Red And White Lesions of The Oral Mucosa PDF

Red And White Lesions of The Oral Mucosa Dr. Gillan El-Kimary BDS, MSc, PhD Lecturer of Periodontology & Oral Medicine...

Red And White Lesions of The Oral Mucosa Dr. Gillan El-Kimary BDS, MSc, PhD Lecturer of Periodontology & Oral Medicine Faculty Of Dentistry Alexandria University Outline Red and white tissue reaction Classification of red and white lesions 1- Infectious Diseases 2-premalignant Lesions 3- Immunopathologic Diseases 4- Allergic Reations 5-toxic Reactions 6- Reactions To Mechanical Trauma 7- Others Cause of white appearance 1) Increase production of keratin ( hyperkeratosis) 2) Abnormal but benign thickening of stratum spinosum (acanthosis) 3)Intra and extracellular accumulation of fluid in the epithelium 4) White pseudo-membrane Cause of red appearance 1) Atrophic epithelium characterized by a reduction in the number of epithelial cells 2) Increased vascularization Classification of Red & White Lesions 1)Infectious Oral Candidiasis Hairy Leukoplakia 2) Premalignant Oral Leukoplakia & Eryhtroplakia Oral Submucous Fibrosis 3) Immunopathologic Oral Lichen Planus Drug-induced Lichenoid Reactions Lichenoid Reaction Of Graft Versus Host Disease Lupus Erythematosus 1 4)Allergic Lichenoid Contact Reactions Reactions To Dentifrice & Chlorhexidine 5) Toxic Reactions Smokless Tobacco Smokers Palate 6) Reactions To Mechanical Trauma Morsicatio Frictional Hyperkeratosis 7) Others Benign Migratory Glossitis Leukodema White Spongy Nevus Hairy Tongue 1) Infectious Lesions a- Oral Candidiasis The most prevalent opportunistic infection affecting oral mucosa. Caused by Candida Albicans A superficial infection (upper layers of oral mucosal epithelium with formation of patchy white plaque or flecks on mucosa) It is composed of desquamated epithelial inflammatory cell, fibrin and yeast. Candida Albicans tissue invasion Epithelial Adherence Epithelial penetration “ Lipase” Predisposing Factors 1-changes in oral microbial flora followin administration of antibiotics 2-chronic local irritants as denture. 3-corticosteroids 4-radiation of head and neck 5-age(infancy-old age) 6-immune status 7-hospitalization 8- Smoking 9-Xerostomia 2 Classification Of Oral Candidiasis 1) Primary Oral Candidiasis Acute Pseudomembranous Erythematous Chronic Pseudomem. Erythematous Plaque-like Nodular Candida associated lesions Denture Stomatitis Angular Chelitis Median Rhomboid glossitis 2) Secondary Oral Candidiasis Accompanied by systemic mucocutaneous manifestations e.g AIDS, DiGeorge syndrome Pseudomembranous Candidiasis (Thrush) Acute form “Thrush” - primary oral candidiasis - predominantly affects patients medicated with antibiotics and immunosuppressant drugs Chronic form - associated with human immunodeficiency virus ( HIV patient) - Steroid inhalers Clinical presentation 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. The clinical presentations of acute and chronic pseudomembranous candidiasis are indistinguishable. Erythematous Candidiasis “Atrophic” Clinical presentation Explained by increased vascularity Having diffuse border ,which help distinguishing it from erythroplakia, which has a sharper demarcation Infection is found in the palate, and dorsum of the tongue of patient using broad spectrum antibiotics, and smoking or using inhalation steroids 3 Chronic Plaque-Type and Nodular Candidiasis “ Candidal leukoplakia” Characterized by white irremovable plaque, indistinguishable from oral leukoplakia Has been associated with malignant transformation. Candida Associated Lesions 1- Denture Stomatitis The most prevalent site for denture stomatitis is the denture-bearing palatal mucosa ØThe denture serves as a vehicle that accumulates sloughed epithelial cells and protects the microorganisms from physical influences such as salivary flow. ØThe microflora is complex and may, in addition to C. albicans contain bacteria from several genera, such as Streptococcus, Lactobacillus, Prevotella, and Actinomyces-strains. ”Mixed Infection” Clinical presentation ØType I is limited to minor