNOSTIC DILEMMA

Dr. Prerana V. Waghmare1, Dr. Deepa L. Raut2.

Post graduate student1, Prof. and HOD2. Department of and Radiology, Saraswati Dhanwantari Dental College & Hospital & Post Graduate Research Institute, Parbhani, Maharashtra, India.

ABSTRACT- White lesions of the oral cavity are commonly encountered in routine clinical dental practice. Common white lesions may cause diagnostic dilemma. White lesions are usually focal, multifocal, striated or diffuse. Diagnosis of these lesions is extremely important, as some of these lesions may represent early stages of malignancies. Clinical diagnostic skills and good judgment forms the key to successful diagnosis and management of white lesions of the oral cavity. This review article lists the non scrapable white lesions affecting or pharyngeal mucosa ranging from normal variants of to those which are malignant; it also highlights the specific features of each of these lesions.

KEY WORDS- Potentially malignant disorders, Non scrapable lesions, White lesions, malignant transformation.

INTRODUCTION- are very few epidemiological studies on oral mucosal lesions and in particular white White lesions of the oral cavity are most lesions. Few prevalence related studies have commonly seen by dental professionals in day been done on potentially malignant conditions, to day dental practice. It includes some rarely correlating their clinic pathologic physiological variations, systemic conditions, correlation [3, 4]. , malignancies and other lesions. The importance of early diagnosis of these COMMON NON-SCRAPABLE WHITE will lesions help in preventing its LESIONS complications. White lesions of the oral mucosa obtain their characteristic appearance 1. LINEA ALBA- because of a thickened layer of The linea Alba (Latin for white line), is a (), superficial debris on oral horizontal streak on the buccal mucosa at the mucosa, blanching caused by reduced level of occlusal plane. It usually extends from vascularity and loss of pigmentation due to [5] [1] the commissure to the posterior teeth. It acquired causes . The treatment ranges from is a common finding and most likely reassurance by the clinician to management of associated with pressure, frictional irritation, potentially malignant disorders. or trauma from the facial surfaces of the teeth. The consensus views of the Working It may be found in individuals who chew Group are presented here. The term, tobacco, and may be mistaken for a lesion potentially malignant disorders, was [5] requiring treatment. recommended to refer to precancer as it conveys that not all disorders described under CLINICAL MANIFESTATIONS [5]- this term may transform into [2]. White lesions are seen in the oral  The linea alba is usually present bilaterally cavity and are mainly found as an incidental  It is restricted to dentulous areas finding on routine examination. They may be benign, potentially malignant in nature. Review of the literature has shown that there

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 10  It presents an asymptomatic, linear irritants such as spices, oral debris or tobacco elevation, with a whitish colour, at the [8]. level of the occlusal line of the teeth CLINICAL MANIFESTATIONS- TREATMENT [5]- There is a diffuse, gray-white, milky Treatment is not required. opalescent appearance of the mucosa which usually occurs bilaterally on the buccal mucosa. Less often, the labial mucosa, the or the floor of may be affected. The surface of the area is folded, creating a wrinkled, white streaked lesion.[7] usually start to appear around age 2 to 5; however, it is not often noticeable until adulthood. [8] Clinically Leukoedema presents as asymptomatic, folds or white lines crisscross the affected area. The buccal F Fig.1 White keratotic linear line at occlusal level. mucosa is the most common site for

Leukoedema; however, it can extend to the labial mucosa, floor of the mouth, and pharyngeal areas. [8] Other mucosal surfaces can be affected, such as vagina and . Leukoedema cannot be wiped off; however, it can be eliminated temporarily by stretching of the mucosa, which is referred to as clinical [8] stretch test.

