W8 Lichen Planus & Red & White Lesions (1) PDF

1 Lesions of oral Mucosa OTHER RED and WHITE LESIONS and CONDITIONS COMPILATION FROM Burkett's and Color atlas LECTURE OBJECTIVE To enumerate etiology, pathogenesis , differential diagnosis of red oral lesions 1. INTRODUCTION 2. CLASSIFICATION 3. DESCRIPTION...

1 Lesions of oral Mucosa OTHER RED and WHITE LESIONS and CONDITIONS COMPILATION FROM Burkett's and Color atlas LECTURE OBJECTIVE To enumerate etiology, pathogenesis , differential diagnosis of red oral lesions 1. INTRODUCTION 2. CLASSIFICATION 3. DESCRIPTION OF INDIVIDUAL LESIONS 4. DIFFERENTIAL DIAGNOSIS A white appearance of the oral mucosa may be caused by a variety of factors. The oral epithelium may be stimulated to an increased production of keratin (hyperkeratosis, Composition 1) or an abnormal but benign thickening of stratum spinosum (acanthosis, Composition 2). Intra- (Composition 3) and extracellular accumulation of fluid in the epithelium may also result in clinical whitening. Necrosis of the oral epithelium, which may also be perceived as a white lesion, may occur when the oral mucosa is exposed to toxic chemicals. Microbes, particularly fungi, can produce whitish pseudomembranes consisting of sloughed epithelial cells, fungal mycelium, and neutrophils, which are loosely attached to the oral mucosa (Composition 4). A red lesion of the oral mucosa may develop as the result of atrophic epithelium (Composition 5), characterized by a reduction in the number of epithelial cells (Composition 6) or increased vascularization. 2  3 A lesion is a localized area of disease or injury in any organ or tissue of the body” Papule: Well circumscribed, solid, raised lesion up to 1 cm in diameter Plaque: Well circumscribed solid raised lesion more than 1 cm in diameter Classification red and white lesions 1. Variations from normal Linea alba Fordyce granules Leukoedema 2. Non-Keratotic white lesions Habitual cheek & Lip biting Burns  4 Uremic stomatitis Radiation mucosistis Lesions of specific infections like measels, mucous patches in secondary syphilis 3. Oral candidiasis ~ Acute pseudomembranous ~ Acute atrophic ~ Chronic atrophic ~ Chronic hypertrophic 4. Keratotic white lesions with no increased potential for oral cancer ~ Stomatitis nicotina palati ~ Traumatic keratosis ~ Focal epithelial hyperplasia ~ Psoriasiform lesions ~ Psoriasis, Geographic tongue ~ Oral genodermatosis 5. Red and white lesions with unknown or increased malignant potential ~ Leukoplakia ~ Erythroplakia ~ Oral submucous fibrosis ~ Lichen planus ~ Actinic keratosis, Cheilitis ~ Discoid lupus erythematosus ~ Dyskeratosis congenita ~ Carcinoma in situ ~ Bowen’s disease ~ Erythema multiforme, lupus erythematosus  5 Linea alba (WHITE LINE) Linea alba White line ,a horizontal streak on the buccal Mucosa at the level of occlusal plane extending from commisure to posterior teeth. Etiology: pressure, frictional irritation or sucking trauma No treatment required Fordyce’s granules/spots Fordyce’s granules/spots Ectopic sebacious glands with in normal mucosa Present in 80 to 90% of population Present as multiple yellowish white or white papules Seen in buccal mucosa, vermillion border of upper lip, Retromolar pad area and anterior to tonsillar area More common in men Appear at puberty and increase with age  6 Leukoedema Leukoedema (increase edema in epithelium) Common mucosal alteration seen on buccal mucosa Bilaterally Faint white diffuse and filmy appearance with Many surface folds resulting in surface wrinkling cannot be scrapped Dissapears on streching Differential diagnosis Leukoplakia, cheek biting lesion Habitual cheek/lip biting Habitual cheek/lip biting White plaque with rough surface on buccal mucosa or lips Appear paler than sorrounding tissue Because of stress person keeps biting Differential diagnosis Leukoplakia, Candidiasis, chemical burn  7 Burns- thermal, Results from intake of hot beverages or foods. Most commonly due to hot pizzas and cheese dishes. Burns can also occur from hot dental instruments or molten impression compound – Commonly seen on the lips and commisures. Burns- , chemical, Causes of chemical burns: aspirin burn, hydrogen peroxide, sodium hypochlorite, Irregularly shaped with white pseudomembrane covered lesion Lesion are pain full Gentle pressure causes white material to slide and ulceration Develops with erythema Lesion is scrappable Differential diagnosis candidiasis Treatment Prevention Palliative treatment Topical anesthetic mouth rinse diphen hydramine hydrochloride Lignocaine gel  8 If secondary infection antibiotic Uremic stomatitis Occurs in severe untreated renal failure (chronic) patients. Barries classification of uremic stomatitis consists of – – Type I – Erythemopultaceous – Type II – Ulcerative form Lichenoid reactions  Lichenoid reactions represent a family of lesions with different etiologies with a common clinical and histologic appearence.  Oral lichenoid reactions include the following disorders:  Lichen planus  Lichenoid contact reactions  Lichenoid drug eruptions  Lichenoid reactions of graft-versus-host disease (GVHD) Oral lichen Planus (OLP)  Oral lichen planus (OLP) may contain both red and white elements and provide, together with the different textures, the basis for the clinical classification of this disorder.  The white and red components of the lesion can be a part of the following textures and types  9  Reticulum  Papules  Plaque-like  Bullous  Erythematous  Ulcerative  The Reticular form of OLP is characterized by fine white lines or striae  The striae may form a network but can also show annular (circular) patterns.  Although reticular OLP may be encountered in all regions of the oral mucosa, most frequently this form is observed bilaterally in the buccal mucosa and rarely on the mucosal side of the lips.  Reticular OLP can sometimes be observed at the vermilion border. The Papular type of OLP is usually present in the initial phase of the disease.  