Red and White Lesions of the Oral Mucosa PDF

Red and White Lesions of the Oral Mucosa Dr. Omar Soliman Lecturer of Oral medicine and Periodontology,South Vally University  2 Dr. Omar Soliman  3 Dr. Omar Soliman  A white appearance of the oral mucosa m...

Red and White Lesions of the Oral Mucosa Dr. Omar Soliman Lecturer of Oral medicine and Periodontology,South Vally University  2 Dr. Omar Soliman  3 Dr. Omar Soliman  A white appearance of the oral mucosa may be caused by a variety of factors. 1. The oral epithelium may be stimulated to an increased production of keratin (hyperkeratosis, Composition 1). 4 Dr. Omar Soliman  A white appearance of the oral mucosa may be caused by a variety of factors. 2. An abnormal but benign thickening of stratum spinosum (acanthosis, Composition 2). 5 Dr. Omar Soliman  A white appearance of the oral mucosa may be caused by a variety of factors. 3. Intra- (Composition 3) and extracellular accumulation of fluid in the epithelium may also result in clinical whitening. 6 Dr. Omar Soliman  A white appearance of the oral mucosa may be caused by a variety of factors. 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). 7 Dr. Omar Soliman  A red appearance of the oral mucosa may be caused by a variety of factors. A red lesion of the oral mucosa may develop as the result of: 1. Atrophic epithelium (Composition 5), characterized by a reduction in the number of epithelial cells (Composition 6) or 2. Increased vascularization that is dilatation of vessels and/ or proliferation of vessels. 8 Dr. Omar Soliman  Composition 7 and 8 describe the immune pathogenesis of oral lichen planus (OLP) and lichenoid contact reactions (LCRs). Oral mucosal lesions also present with different tissue textures as reticular, plaque-like, papular, or pseudomembranous, which affect the clinical appearance of the lesions. 9 Dr. Omar Soliman  10 Dr. Omar Soliman  Frequently used terms in the oral diseases: 11 Dr. Omar Soliman  Macules. These are lesions that are flush with the adjacent mucosa and that are noticeable because of their difference in color from normal skin or mucosa. They may be red due to increased vascularity or inflammation, or pigmented due to the presence of melanin, hemosiderin, and foreign materials (including the breakdown products of medications). A good example in the oral cavity is the melanotic macule. 12 Dr. Omar Soliman  Plaques. These are raised lesions that are greater than 1 cm in diameter; they are essentially large papules. 13 Dr. Omar Soliman  Papules. These are lesions raised above the skin or mucosal surface that are smaller than 1.0 cm in diameter (some use 0.5 cm for oral mucosal lesions). They may be slightly domed or flat-topped. Papules are seen in a wide variety of diseases, such as the yellow-white papules of pseudomembranous candidiasis. 14 Dr. Omar Soliman  Nodules. These lesions are present within the dermis or mucosa. The lesions may also protrude above the skin or mucosa forming a characteristic dome-shaped structure. A good example of an oral mucosal nodule is the irritation fibroma. 15 Dr. Omar Soliman  Vesicles. These are small blisters containing clear fluid that are less than 1 cm in diameter. Bullae. These are elevated blisters containing clear fluid that are greater than 1 cm in diameter (some use 0.5 cm for oral lesions). 16 Dr. Omar Soliman  17 Dr. Omar Soliman  Erosions. These are red lesions often caused by the rupture of vesicles or bullae, or trauma and are generally moist on the skin. However, they may also result from thinning or atrophy of the epithelium in inflammatory diseases such as lichen planus. These should not be mistaken for ulcers that are covered with fibrin and are yellow although erosions may develop into ulcers. 18 Dr. Omar Soliman  Ulcers. These are well-circumscribed, sometimes depressed lesions with an epithelial defect that is covered by a fibrin clot, resulting in a yellow-white appearance. A good example is an aphthous ulcer. 19 Dr. Omar Soliman  Pustules. These are blisters containing purulent material and appear yellow. Purpura. These are reddish to purple discolorations caused by blood from vessels leaking into the connective tissue. These lesions do not blanch when pressure is applied and are classified by size as petechiae (less than 0.3 cm), purpura (0.4–0.9 cm), or ecchymoses (greater than 1 cm). 20 Dr. Omar Soliman  21 Dr. Omar Soliman  Red And WhiteLesions. 22 Dr. Omar Soliman  23 Dr. Omar Soliman  1. INFECTIOUS DISEASES. A.Oral Candidiasis. B.Oral Hairy Leukoplakia. 