Oral Mucosa Lesions PDF

 Macules Well-circumscribed, flat lesions that noticeable because of their change from normal skin color. They may be red due to the presence of vascular lesions or inflammation, or pigmented due to the presence melanin, hemosiderin and any foreign material.  Pap...

 Macules Well-circumscribed, flat lesions that noticeable because of their change from normal skin color. They may be red due to the presence of vascular lesions or inflammation, or pigmented due to the presence melanin, hemosiderin and any foreign material.  Papules &Plaques  Papules: Solid lesions raised above the skin surface that are smaller than 1 cm in diameter.  Plaques: Solid raised lesions that are over 1 cm in diameter; they are large papules.  Nodules These lesions are present deep in the dermis, and the epidermis can be easily moved over them.  Vesicles & Bullae  Vesicles: Elevated blisters containing clear fluid that are under 1 cm in diameter.  Bullae: Elevated blister like lesions containing clear fluid that are over 1 cm in diameter  Pustules Pustules : Raised lesions containing purulent material.  Erosions & Ulcers Erosions: Moist red lesions often caused by the rupture of vesicles or bullae as well as trauma. Ulcers: A defect in the epithelium; it is a well- circumscribed depressed lesion over which the epidermal layer has been lost.  The normal colour of the oral mucosa The color of the oral mucosa is pink due to the passage of light through the translucent superficial layer of soft tissue. The light strikes the capillary bed and reflects back resulting in the pink color of the oral mucosa. Four factors contribute to the color of the oral mucosa: 1- Quantity and quality of blood 2- Thickness of oral mucosa 3- Presence of melanin 4- Degree of keratinization White colour of the oral mucosa is due to: 1.Keratin or parakeratin (hyperkeratosis or hyperparakeratosis). 2.  Prickle cell layer (acanthosis). 3. Intracellular edema (spongiosis). 4. Intercellular edema. 5.  Collagen fibers (fibrosis). 6. Pseudomembrane over the oral mucosa. 1- Keratin layer 2- Granular cell layer 3- Prickle cell layer 4- Basal cell layers Red colour of the oral mucosa is due to: 1. Thinning of the epithelium (atrophy). 2.  Vascularity: as in inflammation due to vasodilatation  WHITE AND RED LESIONS OF THE ORAL MUCOSA ➔White lesion of the oral mucosa is due to changes Over the epithelium Within Under the epithelium epithelium Pseudomembraneous Oral keratosis Oral submucous candidiasis fibrosis  CLINICAL CLASSIFICATION OF WHITE AND RED LESIONS I. Variation in structure and appearance of normal oral mucosa: Linea alba buccalis, leukoedema and fordyce's granules. II. Non keratotic white lesions (white lesions that can be rubbed off ): Aspirin Burns. Thrush  CLINICAL CLASSIFICATION OF WHITE AND RED LESIONS III. Keratotic white lesions (white lesions that cannot be rubbed off ): A. Keratotic white lesions WITH precancerous potential Smoker's keratosis. Smokeless tobacco induced keratosis. Syphilitic keratosis. Actinic keratosis. Leukoplakia. Lichen planus. Lupus erythematosus.  CLINICAL CLASSIFICATION OF WHITE AND RED LESIONS B. Keratotic White lesion Without Precancerous Potential Frictional (traumatic) keratosis. Glass blower's keratosis Keratotic lesion associate with dental restoration (electro galvanic keratosis) Nicotinic Stomatitis. IV. Oral Candidiasis.  Classification of red and white lesions Hereditary Infectious Leukoplakia Erythroplakia 1- Leukoedema 1- Oral Hairy Leukoplakia 2- White Sponge Nevus 2- Koplik’s spots 3- Hereditary Benign 3- Candidiasis Intraepithelial Dyskeratosis 4- Mucous Patches Autoimmune 4- Dyskeratosis Congenita 5- Parulis 1. Oral Lichen Planus 2. Lichenoid Reactions Reactive/Inflammatory 3. Lupus Erythematosus 1- Linea Alba (White Line) 2- Frictional (Traumatic) Keratosis 3- Cheek Chewing 4- Chemical Injuries of the Oral Mucosa 5- uremic stomatitis 6-Actinic Keratosis (Cheilitis) Miscellaneous Lesions 7- Smokeless Tobacco–Induced Keratosis Fordyce’s Granules 8- Nicotine Stomatitis Geographic Tongue Hairy Tongue (Black Hairy Tongue) Oral Submucous Fibrosis Hereditary White Lesions 1- Leukoedema 2- White Sponge Nevus 3- Hereditary Benign Intraepithelial Dyskeratosis 4- Dyskeratosis Congenita  Hereditary White Lesions 1-Leukoedema Leukoedema is a common mucosal alteration that represents a variation of the normal condition rather than a true pathologic change Clinical features:  The buccal mucosa bilaterally, and it may be seen rarely on the labial mucosa, soft palate, and floor of the mouth.  Leukoedema ▪It usually has a faint, whitish-grey, diffuse, and filmy appearance, with numerous surface folds resulting in wrinkling of the mucosa. ▪It cannot be scraped off, and it disappears or fades upon stretching the mucosa. It increases in black races.  Leukoedema  Microscopic examination: Thickening of the epithelium, with significant intracellular edema of the stratum spinosum. The surface of the epithelium may demonstrate a thickened layer of parakeratin.  Treatment No treatment is indicated for leukoedema since it is a variation of the normal condition. No malignant change has been reported. Leukoedema What is meaning of autosomal dominant? Autosomal dominant inheritance is a genetic trait or condition can be passed down from parent to child. One copy of a mutated (changed) gene from one parent can cause the genetic condition What is the meaning of autosomal recessive? In autosomal recessive inheritance is a genetic condition occurs when the child inherits one mutated copy of a gene from each parent What is difference between autosomal dominant and recessive? Autosomal dominant traits pass from one parent onto their child. Autosomal recessive traits pass from both parents onto their child.  2- White Sponge Nevus  White sponge nevus (WSN) is a rare autosomal dominant disorder.  The disease usually involves the oral mucosa and (less frequently) the mucous membranes of the nose, esophagus, genitalia, and rectum.  The lesions of WSN may be present at birth or may first manifest or become more intense at puberty.  Genetic analyses of families with WSN have identified a mutation in one allele of keratin 4 and keratin 13 gens, that leads to proline substitution for leucine within the keratin gene cluster on chromosome. Which usually occur in the oral mucosa  2- White Sponge Nevus Clinical features: White sponge nevus presents as bilateral symmetric white, soft, “spongy,” or velvety thick plaques of the buccal mucosa. Other sites in the oral cavity may be involved as the ventral tongue, floor of the mouth, labial mucosa, soft palate, and alveolar mucosa. The condition is usually asymptomatic and does not exhibit tendencies toward malignant change. White Sponge Nevus It is a rare autosomal-dominant disorder of the conjunctiva & oral mucosa. This disorder progresses during childhood with oral manifestations being similar to WSN as thick, corrugated white plaques affecting the buccal and labial mucosa (Symptomless). Candida superinfection is possible on oral lesions. White thick opaque gelatinous plaques may affect the conjunctiva with occasional corneal involvement. Eye lesions are found very early in life and increase over time. Patients might complain from tearing, photophobia, and itching of the eyes when the lesions are active (Should be evaluated by ophthalmologist) Hereditary benign intraepithelial dyskeratosis (HBID) also called Witkop-Von Sallmann syndrome, Dyskeratosis Congenita Abnormal skin pigmentation Nail dystrophy (approximately 90%) Oral premalignant leukoplakia Elevated risk for squamous cell carcinoma (80%) Dyskeratosis Congenita: an X-linked recessive trait with a marked male predilection & women showing less serious clinical manifestations.  