Oral Candidiasis: Types, Symptoms, and Management PDF
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Ass Prof Shereen Ali
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This document provides a classification of candidiasis, detailing various types, including acute and chronic pseudomembranous and erythematous candidiasis. It also discusses predisposing factors and systemic conditions, such as malnutrition and diabetes, that can increase the risk of developing oral candidosis. The document covers different types of oral lesions and candidiasis-associated conditions.
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The normal pink color of oral mucosa is due to passing through the epithelium strikes the capillary bed in connective tissue and reflects back. Ass Prof Shereen Ali – Dentistry integrated program ...
The normal pink color of oral mucosa is due to passing through the epithelium strikes the capillary bed in connective tissue and reflects back. Ass Prof Shereen Ali – Dentistry integrated program White lesions 1. Changes Over the 2. Changes within the 3. Changes under epithelium epithelium the epithelium -Fungi produce -Hyperkeratosis: increased -Reduced pseudomembranes production of keratin vascularity of the [candidiasis] -Acanthosis: thickening of connective tissue. -Coagulative necrosis due to stratum spinosum [Oral [palor due to burns & toxic chemicals keratosis] anemia] “desquamated epithelial cells, -Intracellular & fibrin, inflammatory cells, Extracellular edema of the microorganisms, food debris” epithelial cells Ass Prof Shereen Ali – Dentistry integrated program Red lesions 1. Changes within the 2. Changes under the epithelium epithelium -Atrophic epithelium -Increased vascularity of the characterized by reduction in connective tissue. [vascular number of epithelial cells. pigmented lesions] [atrophic OLP] Ass Prof Shereen Ali – Dentistry integrated program 1) Infectious diseases: Oral Candidiasis Hairy Leukoplakia 2) Premalignant lesions: Oral Leukoplakia and Erythroplakia Oral Submucous Fibrosis Ass Prof Shereen Ali – Dentistry integrated program 3) Immunopathologic diseases: Oral Lichen Planus Drug-Induced Lichenoid Reactions Lichenoid Reactions of Graft-versus-Host Disease Lupus Erythematosus 4) Allergic reactions: Lichenoid Contact Reactions Reactions to Dentifrice and Chlorhexidine Ass Prof Shereen Ali – Dentistry integrated program 5) Toxic reactions: Reactions to Smokeless Tobacco Smoker’s Palate Chemical burn* 6) Reactions to mechanical trauma: Frictional keratosis* Morsicatio Ass Prof Shereen Ali – Dentistry integrated program 7) Other red and white lesions: Actinic keratosis* Glass blower keratosis* Syphilitic keratosis* Benign Migratory Glossitis (Geographic Tongue)* Leukoedema White Sponge Nevus Hairy Tongue Ass Prof Shereen Ali – Dentistry integrated program Oral candidiasis is the most prevalent opportunistic infection affecting the oral mucosa. In the vast majority of cases, the lesions are caused by the yeast Candida albicans. C. albicans > 80% of the species isolated C. tropicalis from human Candida infections C. glabrata Ass Prof Shereen Ali – Dentistry integrated program Etiology: Predisposing factors have the capacity to convert Candida Candida normal commensal flora pathogenic organism (saprophytic stage) (parasitic stage) Ass Prof Shereen Ali – Dentistry integrated program I- Local predisposing factors: promote growth of Candida 1. Denture wearing OR affect immune 2. Smoking response of oral mucosa 3. Steroids “Inhalation and Topical” 4. Hyperkeratosis 5. Imbalance of oral microflora ?? *Antibiotics [especially broad-spectrum antibiotics], *Excessive use of antibacterial mouth rinses, *xerostomia causing reduced IgA. 6. Quality and quantity of saliva Ass Prof Shereen Ali – Dentistry integrated program II- Systemic predisposing factors: 1. Immunosuppressive diseases “Leukemia, lymphomas, AIDS” 2. Malabsorption and malnutrition 3. Immunosuppressive drugs related to the patient’s 4. Chemotherapy immune and endocrine 5. Endocrine disorders status 6. Diabetes mellitus Ass Prof Shereen Ali – Dentistry integrated program Malnutrition & malabsorption: ????????? Malnutrition may lead to * lymphoid hypoplasia reduction in lymphocyte number and phagocytosis. Malabsorption * iron deficiency anemia reduced epithelial maturation and decreased T-cell response. Ass Prof Shereen Ali – Dentistry integrated program Diabetes mellitus: ????????? i. Hyperglycemia: decreases phagocytic function of neutrophils ii. Ketoacidosis: decreases chemotaxis & phagocytic function of neutrophils. iii. Vascular wall disease: decrease blood flow & oxygen tension, impair chemotaxis. Ass Prof Shereen Ali – Dentistry integrated program Candidiasis is said to affect the very young, the very old, and the very sick Ass Prof Shereen Ali – Dentistry integrated program CLASSIFICATION OF CANDIDOSIS I. Primary oral candidosis: confined to oral & perioral tissues 1. Acute : a- Pseudomembranous. (Thrush) b- Erythematous. (previouslyAtrophic) Ass Prof Shereen Ali – Dentistry integrated program 2. Chronic : a-Pseudomembranous. b- Erythematous. c- Plaque-like. d- Nodular. 3. Candida associated: a- Denture stomatitis. b- Angular cheilitis. c- Median rhomboid glossitis. Ass Prof Shereen Ali – Dentistry integrated program II. Secondary oral candisidosis: accompanied by systemic mucocutaneous manifestations 1. Familial chronic mucocutaneous candidiasis 2. Diffuse chronic mucocutaneous candidiasis 3. Candidiasis endocrinopathy syndrome 4. Severe combined immunodeficiency 5. DiGeorge syndrome 6. Chronic granulomatous disease 7. Acquired immune deficiency syndrome (AIDS) Ass Prof Shereen Ali – Dentistry integrated program Acute pseudomembranous candidiasis (Thush) Predominantly affects: patients medicated with antibiotics, patients medicated with immunosuppressant drugs, or patients suffering from a disease that suppresses the immune system. Ass Prof Shereen Ali – Dentistry integrated program Typical lesion: Loosely attached soft, white creamy membranes “pseudomembrane” comprising candidal hyphae and cellular debris. Removing the pseudomembrane, will reveal an erythematous inflamed, sometimes bleeding area. Site: Any mucosal surface may be involved localized or diffuse “patient’s body resistance”. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Symptoms: Asymptomatic, some discomfort may be experienced from the pseudomembranes. Generally painless, unless the pseudomembrane is torn off or removed. Ass Prof Shereen Ali – Dentistry integrated program Chronic pseudomembranous candidiasis Affects: Patients suffering from human immunodeficiency virus (HIV) infections. Patients using steroid inhalers. Ass Prof Shereen Ali – Dentistry integrated program Acute erythematous candidiasis Occur: As a successor to pseudomembranous candidiasis OR Emerge de novo: * Broad-spectrum antibiotic * Inhaled steroids * Smoking Ass Prof Shereen Ali – Dentistry integrated program Lesion: erythematous, with painful eroded areas. diffuse border, which helps distinguish it from erythroplakia, which has a sharper demarcation. Site: Inhaled steroids palate & dorsum of the tongue Antibiotics dorsum of the tongue (antibiotic glossitis) Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Symptoms: Burning sensation “marked compared with thrush because of the erosions & intense inflammation”. Chronic erythematous candidiasis Clinical features: Identical to the acute form Ass Prof Shereen Ali – Dentistry integrated program N.B. Oral lesions tend to be localized with systemic antibiotic and diffuse with topical antibiotic mouth rinse. A similar picture of generalized redness and soreness of the oral mucosa are the typical features of candidosis associated with xerostomia. Ass Prof Shereen Ali – Dentistry integrated program Lesion: thick, white leathery plaque of irregular thickness, with rough or nodular surface. Difficult to differentiate it from leukoplakia: *similar clinically, *differentiate by finding: -periodic acid-schiff (PAS)-positive hyphae -high candidal antibody titre “serum & saliva” Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Malignant transformation: positive correlation between oral candidiasis and moderate to severe epithelial dysplasia has been observed, both the chronic plaque-type & nodular candidiasis have been associated with malignant transformation Ass Prof Shereen Ali – Dentistry integrated program Denture Stomatitis (Sore Mouth) Site: Most prevalent site: denture-bearing palatal mucosa + [inadequate cleaning & wearing denture day & night] Unusual: for mandibular mucosa to be involved intimate contact between upper denture & palatal mucosa serves as a vehicle protects microorganisms from salivary flow & salivary Abs (IgA) Ass Prof Shereen Ali – Dentistry integrated program Lesion: Classified into 3 different types: *Type I: localized to minor erythematous sites. *Type II: major part of the denture covered mucosa. *Type III: type II features + a granular mucosa in the central part of the palate. Angular cheilitis is seen in many cases. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Symptoms: Are usually absent, but occasionally there may be soreness, or burning sensation which is reported during period of exacerbation. Ass Prof Shereen Ali – Dentistry integrated program Angular cheilitis Lesion: infected fissures affecting the lip commissure, often surrounded by erythema. Lip-licking habits: it extends onto the surrounding skin folds producing erythematous fissuring. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Frequently coinfected with: both Candida and Staphylococcus aureus Associated with: Vitamin B12, iron deficiencies, loss of vertical dimension Ass Prof Shereen Ali – Dentistry integrated program N.B. Angular cheilitis can be seen with any type of intraoral candidosis & this is the only feature which they all share in common. Angular cheilitis may occasionally be seen in isolation, & then it is likely to be staphylococcus or streptococcus rather than candida. Ass Prof Shereen Ali – Dentistry integrated program Median Rhomboid glossitis Etiology: not fully clarified, but Lesion: shows a mixed microflora - Candida hyphea >85% of the lesions. Increased risk: Smokers - Denture-wearers - Patients using inhalation steroids Ass Prof Shereen Ali – Dentistry integrated program Lesion: oval erythematous lesion resulting from atrophy of the filiform papillae and the surface may be lobulated. Lesion: center of the posterior part of tongue dorsum Sometimes a concurrent erythematous lesion in the palatal mucosa (kissing lesions) Treatment: restricted to a reduction in predisposing factors Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program >90% AIDS patients have had oral candidiasis during the course of their HIV infection. Most common types of oral candidiasis in conjunction with HIV: Pseudomembranous candidiasis, Erythematous candidiasis, Chronic hyperplastic candidiasis, Angular cheilitis. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program A. Clinical findings Check previously B. Laboratory investigations: 1) Smear: from the infected area detect candidal hyphae via PAS stain Ass Prof Shereen Ali – Dentistry integrated program 2) Culture: on Sabouraud medium Creamy white colonies, flat or hemispherical in shape with a beer-like aroma Ass Prof Shereen Ali – Dentistry integrated program 3) Serology: high candidal Ab titre in serum and saliva 4) Histopathologic examination: in chronic plaque-type and nodular candidiasis, identify the possible presence of epithelial dysplasia identify invading Candida organisms by PAS staining Ass Prof Shereen Ali – Dentistry integrated program A. Elimination / Reduction of predisposing factors: 1) Stop antibiotic and steroids if possible. 2) Improve oral hygiene. 3) Make new denture. 4) Control of diabetes and other systemic diseases. B. Anti-fungal drugs: Names + mechanism Specific treatment of each type Ass Prof Shereen Ali – Dentistry integrated program B. Anti-fungal drugs: Amphotericin B Acute 1ry lesions *4 times daily for 3 Polyenes Nystatin weeks. “Mycostatin Topical *respond rapidly suspension” within 7 days but must Miconazole continue for 2 weeks “Daktarin gel” Ketoconazole 200mg Azoles Resistant 1ry lesions, Fluconazole Systemic deeply seated lesions & 50-100mg 2ry lesions Itraconazole *once daily for 2 100 mg weeks. Ass Prof Shereen Ali – Dentistry integrated program 1) Amphotericin B & Nystatin: 1st alternatives in treatment of 1ry oral candidiasis Act by local contact: linking drugs to the fungal cell membrane holes form in the cell membranes unable to protect the normal fluid and electrolyte balance of the cell content. 