Fig. 2 White keratotic line at occlusal level

LEUKOEDEMA- Leukoedema (also spelled leucoedema)[6] is a blue, grey or white appearance of mucosa, particularly buccal mucosa.It is a harmless and very common condition. Because it is so common, it has been argued that it may in fact represent a variation of the normal appearance Fig.3 Folded appearance of leucoedema on buccal rather than a disease [7] but empirical mucosa evidence suggests that leukoedema is TREATMENT- an acquired condition caused by local [8] Leukoedema is considered to be a normal irritation. variation; therefore, no treatment is required [8] ETIOLOGY- for this condition. The cause is unknown [7] but it is thought to be DIFFERENTIAL DIAGNOSIS- caused by intracellular of the Clinical examination readily differentiates superficial epithelial cells coupled with leukoedema from since there is no retention of superficial parakeratin. Although loss of pliability or flexibility of the involved leukoedema is thought to be a developmental tissues. [9] Leukoedema is distinguished from condition, it may be more common and more by stretching the buccal mucosa pronounced in smokers, and becomes less [10]. Areas exhibiting leukoedema will either noticeable when smoking is stopped. It may disappear or persist upon stretching, whereas also develop in areas subject to repeated lesions of lichen planus will become more subclinical irritation, caused by low grade

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 11 pronounced. Leukoedema should also be clinician. But still a small minority roughly differentiated from white sponge and 4% are potentially dangerous if left habitual cheek-biting (pathomimia morsicatio unattended.[15]Following diagnostic algorithm buccarum) [11, 12] . is a for oral white lesions, if the lesion after monitoring for 6 weeks still persists, relatively uncommon lesion, and the buccal [13] has to be performed and if results indicate mucosa appears thickened and folded. with no then proper [17] FRICTIONAL KERATOSIS- follow-up and review are necessary. Frictional keratosis is a reactive white lesion caused by prolonged mild irritation of the . It shows rough and frayed LEUKOPLAKIA- surface, upon removal of the offending agent, DEFINITION AND TERMINOLOGY- the lesion resolves in 2 weeks. In 1978, oral leukoplakia has been defined by should be performed on these lesions that do [14, 15] the World Health Organization (WHO) as: ‘A not heal to rule out a dysplastic lesion . white patch or plaque that cannot be ETIOLOGY- characterized clinically or pathologically as [18] It is mostly caused by acute trauma which in any other disease. turn causes ulcers while chronic trauma causes ETIOLOGY - hyperkeratosis. The etiology for frictional Tobacco plays important role in etiology. keratosis is habitual cheek biting, orthodontic Whether the use of alcohol by itself is an appliance, ill-fitting denture, broken cusp, independent etiological factor in the rough edges of a carious tooth or malaligned development of oral leukoplakia, is still teeth [16]. questionable [20-24].The role of Candida. CLINICAL MANIFESTATIONS- albicans as a possible etiological factor in leukoplakia and its possible role in malignant Clinical features are at first a patch which is [24-28] pale translucent later it becomes dense and transformation is still unclear. The role of white, mostly they occur in areas that are viral agents in the pathogenesis of oral commonly traumatized like buccal mucosa leukoplakia has been noticed, particularly with regard to exophytic, verrucous along the occlusal line, , lateral margins of [29,30] [16] leukoplakia. In a study from India, serum . vitamin levels of vitamin A, B12, C, beta carotene and folate acid were significantly decreased in patients with oral leukoplakia compared to controls, whereas serum vitamin E was not.[31]Loss of heterozygosity (LOH) of the arms 3p and 9p are associated with increased malignant potential in oral leukoplakia (Emilion et al, 1996; Mao, 1997; Zhang and Rosin, 2001). Fifty percent of leukoplakia contains allelic loss of either Fig.4 Frictional keratosis in retromolar region the 3p or 9p chromosome arms 4(Rosin et al, [32] adjacent to sharp tooth 2000; van der Riet, 1994) . TREATMENT- Frictional keratosis is one of the most CLINICAL MANIFESTATIONS- commonly associated traumatic oral lesions by The site distribution shows world-wide sharp edges of the tooth. Removal of cause for differences, that are partly related to gender irritation is required. Many of them are and tobacco habits [19, 33, 34, 38].In general, two harmless and do not require any treatment clinical variants of leukoplakia are being other than reassurance from the side of the recognized, the homogeneous and the non-