24 Dr. Omar Soliman  A. Oral Candidiasis. Oral candidiasis is the most prevalent opportunistic infection affecting the oral mucosa. In the vast majority of cases, the lesions are caused by Candida albicans. The pathogenesis is not fully understood, but a number of predisposing factors have been shown to convert C. albicans from the normal commensal flora (saprophytic stage) to a pathogenic organism (parasitic stage). C. albicans is usually a weak pathogen, and candidiasis is said to affect the very young, the very old, and the very sick. Most candidal infections only affect mucosal linings, but rare systemic manifestations may have a fatal course. Oral candidiasis is divided into primary and secondary infections. The primary infections are restricted to the oral and perioral sites, whereas secondary infections are accompanied by systemic mucocutaneous manifestations. 25 Dr. Omar Soliman  26 Dr. Omar Soliman  Etiology and Pathogenesis of Oral Candidiasis. C. albicans, C. tropicalis, and C. glabrata comprise together over 80% of the species isolated from human candidal infections. To invade the mucosal lining, the microorganisms must adhere to the epithelial surface; therefore, candidal strains with better adhesion potential are more virulent than strains with poorer adhesion ability. The yeasts’ penetration of the epithelial cells is facilitated by their production of lipases, and for the yeasts to remain within the epithelium, they must overcome constant desquamation of surface epithelial cells. There is an apparent association between oral candidiasis and the influence of local and general predisposing factors. The local predisposing factors are able to promote growth of the yeast or to affect the immune response of the oral mucosa. General predisposing factors are often related to an individual’s immune status and endocrine 27 status. Dr. Omar Soliman  Etiology and Pathogenesis of Oral Candidiasis. Drugs as well as diseases, which suppress the adaptive or the innate immune system can affect the susceptibility of the mucosal lining. Pseudomembranous candidiasis is also associated with fungal infections in young children, who neither have a fully developed immune system nor a fully developed oral microflora. Denture stomatitis, angular cheilitis, and median rhomboid glossitis are referred to as Candida-associated infections as bacteria may also cause these infections. 28 Dr. Omar Soliman  29 Dr. Omar Soliman  Clinical Findings of Oral Candidiasis. Pseudomembranous Candidiasis The acute form of pseudomembranous candidiasis (thrush) is grouped with the primary oral candidiasis and is recognized as the classic candidal infection. The infection predominantly affects patients taking antibiotics, immunosuppressant drugs, or having a disease that suppresses the immune system. The infection typically presents with loosely attached membranes comprising fungal organisms and cellular debris, which leaves an inflamed, sometimes bleeding area if the pseudomembrane is removed. 30 Dr. Omar Soliman Dr. Omar Soliman 31 Dr. Omar Soliman  Clinical Findings of Oral Candidiasis. Erythematous Candidiasis The erythematous form of candidiasis was previously referred to as atrophic oral candidiasis. However, an erythematous surface may not just reflect atrophy but can also be explained by increased vascularization. The lesion has a diffuse border, which helps distinguish it from erythroplakia, which usually has a sharper demarcation and often appears as a slightly submerged lesion. Erythematous candidiasis may be considered a successor to pseudomembranous candidiasis but may also emerge de novo. The infection is predominantly seen in the palate and the dorsum of the tongue of patients who are using inhalation steroids. Other predisposing factors that can cause erythematous candidiasis are smoking and treatment with broad-spectrum antibiotics. The acute and chronic forms present with identical clinical features. 32 Dr. Omar Soliman  33 Dr. Omar Soliman  Clinical Findings of Oral Candidiasis. Chronic Plaque-Type and Nodular Candidiasis: The chronic plaque type of oral candidiasis replaces the older term, candidal leukoplakia. A white irremovable plaque characterizes the typical clinical presentation, which may be indistinguishable from oral leukoplakia. A positive correlation between oral candidiasis and moderate to severe epithelial dysplasia has been observed and both the chronic plaque-type and the nodular type of oral candidiasis have been associated with malignant transformation, but the possible role of yeasts in oral carcinogenesis is unclear. It has been hypothesized that it may act through its capacity to catalyze nitrosamine production. 34 Dr. Omar Soliman  35 Dr. Omar Soliman  36 Dr. Omar Soliman  Clinical Findings of Oral Candidiasis. Denture Stomatitis The most prevalent site for denture stomatitis is the denture-bearing palatal mucosa. It is unusual for the mandibular mucosa to be involved. Denture stomatitis is classified into three different types 1. Type I is limited to minor erythematous sites caused by trauma from the denture. 2. Type II affects a major part of the denture-covered mucosa. 