Lichenoid contact reaction in buccal mucosa and alveolar ridge due to amalgam build-up of 1st and 2nd mandibular molar. No prevalence rate has been reported for LCR yet. Women are affected more frequently than men. Clinically, LCRs show the same features as seen in OLP, that is, reticulum, papules, plaques, erythema, and ulcers [ 4 , 5 ].
The majority of LCRs are confined to sites just in contact with dental materials, such as the buccal mucosa and the lateral borders of the tongue. Lesions are hardly ever observed in sites such as the gingivae, palatal mucosa, floor of the mouth, or dorsum of the tongue.
Most LCRs are non-symptomatic, but the patient might experience discomfort from spicy and hot food when the lesion converts to erythematous or ulcerative forms. The duration of contact with dental material has the key role to develop LCRs on the oral mucosa. Lichenoid reactions caused by dental composites have been observed on the mucosal side of both upper and lower lips. However, it is not necessary to replace restorative materials that are not in direct contact with LCRs.
While a malignant potential for LCRs has been suggested, no prospective studies have been conducted to support this hypothesis [ 4 ]. It has been suggested that drugs or their metabolites precipitate the lichenoid reaction. DILRs are uncommon and account for a very low percentage of this entity [ 4 ]. There are many drugs responsible for the development of these lesions such as non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors. Other medications, such as anti-malarial and antihypertensive drugs, diuretics, oral hypoglycemic agents, gold salts, penicillamine, and beta blockers are also related to the evolution of DILRs [ 30 ].
Usually the lesions evolve several months after the patient starts a new drug. DILRs are not generally severe; however, if a patient has serious symptoms withdrawal of the drug and use of topical steroids are often recommended [ 4 ]. Graft-versus-host disease GVHD is a major complication of allogeneic hematopoietic cell transplantation.
Oral GVHD mimics clinical features of OLP, but with a more generalized distribution and concomitant involvement of other organs such as skin and liver. It is characterized by lichenoid inflammation that can involve all intraoral sites, but particularly affects the tongue, buccal mucosa and lips.
Clinical signs ranged from only mild reticulation to more extensive disease with painful ulcerations. The soft palate is infrequently affected and it rarely extends posteriorly to the oropharynx. The clinical manifestations of SCLE are intermediate compared to the aforementioned types [ 5 ]. The prevalence of LE in the United States is more than 1. SLE affects nearly 1 in every people with a female to male ratio of and the mean age of 31 years at the time of diagnosis.
The etiology remains unknown, however increased action of B lymphocytes and autoantibody production with the imbalanced function of T lymphocytes have been identified. Genetic and environmental factors such as infections mostly with EBV and other viruses, contact with pollutants, hormonal factors, ultraviolet light, smoking, diet, and use of some drugs are the predisposing factors for this condition [ 4 , 5 ].
There is an extensive range of clinical symptoms for SLE. Sunlight often aggravates the malar rash [ 4 , 5 ]. The lesions generally involve the palate, buccal mucosa, and gingivae. Sometimes, vermilion zone of the lower lip lupus cheilitis is also affected [ 4 , 5 , 32 ]. Ulcers are often aphthous-like with a white to yellow coating and a peripheral red rim especially in the hard palate [ 32 ].
A honeycomb plaque is a rare condition, revealed as a chronic, well-defined plaque along with white lacy hyperkeratosis and buccal erythema.
The lesions generally affect both lining and masticatory mucosa, however they are less hyperkeratotic on the lining mucosa e. Lupus cheilitis is an inflammatory condition of the lips presenting as a small or diffuse, erythematous and edematous lesion that might develop into crusty painful ulcers.
This condition usually affects the vermilion zone of the lower lip [ 32 ]. Oral manifestations of CCLE are similar to erosive OLP with an ulcerated or atrophic, erythematous central area and peripheral white, fine, radiating striae. Occasionally the central region shows a fine stippling of white dots along with erythema. However, the oral features are generally accompanied with skin lesions. When ulcerative and atrophic oral lesions come into contact to acidic or salty foods pain might arise similar to erosive OLP.
Diagnosis of SLE can be quite challenging in primary stages because of its ambiguous clinical course usually with remission phases. American Rheumatism Association has set some clinical and laboratory criteria for the diagnosis of SLE [ 5 ].