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 12 homogeneous type. Transitions or changes and may do so in a protracted among the different clinical variants of oral course of over 10–15 years. [36, 37] leukoplakia may occur Homogeneous leukoplakia has been defined as Reported risk factors of statistical a predominantly white lesion of uniform flat, significance for malignant transformation of leukoplakia, listed in an at random order thin appearance that may exhibit shallow [35] cracks and has a smooth, wrinkled or (not applicable in the individual patient) corrugated surface with a constant texture  Female gender throughout [18]. Non-homogeneous leukoplakia  Long duration of leukoplakia has been defined as a predominantly white or  Leukoplakia in non-smokers white-and-red lesion ("erythroleukoplakia") (idiopathic leukoplakia) that may be irregularly flat, nodular or  Location on the tongue and/or floor of exophytic. The nodular lesions are the mouth 2 characterized by white patches or nodules on a  Size > 200 mm erythematous base [39], while the exophytic  Non-homogeneous type lesions have irregular blunt or sharp  Presence of Candida albicans projections [18].  Presence of The adjective "non-homogeneous" is applicable both to the aspect of colour, i.e. a VARIOUS FORMS OF LEUKOPLAKIA - [2] mixture of white and red changes Clinical types - ("erythroleukoplakia") and to the aspect of Two main clinical types of leukoplakia are texture, i.e. exophytic, papillary or verrucous. recognized With regard to the latter lesions, no 1. Homogeneous reproducible clinical criteria can be provided 2. Non-homogeneous leukoplakia. to distinguish (proliferative) verrucous leukoplakia from the clinical aspect of Non homogeneous varieties includes verrucous hyperplasia or  speckled: mixed, white and red, but [40, 41]. Furthermore, a diagnosis of retaining predominantly white proliferative verrucous leukoplakia can only character be made retrospectively after new lesions have  Nodular: small polypoid outgrowths, developed [2].The homogeneous type is usually rounded red or white excrescences otherwise asymptomatic, whereas the non-  Verrucous: wrinkled or corrugated homogeneous (mixed white and red) surface appearance. leukoplakias are often associated with mild complaints of localised pain or discomfort. In However, those with mixed white and red the presence of redness or palpable induration, plaques should be recognized as having a [38] malignacy may already be present . higher risk status. These are to be denoted as erythroleukoplakia. MALIGNANT TRANSFORMATION- • Proliferative verrucous leukoplakia (PVL) presents with multiple, In a study from India, an annual malignant transformation rate of 0.3% has been simultaneous leukoplakias ; as the reported.[35]In studies from Western countries disease is visibly multifocal and somewhat higher figures have been frequently covers a wide area. This mentioned; an annual malignant clearly fits with the proposed transformation rate of approximately 1% is terminology of potentially malignant probably a reasonable average figure for all disorder’ rather than struggling to list types of leukoplakia together. Non PVL under lesions’ or as a condition homogenous type [35] nearly always transforms into verrucous carcinoma or squamous cell

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 13 Carotenoids[39]

1. Beta-Carotene- Betacarotene is a vitamin

A precursor. The use of beta-carotene has been recommended in order to prevent Oral Leukoplakia and possibly . The potential benefits and protective

effects against cancer are possibly related to its antioxidizing action. This function is accomplished through a ligation between beta-carotene and oxygen, which is an Fig.5 Homogenous leukoplakia on buccal mucosa unstable reactive molecule, thus diminishing the damaging effects of free radicals.

2. Lycopene- Lycopene is a carotenoid without provitamin A action. This is a fat-soluble red pigment found in some fruit and vegetables. The greatest known source of licopene is tomatoes, which are widely employed in cooking. There is a positive relationship Fig.6 Non-homogenous leukoplakia between lycopene consumption and a TREATMENT [2] – reduction in the risk of the development of White patch degenerative diseases caused by free Exclude other known radicals, such as cancer and cardiovascular diseases. Lycopene has the uncommon conditions /disorders/diseases feature of becoming bound to chemical based on history and species that react to oxygen, thus being the examination most efficient biological antioxidizing agent. Provisional clinical Due to this property, studies have been Diagnosis of leukoplakia enthusiastically conducted with lycopene, in order to find out whether or not it could be an alternative to protect patients against the Biopsy Other known damaging effects of free radicals. In addition disorder confirmed to its antioxidizing property, lycopene also has the capacity to modify intercellular exchange junctions, and this is considered to Other known disorder Revise diagnosis be an anticancer mechanism. Excluded to other disease/ No systemic significant toxical effect of disorder lycopene has been observed and there is no evidence of side effects from the treatment with lycopene. Lycopene is a promising candidate in reducing cancer and chronic diseases in human beings; however, further Leukoplakia with dysplasia research is needed to clarify its potential Leukoplakia without dysplasia