3. Type III has a granular mucosa. The denture serves as a vehicle that accumulates sloughed epithelial cells and protects the microorganisms from physical influences such as salivary flow. The micro- flora is complex and may, in addition to C. albicans contain bacteria from several genera, such as Streptococcus. It is not known to what extent these bacteria participate in the pathogenesis of 37 denture stomatitis. Dr. Omar Soliman  38 Dr. Omar Soliman  Clinical Findings of Oral Candidiasis. Angular Cheilitis Angular cheilitis presents as infected fissures of the commissures of the mouth, often surrounded by erythema. The lesions are frequently coinfected with both Candida albicans and Staphylococcus aureus. VitaminB deficiency, iron deficiencies, and loss of vertical dimension have been 12 associated with this disorder. Dry skin may promote the development of fissures in the commissures, allowing invasion by the microorganisms. Thirty percent of patients with denture stomatitis also have angular cheilitis, but this infection is only seen in 10% of denture-wearing patients without denture stomatitis. 39 Dr. Omar Soliman  40 Dr. Omar Soliman  Clinical Findings of Oral Candidiasis. Median Rhomboid Glossitis Median rhomboid glossitis is clinically characterized by an erythematous lesion in the center of the posterior part of the dorsum of the tongue. As the name indicates, the lesion has an oval configuration. This area of erythema results from atrophy of the filiform papillae and the surface may be lobulated. The etiology is not fully clarified, but the lesion frequently shows a mixed bacterial/ fungal microflora. Biopsies yield candidal hyphae in more than 85% of the lesions. Smokers and denture-wearers have an increased risk of developing median rhomboid glossitis as well as patients using inhalation steroids. Sometimes a concurrent erythematous lesion may be observed in the palatal mucosa (kissing lesions). Median rhomboid glossitis is asymptomatic, and management is restricted to a reduction of predisposing factors. The lesion does not entail any increased risk for malignant transformation. 41 Dr. Omar Soliman  42 Dr. Omar Soliman  Clinical Findings of Oral Candidiasis. Oral Candidiasis Associated with HIV More than 90% of acquired immune deficiency syndrome (AIDS) patients have had oral candidiasis during the course of their HIV infection, and the infection is considered a portent of AIDS development. The most common types of oral candidiasis in conjunction with HIV are pseudomembranous candidiasis, erythematous candidiasis, angular cheilitis, and chronic plaque-like candidiasis. As a result of the highly active antiretroviral therapy (HAART), the prevalence of oral candidiasis has decreased substantially. 43 Dr. Omar Soliman  44 Dr. Omar Soliman  Clinical Manifestations of Oral Candidiasis. Secondary oral candidiasis is accompanied by systemic mucocutaneous candidiasis and other immune deficiencies. Chronic mucocutaneous candidiasis (CMC) embraces a heterogeneous group of disorders, which, in addition to oral candidiasis, also affect the skin, typically the nail bed and other mucosal linings, such as the genital mucosa. The face and scalp may be involved, and granulomatous masses can be seen at these sites. Approximately 90% of the patients with CMC also present with oral candidiasis. The oral manifestations may involve the tongue, and white plaque-like lesions are seen in conjunction with fissures. CMC can occur as part of endocrine disorders, including hyperparathyroidism and Addison’s disease. Impaired phagocytic function by neutrophilic granulocytes and macrophages caused by myeloperoxidase deficiency have also been associated with CMC. 45 Dr. Omar Soliman  Diagnosis and Laboratory Findings of Oral Candidiasis. The presence of candidal microorganisms as a member of the commensal flora complicates the discrimination of the normal state from infection. It is imperative that both clinical findings and laboratory data are balanced in order to arrive at a correct diagnosis. Sometimes antifungal treatment has to be initiated to assist in the diagnostic process. 46 Dr. Omar Soliman  1. Smear. Smear from the infected area comprising epithelial cells, creates opportunities for detection of the yeasts. The material is fixed in isopropyl alcohol and air-dried before staining with periodic acid–Schiff (PAS). The detection of yeast organisms in the form of hyphae- or pseudohyphae-like structures is usually considered a sign of infection although these structures have also been identified in normal oral mucosa. This technique is particularly useful when pseudomembranous oral candidiasis and angular cheilitis are suspected. To increase the sensitivity, a second scrape can be transferred to a transport medium followed by cultivation on Sabouraud agar. To discriminate between different candidal species, an additional examination can be performed on Pagano-Levin