Systemic corticosteroids in combination with other immunosuppressive agents and immunomodulators are frequently used for more severe conditions. Meanwhile, systemic therapy would lead to the amelioration of oral lesions if any [ 5 ] Table 3. Frictional traumatic keratosis is defined as white plaques with a rough and frayed surface clearly related to an identifiable source of mechanical irritation.
These lesions can occasionally mimic dysplastic leukoplakia. The prevalence has been reported as high as 5. This category includes linea alba, and cheek, lip, and tongue chewing. Traumatic keratosis has never been shown to undergo malignant changes. Once the irritant is removed the lesion must resolve within two weeks; otherwise, biopsy is mandatory to rule out a dysplastic lesion [ 6 ]. Oral leukoplakia OL has been defined as a white patch or plaque that cannot be attributed to any clinically or histologically definite lesion [ 22 , 33 ].
The prevalence of OL is reported 2. Most lesions are seen above the age of 50 with men being more commonly affected; however, a slight predilection for women has been found in some studies [ 4 ]. While the etiology of these lesions remained unexplained some authors mentioned the relationship between leukoplakia and tobacco, alcohol, sanguinaria, ultraviolet radiation, trauma, betel quid chewing, genetic factors, and microorganisms [ 4 , 5 , 33 , 34 ].
These lesions are divided into homogenous or non-homogenous types. The homogenous type has a regular, smooth whitish surface and well-defined margins. The non-homogenous form of leukoplakia consists of an erythematous part erythroleukoplakia or speckled type or a nodular, erosive, ulcerated, or verrucous exophytic component. In the speckled type the lesion is predominantly white. The verrucous leukoplakia has an elevated, proliferative, or corrugated surface, and the nodular type develops small polypoid enlargements or rounded mostly white excrescences [ 7 , 22 , 34 ] Figure 8.
Oral leukoplakia is generally localized or widespread on the buccal mucosa, lip vermilion, and gingivae. Characteristics of acquired white lesions that cannot be scraped off, without specific pattern. OHL is an indicator of progress towards AIDS stage in HIV infection, but it might occur in other states of immune deficiencies and very rarely in immune competent individuals [ 4 , 5 , 17 , 34 ]. OHL is more commonly observed among men with no potential for malignant transformation [ 4 , 17 ]. It is clinically described as whitish nonscrapable velvety plaques that symmetrically involve the borders of the tongue unilaterally or bilaterally.
The shape of plaques varies from slight, white vertical bands to thickened, furrowed areas with a shaggy surface [ 5 , 34 , 35 ] Figure 9. OHL infrequently spread to cover the entire dorsal and lateral surfaces of the tongue. Rarely, the buccal mucosa, soft palate, pharynx, or esophagus can be affected [ 5 ]. While oral hairy leukoplakia is asymptomatic, superimposed infection with candida create symptoms of mild pain and taste alteration [ 4 , 35 ].
Treatment of OHL generally is not needed, and it has been reported to display spontaneous regression; however minor discomfort or esthetic concerns may require therapy. Therapeutic interventions include systemic anti-herpes virus drugs, topical retinoids or podophyllum resin, combination therapy with acyclovir cream and podophyllum resin, gentian violet, surgical excision, or cryotherapy [ 5 , 35 ] Table 4.
Proliferative verrucous leukoplakia commonly appears in the elderly women with no racial preference. The mean age of patients with long-lasting lesions of PVL was reported over 60 years [ 4 , 5 , 34 , 37 ]. While the etiology of this condition is uncertain genetic factors and viral infections such as Human Papilloma Virus especially type 16 and 18 and Epstein-Barr Virus have been proposed [ 36 , 37 ].
Clinical appearance in the early stage contains small whitish and well-defined patches or plaques appearing as focal and homogeneous keratotic lesions Figure The lesions enlarge slowly and constantly over time involving diffuse surfaces of the mucosa.
Meanwhile, non-homogeneous multifocal areas with speckled and rough surface might appear in the form of exophytic, wart-like, verrucous, polypoid projections or erythematous features [ 5 , 34 , 36 , 37 ]. PVL usually develops bilaterally, which affects the buccal mucosa, gingivae, and alveolar ridges. The gingivae have been reported as the most affected area; hence a PVL subtype named proliferative verrucous leukoplakia of the gingivae has been proposed [ 22 , 36 , 37 ].