Classification of red and white lesions Hereditary Infectious Leukoplakia Erythroplakia 1- Leukoedema 1- Oral Hairy Leukoplakia 2- White Sponge Nevus 2- Koplik’s spots 3- Hereditary Benign 3- Candidiasis Intraepithelial Dyskeratosis 4- Mucous Patches Autoimmune 4- Dyskeratosis Congenita 5- Parulis 1. Oral Lichen Planus 2. Lichenoid Reactions Reactive/Inflammatory 3. Lupus Erythematosus 1- Linea Alba (White Line) 2- Frictional (Traumatic) Keratosis 3- Cheek Chewing 4- Chemical Injuries of the Oral Mucosa 5- uremic stomatitis 6-Actinic Keratosis (Cheilitis) Miscellaneous Lesions 7- Smokeless Tobacco–Induced Keratosis Fordyce’s Granules 8- Nicotine Stomatitis Geographic Tongue Hairy Tongue (Black Hairy Tongue) Oral Submucous Fibrosis ORAL KERATOSIS ➔Is a group of white lesions that can not rupped or stripped off and have definite etiological factor. It is a reversible condition. Response of oral mucosa to insult:- ➔ Low grade insult + Long duration→ Keratosis. ➔ High grade insult + Short duration → Erosion & Ulceration Reactive/inflammatory white lesions  Linea Alba (White Line)  Frictional (Traumatic) Keratosis  Cheek Chewing  Chemical Injuries of the Oral Mucosa  Actinic Keratosis (Cheilitis)  Smokeless Tobacco–Induced Keratosis  Nicotine Stomatitis  Uremic stomatitis  Reactive and inflammatory white lesions 1- linea Alba (White Line) It is a horizontal streak on the buccal mucosa bilaterally at the level of the occlusal plane extending from the commissure to the posterior teeth. Treatment: No treatment is indicated for patients with linea Alba. 2- Frictional (Traumatic) Keratosis Clinical features:  Frictional (traumatic) keratosis is defined as a white plaque with a rough surface that is clearly related to an identifiable source of mechanical irritation.  Frictional keratosis is frequently associated with rough or maladjusted dentures and with sharp cusps and edges of broken teeth. Frictional (Traumatic) Keratosis Treatment:  Traumatic keratosis has never been shown to undergo malignant transformation.  Upon removal of the offending agent, the lesion should resolve within 2 weeks. Biopsies should be performed on lesions that do not heal to rule out a dysplastic lesion. 3- Cheek Chewing Cheek chewing is most commonly seen in people who are under stress or in psychological situations in which cheek and lip biting become habitual. The occurrence is twice as prevalent in females and three times more common after the age of 35 years.  Cheek Chewing  The lesions are most frequently found bilaterally on the posterior buccal mucosa along the plane of occlusion.  Patients often complain of roughness or small tags of tissue that they actually tear free from the surface. The lesions are poorly outlined whitish patches that may be intermixed with areas of erythema or ulceration. Treatment and prognosis:  Since the lesions result from an unconscious and/or nervous habit, no treatment is indicated.  A plastic occlusal night guard may be fabricated. 4- Chemical Injuries of the Oral Mucosa Transient non-keratotic white lesions of the oral mucosa are often a result of a variety of agents that are caustic when retained in the mouth for long periods of time, such as  Aspirin,  Silver Nitrate,  Formocresol,  Sodium Hypochlorite,  Dental Cavity Varnishes,  Acid Etching Materials,  Hydrogen Peroxide  Dentifrices & Mouthwashes (Cinnamon-flavored Dentifrice).  Chemical Injuries of the Oral Mucosa Typical features: ❑The lesions are usually located on the mucobuccal fold area and gingiva. ❑The injured area is irregular in shape, white, covered with a pseudo membrane, and very painful.  Chemical Injuries of the Oral Mucosa Treatment and prognosis: ▪ The best treatment of chemical burns of the oral cavity is prevention. ▪ The proper use of a rubber dam during endodontic procedures reduces the risk of iatrogenic chemical burns. ▪ Most superficial burns heal within 1 or 2 weeks. ▪ A protective emollient agent such as a film of methyl cellulose may provide relief. Deep-tissue burns and necrosis may require careful débridement of the surface, followed by antibiotic coverage.  Uremic Stomatitis Uremic stomatitis is considered as chemical burn. It is a rare disorder that may occur in patients with acute or chronic renal failure due to increased concentration of urea and its products in the blood and saliva. The pathogenesis of oral lesions is not clear. It usually appears when blood concentration of urea exceeds 30 mmol/1. Treatment:  The oral lesions usually improve after hemodialysis.  A high level of oral hygiene, mouthwashes. 6- Actinic Keratosis (Cheilitis)  Actinic (or solar) keratosis is a premalignant epithelial lesion that is directly related to long-term sun exposure.  These lesions are classically found on the vermilion border of the lower lip as well as on other sun-exposed areas of the skin (forehead, cheeks, forearms). The surface may be crusted and rough to the touch.  Actinic Keratosis (Cheilitis) Treatment and prognosis:  A small percentage of these lesions will transform into squamous cell carcinoma. Biopsies should be performed on lesions that repeatedly ulcerate, crust over, or show a thickened white area.  Avoid exposure to solar radiation.  Use sun screen lotion or cream (Para aminobenzoic acid), absorbs sunlight.  Use of sun blockers (zinc oxide), scatters the sunlight.  Periodic recall is mandatory.  Biopsy should be performed on lip lesions that do not show regression after stop the sun light exposure. If biopsy reveals epithelial dysplasia, laser surgery, cryotherapy may be performed.  Chemotherapeutic agents such as topical 5% fluorouracil (antimetabolite) have been used with some success.  7-Smokeless Tobacco–Induced Keratosis snuff dipper’s keratosis tobacco pouch keratosis Typical features: ❖Smokeless tobacco are seen in the area contacting the tobacco. ❖The most common area of involvement is the anterior mandibular vestibule, followed by the posterior vestibule. ❖The surface of the mucosa appears white and is granular or wrinkled. ❖These lesions are accepted as precancerous Smokeless Tobacco–Induced Keratosis ❖Commonly noted is a characteristic area of gingival recession with periodontal-tissue destruction in the immediate area of contact. This recession involves the facial aspect of the tooth or teeth and is related to the amount and duration of tobacco use. ❖The lesion is usually asymptomatic and is discovered on routine examination. Smokeless Tobacco–Induced Keratosis Treatment and prognosis: Cessation of use almost always leads to a normal mucosal appearance within 1 to 2 weeks. Biopsy specimens should be obtained from lesions that remain after 1 month.  8- Nicotine Stomatitis stomatitis nicotina palati smoker’s palate  White lesion that develops on the hard and soft palate in heavy cigarette, pipe, and cigar smokers.  