2) Miconazole: is the treatment of choice in angular cheilitis Ass Prof Shereen Ali – Dentistry integrated program 3) Systemic Azoles: used for deeply seated 1ry candidiasis “chronic hyperplastic candidiasis, DSM, median rhomboid glossitis with a granular appearance” – therapy-resistant infections – 2ry candidiasis Adverse effects: e.g. Ketoconazole is contraindicated in acute liver disease - Fluconazole interact with warfarin leading to an increased bleeding tendency Ass Prof Shereen Ali – Dentistry integrated program It is a white lesion that occurs on the lateral or ventral surfaces of the tongue in patients with severe immunodeficiency. Ass Prof Shereen Ali – Dentistry integrated program The most common disease associated with oral hairy leukoplakia is HIV infection. Hairy leukoplakia has also been reported with other immunosuppressive conditions such as *patients undergoing organ transplantation and *patients undergoing prolonged steroid therapy. Ass Prof Shereen Ali – Dentistry integrated program Etiology: strongly associated with EBV and with CD4+ T lymphocytes. Clinical picture: Most commonly: lateral border of the tongue “bilateral” Appear as: well-demarcated asymptomatic white lesion that varies from a flat, plaque-like lesion to a lesion with papillary hair-like projections. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program The most common disease associated with oral hairy leukoplakia is HIV infection. Hairy leukoplakia has also been reported with other immunosuppressive conditions such as *patients undergoing organ transplantation and *patients undergoing prolonged steroid therapy. Ass Prof Shereen Ali – Dentistry integrated program Histopathology: Hyperkeratosis and acanthosis. Hairy projections are common. Koilocytosis, with edematous epithelial cells and pyknotic nuclei. Ass Prof Shereen Ali – Dentistry integrated program Diagnosis: Clinical characteristics, Histopathologic examination, Detection of EBV by in situ hybridization, electron microscopy or PCR. Treatment: No treatment is indicated. The condition usually disappears when antiviral drugs such as acyclovir are used in treatment of HIV. Ass Prof Shereen Ali – Dentistry integrated program Frictional keratosis is a white plaque with a rough surface that is related to a source of mechanical irritation and that resolve on elimination of the irritant. “physiologic response” Etiology: Chronic rubbing or friction against oral mucosa stimulates the epithelium to respond with an increased production of keratin. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Site: commonly traumatized: o lips, associated with o lateral borders of tongue, *rough or misadjusted dentures o buccal mucosa along *sharp cusps *edges of broken teeth the occlusal line o edentulous ridges chewing on it will lead to keratinization Ass Prof Shereen Ali – Dentistry integrated program Differential diagnosis: homogeneous leukoplakia Frictional keratosis the affected site and a more diffuse demarcation Ass Prof Shereen Ali – Dentistry integrated program Management: Removal of the cause or habit should result in clinical improvement within 2 weeks. Follow up is mandatory, Biopsies should be performed on lesions that do not heal to rule out a dysplastic lesion. Ass Prof Shereen Ali – Dentistry integrated program Frictional keratosis is a reversible lesion since the lesion eventually disappears once the local factor is removed or corrected. If the lesion persists, it should be considered as leukoplakia. Ass Prof Shereen Ali – Dentistry integrated program Caused by: Habitual chewing “parafunctional behavior done unconsciously” Site: Most frequently: buccal and lip mucosa Less frequently: lateral surface of the tongue Never encountered: areas that are not possible to traumatize by habitual chewing Ass Prof Shereen Ali – Dentistry integrated program Lesion: F: M 3:1 Very typical clinical appearance Bilateral shredded area, does not entail ulcerations Patients complain of roughness or small tags of tissue Ass Prof Shereen Ali – Dentistry integrated program Management: Assurance of patient and inform about the parafunctional behavior. Instruct patient to stop habit, For those unable to stop the chewing habit, make an occlusal night guard. In cases of more extensive destruction, a psychiatric disorder should be suspected. Ass Prof Shereen Ali – Dentistry integrated program Lichenoid reactions represent a family of lesions with different etiologies with a common clinical and histologic appearence. Include: a) Lichen planus, b) Lichenoid contact reactions, c) Lichenoid drug eruptions d) Lichenoid reactions of graft-versus-host disease (GVHD). Ass Prof Shereen Ali – Dentistry integrated program Oral lichenoid contact reactions (LCRs) are included with allergic reactions since these lesions represent a delayed hypersensitivity reaction to dental materials or flavoring agents in foods. Ass Prof Shereen Ali – Dentistry integrated program OLP is a common chronic immunologic inflammatory mucocutaneous disease that varies in appearance from keratotic (reticular or plaque-like) to erythematous (atrophic) to ulcerative lesion. Ass Prof Shereen Ali – Dentistry integrated program Etiology: Emotional stress and cell mediated immune response. Ass Prof Shereen Ali – Dentistry integrated program Age: over 40 years. More common in females. Cutaneous manifestation: Most common site: flexor surface of extremities. Purple, pruritic polygonal papules. Skin lesion is characterized by Kobner's phenomena; the development of new lesion on normal looking skin following trauma (e.g. scratching). Ass Prof Shereen Ali – Dentistry integrated program Oral manifestation: Sites: buccal mucosa “most common” tongue, lips, gingiva and floor of the mouth. Lesions are often bilateral. Characterized by: remission and exacerbation. Persist for: years (8-15 years). Ass Prof Shereen Ali – Dentistry integrated program Lesions: don't disappear on stretching, can't be rubbed off, no loss of pliability and flexibility of oral mucosa surrounded by a network of bluish white lines called Wickham's striae radiating from the periphery of lesion.Ass Prof Shereen Ali – Dentistry integrated program Seven forms of OLP are seen: 1) papular, 2) reticular, Papular OLP 3) hypertrophic (plaque like), 4) atrophic / erythematous, Atrophic OLP 5) erosive, Bullous- 6) bullous, Erosive OLP 7) pigmented. Ass Prof Shereen Ali – Dentistry integrated program Papular OLP Pin head size white keratotic papules. Papules maybe discrete or arranged in various clinical patterns such as linear, reticular, annular or plaque like pattern. Ass Prof Shereen Ali – Dentistry integrated program Plaque pattern: appears as raised, thick white patches which may be mistaken with leukoplakia but in OLP there is no loss of pliability and flexibility while in leukolplakia there is loss of pliability and flexibility. Plaque Pattern may affect dorsal surface of the tongue. Ass Prof Shereen Ali – Dentistry integrated program Wickham striae This is the most common form of lichen planus painless lesion that is asymptomatic and is identified during a routine oral examination. no complain or patient complains of change in color of lips or roughness of buccal mucosa. Ass Prof Shereen Ali – Dentistry integrated program Bullous OLP Presents as chronic multiple oral ulcers (stay weeks- months. Lesions start by the development of vesicles or bullae as a result of severe degenerative changes in the basal layer of epithelium with separation of the epithelium from underlying C.T. Ass Prof Shereen Ali – Dentistry integrated program Bullous OLP Bullae soon rupture chronic multiple, shallow, irregular ulcers covered by pseudomembrane and surrounded by erythematous halo around which bluish Wickham striae are seen. Chief complaint: Symptomatic Pain that interferes with function (eating, speaking) and quality of life. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Atrophic OLP It presents as inflamed red areas of the oral mucosa. Erosive OLP may develop as a complication of the atrophy when the thin epithelium is abraded. Chief complaint: Symptomatic with symptoms that range from mild burning sensation to severe pain. Ass Prof Shereen Ali – Dentistry integrated program Atrophic, Ulcerative OLP on dorsum of the tongue Bloody crust Wickham’s stria Ulcerative OLP (developed from atrophic OLP as previously shown), the ulcer is present extraoral, so it becomes Ass Prof Shereen Ali – covered by a bloody crust Dentistry integrated program Desquamative gingivitis Occurs due to atrophic or bullous OLP involving the gingiva It appears as bright red edematous patches that involve the entire width of the attached gingiva. It is not a disease entity but as sign of disease that can be seen in LP, PV or MMP. Desquamative gingivitis caused by OLP is accompanied by Wickham's striae. Ass Prof Shereen Ali – Dentistry integrated program Prognosis: Malignant transformation is more likely in erosive, atrophic and bullous lesions possibly due to exposure of deeper layers of the epithelium to oral environmental carcinogens. Therefore, periodic recall, repeated biopsy and removal of lesions with dysplastic changes is mandatory. Ass Prof Shereen Ali – Dentistry integrated program Histopathology: Three features are essential for LP a) Hyperkeratosis with thickening of the granular cell layer and a saw-toothed appearance of the rete pegs. b) "Liquefaction degeneration" or necrosis of the basal cell layer which is often replaced by an eosinophilic band. c) A dense subepithelial band of lymphocytes composed mainly of T-cells. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Treatment of OLP: There is no known cure for OLP Patient education about nature of Medical Drugs which are the disease history prescribed Unpredictable clinical course Control Corticosteroids associated are the most Rationale of therapeutic systemic successful drugs diseases for controlling drugs i.e. controlling rather signs and than curing the disease. symptoms of OLP. The hyperkeratotic striae will Periodic Recall persist during periods of remission Ass Prof Shereen Ali – Dentistry integrated program 1. Steroids: a. Topical corticosteroids 0.1% triamcinolone ointment in orabase. Triamcinolone acetonide 0.1 - 0.2% mouth bath for 10 minutes. Betamethazone 0.1 mg lozenges. Betamethazone aerosol. Ass Prof Shereen Ali – Dentistry integrated program Application: four times daily; three times after meals and once at bed time nothing by mouth for at least 1 hr after application. Applied to the lesions with cotton swabs or with gauze pads impregnated with steroid. Extensive erosive OLP on gingiva (desquamative gingivitis) may be treated by using splints as carriers for the topical steroids. Ass Prof Shereen Ali – Dentistry integrated program b. Systemic steroids Indication: severe lesions or cases that fail to respond to topical steroids. Consultation with patient's physician is important when underlying medical problems are present e.g. diabetes mellitus and hypertension. Prednisone tablets 40 mg 1 ½ hr after arising as a single dose for 7 days, then 10 - 20 mg every other day (alternate day therapy) for 2 weeks. Ass Prof Shereen Ali – Dentistry integrated program c. Low-dose systemic steroids combined with non- steroidal anti-inflammatory drugs: Used: in case there is any contraindication for the use of steroids (e.g. diabetes, hypertension, TB,...etc) In the form of: 10 - 20 mg prednisone 1 ½ hr after arising + 1000 mg of a NSAID in divided doses for 2 weeks. Ass Prof Shereen Ali – Dentistry integrated program d. Intralesional injection of steroids “triamcinolone acetonide”: Helpful in resistant ulcers (those not responding to topical or systemic corticosteroid therapy). Pain of the injection is controlled by injecting the steroid in a 50% mixture with lidocaine. Three injections (one week interval) are required. Ass Prof Shereen Ali – Dentistry integrated program 2.Topical application of cyclosporine: It appears to be helpful in managing extensive cases of OLP. The ability of the drug to promote viral reproduction and malignant change in epithelial cells had limited its use except for extensive oral lesions. Ass Prof Shereen Ali – Dentistry integrated program 3. Antifungal drugs: Topical antifungal drugs should be given for at least one week out of every four weeks of steroid therapy. 4. Tranquilizers. 5. Benzydamine hydrochloride mouthwash. Ass Prof Shereen Ali – Dentistry integrated program They are oral mucosal lesions that have clinical and histopathologic features of lichen planus that are associated with the administration of a drug and that resolve after the withdrawal of the drug. Causes: *Gold therapy, *non-steroidal anti-inflammatory drugs, *antihypertensive, *oral hypoglycemic agents. Ass Prof Shereen Ali – Dentistry integrated program GVHD is a multisystem immunologic phenomenon characterized by the interaction of immunocompetent cells from one individual (the donor) to a host (the recipient) who is immunodeficient. It is a multisystem immunologic mediated reaction in which lymphocytes in a donor graft cause an immunologic reaction against the recipient tissue. Ass Prof Shereen Ali – Dentistry integrated program It occurs in 70% of patients who undergo bone marrow transplantation, usually for treatment of acute leukemia. Forms of GVHD: o Acute GVHD (< 100 days post-transplantation) o Chronic GVHD (>day 100, post-transplantation): is associated with lichenoid lesions “both skin and mucous membranes” Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program LE represents the classic prototype of an autoimmune disease involving immune complexes. SLE DLE immune complex mediated the less aggressive form inflammatory disease that affecting predominantly the causes multi-organ/ skin and/or oral mucosa multisystem damage Ass Prof Shereen Ali – Dentistry integrated program Etiology: Autoimmune process that may be influenced by Environmental Infectious Genetic factors factors