erythematous sites caused by trauma from the denture. ØType II affects a major part of the denture-covered mucosa ØType III has a granular mucosa (In addition to the features of type II) “Papillary Hyperplasia” 2- Angular Chelitis -It 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 Etiology Loss of vertical dimension Vit. B deficiency Iron deficiencies DM, HIV, neutropenia 3- Median Rhomboid Glossitis MRG is clinically characterized by an erythematous lesion in the center of the posterior part of the dorsum of the tongue oval configuration. This area of erythema results from atrophy of the filiform papillae and the surface may be lobulated. A concurrent erythematous lesion may be observed in the palatal mucosa (kissing lesions) MRG is asymptomatic, and management is restricted to a reduction of predisposing factors. The lesion does not entail any increased risk for malignant transformation. 4 Management Of Oral Candidiasis Antifungal + remove predisposing factor The most commonly used antifungal drugs belong to the groups of polyenes or azoles polyenes such as nystatin and amphotericin B (well tolerated, not ass. with resistance) , they affect the yeast’s cell membrane integrity and also affect adherence of fungi. Azoles such as miconazole, fluconazole. (can be used systemically in deeply seated infections) There are several disadvantages with the use of azoles. They are known to interact with warfarin, leading to an increased bleeding propensity and development of resistance 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 NB: Chlorhexidine may also be used but can discolor the denture and also counteracts the effect of nystatin Antifungal (Systemic) In cases of inaccessible areas ”Oropharyngeal candidiasis” (soft palate, posterior third of tongue) C/I in liver and renal patients ( referral) Dosage (1st day 200mg then 100 mg daily for 1-2 weeks ) b- Oral Hairy Leukoplakia OHL is a common HIV-associated oral mucosal lesion. OHL has been used as a marker of disease activity since the lesion is associated with low CD4+ Tlymphocyte counts. The lesion is not pathognomonic for HIV disease since other states of immune deficiencies, such as caused by immunosuppressive drugs and cancer chemotherapy OHL is strongly associated with Epstein Barr virus (EBV) and with low levels of CD4+ T lymphocytes. Antiviral medication, which prevents EBV replication, is curative Clinical presentation Frequent site: lateral borders of the tongue as a vertical white folds ØThe lesions may also be seen as white and somewhat elevated plaque, which cannot be scraped off. ØOHL is asymptomatic. (unless superinfected with candidal strains) Dx & management ØDx of OHL is usually based on clinical characteristics, but histopathologic examination and detection of EBV can be performed to confirm the clinical diagnosis. ØCan be treated successfully with antiviral medication. ØIn addition, the disorder has also been reported to show spontaneous regression. ØOHL is not related to increased risk of malignant transformation 5 2) Premalignant Lesions The development of oral leukoplakia & erythroplakia as premalignant lesions involves different genetic events. Activation of oncogenes and deletion and injuries to suppressor genes and genes responsible for DNA repair will all contribute to a defective functioning of the genome that governs cell division. Following a series of mutations, a malignant transformation may occur Oral Leukoplakia Clinical presentation A) Homogenous Leukoplakia Ø Def: White plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer. Ø Clinically characterized as a white, often well-demarcated plaque with an identical reaction pattern throughout the entire lesion. The surface texture can vary from a smooth and thin to a leathery appearance with surface fissures “cracked mud” Ø Asymptomatic DDx.. OLP B) Non-homogenous Leukoplakia Other names: erythroleukoplakia & speckled leukoplakia white patches or plaques intermingled with red elements The clinical manifestation of the white component may vary from large white verrucous areas to