The lesion is not considered to be premalignant.  Reverse smoking” produces significantly more pronounced palatal alterations that may be erythroleukoplakia and that are definitely considered premalignant.  Nicotine Stomatitis Typical features:  This condition is most often found in older males with a history of heavy long-term cigar, pipe, or cigarette smoking.  Due to the chronic insult, the palatal mucosa becomes diffusely gray or white. Numerous slightly elevated papules with punctate red centers that represent inflamed altered minor salivary gland ducts are noted. Nicotine Stomatitis Treatment and prognosis: Nicotine stomatitis is completely reversible once the habit is discontinued. The lesions usually resolve within 2 weeks of cessation of smoking. The severity of inflammation is proportional to the duration and amount of smoking. A biopsy should be performed on any white lesion of the palatal mucosa that persists after 1 month of discontinuation of smoking habit.  Classification of red and white lesions Hereditary Infectious Leukoplakia Erythroplakia 1- Leukoedema 1- Oral Hairy Leukoplakia 2- White Sponge Nevus 2- Koplik’s spots 3- Hereditary Benign 3- Candidiasis Intraepithelial Dyskeratosis 4- Mucous Patches Autoimmune 4- Dyskeratosis Congenita 5- Parulis 1. Oral Lichen Planus 2. Lichenoid Reactions Reactive/Inflammatory 3. Lupus Erythematosus 1- Linea Alba (White Line) 2- Frictional (Traumatic) Keratosis 3- Cheek Chewing 4- Chemical Injuries of the Oral Mucosa 5- uremic stomatitis 6-Actinic Keratosis (Cheilitis) Miscellaneous Lesions 7- Smokeless Tobacco–Induced Keratosis Fordyce’s Granules 8- Nicotine Stomatitis Geographic Tongue Hairy Tongue (Black Hairy Tongue) Oral Submucous Fibrosis Infectious white lesions and white and red lesions  Oral Hairy Leukoplakia  Koplik’s spots  Candidiasis  Mucous Patches  Parulis  Oral Hairy Leukoplakia  Oral hairy leukoplakia is a corrugated white lesion that usually occurs on the lateral or ventral surfaces of the tongue in patients with severe immunodeficiency.  The most common disease associated with oral hairy leukoplakia is HIV infection.  Epstein-Barr virus (EBV) is implicated as the causative agent in oral hairy leukoplakia.  Oral hairy leukoplakia may present as a plaque-like lesion and is often bilateral.  Diagnosis  The definitive diagnosis can be established by demonstrating the presence of EBV through in situ hybridization, electron microscopy, or polymerase chain reaction (PCR).  Treatment and prognosis  No treatment is indicated. The condition usually disappears when antiviral medications such as zidovudine, acyclovir, or gancyclovir are used in the treatment of the HIV infection and its complicating viral infections.  Koplik’s spots  Measles is a virus infection caused by Paramyxovirus.  Measles is predominantly the disease of children, which appear in winter and spring following incubation period of 7-10 days.  Koplik’s spots have been reported in 97% of children. After 1-2 days follow prodromal symptoms and 2-3 days before the developments of skin lesion (cutaneous rash of measles) Koplik’s spots begin to exist.  Koplik’s spots  As soon as the skin rash develops Koplik’s spots disappear.  Koplik’s spots do not appear in German measles.  Koplik’s spots are commonly seen on mucosa of the cheeks and lips as a small bluish white specks surrounded by a bright red margin or a grain of rice on an erythematous base.  Complications of measles are encephalitis and thrombocytopenia purpura.  Candidiasis  Candidiasis” refers to a multiplicity of diseases caused by a yeast like fungus, Candida albicans, and is the most common oral fungal infection in humans.  Candida species are normal inhabitants of oral flora in 40% -60% of the population at low concentration.  Candida is predominantly an opportunistic infectious agent that is poorly equipped to invade and destroy tissue.  The disease may be either acute or chronic in nature according to the course of the disease.  Predisposing factors Marked changes in oral microbial flora occur following Antibiotics administration of antibiotics Topical or systemic antibiotics reduce the count of oral bacteria so give a chance for Candida to grow causing infection. Smoking localized epithelial alterations allowing candidal colonization. Cigarette smoke may also provide nutrition for candida albicans. Xerostomia may be secondary to smoking, salivary gland Xerostomia disease, certain drugs, radiation,..... Reduced salivary secretion that reduced salivary IgA which allows for candidal invasion into the tissue. Corticosteroids are immunosuppressive drugs which inhibit Corticosteroid lymphocytes.. therapy Topical or systemic corticosteroids results in candidal infection so, use of antifungal drug for one week out of four weeks of corticosteroid therapy.  Predisposing factrors Infants acquire the infection from: their mothers during labor or Age defective hygiene of bottles. -The immune system is not well developed in infants, thus they are liable for infection. Old age due to: Malnutrition and malabsorption, defective immune response or low vertical dimension. During pregnancy the following changes may be responsible for Pregnancy candidal infection: -Increased estrogen and progesterone which may act as substrate for pathogens. - Defective cell mediated immunity. Diabetes Diabetic individuals are liable to develop oral candidiasis due to the defect in immunity (especially neutrophils).  Classification of Oral Candidiasis Acute Chronic Pseudomembranous Atrophic Atrophic Hyperplastic 1-Denture sore mouth 1-Candidal leukoplakia Thrush 2-Angular cheilitis 2-Papillary hyperplasia 3-Median rhomboid of the palate glossitis 3-Median rhomboid glossitis (nodular) Candida antibiotic Iron deficiency Antibiotic sore anemia mouth  Acute Candidiasis 1- Acute Pseudomembranous Candidiasis (Thrush) Clinical Features:  It is a superficial infection of the outer layers of the epithelium, and it results in the formation of patchy white plaques or flecks on the mucosal surface.  Removal of the plaques by gentle rubbing or scraping usually reveals an area of erythema or even shallow ulceration.  Diagnosis and DD  A smear demonstrating a yeast or myelin is helpful when the diagnosis is uncertain.  The differential diagnosis of thrush includes food debris, habitual cheek biting, and rarely, a genetically determined epithelial abnormality such as white sponge nevus.  Acute Atrophic Candidiasis  Acute atrophic candidiasis presents as a red patch of atrophic or erythematous raw and painful mucosa, with minimal evidence of the white pseudomembranous lesions observed in thrush.  Acute Atrophic Candidiasis  Forms: - Antibiotic sore mouth, develops symptoms of oral burning, bad taste, or sore throat during or after therapy with broad- spectrum antibiotics. - Patients with chronic iron deficiency anemia may also develop atrophic candidiasis.  Removal of the cause such as withdrawal of the offending antibiotic and institution of appropriate oral hygiene leads to improvement.  Chronic Candidiasis Atrophic:  Denture sore mouth  Angular cheilitis  Median rhomboid glossitis Hypertrophic/hyperplastic:  Candidal leukoplakia  Papillary hyperplasia of the palate  Median rhomboid glossitis (nodular)  Denture Stomatitis (Denture Sore Mouth)  Denture stomatitis is a common form of oral candidiasis that manifests as a diffuse inflammation of the maxillary denture-bearing areas and that is often (15 to 65% of cases) associated with angular cheilitis.  