agar 47 Dr. Omar Soliman  2. Imprint culture technique. Imprint culture technique can also be used where sterile plastic foam pads (2.5 × 2.5 cm) are submerged in Sabouraud broth and placed on the infected surface for 60 seconds. The pad is then firmly pressed onto Sabouraud agar, which will be cultivated at 37°C. The result is expressed as colony forming units per cubic millimeter (CFU/mm2). This method is a valuable adjunct in the diagnostic process of erythematous candidiasis and denture stomatitis as these infections consist of fairly homogeneous erythematous lesions. Salivary culture techniques are primarily used in parallel with other diagnostic methods to obtain an adequate quantification of candidal organisms. Patients who display clinical signs of oral candidiasis usually have more than 400 CFU/ mL. In chronic plaque-type and nodular candidiasis, cultivation techniques have to be supplemented by a histopathologic examination. This examination is primarily performed to identify the presence of epithelial dysplasia and to identify invading candidal organisms by PAS staining. However, for the latter, there is a definitive risk of false-negative results. 48 Dr. Omar Soliman  Diagnosis and Laboratory Findings of Oral Candidiasis. 49 Dr. Omar Soliman  Management of Oral Candidiasis. Treatment for fungal infections, which usually include anti-fungal regimens, will not always be successful unless the clinician addresses predisposing factors that may cause recurrence. Local factors are often easy to identify but sometimes not possible to reduce or eradicate. Antifungal drugs have a primary role in such cases. In smokers, cessation of the habit may result in disappearance of the infection even without antifungal treatment. The most commonly used antifungal drugs belong to the groups of polyenes or azoles Polyenes such as nystatin and amphotericin B are usually the first choices in treatment of primary oral candidiasis and are both well tolerated. Polyenes are not absorbed from the gastrointestinal tract and are not associated with development of resistance. They exert the action through a negative effect on the production of ergosterol, which is critical for the yeast’s cell membrane integrity. Polyenes can also affect the adherence of the fungi. 50 Dr. Omar Soliman  Whenever possible, elimination or reduction of predisposing factors should always be the first goal for treatment of denture stomatitis as well as other opportunistic infections. This involves improved denture hygiene and a recommendation not to use the denture while sleeping. The denture hygiene is important to remove nutrients, including desquamated epithelial cells, which may serve as a source of nitrogen, which is essential for the growth of the yeasts. Denture cleaning also disturbs the maturity of a microbial environment established under the denture. As porosities in the denture can harbor microorganisms, which may not be removed by physical cleaning, the denture should be stored in antimicrobial solutions during the night. Different solutions, including alkaline peroxides, alkaline hypochlorites, acids, disinfectants, and enzymes, have been suggested. The latter seems to be most effective against candidal strains. Chlorhexidine may also be used but can discolor the denture and also counteracts the effect of nystatin. Type III denture stomatitis may be treated with surgical excision in an attempt to eradicate microorganisms present in the deeper fissures of the granular tissue. If this is not sufficient, continuous treatment with topical antifungal drugs should be considered. Patients with no symptoms are rarely motivated for treatment, and the infection often persists without the patients being aware of its presence. However, the chronic inflammation may result in increased resorption of the denture-bearing bone. 51 Dr. Omar Soliman  Topical treatment with azoles such as miconazole is the treatment of choice for angular cheilitis often infected by both S. aureus and candidal strains. This drug has a biostatic effect on S. aureus in addition to the fungistatic effect. Retapamulin can be used as a complement to the antifungal drugs. If angular cheilitis comprises an erythema surrounding the fissure, a mild steroid ointment may be required to suppress the inflammation. To prevent recurrences, patients have to apply a moisturizing cream, which may prevent new fissure formation. Systemic azoles may be used for deeply seated primary candidiasis, such as chronic hyperplastic candidiasis, denture stomatitis, and median rhomboid glossitis with a granular appearance, and for therapy-resistant infections, mostly related to compliance failure. There are several disadvantages with the use of azoles. They are known to interact with warfarin, leading to an increased bleeding propensity. This adverse effect may also be present with topical application as the azoles are fully or partly resorbed from the gastrointestinal tract. Development of resistance is particularly compelling for fluconazole in individuals with HIV disease. In such cases, ketoconazole and itraconazole have been recommended as alternatives. However, cross-resistance has been reported between fluconazole on the one hand and ketoconazole, miconazole, and itraconazole on the other. The azoles are also used in the treatment of secondary oral candidiasis associated with systemic predisposing factors and for systemic candidiasis. 