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 14 function in human health, according to the high levels of oxygen,protecting cellular following criteria. membranes fromlipidic peroxidation. (1) Factors influencing the uptake of lycopene in the diet, including the way it 3. Retinoic Acid (Vitamin A)- interacts with othercarotenoids. The current definition of retinoid includes (2) Human metabolism and the possible all the natural and synthetic compounds with function of the metabolites and cis-trans an activity similar to that of Vitamin A. isomers. Vitamin A exists in the human body as (3) Mechanisms of the direct or indirect various interconvertible compounds, notably modulation of cancer. retinal (essential for vision) and retinol, which (4) Studies based on evidences of treatment is the most potent analogue and the main form in human beings. of storage and transportation. Retinoic acid is (5) Mechanisms of lycopene deposition in obtained from carotene and animal products human tissues. such as meat, milk, and eggs, which, while in (6) Lycopene effects in the immunological the intestine, are converted, respectively, into system. retinal and retinol. The absorption of retinoids increases by up to 50% when ingested with Vitamins [39] food. Retinoids are transported in the blood by 1.L-Ascorbic Acid (Vitamin C)- plasmatic proteins. Hepatic metabolization is L-ascorbic acid (L-AA), the so-called achieved via the action of cytochrome P- 450. vitamin C, is found in citrus fruits such as Hypervitaminosis occurs when consumption kiwi, strawberries, papaya, and mango. exceeds the liver’s capacity to store retinoids. The current US recommended daily Topic retinoids were initially tested against allowance for ascorbic acid ranges diseases related to keratinization. 13-cRA was between 100–120 mg/per day for adults. It used for the first time against , in 1969. has been suggested that a daily intake of at The so-called “retinoic ” is the main least 140 mg/day is required for smokers side effect of tretinoin, this leads to cutaneous because they usually present a reduction of irritation characterized by , scaling, the L-AA(L-ascorbic acid )concentration ardency, and/or pruritus. “Retinoic dermatitis” in serum leukocytes. L-AA has occurs frequently, and patients ought to be antioxidizing properties and reacts with previously instructed with regard to superoxide produced as a result of the itsoccurrence. cells’ normal metabolic processes; this inactivation of superoxide inhibits the Bleomycin[39] formation of nitrosamines during protein Bleomycin, a cytotoxic .The use of digestion and helps avoid damage to DNA topical 1% bleomycin in dimethyl sulphoxide and cellular proteins. L-AA toxicity does DMSO was evaluated for the treatment of not occur, since vitamin is water-soluble and a decrease in absorption efficiency dysplastic OL. Bleomycin was applied once occurs when consumption exceeds 180 daily for 14 consecutive days to lesions of the mg/day. oralmucosa in 19 patients. It was well tolerated with minor mucosal reactions. 2.α-Tocoferol (Vitamin E)- Immediate posttreatment biopsies showed that α-Tocoferol (AT) is the commonest and 75% of patients had resolution of dysplasia. most active form of vitamin E. It is found Ninety-four percent of the patients attained at in plant oil, margarine, and green leaves. The recommended daily limit rates are 10 least partial clinical resolution. After a mean mg/day for adult men and 8 mg/day for follow-up period of 3.4 years, 31.6% of adult women. Its absorption rate is reduced patients had no clinically visible lesions. In 2 when consumption exceeds 30mg/day. α- patients (11%), malignant transformation Tocoferol is an effective antioxidant at occurred. Topical bleomycin in treatment of OL was used in dosages of

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 15 0.5%/day for 12 to 15 days or 1%/day for 14 a. RETICULAR ORAL LICHEN days. PLANUS- The most common type of oral lichen TREATMENT GUIDELINES FOR planus is the reticular form. LEUKOPLAKIA Characteristically, it presents as a series of [42] Longshore and Camisa fine, radiant, white striae known as 1. Eliminate all contributing factors ‘Wickham striae’, which may be 2. Absence of dysplasia or presence of mild surrounded by a discrete erythematous [45, 46] dysplasia -surgical excision/laser surgery of border. The buccal mucosa is the site the lesions on the ventral/lateral tongue, floor most commonly involved. The striae are of the mouth, , and oropharynx. typically bilateral in a symmetrical form Close observation and follow-up for all other on the buccal mucosa. They may also be anatomic locations seen on the lateral border of the tongue 3. Presence of moderate or severe dysplasia - and less often on the gingiva and the lips. surgical excision or laser therapy is preferred Reticular lichen planus is likely to resolve [47] treatments in 41% of cases. 4. Red lesions (/ leukoerythroplakia) - Surgical removal is best b. PAPULAR ORAL LICHEN 5. Proliferative verrucous leukoplakia - PLANUS - Complete surgical excision/laser surgery if The papular form presents as small white possible pinpoint about 0.5 mm in size. It is rarely seen and because the lesions are 6. Follow-up for all lesions. small it is possible to overlook them [47] during a routine oral examination.