Candida act as an endogenous infecting agent on tissue predisposed by chronic trauma to microbial invasion.  Denture Stomatitis  Soft liners in dentures provide a porous surface and an opportunity for additional mechanical locking of plaque and yeast to the appliance. In general, soft liners are considered to be an additional hazard for patients who are susceptible to oral candidiasis.  Denture sore mouth is rarely found under a mandibular denture due to the negative pressure that forms under the maxillary denture excludes salivary antibody (IgA) from this region, and yeast may reproduce, undisturbed, in the space between the denture and mucosa.  Lesions of chronic atrophic candidiasis have also been frequently reported in HIV-positive and AIDS patients.  Clinical Stages  The first stage consists of numerous palatal petechiae  The second stage displays a more diffuse erythema involving most of the denture- covered mucosa  The third stage includes the development of tissue granulation or nodularity (papillary hyperplasia). Denture sore mouth has to be differentiate from contact stomatitis in denture wearer Denture sore mouth Contact stomatitis Onset After long time of wearing 24-48 hrs after wearing denture denture Site Denture bearing areas mainly Denture bearing and upper denture contacting areas, both arches Patch test Negative Positive Treatment Antifungal drugs Antihistaminic  Treatment  Antifungal treatment will modify the bright red appearance of denture sore mouth and papillary hyperplasia specifically but will not resolve the basic papillomatous lesion where surgical excision may be required.  Antifungal therapy and cessation of denture wearing usually is advisable before surgical excision since elimination of the mucosal inflammation often reduces the amount of tissue that needs to be excised.  Yeast attached to the denture plays an important etiologic role in chronic atrophic candidiasis. Rinsing the appliance with a dilute (10%) solution of household bleach, soaking it in boric acid, or applying nystatin cream before inserting the denture will eliminate the yeast.  Angular Cheilitis  Angular cheilitis is the term used for an infection involving the lip commissures. The majority of cases is Candida associated and respond promptly to antifungal therapy.  Lesions are moderately painful, fissured due to accumulation of saliva in the skin folds at the commissural angles.  Angular Cheilitis Etiologic cofactors include:  Reduced vertical dimension  A nutritional deficiency (iron deficiency anemia and vitamin B or folic acid deficiency)  Diabetes  AIDS  Co-infection with staphylococcus and beta-hemolytic streptococcus.  Median Rhomboid Glossitis  Erythematous patches of atrophic papillae located in the central area of the dorsum of the tongue are considered a form of chronic atrophic candidiasis. When these lesions become more nodular, the condition is referred to as hyperplastic median rhomboid glossitis.  Chronic Hyperplastic Candidiasis  mycelial invasion of the deeper layers of the mucosa and skin occurs, causing a proliferative response of host tissue  Candidal leukoplakia is considered a chronic form of oral candidiasis in which firm white leathery plaques are detected on the cheeks, lips, palate, and tongue.  The differentiation of candidal leukoplakia from other forms of leukoplakia is based on finding periodic acid– Schiff (PAS)–positive hyphae in leukoplakic lesions.  IV-Immunocompromised (HIV)- associated candidiasis  patients who are on immunosuppressive drug regimens or who have HIV infection, cancer, or hematologic malignancies have an increased susceptibility to oral candidiasis.  This supports an important role for T lymphocytes in immunity to Candida, especially in regard to chronic candidiasis.  In HIV-infected patients who develop oral candidiasis, the level of salivary anti-Candida IgG is increased while serum and salivary IgA decrease.  Candidiasis in AIDS patient caused by …………………………. & ……………………………………………..  Treatment of oral candidiasis  Removal of predisposing factor but in patients whom cannot eliminate predisposing factors such as xerostomia and immunodeficiency may need either continuous or repeated treatment to prevent recurrences.  The consumption of yogurt (Lactobacillus acidophilus ) two to three times per week and improved oral hygiene can also help, especially if underlying predisposing factors cannot be eliminated. L. acidophilus is producing lactic acid, which keeps the pH level low and inhospitable to Candida  Treatment of oral candidiasis  topical administered medications are now available as nystatin and amphotericin B. The majority of acute oral Candida infections respond rapidly to topical nystatin 4 times daily for three weeks and will not recur.  Nystatin in cream form may also be applied directly to the denture or to the corners of the mouth  Systemic therapy includes the use of any one of these three: ketoconazole, itraconazole, and fluconazole.  A once-daily dose of 200 mg of ketoconazole, 100 mg of fluconazole, or itraconazole oral suspension (100 to 200 mg/d) for 2 weeks. When these medications are used for this short period, side effects such as increased liver enzymes, abdominal pain, and pruritus are rare.  Classification of red and white lesions Hereditary Infectious Leukoplakia Erythroplakia 1- Leukoedema 1- Oral Hairy Leukoplakia 2- White Sponge Nevus 2- Koplik’s spots 3- Hereditary Benign 3- Candidiasis Intraepithelial Dyskeratosis 4- Mucous Patches Autoimmune 4- Dyskeratosis Congenita 5- Parulis 1. Oral Lichen Planus 2. Lichenoid Reactions Reactive/Inflammatory 3. Lupus Erythematosus 1- Linea Alba (White Line) 2- Frictional (Traumatic) Keratosis 3- Cheek Chewing 4- Chemical Injuries of the Oral Mucosa 5- uremic stomatitis 6-Actinic Keratosis (Cheilitis) Miscellaneous Lesions 7- Smokeless Tobacco–Induced Keratosis Fordyce’s Granules 8- Nicotine Stomatitis Geographic Tongue Hairy Tongue (Black Hairy Tongue) Oral Submucous Fibrosis Idiopathic “True” Leukoplakia  Leukoplakia is a white keratotic patches that cannot be rubbed off and a precancerous lesion with a recognizable risk for malignant transformation.  Precancerous lesion as a “morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart.”  Leukoplakia is defined as “a white patch or plaque that cannot be characterized clinically or pathologically as any other disease”.  Etiology Unknown Tobacco usage Alcohol consumption Sunlight  Etiology  Candida albicans  Human papilloma virus (HPV)  Electrogalvanic current  Chemical irritation  Systemic predisposing factors: nutritional deficiency (Vit B 12, Iron deficiency) when exposed to various local insults may predispose to both leukoplakia and carcinoma.  Clinical Features  Leukoplakia: adult men older than 50 years of age.  Occur on any mucosal surface, buccal mucosa, vermilion border of the lower lip, and gingiva. They are less common on the palate, maxillary mucosa, retromolar area, floor of the mouth, and tongue and infrequently causes discomfort or pain.  Lesions of the tongue and the floor of the mouth account for more than 90% of cases that show dysplasia or carcinoma.  