predisposition Ass Prof Shereen Ali – Dentistry integrated program 1. Immunologic factor: hyperactive B-cells & impaired function of suppressor T-cells autoantibodies formation formation of immune complexes “autoAbs + Ags” activation of the complement leading to tissue damage precipitate in and around the blood vessels causing vasculitis, thrombosis and ischemia Ass Prof Shereen Ali – Dentistry integrated program Autoantibodies directed against: various cellular antigens in both the nucleus and the cytoplasm Include: Anti-nuclear Abs (ANA) Anti-cytoplasmic Abs Anti-erythrocytes Abs Anti-lymphocytes Abs Anti-platelets Abs Ass Prof Shereen Ali – Dentistry integrated program 2. Environmental factors: sun exposure, drugs, chemical substances, hormones aggravate the disease Drugs: e.g. hydralazine, chlorpromazine, isoniazid, quinidine, procainamide Hormonal: *high incidence in women in their child bearing years, *prevalence decreases during the menopause Ass Prof Shereen Ali – Dentistry integrated program 3. Genetic predisposition: Supported by: *elevated risk for siblings to develop LE *increased disease concordance in monozygotic twins 4. Infectious factors: RNA viruses are thought to initiate the abnormal immune response. [EBV, CMV & VZV] Ass Prof Shereen Ali – Dentistry integrated program Age: reproductive age. Sex: females. Cutaneous manifestation: Typical cutaneous lesions: red macules covered with yellow or grey scales. Removal of the scales reveals numerous extensions "carpet tack" favor sun-exposed areas, such as face & extremities Ass Prof Shereen Ali – Dentistry integrated program Skin lesions occur on the face, it involves malar regions and cross the bridge of the nose which gives Butterfly Distribution. Lesions are also seen on scalp, ears, chest, back and extremities. Ass Prof Shereen Ali – Dentistry integrated program Oral manifestation: Sites: buccal mucosa, palate, tongue and vermillion border of the lips A radiating pattern of very delicate white lines (Wickham's striae). Unlike lichen planus, *the distribution of DLE lesions is usually asymmetric *the Wickham's striae are less well defined. Ass Prof Shereen Ali – Dentistry integrated program Typical oral lesions: White patches that may be surrounded by a red halo. Red lesion (central atrophic area) with white dots surrounded by a white border. Alternating red (atrophic), white (keratotic) and red (telangiectatic) zones. [Characteristic] Ass Prof Shereen Ali – Dentistry integrated program Tongue: Atrophy of tongue coating Lower lip: may show atrophic plaques surrounded by keratotic border which may involve the entire vermilion border and extend to circumoral skin. Malignant transformation of lip lesion has been reported. Ass Prof Shereen Ali – Dentistry integrated program Prognosis Slowly progressive disease over many years. Sometimes spontaneous remission or in rare cases it develops into SLE. Oral DLE must be followed up at least once yearly: ?? Detect developing sign of skin DLE. “early lesions responds better to local treatment” Occurrence of oral ulceration which indicate presence of or later development of SLE. Malignant transformation of lip lesion. Ass Prof Shereen Ali – Dentistry integrated program Treatment: Topical steroids are used for both oral and skin lesions of DLE. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Skin manifestations: Erythematous rash over the malar region and bridge of the nose (butterfly distribution) usually associated with SLE. Skin manifestations include *photosensitive rashes, *alopecia, *Raynaud's phenomenon, *skin ulcerations secondary to vasculitis. Ass Prof Shereen Ali – Dentistry integrated program Oral manifestations: Similar to those of DLE More prevalent on buccal mucosa, followed by gingiva, vermillion border of lip and palate. Appear as: Erythema, ulceration, white keratotic plaques or papules. Xerostomia 2ry to Sjogren's syndrome which increases incidence of caries and candidiasis. TMJ involvement commonly occurs in SLE and may cause pain and mechanical dysfunction. Ass Prof Shereen Ali – Dentistry integrated program Renal manifestations Glomerulonephritis results from the deposition of complement and immune complexes. 50% of patients: glomerular destruction is seen in. 5 - 20% of patients: progress to end-stage renal disease and require hemodialysis or transplantation. Nephrotic syndrome results from massive destruction and is a common cause of death in SLE patients. Ass Prof Shereen Ali – Dentistry integrated program Cardiac manifestations: Atherosclerosis. The most common cardiac lesion -involves the endocardium -was originally described by Libman and Sacks as verrucous valve lesions "Libman-Sacks endocarditis". Ass Prof Shereen Ali – Dentistry integrated program Hematologic manifestations Leukopenia, Anemia, Thrombocytopenia. Musculoskeletal manifestations Arthritis and arthralgia with morning stiffness is the most common initial manifestation. CNS manifestations Cerebral dysfunction (psychosis - seizures) Peripheral neuropathy. Ass Prof Shereen Ali – Dentistry integrated program Thus, whenever a patient demonstrates signs and symptoms of multi-organ involvement, SLE should be considered, especially for a female who is 20 - 40 years of age. Diagnosis is made when at least 4 of the previous system involvement criteria are present. Ass Prof Shereen Ali – Dentistry integrated program Diagnosis: The most important diagnostic laboratory test for SLE is the test for antinuclear antibody (ANA) in the serum. Routine laboratory tests show signs of anemia, thrombocytopenia, lymphopenia (Pancytopenia). Ass Prof Shereen Ali – Dentistry integrated program Treatment: Oral lesion is treated by: topical steroids or intralesional steroid injections. Systemic steroids are used in case of SLE or may be combined with immunosuppressive drugs. Ass Prof Shereen Ali – Dentistry integrated program Dental considerations: ”Problems in SLE patients” 1. Adrenal suppression adrenal-suppressive doses of corticosteroids patient susceptible to adrenal crisis. 2. Infection Immunosuppressive drugs increased risk of infection preoperative prophylactic antibiotics Ass Prof Shereen Ali – Dentistry integrated program 3.Hematologic abnormalities Develop anemia, leukopenia & thrombocytopenia Prior to any extensive dental procedures, CBC: screen for thrombocytopenia, anemia & leukopenia Prothrombin time/partial thromboplastin time: screen for a coagulopathy. Ass Prof Shereen Ali – Dentistry integrated program 4. Cardiac disease Libman-Sacks vegetations infective endocarditis antibiotic prophylaxis prior to dental treatment that causes bacteremia. 