ORAL LICHEN PLANUS- c. PLAQUE-LIKE ORAL LICHEN Lichen planus is a common mucocutaneous PLANUS disease. It was first described by Wilson in Plaque-like lesions resemble leukoplakia and occur as homogenous white patches.It 1869 and is thought to affect 0.5–1% of the may can be slightly elevated or smooth, [43] world’s population. Oral lichen planus is a irregular and multifocal. The primary sites chronic disease that can persist in some are dorsum of tongue and buccal mucosa. patients for a long time. In contrast to This form is significantly more common cutaneous lichen planus, the oral form may among tobacco smokers. [48] The lesions persist for up to 25 years.[89] It affects woman are often discovered incidentally by the [45,46] patient or by a clinician during a routine more often than men in a ratio 2:3. oral examination.

CLASSIFICATION- d. ATROPHIC ORAL LICHEN [44] Andreasen divided oral lichen planus into PLANUS six types: reticular, papular, plaque-like, The atrophic type of oral lichen planus is erosive, atrophic, and bullous. The reticular, diffuse, red and there are usually white papular and plaque-like forms are usually striae around the lesion. Such striae that painless and appear clinically as white radiate peripherally are usually evident at keratotic lesions. The erosive, atrophic and the margins of the atrophic zones of the bullous forms are often associated with a lesion. The atrophic form can display a burning sensation and in many cases can cause symmetrical patchy distribution over all severe pain. A detailed history and four quadrants. The lingual gingiva is observation of the clinical features of the usually less severely involved. This disease are usually sufficient to establish the condition can cause a burning sensation diagnosis. particularly when in contact with certain

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 16 foods. About 12% of atrophic lesions will ETIOLOGY OF ORAL LICHEN PLANUS [47] resolve spontaneously. Although the aetiology has not been fully e. BULLOUS ORAL LICHEN elucidated, an immunologically induced PLANUS - degeneration of the basal cell layer of the oral mucosa has been suggested. In the past, Bullous oral lichen planus appears as small bullae or vesicles that tend to rupture easily. The bullae or vesicles range from a few millimetres to several centimetres in diameter. When they rupture they leave an ulcerated, painful surface. This form is rarer than the other forms of oral lichen planus. It is commonly seen on the buccal mucosa, particularly in the posteroinferior areas adjacent to the second and third molar teeth. The next most common site is the Fig.8 Erosive lichen planus on buccal mucosa lateral margins of the tongue. The lesions speculation about the aetiology covered a are rarely seen on the gingiva or inner wide range of possibilities including trauma, [47] aspect of the lips. specific bacteria, , parasites, viruses, mycotics, allergies, toxicity, neurogenic, [51] f. EROSIVE ORAL LICHEN hereditary and psychosomatic disorders. PLANUS- Erosive oral lichen planus is the second Diabetes mellitus and hypertension have most common type. The lesions are been described when associated with oral usually irregular in shape and covered lichen planus as ‘Grinspan syndrome’. [52] In with a fibrinous plaque or addition, it can be seen in several members pseudomembrane where there is erosion. of one family, but this does not suggest that The periphery of the lesion is usually oral lichen planus is a hereditary disease. surrounded by reticular or finely radiating keratotic striae. It is painful when the DIFFERENTIAL DIAGNOSIS OF pseudomembrane or fibrinous plaque is ORAL LICHEN PLANUS – disturbed. It is thought that erosive oral Clinically, the differential diagnoses should lichen planus has a greater potential to include undergo malignant change. [96] It has been

reported that only the atrophic and erosive  lichenoid reactions forms of lichen planus undergo malignant  leukoplakia change, and this may be because of the  atrophic nature of the mucosa rather than  [47] the specific disease.  mucous membrane Lichenoid reactions in the oral cavity are invariably drug-induced lesions.The erosive or atrophic types that affect the gingiva should be differentiated from pemphigoid, as both may have a desquamative clinical appearance. erythematosus often has white plaque-like lesions with an erythematous border. In some cases, can resemble bullous lichen planus, but it is more acute and Fig.7 Reticular pattern in lichen planus generally involves the labial mucosa.