Early lesions are usually soft in consistency, while late appears as a leathery white patch and may show evidence of loss of elasticity and flexibility.  Borders may be well or ill defined and surface may be smooth or rough, flat or elevated or verrucous.  Subtypes  “Homogeneous leukoplakia” (or “thick leukoplakia”) well-defined white patch, localized or extensive, that is slightly elevated and that has a fissured, wrinkled, or corrugated surface. On palpation, these lesions may feel leathery to “dry, or cracked mud- like.”  Subtypes  Nodular (speckled) leukoplakia (Candida leukoplakia) is granular or non-homogeneous. It is a mixed red-and-white lesion in which keratotic white nodules or patches are distributed over an atrophic erythematous background. This type of leukoplakia is associated with a higher malignant transformation rate.  Subtypes  Verrucous leukoplakia” or “verruciform leukoplakia” is a thick white lesion with papillary surfaces in the oral cavity. These lesions are usually heavily keratinized and are most often seen in older adults in the sixth to eighth decades of life.  Histopathologic Features Benign form: there may be various combinations of hyperkeratosis, hyperparakeratosis and acanthosis and the basal cell layer is always intact. There is diffused chronic inflammatory cell infiltration into the underlying connective tissue.  Histopathologic Features  Epithelial dysplasia: the diagnosis is made when less than the complete thickness of the epithelium demonstrates the characteristic features of dysplasia, this includes the presence of:  Mitosis is increased and abnormal  Individual cell keratinization  Alteration in the nuclear cytoplamic ratio  Loss of polarity and disorientation of the cells  Hyperchromatism  Large prominent nucleoli  Basiar hyperplasia  Division of nucleus without division of cytoplasm Classification of epithelial dysplasia  Mild: Changes involve only the basal one-third of the epithelium  Moderate: Changes involve up to the basal two- thirds of the epithelium  Severe: Changes involve more than the basal two- thirds of the epithelium  Carcinoma-in-situ: Changes involve the full thickness of the epithelium; however, the basement membrane is intact Classification of epithelial dysplasia Carcinoma in situ & Carcinoma  Carcinoma in situ: the epithelium demonstrates dyplasia throughout its full thickness (from top to bottom), but the basement membrane is intact,  Carcinoma: a loss of basement membrane and invasion of the underlying tissue. leukoplakia  Diagnosis and Management elimination of an irritant the persistent lesion, Topical antifungal drugs for leukoplakic lesion disappears 2 weeks. Re-evaluation after antifungal No treatment and follow up the lesion regress the follow up Lesions that are not respond to therapy; of the lesion would be enough. biopsy has to be performed. toluidine blue and cytobrush techniques No sign of dysplasia No time should be wasted, and the lesion should be removed and follow up. Small lesion removed by Large lesion excisional biopsy Leave lesion and reevaluation Remove remainder of lesion surgical , Repeated biopsy 6-12 months follow up  Diagnosis and Management 1) A diagnosis of leukoplakia is made when adequate clinical and histologic examination fails to reveal an alternative diagnosis and when characteristic histopathologic findings for leukoplakia are present. 2)The use of antioxidant nutrients and vitamins have not been reproducibly effective in management. Programs have included single and combination dosages of vitamins A, C, and E.  Toluidine blue 1- The patient rinses for 20 seconds with 1% acetic acid to. clean the area; 2- then 20 seconds with plain water; 3- then 60 seconds with 1% aqueous toluidine blue solution; 4- then again 20 seconds with a 1% acetic acid; and finally with water for 20 seconds.  MECHANISM DYE Affinity Towards Nucleic Acid DNA On Applying Dysplastic and Anaplastic Cells Contain Toluidine more DNA Than Normal Cells Blue Increased So, It Delineates Areas Uptake In These Of Malignancy Areas INDICATIONS  Suspicious Lesions  Premalignant Lesions  To Select The Site For Biopsy  Mark The Extent Of The Lesion For Biopsy  Post Operative Evaluation - Recurrence INTERPRETATION  Dark Blue In Solid/Stippled Fashion – Malignancy  Light Blue Equivocal Stain – Malignancy Unless Proved Otherwise By Biopsy  LIMITATIONS  FALSE +VE – Traumatic and Inflammatory Ulcers  FALSE –VE – Keratotic White Lesion/Dysplasia Confined to Basal Layer Toluidine Blue and Cytobrush Techniques  Erythroplakia  “bright red velvety plaque or patch which cannot be characterized clinically or pathologically as being due to any other condition.  The majority of Erythroplakia (particularly those located under the tongue, on the floor of the mouth, and on the soft palate and anterior tonsillar pillars) exhibit a high frequency of premalignant and malignant changes.  The etiology of Erythroplakia is uncertain, most cases of Erythroplakia are associated with heavy smoking, (reverse smoking) with or without concomitant alcohol abuse.  Clinical Features  Older men, in the sixth and seventh decades of life.  Almost all the lesions are asymptomatic  Erythroplakia are more commonly seen on the floor of the mouth, the ventral tongue, the soft palate, and the tonsillar fauces, all prime areas for the development of carcinoma.  Clinical Features 1. “Homogeneous Erythroplakia, 2. Erythroplakia interspersed with patches of leukoplakia, 3. Granular or speckled Erythroplakia”.  Erythroplakia Histopathologic Features: Erythroplakia are histopathologically demonstrating severe epithelial dysplasia, carcinoma in situ, or invasive carcinoma. Differential Diagnosis:  Differentiation of Erythroplakia from benign inflammatory lesions of the oral mucosa can be enhanced using a 1% solution of toluidine blue, applied topically with a swab or as an oral rinse.  Clinically similar lesions may include erythematous candidiasis, areas of mechanical irritation, denture stomatitis, vascular lesions, and a variety of nonspecific inflammatory lesions.  Treatment and Prognosis  The treatment of Erythroplakia should follow the same principles outlined for that of leukoplakia.  Observation for 1 to 2 weeks following the elimination of suspected irritants is acceptable, but prompt biopsy at that time is mandatory for lesions that persist  Epithelial dysplasia or carcinoma in situ warrants complete removal of the lesion. Actual invasive carcinoma must be treated promptly according to guidelines for the treatment of cancer.  Since recurrence and multifocal involvement is common, long-term follow-up is mandatory.  