It is clinically characterized by small white dots, which in most occasions intermingle with the reticular form.  Sometimes the papular elements merge with striae as part of the natural course.  11 Plaque-type OLP shows a homogeneous well-demarcated white plaque often, but not always, surrounded by striae.  Plaque-type lesions may clinically be very similar to homogeneous oral leukoplakias.  The difference between these two mucosal disorders is the simultaneous presence of reticular or papular structures in the case of plaque-like OLP.  This form is most often encountered in smokers and the lesions can transfer into oral squamous cell carcinomas. Erythematous (atrophic) OLP is characterized by a homogeneous red area.  When this type of OLP is present in the buccal mucosa or in the palate, striae are frequently seen in the periphery.  Some patients may display erythematous OLP exclusively affecting attached gingiva.  This form of lesion may occur without any papules or striae and presents as desquamative gingivitis. Ulcerative lesions are the most disabling form of OLP  Clinically, the fibrin-coated ulcers are surrounded by an erythematous zone frequently displaying radiating white striae.  As for the erythematous form of OLP, the affected patient complains of a smarting sensation in conjunction with food intake.  11  Differential Diagnosis  Discoid lupus erythematosus (DLE)- The striae present in DLE are typically more prominent, with a more marked hyperkeratinization, and the striae may abruptly terminate against a sharp demarcation  Homogeneous oral leukoplakia- is not featured with papular or reticular elements.  Mucous membrane pemphigoid -the epithelium is easily detached from the connective tissue by a probe or a gentle searing force (Nikolsky’s phenomenon).  Erythema multiforme- Do not typically appear with reticular or papular elements in the periphery of the ulcerations. Management  Since the etiology behind OLP is unknown, current treatment strategies are aiming at reducing or eliminating symptoms.  Several topical drugs have been suggested, including steroids, calcineurin inhibitors (cyclosporine and tacrolimus), retinoids, and ultraviolet phototherapy  12 Radiation mucositis Secondary to radiation therapy for head and neck cancers Develops at the end of first week of therapy There will be redness followed by pseudomembrane covered With greyish white slough Differential diagnosis: (history of radiation therapy) leads to diagnosis Treatment : Topical anesthetics mouth rinse Lesions of specific infections Koplik’s spot- Measles Kopliks spots caused by measels virus Common in children Focal white spot less than 1cm oval or round in shape on buccal mucosa or gingiva Differential diagnosis Fordyces spot Cheek biting keratosis Mucous patches- Secondary syphilis Appears as small discrete white lesions D/D: Candidiasis  13 Stomatitis nicotina palati (smokers palate)  Stomatitis nicotina palate refers to a specific white lesion that develops on the hard and soft palate in heavy cigarette, pipe and cigar smokers.  The lesions are restricted to areas that are exposed to a relatively concentrated amount of hot smoke during inhalation. Although it is associated closely with tobacco smoking, the lesion is not considered to be premalignant Reverse smoking seen in South American and Asian populations, produces significantly more pronounced palatal alterations that are definitely considered pre-malignant. Clinical features Age: Adults Sex: Males > females Site: palatal mucosa (‘nicotina palatini’ Symptoms: mostly asymptomatic  14 Signs: initial stages red burn like lesion (spots) ~ it is seen as well-defined, white or gray patch/plaque, which is non-scrapable. ~ Small nodular elevations with red spots in the centre are interspersed in the white lesion. ~ Erosion/ulceration may be seen in reverse smokers Treatment: In conventional smokers 1. Stoppage of smoking habit 2. Patient education 3. Covering of palatal mucosa with acrylic plate/denture 4. If the lesion doesn’t disappear after 3-4 weeks, periodic observation or histological examination is indicated. Treatment: In reverse smokers 1. Stoppage of smoking habit 2. Patient education 3. Surgical excision if dysplastic on histological examination 4. Periodic observation Traumatic keratosis Clinical features Age: young adults, adults, Sex: No predilection Site: buccal mucosa, gingiva, lateral aspect of tongue Symptoms: mostly asymptomatic Signs:  15 ~ appears as a well-defined, white plaque, which is non-scrapable. ~ Loss of strechability of affected mucosa Differential diagnosis Leukoplakia White spongy nevus Treatment: 1. Removal of cause If lesion does not disappear after 2-3 weeks, surgical excision and histological examination White spongy nevus (oral genodermatosis) Clinical features: Rare genetic disease May be present at birth Appear as bilaterally symmetrical white spongy thick plaques on buccal mucosa Lesion is asymptomatic Differential diagnosis: Candidiasis Cheek biting Chemical burn Denture sore mouth (DSM) and Papillary hyperplasia (PH)  16 Both are related to the wearing of dentures. The mildest form of denture sore mouth appears as small, localized and asymptomatic red spots on the posterior palatal mucosa. As the condition worsens, large confluent areas turn crimson red (Fig. 1).) This is the classic form of DSM. In later stages, hyperplasia of palatal mucosa occurs and produces the red, pebbly appearances of papillary hyperplasia (Fig. 2). ETIOLOGY: The cause is unknown but there is evidence that Candida albicans is at least contributory. DSM has been called chronic atrophic candidiasis. Organisms are found more often in PH and DSM than in normal controls. TREATMENT: We know of no effective therapy other than fungicides such as nystatin, clotrimazole, ketoconazole or fluconazole in the usual doses for oral candidiasis. Good oral and denture hygiene may help. The denture should fit well and not be worn at night. In cases of excessively redundant papillary hyperplasia, surgical reduction may provide a better denture base.