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 17 MALIGNANT TRANSFORMATION I. Non-Surgical Management Of Oral OF ORAL LICHEN PLANUS - Lichen Planus- There is some controversy regarding its malignant potential. There seems to be a Corticosteroids – slightly higher incidence of oral squamous Intralesional corticosteroids- cell carcinoma in patients with oral lichen Topical corticosteroids are of limited planus than in the general population.[53] value for some cases of oral lichen The actual overall frequency of malignant planus. In such cases, it may be transformation is low, varying between appropriate to use topical corticosteroids 0.3% and 3%.[55] The forms that more in combination with intralesional commonly undergo malignant preparations. Zegarelli[63] combined the transformation are the erosive and use of topical and intralesional [49,54] corticosteroids in seven patients, atrophic forms. resulting in complete improvement in

[58] five patients. However, intralesional  Silverman et al., in a survey of 570 corticosteroids have some patients followed for a mean of 5.6 contraindications, including atrophy of years, reported malignant transformation tissue and secondary candidiasis after in seven patients. The lichen lesions in frequent injections. five of the seven patients were considered to be either erosive or Systemic corticosteroids - atrophic. Systemic corticosteroids are of great value when there has been an acute  Holmstrup et al., in a survey of 611 exacerbation of symptoms and are often patients followed for a mean of 7.5 used in combination with topical years, reported nine cases of malignant corticosteroids. Because of the transformation. Six of these patients had immediate effect of systemic a combination of the reticular and corticosteroids and their inherent atrophic forms, one had a combination of toxicity, adverse effects are common the reticular, atrophic and erosive forms even after a course as short as two and two had a combination of the weeks.[64] The most common adverse reticular and plaque-like forms. effects include gastrointestinal upset,  The numerous reports range from 0.4% mood alteration, polyuria, insomnia and to 5.6%.[57,58] shakes.[65] Changes in blood pressure  About 2% of patients develop squamous [60] and blood glucose concentrations have cell carcinoma. been reported in a few patients.[61]  Nevertheless, Eisenberg and Patients who take systemic steroids for a Krutchkoff[59] reported in their review long time, particularly in high doses, that there was ‘no inherent should be monitored regularly. predisposition for oral lichen planus to

become malignant’, whereas in the same Retinoids - journal Holmstrup stated that the Retinoids were first used for the controversy was over because there was treatment of asymptomatic, white, an ‘increased risk of oral cancer reticulated oral lichen planus by Gunther. development’. [66] Vitamin A was applied locally to the

MANAGEMENT OF ORAL LICHEN lesions with good results. Tretinoin is the PLANUS- most readily available topical retinoid.

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 18 Cyclosporin- appears to have lost currency, and most histopathologists prefer the term "chronic Damage to the basement membrane in hyperplastic candidosis/candidiasis". oral lichen planus is the result of the production of lymphokines such as CLINICAL MANIFESTATIONS- interferon gamma by activated T lymphocytes. Cyclosporin is an The most common and arguably the classic immunosuppressant and reduces the clinical presentation of CHC is a white plaque production of lymphokines.[61] It inhibits that cannot be scraped off and presenting most the proliferation and function of T frequently in the commissural regions of the lymphocytes. Its main adverse reaction is oral mucosa. However, other oral sites can be renal dysfunction as a result of prolonged infrequently affected. The lesion can be use, so patients taking cyclosporin need differentiated from oral leukoplakia of to be monitored closely The primary idiopathic origin, since appropriate antifungal side-effect of cyclosporin therapy was therapy usually leads to resolution of the reported to be transient sensations of condition. burning on the mucosal surface of the [67] lesion. CHC presenting as leukoplakia appears as well-demarcated, palpable, raised lesions that THE SURGICAL MANAGEMENT may vary from small translucent whitish areas OF ORAL LICHEN PLANUS- to large opaque plaques that cannot be rubbed off. Cryosurgery and carbon dioxide laser Some or all areas of the plaque may have a ablation have been suggested for the smooth, homogenously white surface, and if surgical treatment of oral lichen planus. this feature predominates, the lesion is However, excision should not be a referred to as a homogenous leukoplakia. primary method of treatment as it is an However, the inflammatory condition that can recur. In Surface often has erythematous areas addition, surgical management is not intermingled with white areas that, more often suitable for the erosive and atrophic than not, possess a nodular characteristic. types because the surface is Such lesions are referred to as nodular or eroded. Surgical treatment is more speckled leukoplakia. applicable to the plaquelike lesions, because the affected surface epithelium [67] can be removed easily.