elimination of an irritant Lesions that are not respond to therapy; Erythroplakia lesion biopsy has to be performed. toluidine blue disappears and cytobrush techniques No treatment and follow up No sign of dysplasia No time should be wasted, and the lesion should be removed and follow up. Small lesion removed by Large lesion excisional biopsy Leave lesion and reevaluation Repeated biopsy 6-12 months  Classification of red and white lesions Hereditary Infectious Leukoplakia Erythroplakia 1- Leukoedema 1- Oral Hairy Leukoplakia 2- White Sponge Nevus 2- Koplik’s spots 3- Hereditary Benign 3- Candidiasis Intraepithelial Dyskeratosis 4- Mucous Patches Autoimmune 4- Dyskeratosis Congenita 5- Parulis 1. Oral Lichen Planus 2. Lichenoid Reactions Reactive/Inflammatory 3. Lupus Erythematosus 1- Linea Alba (White Line) 2- Frictional (Traumatic) Keratosis 3- Cheek Chewing 4- Chemical Injuries of the Oral Mucosa 5- uremic stomatitis 6-Actinic Keratosis (Cheilitis) Miscellaneous Lesions 7- Smokeless Tobacco–Induced Keratosis Fordyce’s Granules 8- Nicotine Stomatitis Geographic Tongue Hairy Tongue (Black Hairy Tongue) Oral Submucous Fibrosis  Oral Lichen Planus  Oral lichen planus (OLP) is a common chronic immunologic inflammatory mucocutaneous disorder that varies in appearance from keratotic (reticular or plaque like) to erythematous and ulcerative.  About 28% of patients who have OLP have skin lesions. The skin lesions are flat violaceous papules with a fine scaling on the surface. Unlike oral lesions, skin lesions are usually self-limiting, lasting only 1 year or less.  Etiology and Diagnosis The etiology of lichen planus is not fully understood and can be divided into:  Idiopathic lichen planus: psychological stress and cell mediated immune response.  Lichnoid reaction: drug induced or graft versus host disease.  Virus C  Idiopathic Lichen Planus  Emotional stress has been implicated in the development of lichen planus as death of close relative or new environment, job.  Also, Diabetes, Hypertension and Lichen planus are disorder sharing emotional stress factor were found to be associated together ‟ Grinspan Syndrome.”  Cell mediated immune response: due to lymphocyte- epidermal interaction resulting in degeneration of basal cell layer. Langerhans cell recognize, process and present appropriate antigen altered kerationcytes to lymphocytes which has been attracted to the area by interleukin-1 secreated by Langerhans\ macrophages. Interleukin-1 can also stimulate T-cells to produce interleukin-2 which causes T-cells proliferation  Cytotoxic T-cells can damage basal cells by two mechanisms  Cytotoxic T-cells release cytotoxic proteins called perforin which form pores in the cell membrane of basal cells so basal cells absorb extracellular fluid and swell. Cell death occur by dilution of cytoplasmic components(liquefaction degeneration of basal cell layer).  Cytotoxic T-cells stimulate basal cells to undergo apoptosis or programmed cell death. The basal cells become shrunken with little eosinophilic cytoplasm and pyknotic nuclear fragments. - Those dead basal cells are called Civatte bodies which will be phagocytosed by adjacent basal cells or by macrophages. - Dead cells which are not phagocytosed are extruded into connective tissue and become coated with IgM and are called Colloid bodies.  Clinical Features  Age of onset: 50 years female  The skin lesions of lichen planus have been classically described as purple, pruritic, and polygonal papules and most common in the flexor surface of extremities.  The skin lesion resolves within 1-2 years, most commonly leaving hyper-pigmentation.  Kobner’s phenomena  Skin lesion characterized by Kobner’s phenomena (development of new lesion on normal looking skin following trauma as scratching). Heinrich Köbner  Clinical Features  OLP may occur at any oral mucosal site, but the buccal mucosa is the most common site followed by tongue and gingiva.  OLP may be associated with pain or discomfort, which interferes with function and with quality of life.  Lesions are bilateral and characterized by remission and exacerbation.  Clinical Features Lesions do not disappear on stretching, cannot be rubbed off, do not cause loss of flexibility of the oral mucosa.  Clinical Features  Lesions are surrounded by a network of bluish white lines called Wickham’s striae radiating from the periphery of the lesion. louis frédéric wickham  Reticular from  It consists of slightly elevated fine white lines (Wickham's striae) that produce lace-like pattern, fine radiating lines or annular lesion.  The patients may feel roughness while rubbing the tongue against the buccal mucosa or may notice change in the lip colour.  Papular form  It appears as discrete papules 0.5-1 mm in diameter on the well keratinized areas of the oral mucosa.  Plaque form  It appears as homogenous white patches which may resemble leukoplakia but there is no loss of pliability and flexibility.  Atrophic form  It appears as diffused, erythematous patches. Wickham's striae may radiate from the lesion.  Atrophic lichen planus involving the gingiva results in desquamative gingivitis (bright red edematous).  Atrophic lichen planus may be seen on the dorsum of the tongue resulting in atrophy of filiform and fungiform papillae.  Symptoms ranged from mild burning to severe pain.  Erosive from  It appears as an ulcerated area with irregular borders and covered by pseudomembrane. Erosive lesions probably develop as a complication of the atrophic process when the thin epithelium is abraded or ulcerated.  The periphery of the lesion is usually surrounded by wickham's striae.  The malignant transformation is more commonly noted in the erosive and the atrophic form.  Bullous form  It is a rare form of lichen planus that appears as vesicle or bullae that rupture resulting in chronic irregular ulcer.  Bullous and erosive form of lichen planus occur in the severe form of the disease when extensive degeneration of the basal layer of epithelium causes a separation of the epithelium from the underlying connective tissue.  Histopathologic Features (1) Areas of hyperparakeratosis or hyperorthokeratosis, often with a thickening of the granular cell layer and a saw-toothed appearance to the rete pegs. (2) “Liquefaction degeneration,” or necrosis of the basal cell layer, which is often replaced by an eosinophilic band. (3) A dense subepithelial band of lymphocytes. Isolated epithelial cells, shrunken with eosinophilic cytoplasm and one or more pyknotic nuclear fragments (Civatte bodies), are often scattered within the epithelium and superficial lamina propria. These represent cells that have undergone apoptosis. The linear sub-basilar lymphocytic infiltration is composed largely of T cells.  Immunofluorescent Studies  Direct immunofluorescence demonstrates a shaggy band of fibrinogen in the basement membrane zone in 90 to 100% of cases. Patients also may have multiple mainly IgM-staining cytoid bodies, usually located in the dermal papilla (Skin) or in the peribasalar area.  Differential Diagnosis  Lichenoid lesions (eg, drug-induced lesions, contact mercury hypersensitivity)  Erythema multiforme,  Lupus erythematosus,  Graft-versus-host reaction  Leukoplakia,  Squamous cell carcinoma,  Mucous membrane pemphigoid,  Candidiasis.  Management of lichen planus elimination of an irritant Reticular, plaque, papules Atrophic, bullous , erosive No treatment and follow up Corticosteroids + Retinoids Topical Systemic Intra lesional injection kenalog in orabase prednisone 5 mg-10 mg kenacort A diabetes and hypertension. Low dose systemic steroids and nonsteroidal anti-inflammatory drugs Candida overgrowth with clinical thrush may develop, requiring concomitant topical or systemic antifungal therapy. Other topical and systemic therapies Topical application of cyclosporine or reported to be useful, such as dapsone, tacrolimus appears to be helpful in doxycycline, and antimalarials. managing cases of OLP not response retinoid. to steroid.  