5. Renal disease Perform renal function tests (creatinine clearance, serum creatinine and blood urea nitrogen) Patients who are undergoing hemodialysis: dental treatment on non-dialysis day Ass Prof Shereen Ali – Dentistry integrated program 6. Exacerbation by drug therapy Drugs that have been related to acute lupus flares include penicillin, sulfonamides , NSAIDs. Ass Prof Shereen Ali – Dentistry integrated program Definition: It is a predominantly white lesion of the oral mucosa that cannot be characterized as any other definable lesion. It is a precancerous white lesion of the oral mucosa with risk of malignant transformation. Ass Prof Shereen Ali – Dentistry integrated program Etiology: Exact etiology unknown (idiopathic keratosis) Local predisposing factors: tobacco (>80% of patients are smokers), alcohol, spicy food, excessive exposure to sunlight, candidiasis. Systemic predisposing factors: nutritional deficiency as vitamin B12 and iron deficiency. Ass Prof Shereen Ali – Dentistry integrated program Clinical picture: Age: adults > 50 years of age. Gender: more frequently in men. Size: variable. Painless unless there is ulceration. Ass Prof Shereen Ali – Dentistry integrated program It may cause loss of pliability and flexibility of the oral mucosa. Site: Buccal mucosa, vermillion border of the lower lip, gingiva, floor of the mouth and tongue. Lesions of tongue & floor of the mouth account for >90% of the cases that show dysplasia. Ass Prof Shereen Ali – Dentistry integrated program Types: 1. Homogenous leukoplakia: It is a white, well-demarcated plaque with an identical pattern throughout the entire lesion. Surface texture: vary from a smooth thin surface to a leathery appearance with surface fissures sometimes referred to as “cracked mud”. Ass Prof Shereen Ali – Dentistry integrated program 2. Non-homogenous leukoplakia (Speckled leukoplakia / Erythroleukoplakia): It is a white patches or plaque intermixed with red tissue elements. The white component may vary from large white verrucous areas to small nodular structures. Ass Prof Shereen Ali – Dentistry integrated program 3. Verrucous / verruciform leukoplakia: It is oral leukoplakia, where the white component is dominated by papillary projections, similar to oral papillomas. Ass Prof Shereen Ali – Dentistry integrated program 4. Proliferative verrucous leukoplakia (PVL): It is similar to the verrucous type but with a more aggressive proliferation pattern and recurrence rate. More common: older women Predilection site: lower gingiva Ass Prof Shereen Ali – Dentistry integrated program Clinical changes suggestive of malignant transformation in leukoplakia are: ulceration, erythroplakia, Induration, lymphadenopathy. Ass Prof Shereen Ali – Dentistry integrated program Histopathtology: Changes range from hyperkeratosis, acanthosis, dysplasia and carcinoma in situ to invasive squamous cell carcinoma. Ass Prof Shereen Ali – Dentistry integrated program Diagnosis & Management: Diagnosis is based on the clinical observation of a white or red patch that is not explained by a definable cause, such as trauma. If trauma is suspected, the cause “sharp tooth cusp or restoration” should be eliminated. If healing does not occur in 2 weeks, biopsy is essential to rule out malignancy. Ass Prof Shereen Ali – Dentistry integrated program Diagnosis of leukoplakia is made when clinical and histologic examination fails to reveal another diagnosis. Definitive treatment involves surgical excision. After surgical removal, long term follow up is important since recurrence is frequent Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program It is defined as a red lesion of the oral mucosa that cannot be characterized as any other definable lesion. Clinical picture: an eroded red lesion that is frequently observed with a distinct demarcation against the normal-appearing mucosa. non-symptomatic, although some patients may experience a burning sensation with food intake. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Definition: It is a chronic disease that affects the oral mucosa as well as the pharynx and the upper 2/3 of the esophagus. Ass Prof Shereen Ali – Dentistry integrated program Etiology: 1. There is a critical role for betel nut chewing habit. Betel nuts affects metabolism of collagen, which leads to an increased fibrosis. 2. There is also evidence of a genetic predisposition, namely gene polymorphism of the gene coding for tumor necrosis factor-a (TNF-a). Ass Prof Shereen Ali – Dentistry integrated program Clinical picture: First sign: erythematous lesions sometimes in conjunction with petechiae, pigmentations & vesicles. Followed by: a paler mucosa, which may comprise white marbling. Ass Prof Shereen Ali – Dentistry integrated program Later: fibrotic bands located beneath an atrophic epithelium “most prominent clinical characteristics”. Increased fibrosis leads to: loss of resilience, which -interferes with speech, tongue mobility, - decrease ability to open the mouth. Ass Prof Shereen Ali – Dentistry integrated program The atrophic epithelium may cause a smarting sensation and inability to eat hot and spicy food. >25% of the patients exhibit also oral leukoplakias. Ass Prof Shereen Ali – Dentistry integrated program Histopathology: Early characteristics: fine fibrils of collagen, edema, hypertrophic fibroblasts, dilatated and congested blood vessels, an infiltration of neutrophilic and eosinophilic granulocytes. Followed by: a down-regulation of fibroblasts, epithelial atrophy, loss of rete pegs, early signs of hyalinization in concert with an infiltration of inflammatory cells. Epithelial dysplasia varies from 7 to 26%. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Treatment: It is focused on cessation of the chewing habits. Early lesions have a good prognosis as they may regress. Ass Prof Shereen Ali – Dentistry integrated program Habitually chewing tobacco or dipping snuff (finely powdered tobacco) results in a white mucosal lesion in the area of tobacco contact, called smokeless tobacco keratosis or snuff dipper’s keratosis Ass Prof Shereen Ali – Dentistry integrated program Etiology: Smokeless tobacco contains several known carcinogens including N-nitroso-nornicotine (NNN). “this habit is common in the US, India & South East Asia” Ass Prof Shereen Ali – Dentistry integrated program Clinical picture: Asymptomatic wrinkled white lesion in the vestibule. Discoloration of teeth Gingival recession with periodontal tissue destruction involving the facial aspect of teeth in the immediate area of contact. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Histopathology: Hyperkeratinization, acanthosis, and epithelial vacuolizations are common histopathologic features together with different degrees of subepithelial inflammation. Ass Prof Shereen Ali – Dentistry integrated program Treatment: Cessation of use of tobacco leads to normal mucosal appearance within 1 - 2 weeks. Biopsy *obtained from lesions that remain after 1 month. *indicated for lesions that show: -surface ulceration -erythroplakia -intense whiteness -papillary surface Ass Prof Shereen Ali – Dentistry integrated program It is a white lesion that develops on the hard and soft palate in heavy cigarette, pipe and cigar smokers. Ass Prof Shereen Ali – Dentistry integrated program Reverse smoking (placing burning end of the cigarette in the oral cavity) seen in America and Asia produces premalignant palatal lesions. Ass Prof Shereen Ali – Dentistry integrated program This lesion also develops in individuals with a long history of drinking extremely hot beverages. This suggests that heat, rather than toxic chemicals in tobacco smoke, is the primary cause. Ass Prof Shereen Ali – Dentistry integrated program Clinical picture: erythematous irritation is initially seen, followed by a whitish palatal mucosa reflecting a hyperkeratosis. + slightly elevated white papules with red dots representing orifices of accessory salivary glands, which can be enlarged and display metaplasia. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Treatment: Nicotine stomatitis is reversible once the habit is stopped. This condition rarely evolves into malignancy except in individuals who reverse smoke. A biopsy should be performed in any white lesion of the palatal mucosa that persists after 1 month of discontinuation of smoking habit. Ass Prof Shereen Ali – Dentistry integrated program Smoker’s patches Are white patches on the upper and lower lips produced by cigarette smoking. Smoker’s keratosis Is a diffuse milky white lesion on the buccal mucosa, more pronounced at the commissures. It is due to heat, tobacco constituents and NNN. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Caustic chemicals aspirin, formocresol, sodium hypochlorite, acid etching material and hydrogen peroxide cause non keratotic white lesions of the oral mucosa “rubbed off leaving red raw painful bleeding surface” Ass Prof Shereen Ali – Dentistry integrated program The white lesions seen in burns are due to: the formation of a superficial pseudomembrane composed of *a coagulated necrotic surface tissue *an inflammatory exudate Ass Prof Shereen Ali – Dentistry integrated program Acetylsalicylic acid (Aspirin): is a common source of burns of the oral mucosa. Usually, the tissue is damaged when aspirin is held in for prolonged periods of time for relief of dental pain. Site: where aspirin touches the oral mucosa. Ass Prof Shereen Ali – Dentistry integrated program Prevention of chemical burns : Avoid using aspirin topically on the oral tissues. Use a rubber dam during endodontic treatment. Treatment of chemical burns: Rinsing with water to remove the chemicals. Topical steroid (0.1% triamcinolone paste). Topical lidocaine gel. Carboxymethyl cellulose. Ass Prof Shereen Ali – Dentistry integrated program Lichenoid contact reactions are considered as a delayed hypersensitivity reaction to constituents derived from dental materials, predominantly amalgam fillings. Ass Prof Shereen Ali – Dentistry integrated program Clinically, it displays the same reaction patterns as seen in OLP. The most apparent clinical difference is the extension of the lesions. The majority are confined to sites that are regularly in contact with dental materials, such as the buccal mucosa and the border of the tongue. Ass Prof Shereen Ali – Dentistry integrated program They are delayed hypersensitivity reactions to toothpastes and mouthwashes, but these reactions are rare. The compounds responsible for the allergic reactions may include flavor additives such as cinnamon or preservatives. Ass Prof Shereen Ali – Dentistry integrated program Clinical manifestations: fiery red edematous gingiva, which may include both ulcerations and white lesions. Similar lesions may involve other sites, such as the labial, buccal, and tongue mucosae. Ass Prof Shereen Ali – Dentistry integrated program Actinic keratosis* From Glass blower keratosis* Assignments Syphilitic keratosis* Benign Migratory Glossitis (Geographic Tongue)* Leukoedema White Sponge Nevus Hairy Tongue Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program I. Variation in structure and appearance of normal oral mucosa: Linea alba buccalis, Leukoedema Fordyce's granules. II. Non keratotic white lesions (white lesions that can be rubbed off): Burns. Some forms of candidiasis ???!!! Ass Prof Shereen Ali – Dentistry integrated program III. Keratotic white lesions (white lesions that cannot be rubbed off): 1) Keratotic white lesions WITH precancerous potential *Syphilitic keratosis *Actinic keratosis *Leukoplakia *Oral submucous fibrosis *Lichen planus ? *Lupus erythematosus ? *Smokeless tobacco induced keratosis *Smoker's keratosis *some forms of candidiasis ? Ass Prof Shereen Ali – Dentistry integrated program 2) Keratotic white lesions WITHOUT precancerous potential *Frictional (traumatic) keratosis. *Glass blower's keratosis *Nicotinic Stomatitis ? “except” *Oral genodermatosis. *Psoriasis. IV. Oral Candidiasis. Ass Prof Shereen Ali – Dentistry integrated program References: Burket`s Oral Medicine 11th edition Essentials of Oral Pathology and Oral Medicine “R. A. Cawson” Oral Medicine by Prof. Dr Samy Sadek. Ass Prof Shereen Ali – Dentistry integrated program Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Gray Black Prof Shereen Ali - DIIP - Fall 2022 Brown Brown Melanin Hemosiderin Bilirubin / Carotene Hemoglobin Blue / Yellow Purple Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 According to the color According to the distribution A- Brown Melanotic lesions B- Brown Heme-associated lesions C- Blue (Purple) Vascular lesions Focal Multi-focal Diffuse D- Black (Grey) lesions Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 1. Focal 2. Multi-focal 3. Diffuse Melanotic macule. Peutz-Jeghers syndrome Physiologic pigmentation Nevus. Café au lait pigments Smoker's melanosis Melanoma. Endocrinopathic Melanoacanthoma. pigmentation Drug induced melanosis HIV oral melanosis Pigmented lichen planus Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 Prof Shereen Ali - DIIP - Fall 2022 A) Multifocal / Focal Petechiae & Ecchymosis Purpura: – discoloration resulting from extravascular bleeding into CT due to abnormal bleeding tendency or trauma – According to size: small pinpoint areas (petechiae), larger areas (ecchymosis) or swellings (hematomas). Ass Prof Shereen Ali – Dentistry integrated program Capillary hemorrhages will appear red initially turning brown in few days once extravasated red cells have lysed and hemoglobin degraded to hemosiderin. Ass Prof Shereen Ali – Dentistry integrated program Petechiae secondary to platelet deficiency or clotting disorders are not limited to oral mucosa but occur also on skin. When traumatic petechiae are suspected, the patient should be instructed to cease the activity contributing to the lesions, and by 2 weeks the lesions should disappear. Failure to do so should arouse suspicion of abnormal hemostasis, and a platelet count and platelet aggregation studies must be ordered. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program B) Diffuse Hemochromatosis Depostion of hemosiderin in multiple organs and tissues. It may be: – hereditary ( error in iron metabolism secondary to increased iron intestinal absorption) or – secondary to diseases and conditions such as chronic anemia, liver cirrhosis and excess iron intake. Ass Prof Shereen Ali – Dentistry integrated program Excess iron is deposited into: Liver: liver cirrhosis. Pancreas: diabetes mellitus. Adrenal gland: Addison’s disease!!!??? Heart: heart failure. Skin: pigmentation. Oral mucosa: brown to grey macules. “gingiva – palate” Ass Prof Shereen Ali – Dentistry integrated program Skin pigmentation is attributed to: – increased iron concentration in circulation & deposition in skin. – increased melanin production secondary to adrenal dysfunction. Ass Prof Shereen Ali – Dentistry integrated program Hemochromatosis is often called “bronze” diabetes because of an accompanying skin discoloration. Its classic manifestations include: – diabetes mellitus. – Liver cirrhosis. – Skin pigmentation. Ass Prof Shereen Ali – Dentistry integrated program Diagnosis: – Oral biopsy is helpful in diagnosis; tissue stained for iron with Prussian blue. – Elevated iron serum level. Ass Prof Shereen Ali – Dentistry integrated program A) Focal Blue (Purple) Vascular lesions 1- Hemangioma Hemangiomas are benign proliferation of blood vessels. Site: Tongue and labial mucosa Appear as: – flat reddish blue macule or – a blue nodule. Ass Prof Shereen Ali – Dentistry integrated program Color of lesion depends on the depth of vascular proliferation within the oral mucosa. – Close to overlying epithelium: reddish blue – Deep in connective tissue: deep blue. Diascopic examination: blanch under pressure. Ass Prof Shereen Ali – Dentistry integrated program 2- Varix / Varices It is abnormally / pathologically dilated vein. Etiology: – Varices increase in number with age – Varix may be the result of trauma. Ass Prof Shereen Ali – Dentistry integrated program Lingual varicosities Thrombosed varix Site ventral surface of the lower lip, B.mucosa tongue Presents Multiple tortuous blue, blue, red, or purple as: red & purple elevations. nodule. Painless. often lobulated or not subject to rupture & nodular. hemorrhage. Ass Prof Shereen Ali – Dentistry integrated program Lingual varicosities Thrombosed varix Diascopy Compressible, blanch on Firm and does not blanch pressure Ass Prof Shereen Ali – Dentistry integrated program B) Multifocal Blue (Purple) Vascular lesions 1- Kaposi's Sarcoma It is a malignant neoplasm of vascular origin. It is the most common neoplasm in HIV. It begins as flat red macules with irregular outline mainly on palate, as lesion increase in size they become nodules. The facial gingiva is the 2nd most common site. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program 2- Hereditary Hemorrhagic Telangiectasia Autosomal dominant trait. Occurs due to weakening defect in coat of venules. [multiple microaneurysms] Ass Prof Shereen Ali – Dentistry integrated program Characterized by: multiple mucocutaneous lesions which are red to purple macules, nodules and telangiectasia Diascopy: blanch on pressure Ass Prof Shereen Ali – Dentistry integrated program A) Focal Black (Grey) lesions 1- Amalgam Tattoo Lesions are focal bluish gray or black macules. Common site: buccal mucosa, gingiva, or palate. They are found adjacent to teeth with large amalgam restorations. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program 2- GraphiteTattoo Graphite tattoos tend to occur on the palate, representing traumatic implantation from a lead pencil. The lesions are focal gray or black macules. Ass Prof Shereen Ali – Dentistry integrated program Ass Prof Shereen Ali – Dentistry integrated program B) Diffuse Black (Grey) lesions 1- Heavy Metal Toxicosis Oral manifestations: 1. Metallic taste. 2. Metallic line affecting interdental papillae and marginal gingiva. 3. Enlarged salivary glands. 4. Increased salivary secretion. Ass Prof Shereen Ali – Dentistry integrated program 5. Itching sensation. 6. Sore, inflamed tongue. 7. Tongue tremors (plumbism-mercurialism). 8. Lip cracking, dryness, swelling (mercurialism). 9. Gingiva is susceptible to ANUG. 10. Alveolar bone destruction. 11. Regional lymph nodes enlargement. Ass Prof Shereen Ali – Dentistry integrated program Pathogenesis of metallic line The metal salts circulate in the blood and reach the capillaries of gingiva. If there is gingival inflammation (increase the capillary permeability), the metal will pass from the capillaries to connective tissue. Metal salts react with hydrogen sulphide (results from food debris decomposition) forming insoluble precipitate of metal sulphide (metallic line). Deposition of metal sulphide interferes with gingival nutrition lowering gingival resistance it is susceptible to ANUG. Ass Prof Shereen Ali – Dentistry integrated program Diagnosis: – History of occupational exposure or therapeutic administration. – Clinical examination: metallic line may be continuous or interrupted. – Paper corner test: Insert the corner of a small piece of white paper into the gingival crevice. If the color disappears: it is subgingival calculus. If the color is accentuated: it is metallic line. Ass Prof Shereen Ali – Dentistry integrated program 2- Black Hairy Tongue Check Assignments References Burket`s Oral Medicine 11th edition Oral Medicine by Prof. Dr Samy Sadek. Kauzman A, Pavone M, Blanas N, Bradley G. Pigmented Lesions of the Oral Cavity: Review, Differential Diagnosis, and Case Presentations. Journal of the Canadian Dental Association. November 2004, Vol. 70, No. 10 Ebanks J, Wickett R and Boissy R. Mechanisms Regulating Skin Pigmentation: The Rise and Fall of Complexion Coloration. Int. J. Mol. Sci. 2009, 10, 4066-4087 Alawi F. Pigmented lesions of the oral cavity: An Update. Dent Clin North Am. 2013 October ; 57(4): 699–710. Ass Prof Shereen Ali – Dentistry integrated program Thank You