The rate of malignant transformation for PVL is reported between It might eventually progress to develop OSCC or verrucous carcinoma [ 22 , 36 ]. Various treatments modalities such as surgery, carbon dioxide laser ablation, topical photodynamic therapy, oral retinoids, topical bleomycin solution, beta-carotene, methisoprinol a synthetic antiviral agent , radiation, and chemotherapy are suggested. None of the treatment methods is effective in quiting relapses and malignant transformation, and therefore a lifelong follow-up is mandatory [ 36 , 37 ].
The incidence has been reported higher among men and patients older than 65 years. Etiology of OSCC is multifactorial including tobacco smoke, alcohol consumption, betel quid, phenol, viral, bacterial and fungal infections, electro-galvanic reaction, radiation, genetics, immunosuppression, expression of oncogenes, deactivation of tumor suppressor genes, malnutrition, iron-deficiency anemia, and some heritable conditions [ 4 , 5 , 22 ].
Oral lesions may present as red, white, or combined red-and-white lesions; alteration of the surface texture into granular, rough, fungating, papillary, and verruciform or crusted lesion may be seen; a mass or irregular ulceration with rolled border and induration on palpation may also exist Figure Squamous Cell Carcinoma with verrucous, plaque like and exophytic clinical manifestations at the lateral border of the tongue, extending to the floor of the mouth.
The lesion can be flat or elevated with some palpability or induration. The Floor of the mouth, posterior lateral borders and ventral surface of the tongue are considered high-risk areas for OSCC.
Involvement of submandibular and digastric lymph nodes due to cancer causes lymphadenopathy with firm to hard consistency, which converts to fixed nodes in later stages [ 4 , 5 ]. Patients are most often diagnosed in advanced phases after progression of symptoms related to disease. Treatment planning depends on clinical staging; therefore, primary stages are treated by surgical process and advanced cases may be managed by radiation therapy or combined chemoradiation therapy with or without surgery [ 5 ] Table 4.
It is found mostly in the elderly men over 55 [ 5 ]. Oral verrucous carcinoma usually shows slow growth rate, local invasion, and a low tendency to metastasize. However, these characteristics depend highly on the size of the tumor and the time of diagnosis [ 38 , 39 ].
Some precursor lesions such as leukoplakia, erythroplakia, and proliferative verrucous leukoplakia can evolve to verrucous carcinoma over time [ 38 ]. Its etiology is not well understood, but some causative habits like smoking, alcohol consumption, betel nut chewing, and smokeless tobacco have been postulated [ 5 , 38 ].
The role of Human Papilloma Virus in the oncogenesis of verrucous carcinoma has yet to be elucidated [ 38 ]. Verrucous carcinoma manifests as an asymptomatic, diffuse, well-demarcated, thick white plaque with papillary or verruciform projections on the surface [ 5 , 38 ].
Sometimes the lesion tends to be pink in coloration due to an inflammatory reaction to the tumor. All parts of oral mucosa can be affected, however mandibular vestibule, buccal mucosa, gingivae, tongue, and hard palate are the most involved sites.
In case of tobacco dipping in the maxillary vestibule or floor of the mouth, these locations are affected more frequently [ 5 ]. A malignant transformation has been related to oral verrucous carcinoma. It is reported that the rate of malignant transformation in gingival lesions is about 21 times higher than tongue lesions [ 38 ]. Surgery is considered the treatment of choice in most cases; however, combination therapy with surgery and radiotherapy is preferred in extensive lesions.
The risk of recurrence rises when surgery or radiotherapy is implemented alone [ 5 , 38 , 39 ] Table 4. This condition is commonly seen among heavy smokers of pipe, tobacco, cigarettes, and reverse smokers as well as patients who drink extremely hot beverages habitually. A frequency of 0. Albeit both high temperature and chemical ingredients of smoke have synergistic effects on developing nicotine stomatitis, the impact of high temperature is much higher than that of chemicals. Nicotine stomatitis primarily presents as an erythematous area on the posterior rugae; then the lesion converts to diffuse leathery grayish-white palatal plaque.