CHRONIC HYPERPLASTIC CANDIDIASIS-

Lehner (1964, 1967)[68,69] recognized the presentation of chronic candidal in the form of leukoplakia and introduced the Fig.9 white hyperplastic candidiasis on lateral term "candidal leukoplakia." The terms border of tongue "chronic hyperplastic candidosis" (CHC) and TREATMENT AND PROGNOSIS "candidal leukoplakia" (CL) appear to have been synonymously used until the mid-1980s GENERAL MEASURES TO ELIMINATE (Cawson, 1966a,b; Cawson and Lehner, 1968) PREDISPOSING FACTORS Since has been clearly [70,71]. Several authors preferred the term shown to be linked to the causation of "candidal leukoplakia" to describe lesions many/most leukoplakias, and to candidal confined to the mouth alone. In recent times, however, the term "candidal leukoplakia"

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 19 leukoplakias in particular, elimination of this are easily recognised and clinically important; habit is an important the lesions appear as bilateral white spongy plaques, typically found on the buccal mucosa, Step in the management of CL- and the patients report no painful symptoms. Prostheses, particularly maxillary dentures, The lesion can be found in other common act as reservoirs of Candida and have been sites, including the tongue, floor of the mouth shown to be linked to a high prevalence of CL. and alveolar mucosa [79]. The disease are Although requesting patients to abandon their characterised by white, thickened, folded and dentures is not a realistic option, preventive spongy lesions of the oral mucosa, although measures such as not wearing the prosthesis at the oesophageal, laryngeal, nasal and night, together with stringent denture hygiene, anogenital mucosa can also be affected [80]. should be encouraged to prevent candidal The WSN plaques are considered benign colonization of the denture surface. Patients because the lesions are asymptomatic and using a steroid inhaler for medical reasons painless in many cases, although they may should be advised to rinse their or undergo alternate periods of remission and drink water soon after using the inhaler exacerbation due to infections. This disorder (Spector et al., 1982; Ellepola and often manifests in early childhood and exhibits Samaranayake, 2001) [72, 73]. no gender preference. WSN occur on the surface of the , including the oral mucosa SPECIFIC TREATMENT OF CHRONIC and anal mucosa, among other areas. HYPERPLASTIC CANDIDAL LEUKOPLAKIA- TREATMENT AND PROGNOSIS- Although WSN patients experience no Antifungal therapy significant physical pain, they often complain of an altered Cawson and Lehner (1968)[74], in their first report on CL, claimed improvement and disappearance of a significant number of their cases of leukoplakia with polyene-nystatin (tablets) dissolved slowly in the mouth. Lamey et al. (1989) [75] reported a case of CL with a significant degree of epithelial dysplasia that resolved within 11 days of systemic treatment with the triazole antifungal, fluconazole. Holmstrup and Bessermann (1983) [76] reported that, following antifungal therapy, nodular lesions of the commissural areas showed the highest recurrence rate after 12 months. Fig.10 White, folded appearance of White sponge nevus

WHITE SPONGE NEVUS- texture to their mucosa. Azithromycin, tetracycline and penicillin have exhibited White sponge nevus (WSN) is a rare some clinical effects [81]. A case of WSN hereditary leucokeratosis that was first exhibiting significant improvement following described by Hyde in 1909[77]; the term white penicillin administration has been reported [82]. sponge nevus was first coined by Cannon in McDonagh et al. first reported that 1935[78].It is also known as cannons disease, tetracycline medicines were effective in four oral epithelial nevus, white folded dysplasia of WSN patients [83]. Another report stated that mucous membrane. oral tetracycline rinse improved the symptoms of WSN [84].Subsequently, WSN was CLINICAL MANIFESTATION- successfully treated with a tetracycline mouth The onset of WSN is early in life, and both rinse [85]. Long-term low dose systemic sexes are affected equally. Lesions of WSN