Lichenoid Reactions Lichenoid reactions were differentiated from lichen planus on the basis of: (1) Their association with the administration of a drug, contact with a metal, the use of a food flavoring, or systemic disease. (2) Their resolution when the drug or other factor was eliminated or when the disease was treated. Lichenoid reaction in buccal mucosa, reaction to amalgam contact Drugs Induce Lichenoid Reaction  Gold therapy(Rheumatoid arthritis)  Non-steroidal anti-inflammatory drugs (NSAIDs)  Diuretics other anti-hypertensives  Oral hypoglycemic agents of the sulfonylurea type Drugs Induce Lichenoid Reaction  Classification of red and white lesions Hereditary Infectious Leukoplakia Erythroplakia 1- Leukoedema 1- Oral Hairy Leukoplakia 2- White Sponge Nevus 2- Koplik’s spots 3- Hereditary Benign 3- Candidiasis Intraepithelial Dyskeratosis 4- Mucous Patches Autoimmune 4- Dyskeratosis Congenita 5- Parulis 1. Oral Lichen Planus 2. Lichenoid Reactions Reactive/Inflammatory 3. Lupus Erythematosus 1- Linea Alba (White Line) 2- Frictional (Traumatic) Keratosis 3- Cheek Chewing 4- Chemical Injuries of the Oral Mucosa 5- uremic stomatitis 6-Actinic Keratosis (Cheilitis) Miscellaneous Lesions 7- Smokeless Tobacco–Induced Keratosis Fordyce’s Granules 8- Nicotine Stomatitis Geographic Tongue Hairy Tongue (Black Hairy Tongue) Oral Submucous Fibrosis  Lupus Erythematosus (Systemic and Discoid)  Systemic lupus erythematosus (SLE) is an immunologically mediated inflammatory condition that causes multi-organ damage and considered as a collagen or connective tissue disease.  Discoid lupus erythematosus (DLE) is a relatively common disease and has a great cosmetic significance because of its predilection for the face. It is less aggressive form affecting the skin and rarely progressing to the systemic form.  Subacute cutaneous lupus erythematosus described as lying intermediate between SLE and DLE. It has a mild systemic involvement and the appearance of some abnormal autoantibodies. Etiology of Lupus Erythromatosus 1-Immunologic factors: Auto-antibody formation 2- Genetic factors 3-Infectious (EBV, CMV, VZV) and environmental factor (sun exposure, drugs, chemical substances). Ex of drugs: hydralazine, methyldopa, chlorpromazine, isoniazid, quinidine and procainamide) 4- Endocrine factors: (hormones) high incidence in women in their childbearing years.  Drugs Hydralazine lowers blood pressure Methyldopa antihypertensive effect Chlorpromazine antipsychotic medication Isoniazid antibiotic used for the treatment of tuberculosis Quinidine antiarrhythmic agent in the heart Procainamide treatment of cardiac arrhythmias Discoid Lupus Erythematosus  Females in the third or fourth decade of life.  DLE is confined to the skin and oral mucous membranes and has a better prognosis than SLE.  DLE can present in both localized and generalized forms and is called chronic cutaneous lupus (CCL).  favor sun-exposed areas such as the face, chest, back, and extremities Discoid Lupus Erythematosus These lesions characteristically: 1- Expand by peripheral extension 2- Disk-shaped 3- Scar formation 4- Central atrophy 5- Loss of skin pigmentation Discoid Lupus Erythematosus  Skin lesions occur on the face, it involves malar regions and cross the bridge of the nose which gives butterfly distribution Discoid Lupus Erythematosus  The oral lesions can occur in the absence of skin lesions, but there is a strong association between the two. As the lesions expand peripherally, there is central atrophy, scar formation, and occasional loss of surface pigmentation.  The primary locations for these lesions include the buccal mucosa, palate, tongue, and vermilion border of the lips. Discoid Lupus Erythematosus Differential diagnosis: 1. Reticular or erosive lichen planus. Unlike lichen planus, the distribution of DLE lesions is usually asymmetric, and the peripheral striae are much thinner. 2. Leukoplakia: the diagnosis must be based not only on the clinical appearance of the lesions but also on the coexistence of skin lesions and on the results of both histologic examination and direct immunofluorescence testing. Systemic lupus Erythematosus  The lesions are frequently symptomatic,  often consist of one or more of the following components: erythema, surface ulceration, keratotic plaques, and white striae or papules.  They typically respond well to topical or systemic steroids. Clobetasol (a potent topical steroid) placed under an occlusive tray is very effective for temporary relief of these lesions. Raynaud's phenomenon is characterized by blood vessel spasms in the fingers, toes, ears or nose, usually brought on by exposure to cold. Raynaud's phenomenon and Raynaud's disease, a similar disorder, may be associated with autoimmune disorders such as rheumatoid arthritis, systemic lupus erythematosus and scleroderma.  Histopathologic Features  hyperorthokeratosis with keratotic plugs, atrophy of the rete ridges, and Liquefaction degeneration of the basal cell layer. Edema of the superficial lamina propria is also quite prominent.  Histopathologic Features  No band-like leukocytic inflammatory infiltrate seen in patients with lichen planus. Immediately subjacent to the surface epithelium is a band of PAS-positive material, and frequently there is a pronounced vasculitis in both superficial and deep connective tissue.  Another important finding in lupus is that direct immunofluorescence testing of lesional tissue shows the deposition of various immunoglobulins and C3 in a granular band involving the basement membrane zone. This is called the positive lupus band test. Diagnosis  Circulating antinuclear antibody (anti DNA) serum  Complement level is decreased c2, c3,c4  LE cell test : detect LE factor (ANA) LE cell is either a neutrophil or a macrophage that has engulfed (phagocytized) degraded nuclear material from another cell. The engulfed nuclear material takes up Haematoxylin stain strongly; this strongly-stained engulfed nuclear material is called LE body.  Photosensitivity:unusually strong reaction to sun light, causing a rash or flare.  Malignant Potential of Oral Lesions  The precancerous potential of intraoral discoid lupus is controversial.  Basal cell and squamous cell carcinomas have been reported to develop in healing scars of discoid lupus. However, this malignant change may have been caused by the radiation and ultraviolet light used in the treatment of lupus.  The development of squamous cell carcinoma has been described in lesions of discoid lupus involving the vermilion border of the lip, and actinic radiation may play an important adjunct role.  Oral Submucous Fibrosis  Oral submucous fibrosis (OSF) is a slowly progressive chronic fibrotic disease of the oral cavity and oropharynx, characterized by fibroelastic change and inflammation of the mucosa, leading to a progressive inability to open the mouth, swallow, or speak.  Causes: direct stimulation from exogenous antigens like Areca alkaloids or changes in tissue antigenicity that may lead to an autoimmune response. The inflammatory response releases cytokines and growth factors that promote fibrosis by inducing the proliferation of fibroblasts, up-regulating collagen synthesis and down- regulating collagenase production.  