Red points can also be seen on the white mucosa that are actually widened and swollen orifices of accessory salivary glands with periductal nodular keratinization Figure White plaques may affect marginal gingivae and interdental papillae as well [ 4 , 5 , 7 , 41 ].
Nicotine stomatitis can entirely regress after cessation of smoking and be replaced with normal mucosa. Therefore, any white lesion of the palatal mucosa lasting longer than one month after habit cessation should be carefully monitored to rule out malignancy [ 5 , 7 ] Table 4.
Actinic Cheilitis AC is a chronic inflammatory condition also called actinic cheilosis or solar cheilosis [ 5 , 42 ]. The basis of etiopathogenesis is UV light exposure; however other risk factors such as old age, fair complexion, immunosuppression, arsenic exposure, and genetic abnormalities are also implicated. A significant male predilection with a male to female ratio of might be attributed to more outdoor occupational activities among men.
Moreover, the border between vermilion and the adjacent skin cannot be easily distinguished. The lesions progress to rough, scaly, crusting areas and keratotic plaques on drier segments of the vermilion. Finally, chronic ulceration appears, and persists for months and progresses to malignant lesions [ 5 , 42 ]. The warning signs of bleeding, induration, recurrence and sustained pain are suggestive of transforming AC to SCC.
Various treatments such as surgery, cryotherapy, electrosurgery, topical retinoids, 5-fluorouracil cream, photodynamic therapy, CO 2 laser ablation, and vermilionectomy have been suggested for AC [ 5 , 22 , 42 ] Table 4. Chronic mucocutaneous candidiasis CMC is described as a recurrent or consistent disease involving the nails, skin, oral, and genital mucosa initiated by Candida spp. Albicans [ 43 ]. The etiology is associated with hereditary or acquired T-cell deficits and alteration in the gene responsible for producing cytokine IL that is related to mucosal immunity against Candida Albicans [ 5 , 43 ].
Chronic mucocutaneous candidiasis appears as whitish plaques, along with crusts and ulcers frequently found in the oral and pharyngeal mucosa as well as gastrointestinal and vaginal mucosa [ 44 ]. These thick, white plaques of oral lesions generally cannot be scraped off similar to chronic hyperplastic candidiasis, however other clinical forms of candidiasis may appear as well [ 4 ].
Various antifungal medications have been suggested for the treatment of oral lesions with some degrees of resistance to antifungal therapy.
Imidazole derivatives such as ketoconazole, fluconazole, and itraconazole can be used to manage CMC [ 5 , 44 ]. Chronic hyperplastic candidiasis CHC also called as candidal leukoplakia, chronic plaque-type and nodular candidiasis is the least common form of oral candidiasis presenting as white patches or plaques which cannot be detached upon scraping and cannot be attributed to any other lesions [ 4 , 5 , 22 , 45 ].
It is mainly a disease of adulthood with the age range between 31—81 years, and the majority of patients are over 50 [ 46 ]. Chronic hyperplastic candidiasis is frequently presented as well-demarcated, palpable, raised lesions from small translucent whitish areas to large opaque plaques. If the plaque has a smooth, homogenous white surface, it is called a homogenous leukoplakia [ 46 ].
However, the surface often has a fine intermixture of red and white areas resembling a speckled leukoplakia usually possessing a nodular component [ 5 , 46 ]. Chronic hyperplastic candidiasis is typically located on the retro commissure areas bilaterally [ 4 , 46 ]. The tongue, palate, and lips can also be involved [ 4 , 5 , 22 , 45 ].
Whether it is simply a candida infection superimposed on a preexisting oral leukoplakia or a newly formed leukoplakia induced by candida species is a matter of debate [ 5 ]. An increased risk of malignancy related to CHC has been found as compared to normal mucosa [ 46 , 47 ]. Moreover, a four—five times risk of malignancy has been found in comparison to leukoplakia not associated with candidal infection [ 22 ].
Several local or systemic predisposing factors have been identified for CHC such as lack of mucosal integrity, wearing dentures, hyposalivation, acidic and high-glucose-content saliva, tobacco smoking or chewing, diabetes mellitus, immunodeficiency, deficiency of iron and folic acid, high-carbohydrate regimen, and non-secretor status of blood group antigen [ 46 ].