Journal of Interdisciplinary Dental Sciences, Vol.7, No.1 Jan-June 2018, 20 antibiotic therapy maintained the remission of treatment and prognosis is highly variable. WSN [86]. To date, systemic or local Many lesions involving the oral mucosa are applications of retinoic acid have provided benign and do not require treatment. These limited benefits, but both are poorly effective. include developmental conditions like white Dufrasne et al. described a case of effective sponge nevus, frictional keratosis, linea Alba, surgical resection, and the patient was free of etc. In contrast potentially malignant lesions recurrence 2 years later [87]. WSN may be like leukoplakia, lichen planus require treated with chlorhexidine [88]. Meanwhile, intervention depending on potential mortality WSN patients should perform a careful oral and morbidity. hygiene to reduce infection in the oral cavity. The proper diagnosis and treatment of this rare REFERENCES- disease will require the combination of clinical 1. Panat SR, Yadav N, Aggarwal A. White history, clinical examination and pathologic lesions of oral mucosa-diagnostic findings. dilemma. Journal of Dental Sciences & Oral Rehabilitation. 2011;08-10. DISCUSSION- 2. Warnakulasuriya S, Johnson NW, van A wrong diagnosis may lead to wrong der Waal I. Nomenclature and treatment, which may not only cause physical classification of potentially malignant trauma to the patient but may also be fatal disorders of the oral mucosa. J Oral especially in lesions with malignant potential. Pathol Med. 2007;36:575-80. Considering the serious nature of the 3. Freitas MD, Blanco- Carrion A, potentially malignant lesions, we suggest thorough clinical examination and accurate Gandara- Vila P, Antunez-Lopez J, diagnosis is essential. Planning appropriate GarciaGarcia A, Gandara Rey JM. treatment can help in prevention of conversion Clinicopathlologic aspects or oral of simple lesions into malignancies. The leukoplakia in smokers and non smokers. primary goal of this article is learning the Oral Surg Oral Med Oral Pathol Oral process of clinical diagnosis of non scrapable Radiol Endod. 2006; 102(2):199-203. white lesions. 4. Mehta FS, Daftary DK, Shroff BC, Linea alba has its unique appearance as seen at occlusal plane on buccal mucosa. The clinical Sanghvi LD. Clinical and histological diagnostic test for leucoedema is it could be study of oral leukoplakia in relation to disappears on stretching and it is racial. The habits: A five year follow up. Oral Surg frictional keratosis is associated with history Oral Med Oral Pathol. 1969;28(3);372- of trauma and etiological cause is apparent, 88. mostly reversible on removing the cause. 5. Martínez AD, García-Pola MV. Leukoplakia is potentially malignant lesion, careful diagnosis and treatment is essential. Epidemiological study of oral mucosa Oral Lichen Planus is usually associated with in patients of the Oviedo Wickham’s striae and can be differentiated School of Stomatology. Medicina oral: from other lesions. Antifungal therapy organo oficial de la Sociedad Espanola resolves Chronic Hyperplastic Candidiasis is de Medicina Oral y de la Academia diagnostic. White Sponge Nevus is noted in Iberoamericana de Pathology Medicina early life, family history, large areas involved, Bucal. 2002;7(1):4-9. genital mucosa may be affected. 6. Scully C. Oral and maxillofacial CONCLUSION- medicine: the basis of diagnosis and White lesions in oropharyngeal region can treatment. Churchill Livingstone range from genetic disorder to potentially Elsevier; 2008. malignant disorders. Differentiating these 7. Neville BW, Damm DD, Allen CM, lesions clinically is extremely important as Bouquot JE. Odontogenic cysts and

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Corresponding Author Details: Dr. Dr. Prerana V. Waghmare, PG students, Department of Oral Medicine and Radiology, Saraswati Dhanwantari Dental College & Hospital & Post Graduate Research Institute, Parbhani, Maharashtra, India.

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