52 Dr. Omar Soliman  Prognosis of Oral Candidiasis. Prognosis of oral candidiasis is good when predisposing factors associated with the infection are reduced or eliminated. Persistent chronic plaque-type and nodular candidiasis have been suggested to be associated with an increased risk for malignant transformation compared with leukoplakia, not infected by candidal strains. Patients with primary candidiasis are also at risk if systemic predisposing factors arise emerge. For example, patients with severe immunosuppression as seen in conjunction with leukemia and AIDS may encounter disseminating candidiasis with a fatal course. 53 Dr. Omar Soliman  1. INFECTIOUS DISEASES. B. Oral Hairy Leukoplakia. 54 Dr. Omar Soliman  B.Oral Hairy Leukoplakia. Oral hairy leukoplakia (OHL) is the second most common HIV-associated oral mucosal lesion. HL has been used as a marker of disease activity since the lesion is associated with low CD4 T-lymphocyte counts. + The lesion is not pathognomonic for HIV disease since other states of immune deficiencies, such as caused by immunosuppressive drugs and cancer chemotherapy, have also been associated with OHL. Rarely, individuals with a normal immune system may present with OHL. 55 Dr. Omar Soliman  56 Dr. Omar Soliman  57 Dr. Omar Soliman  Etiology and Pathogenesis. Oral hairy leukoplakia is strongly associated with Epstein- Barr virus (EBV) and with low levels of CD4 T lymphocytes. Antiviral medication, which prevents EBV + replication, is curative and lends further support to EBV as an etiologic factor. There is also a correlation between EBV replication and a decrease in the number of CD1a Langerhans’ cells, which, together with T lymphocytes, are important cell + populations in the cellular immune defense of the oral mucosa. 58 Dr. Omar Soliman  Clinical Findings. Oral hairy leukoplakia is frequently encountered on the lateral borders of the tongue but may also be observed on the dorsum and in the buccal mucosa. The typical clinical appearance is vertical white folds oriented as a palisade along the borders of the tongue. The lesions may also be seen as white and somewhat elevated plaque, which cannot be scraped off. Oral hairy leukoplakia is asymptomatic, although symptoms may be present when the lesion is superinfected with candidal strains. As OHL may present in different clinical forms, it is important to always consider this mucosal lesion whenever the border of the tongue is affected by white lesions, particularly in immunocompromised patients. 59 Dr. Omar Soliman  Diagnosis A diagnosis of OHL is usually based on clinical characteristics, but histopathologic examination and detection of EBV can be performed to confirm the clinical diagnosis. It may most easily be confused with chronic trauma to the lateral borders of the tongue. Pathology The histopathology of OHL is characterized by hyperkeratosis often with a chevron- pattern surface and acanthosis. Hairy projections are common, which is reflected in the name given to this disorder. Koilocytosis, with edematous epithelial cells and pyknotic nuclei, is also a characteristic histopathologic feature. The complex chromatin arrangements may mirror EBV replication in the nuclei of koilocytic epithelial cells. Candidal hyphae surrounded by polymorphonuclear granulocytes are also a common feature. The number of immunostained Langerhans’ cells is considerably reduced. Mild subepithelial inflammation may also be observed. EBV can be detected by in situ hybridization or by immunohistochemistry. Exfoliative cytology may be of value and can serve as an adjunct to biopsy. 60 Dr. Omar Soliman  Management Oral hairy leukoplakia can be treated successfully with anti-viral medication, but this is not often indicated as this disorder is not associated with adverse symptoms. In addition, the disorder has also been reported to show spontaneous regression. HL is not related to increased risk of malignant transformation. Medication with HAART has reduced the number of HL to a few percent in HIV-infected patients. 61 Dr. Omar Soliman  62 Dr. Omar Soliman  BONE DESTRUCTION CAUSED BY SYSTEMIC DISORDERS. bone loss initiated by local inflammatory processes may be magnified by systemic influence on the response of alveolar bone. This is termed. The bone factor concept. Dr. Omar Soliman