Different modalities have been proposed to treat CHC with various success rates such as antifungal therapy, topical application of retinoids, betacarotene, bleomycin, several surgical techniques like cold-knife surgery, laser therapy, and cryosurgery.
Many clinicians prefer to treat the lesions with antifungals prior to surgical methods [ 46 , 48 ]. Whiteness or pallor of oral mucosa can be seen in some uncommon conditions such as submucous fibrosis, some granulomatous diseases, skin grafts, scar, and uremic stomititis [ 4 , 6 , 19 , 49 , 50 ]. White lesions of the oral cavity constitute a wide variety of entities with different pathogenesis and clinical features.
We proposed a decision tree to classify such lesions according to their clinical manifestations. This helps clinicians to make a more accurate differential diagnoses list. The first major group, congenital non-scrapable white lesions of the oral cavity Table 1 , most commonly appear early in the life with a history of familial involvement [ 10 , 11 , 12 ].
When the white plaque fades with stretching leukoedema should be suspected, especially in a smoker patient with the involvement of buccal mucosa [ 4 , 11 ]. On the other hand, diffuse white plaques in the oral cavity along with extraoral mucosal lesions are in accordance with white sponge nevus [ 8 ]. Oral white plaques accompanied by conjunctival plaques and eye lesions are usually seen in patients with hereditary benign intraepithelial dyskeratosis [ 13 ]. Similarly, dyskeratosis congenita appears as oral white lesions concomitant with nail dystrophy [ 9 , 11 ].
The second major group of oral white lesions is acquired lesions, which can be scraped off Table 2. Some of the lesions in this category such as mucosal burns, morsicatio, and pseudomembranes of ulcers are due to trauma and can be easily diagnosed by detection of the insulting factor on history taking and clinical examination [ 4 , 5 , 13 , 14 , 15 , 21 ].
While pseudomembranous candidiasis in adults and the elderly suggests a systemic or local predisposing factor like debilitating disease or oral microflora imbalance it is quite common in infants and considered somehow normal [ 4 , 16 ]. Noteworthy, scraping a pseudomembrane covering an oral ulcerative lesion will result in a bleeding surface, but in case of candidiasis punctuated bleeding will appear.
However, mucosa under derbies has normal appearance [ 4 ]. Oral aquired white lesions, which are keratotic and cannot be scraped off are further divided into lesions with specific clinical pattern and those without any specific feature. Because of the profound similarity of keratotic lesions with no clinical pattern, it is mandatory to consider some minor characteristics to differentiate them. The third major group of oral white lesions is white keratotic lesions with a specific pattern Table 3 , which can be differentiated from other entities by their special clinical features like discrete papules, annular or reticular forms; however, they are not distinguishable from each other nor clinically neither microscopically.
This group comprises of lichenoid reactions oral lichen planus, lichenoid contact reaction, drug-induced lichenoid reaction, graft versus host disease [ 27 , 28 , 29 , 30 ].
Presence of papules or reticular elements with symmetrical and generalized distribution along with skin or extraoral mucosal genitalia involvement would be in favor of lichen planus [ 4 , 30 ]. On the other hand, LCRs usually develop on the mucosa adjacent to a dental restoration or appliance [ 5 , 30 ].
Drug-induced lichenoid reactions DILRs are mostly unilateral with a positive history of taking medications capable of inducing such lesions. In addition, resolving of the lesions upon withdrawal of the drug and reappearance or exacerbation by re-challenging confirms the diagnosis of lichenoid drug reaction [ 30 ].
Oral GVHD lesions are more widespread than OLP among patients with a past medical history of hematopoietic stem cell transplantation and sometimes with concomitant involvement of other organs such as skin and liver [ 31 ]. Another lesion with a clinical specific pattern similar to lichenoid lesions is chronic cutaneous lupus erythematosus CCLE with a discoid-patterned lesions comprising of a central ulcerated, atrophic, or erythematous area with white, fine, radiating steriae at the periphery, which is more prominent than OLP and may abruptly terminate with a sharp demarcation [ 32 ].
The fourth subgroup of oral white lesions is keratotic lesions that cannot be scraped off without a specific pattern Table 4. The clinical key for diagnosis of frictional keratosis is accordance of the suspected lesion to the site of chronic mechanical trauma. The traumatic factor can be detected either clinically e. Presence of a keratotic plaque with punctuated interspersed red dots on the palate with a history of smoking or drinking hot beverages are diagnostic for nicotinic stomatitis [ 4 , 5 , 41 ].