OSF is regarded as a premalignant condition, and many cases of oral cancer have been found coexisting with submucous fibrosis.  Etiology Several factors are believed to contribute to the development of OSF, including:  General nutritional and vitamin deficiencies.  Hypersensitivity to certain dietary constituents such as chili peppers, chewing tobacco.  The habitual use of betel and its constituents.  Clinical features  The disease first presents with a burning sensation of the mouth, particularly during consumption of spicy foods.  It is often accompanied by the formation of vesicles or ulcerations and by excessive salivation or xerostomia and altered taste sensations.  Gradually, patients develop a stiffening of the mucosa, with a dramatic reduction in mouth opening and with difficulty in swallowing and speaking.  Clinical features  The mucosa appears blanched and opaque with the appearance of fibrotic bands that can easily be palpated. The bands usually involve the buccal mucosa, soft palate, posterior pharynx, lips, and tongue.  OSF usually affects young individuals in the second and third decades of life but may occur at any age.  Limitation of function + marble Diagnosis like appearence Accumelation of palpable fibrotic bands Histopath. → Atrophy of epith. + loss of rete pegs +hyalinization of C.T. 156  Classification of red and white lesions Hereditary Infectious Leukoplakia Erythroplakia 1- Leukoedema 1- Oral Hairy Leukoplakia 2- White Sponge Nevus 2- Koplik’s spots 3- Hereditary Benign 3- Candidiasis Intraepithelial Dyskeratosis 4- Mucous Patches Autoimmune 4- Dyskeratosis Congenita 5- Parulis 1. Oral Lichen Planus 2. Lichenoid Reactions Reactive/Inflammatory 3. Lupus Erythematosus 1- Linea Alba (White Line) 2- Frictional (Traumatic) Keratosis 3- Cheek Chewing 4- Chemical Injuries of the Oral Mucosa 5- uremic stomatitis 6-Actinic Keratosis (Cheilitis) Miscellaneous Lesions 7- Smokeless Tobacco–Induced Keratosis Fordyce’s Granules 8- Nicotine Stomatitis Geographic Tongue Hairy Tongue (Black Hairy Tongue) Oral Submucous Fibrosis  Developmental White Lesions Fordyce’s Granules  Fordyce’s granules are ectopic sebaceous glands within the oral mucosa. Fordyce’s granules do not exhibit any association with hair structures in the oral cavity.  Fordyce’s granules present as multiple yellowish white or white papules. most commonly on the buccal mucosa and vermilion border of the upper lip. Occasionally, these may be seen on the retromolar pad area and the anterior tonsillar pillars.  Fordyce’s Granules  Men ˃ femal  The granules tend to appear during puberty and increase in number with age.  Fordyce’s granules are completely asymptomatic and are often discovered on routine examination. They are bilateral and become accentuated on stretching the oral mucosa.  Histologically: normal sebaceous glands Treatment no treatment is indicated, no biopsy is usually required. Fordyce’s granules on the vermilion border of the upper lip may require surgical removal for esthetic reasons.  Geographic Tongue  Geographic tongue is a common benign condition dorsal surface of the tongue. women more than men.  This condition is characterized initially by the presence of small, round to irregular areas of dekeratinization and desquamation of filiform papillae. The elevated margins around the red zones are white to slighty yellowish white. Etiology of Geographic Tongue 1. Association with psoriasis 2. Atopic patients who have intrinsic asthma and rhinitis. 3. Family history of asthma, eczema, and hay fever. 4. Juvenile diabetes 5. Patients with pernicious associated with folic acid deficiency 6. Pregnant patients: hormonal fluctuations. 7. Reiter’s syndrome. (arthritis, urethritis, conjunctivitis, lesions of the skin and mucosal surfaces) Hairy Tongue (Black Hairy Tongue) Hairy tongue” is a clinical term describing an abnormal coating on the dorsal surface of the tongue. Hairy tongue results from the defective desquamation of cells that make up the secondary filiform papilla. This buildup of keratin results in the formation of highly elongated hairs, which is the hallmark of this entity. The cause of black hairy tongue Unknown may be:  Tobacco (heavy smoking) and psychotropic agents.  Broad-spectrum antibiotics such as penicillin.  The use of systemic steroids.  The use of oxidizing mouthwashes or antacids  The overgrowth of fungal or bacterial organisms.  Radiation therapy for head and neck malignancies  Poor oral hygiene can exacerbate this condition. The common etiologic factor for all these influences may be the alteration of the oral flora by the overgrowth of yeast and chromogenic bacteria.  black hairy tongue  Anterior two-thirds of the dorsum of the tongue, with a predilection for the midline just anterior to the circumvallate papillae. The patient presents with elongated filiform papillae and lack of desquamation of the papillae.  The tongue appears thickened and matted. Depending on the diet and the type of organisms present, the lesions may appear to range from yellow to brown to black or tan and white.  Black Hairy Tongue  Although the lesions are usually asymptomatic, the papillae elongated and may cause a gag reflex or a tickle in the. They may also result in halitosis or an abnormal taste.  A biopsy is usually unnecessary. Treatment consists of eliminating the predisposing factors if any are present. Cessation of smoking or discontinuation of oxygenating mouthwashes or antibiotics will often result in resolution.  Improvement in oral hygiene is important, especially brushing or scraping of tongue.  Classification of red and white lesions Hereditary Infectious Leukoplakia Erythroplakia 1- Leukoedema 1- Oral Hairy Leukoplakia 2- White Sponge Nevus 2- Koplik’s spots 3- Hereditary Benign 3- Candidiasis Intraepithelial Dyskeratosis 4- Mucous Patches Autoimmune 4- Dyskeratosis Congenita 5- Parulis 1. Oral Lichen Planus 2. Lichenoid Reactions Reactive/Inflammatory 3. Lupus Erythematosus 1- Linea Alba (White Line) 2- Frictional (Traumatic) Keratosis 3- Cheek Chewing 4- Chemical Injuries of the Oral Mucosa 5- uremic stomatitis 6-Actinic Keratosis (Cheilitis) Miscellaneous Lesions 7- Smokeless Tobacco–Induced Keratosis Fordyce’s Granules 8- Nicotine Stomatitis Geographic Tongue Hairy Tongue (Black Hairy Tongue) Oral Submucous Fibrosis  Classification of Oral Candidiasis Acute Chronic Pseudomembranous Atrophic Atrophic Hyperplastic 1-Denture sore mouth 1-Candidal leukoplakia Thrush 2-Angular cheilitis 2-Papillary hyperplasia 3-Median rhomboid of the palate glossitis 3-Median rhomboid glossitis (nodular) Candida antibiotic Iron deficiency Antibiotic sore anemia mouth  Classification of red and white lesions white lesions associated with Immunological Variation in normal mucosa Skin lesion white lesions 1- Dyskeratosis Congenita 1- Linea alba 2- Actinic keratosis 2- Leukodema Oral Lichen Planus 3- Mucous patches 3- Fordyce’s granules Lichenoid Reactions 4- Lichen planus Lupus Erythematosus 5- Lupus erythrematousum Graft-versus-host 6- Graft versus host disease Disease Premalignant white lesions 1- Dyskeratosis Congenita 2- Actinic keratosis 3- Smokless tobacco 4- Revese smoking 5- Leukoplakia 6- Erythroplakia 7- Lichen planus 8- Lupus erythrematousum 9- Oral submucous fibrosis THANK YOU