Actinic cheilitis is suspected when white lesions are seen on the lips among patients with a prolonged history of sun exposure like farmers, fishermen, and other out-doors workers [ 42 ]. Chronic hyperplastic candidiasis is considered in patients with underlying disease and simultaneous cutaneous and mucosal candida lesions. A symmetrical white plaque with pigmentation usually with a cracked-mud appearance in the retro commisural area in a smoker patient is suggestive of chronic hyperplastic candidiasis [ 46 , 47 , 48 ].
Rapid growth in combination with various clinical features such as ulceration, tissue necrosis, and surface non-homogeneity would prompt the clinician to consider SCC in the upper rankings of differential diagnosis [ 5 , 22 , 40 ].
Despite SCC, verrucous carcinoma cannot metastatize. It is associated with smokeless tobacco and often exhibits a rough surface [ 38 , 39 , 40 ]. So, self antigen may be recognized as foreign, by host T-lymphocytes resulting in auto immune response.
Clinically:- Age: middle age, rare in children. Site:- 1 skin lesions: any where, bilateral, symmetrical on flexor surface of wrist, inner aspect of thighs, trunk, nails, vulvar mucosa.
Oral lesions:- Lichen planus has patterns in oral cavity:- 1- Reticular lichen planus. Reticular Lichen planus:- The most common type. Site: posterior buccal mucosa bilaterally, lips, palate, gingiva. Shape: radiating white, velvety, thread like papules in a linear, annular or retiform arrangement.
A tiny white elevated dots is present at the intersection of white lines known as striae of wickham. Erosive Lichen Planus:- Site: posterior- inferior aspect of buccal mucosa adjacent to mandibular molar teeth. Shape: atrophic, erythematous areas with central ulceration, the periphery of atrophic regions is bordered by fine, white radiating striae.
Atrophic Lichen planus:- Site: attached gingiva. Shape: smooth red, poorly defined atrophic zones, at its margins there are whitish keratotic striae radiating peripherally and blending into surrounding mucosa. Hypertrophic lichen planus:- Site: dorsum of tongue and buccal mucosa. Shape: well circumscribed white lesions plaque like which range from slightly elevated and smooth to slightly irregular. Histopathology:- 1-Hyperorthokeratosis or hyperparakeratosis. Lichen planus Diabetes mellitus. Vascular hypertension.
Treatment:- No specific systemic or local therapy. Corticosteroids topical, intralesional ,systemic. Antifungal therapy. Prognosis:- It is a benign lesion , it was not considered a premalignant condition But a large number of cases of epidermoid carcinoma developing in oral lesions of lichen planus. The majority of cases of cancer have occurred in erosive and atrophic types. Hairy leukoplakia:- Def. Etiology:- 1-In male homosexuals. Viral particles are present and replicated within the epithelial cells of tongue.
Human papilloma virus present in co-existence with EBV. Clinically:- Site: lateral surface of tongue, dorsum of tongue, floor of mouth, palate. Shape: unilateral or bilateral surface which is folded or corrugated or papillary hairy. No associated symptoms unless it is superimposed by candidal infection. Histopathology:- 1-Epithelial hyperplasia. Diagnosis:- 1 Immunohistochemical staining technique using anti-viral antibodies. Treatment:- Acyclovir Topical corticosteroids.
Candidiasis Moniliasis Def. This is a term that encompasses a group of mucosal and cutaneous conditions with a common etiological agent from the Candida genus of fungi. Etiology:- The causative organism is Candida Albicans.
The predisposing factors are:- 1-topical corticosteroids. C Mucocutanous forms: 1-localized. Thrush Laboratory findings:- 1-remaval of a portion of the candidal plaque. Histopathology:- Histological section is stained with periodic acid Schiff reagent PAS will show presence of yeast cells and hyphae in the superficial and deeper layers of involved epithelium give bright magenta color.
Histological features include:- 1-hyperparakeratosis. Treatment:- 1 Nystatin. Leukodema:- Def. It is an abnormality of the buccal mucosa of unknown cause. It may be considered as variation of the normal rather than a disease. Etiology:- Causative factors as: smoking, alcohol, bacterial infection. Site: buccal mucosa, labial mucosa, floor of the mouth.
Shape: bilateral, symmetrical filmy opalescence mucosa become grayish white in late stage with corrugated surface. Histopathology:- 1-The epithelium is acanthotic, parakeratotic. Diagnosis:- 1-gentle stroking with a gauze pad will not remove it not rub off 2-With stretching of buccal mucosa, the opaque changes will dissipate. Treatment:- No treatment is necessary. Mucosal burns:- Chemical Burns:- Topical applications of chemicals as aspirin tablets which is used in self medication and held locally against a painful tooth and allowed to dissolve slowly.
Thermal Burns:- Common in hard palatal mucosa caused by hot, sticky food. Premalignant lesion:- It is a benign , morphologically altered tissue that has a greater than normal risk of malignant transformation.
Leukoplakia:- Def. It is a white patch or plaque that cannot be characterized clinically or pathologically as any other disease. It is a clinical term. Etiology:- Exact etiology is unknown ,it may be:- 1-tobacco.
Clinically:- Age: middle age decades. Site: Tongue, floor of mouth, buccal mucosa, palate, lower lip, retro molar sites. Shapes:- 1-mild thin leukoplakia. Leukoplakia Proliferative verrucous leukoplakia Speckled Leukoplakia Histopathology:- It varies as follow:- 1-Hyperkeratosis: thickened keratin layer of surface epithelium either hyperparakeratosis or hyperorthokeratosis.
Epithelial dysplasia Epithelial dysplasia is classified according to the severity as follow:- Mild: when alterations limited to basal and parabasal layers. Moderate: when alterations involve from basal layer to midportion of spinous layer. Severe: when alterations involve from basal layer to a level above midpoint of epithelium. Carcinoma in situ:- Def. Dysplastic epithelial cells that extend from basal layer to surface of mucosa Top-to- Bottom changes.
It is called intra-epithelial carcinoma. Treatment:- 1-Identification of the etiological factor discontinuation. Candidal Leukoplakia:- Age: adult Histopathology:- 1-mitotic activity is 4 times higher than that of idiopathic leukoplakia. Treatment: antifungal therapy may improve the condition. Nicotinic Stomatitis:- Def. It is the most frequently leukoplakic lesion of the palate. Your doctor or dentist will examine your lips and mouth to look for abnormalities — areas of irritation, such as sores and white patches leukoplakia.
Removal of tissue for testing biopsy. The most common oral precancerous lesions are oral leukoplakia , oral submucous fibrosis OSMF , and oral erythroplakia. Leukoplakia is different from other causes of white patches such as thrush or lichen planus because it can eventually develop into oral cancer. Common superficial oral lesions include candidiasis, recurrent herpes labialis, recurrent aphthous stomatitis, erythema migrans, hairy tongue, and lichen planus.
Oral cancer is cancer that starts in the mouth or throat. Oral cancer is fairly common and very curable if found and treated at an early stage. A healthcare provider or dentist usually finds oral cancer in its early stages because the mouth can be easily examined.
About one half of people with oral cancer will live more than 5 years after they are diagnosed and treated. More than half of oral cancers have spread when the cancer is detected. Oral cancer appears as a growth or sore in the mouth that does not go away.
Oral cancer , which includes cancers of the lips, tongue, cheeks, floor of the mouth , hard and soft palate, sinuses, and pharynx throat , can be life threatening if not diagnosed and treated early. Precancerous conditions of the mouth are changes to cells of the mouth that make them more likely to develop into cancer. These conditions are not yet cancer.
The most common precancerous conditions of the mouth are leukoplakia and erythroplakia. Why are white lesions white? Category: medical health dental health.
Payne TF. It is proposed that oral keratoses appear white because of the ability of abnormal oral keratin to evenly reflect the visible light spectrum because of the hydration of the keratin layer in a manner similar to the reaction of the stratum corneum of the epidermis to water. What does leukoplakia look like?
Can you scrape leukoplakia off? Can non smokers get leukoplakia? Does HPV cause leukoplakia? What are the first signs of mouth cancer? Signs and symptoms of mouth cancer may include:. A lip or mouth sore that doesn't heal. Who coined the term leukoplakia?
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