small nodular structures. C) Proliferative Verrucous Leukoplakia (PVL) More aggressive proliferation pattern and high recurrence rate older women, and the lower gingiva is a predilection site. The malignant potential is very high, and verrucous carcinoma or squamous cell carcinoma may be present at the primary examination Oral Erythroplakia Clinical presentation A red lesion of the oral mucosa that excludes other known pathologies The lesion comprises an eroded somewhat submerged red lesion that is frequently observed with a distinct demarcation against the normalappearing mucosa. Asymptomatic DDx.. erythematous OLP Highest risk of malignant transformation Floor of the mouth Lateral borders of the tongue Retromolar area 6 Clinically.. loss of flexibility of the affected tissues and induration Predisposing factors.. SMOKING, alcohol, Candidiasis, mechanical trauma (chronic irritation) Oral leukoplakia/ Erythroplakia Diagnosis White or red patch (unexplained ) If trauma is suspected, such as a sharp tooth or restoration, should be eliminated. If healing does not occur in two weeks, a tissue biopsy is essential to rule out malignancy Diagnosis Biopsy : Histopathology reveals, A- No dysplasia: Hyperkeratosis, chronic inflammatory cells infiltration without any other features of a definable diagnosis is compatible with homogeneous OL. (cellular atypia) B- Epithelial dysplasia (mild to severe) Carcinoma in situ Defined as a lesion in which the full thickness of squamous epithelium shows the cellular features of carcinoma without stromal invasion Management tobacco and alcohol should be eliminated if no dysplasia is found, conservative treatment will be acceptable + Close Follow up topical antifungal is given 1-2weeks in case of dysplasia=surgical excision with or without grafting cryo-surgery, laser are preferred for rapid healing 7  Homogeneous OL are associated with a decreased risk for malignant transformation than nonhomogeneous leukoplakias and erythroplakias, and lesions not exceeding 2 cm appear to have a better prognosis than larger lesion Oral Submucous Fibrosis Oral submucous fibrosis is a chronic disease affecting the oral mucosa, as well as the pharynx and the upper two-thirds of the esophagus. Etiology 1- Chewing of areca nuts habit (dose dependence)...contain Alkaloids..modulate MMPs & collagenase..affect collagen metabolism …FIBROSIS 2- Genetic predisposition (Polymorphism of the gene, which is coding for tumor necrosis factor α (TNF-α) N.B.. Fibroblasts are stimulated by TNF-α, thereby participating in the development of fibrosis Clinical presentation Women-20s age Malignant transformation The 1st signs are erythematous lesions + petechiae …then , paler mucosa (white marbling)..Finally, fibrotic bands located beneath an atrophic epithelium.. loss of resiliency, which interferes with speech, tongue mobility, and a decreased ability to open the mouth burning sensation specially with spicy food Oral complications are most commonly observed on the lips, buccal mucosa, retromolar area, and soft palatal mucosa 3) Immunopathologic Diseases 1) Lichenoid Reactions “Delayed hypersensitivity reactions Type IV” oral lichen planus lichenoid contact reactions Lichenoid drug eruptions lichenoid reaction of graft versus host disease 2) Lupus Erythematosus Oral Lichen Planus Relatively common dermatosis occur on the skin, oral mucus membrane 50%of patient have oral and skin lesion Etiology ”multifactorial “ involves a cell mediated immunologically-induced degeneration of the basal cell layer of the epithelium / Stress Skin lesions Flat-topped, pruritic erythematous to violaceus papules with fine scaling on the surface Have a predilection for the trunk and flexor surfaces of arms and legs 8  The most frequent extra-oral mucosa site involved is the genital mucosa The patients report relief following intense scratching of the lesions, but trauma may aggravate the disease, (new skin lesions) which is referred to as “Koebner phenomenon” Clinical Types Reticular Papular Plaque-like Bullous (unusual) Erythematous Ulcerative - To establish a clinical diagnosis of OLP, reticular or papular textures have to be present. - OLP confined to the gingiva may be entirely erythematous, with no reticular or papular elements present, and this type of lesion has to be confirmed by a biopsy Reticular form characterized by fine white lines / striae (Wickham striae) The striae may form a network but can also show annular (circular) patterns. The striae often display a peripheral erythematous zone, which reflects a subepithelial inflammation. most frequent site: bilaterally in the buccal mucosa Asymptomatic Papular form 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 Asymptomatic DDx ? Plaque-type OLP homogeneous well-demarcated white plaque that occurs in conjunction with striae Clinically,,very similar to homogeneous oral leukoplakias. Frequent in smokers (following cessation, the plaque may disappear and convert into the reticular type) overrepresented among OLP lesions transforming into oral SCC Asymptomatic Erythematous (Atrophic) 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 of the lesion. Some patients may display erythematous OLP exclusively affecting attached gingiva. “Desquamative Gingivitis” DDx ? 9 Ulcerative type the most disabling form of OLP Clinically, the fibrin-coated ulcers are surrounded by an erythematous zone with white striae in the periphery Suspected to be ass. With malignant transformation DDx of OLP Other lichenoid reactions (same clinical & histo., must be diff. by history and upon cause removal, the lesions will disappear) Discoid Lupus Erythematosus (DLE) ” shows white radiating striae sometimes resembling those of OLP. The striae present in DLE are typically more prominent, with a more marked hyperkeratinization, and the striae may abruptly terminate against a sharp demarcation” Dx of LE is confirmed by Direct immunofluorescence for immunoglobulin IgM on biopsies of the clinically normal oral mucosa (Lupus Band Test) Plaque-like OLP is discriminated from homogeneous oral leukoplakia Erythematous OLP of the gingiva exhibits a similar clinical presentation as mucous membrane pemphigoid. Dx Reticular/popular forms are pathognomonic , except for erythematous OLP where biopsy is mandatory Histopathologic features 1- subepithelial band–formed infiltrate dominated by T lymphocytes and macrophages 2- degeneration of basal cells known as liquefaction degeneration “Civatte bodies” 3- hyperparakeratosis, thickening of granular cell layer 4- saw-toothed appearance of the rete pegs Management Unknown etiology. (Symptomatic Rx) Phase 1 therapy (esp. in Erythematous OLP) topical analgesic or antihistamine rinses & alkaline mouthwashes Topical & systemic corticosteroids to diminish inflammatory and hypersensitivity reaction ( 1mg/ Kg daily for seven days has been suggested, followed by a reduction of 10 mg each subsequent day maintenance dose with topical steroids may be commenced during the tapering of the systemic steroids) Topical antifungal Lichenoid Drug Eruptions mimics OLP clinically and histologically drugs or their metabolites may have the capacity to act as haptens, trigger a lichenoid reaction. (delayed hypersensitivity reaction) Penicillin, gold, NSAID, and sulfonamides Skin lesions similar to OLP Resolves upon discontinuance of the drug (symptomatic treatment with topical steroids) 10 Main points of the lecture 1-Classification of soft tissue lesions 2-Classification of Ulcerative and Vesiculobullous lesions 3-Acute multiple lesions Oral Mucosal Lesions Soft tissue lesions are classified Flat lesions Depressed lesions Raised lesions Any lesion could be 1ry or 2ry lesions Primary lesions Macule-patch Papule - Plaque Nodule- tumor Vesicle - Bulla Pustule Secondary lesions Erosion Fissure Ulcer Scar crust Flat circumscribed area of epidermis or mucosa < 1cm. Distinguished by color from surroundings, may be: Red Pigmented Blue, brown or black) due to melanin or foreign materials Macule Primary lesions Patch Flat Circumscribed area Neither elevated nor depressed > the macule size (1 cm). Differentiated from surroundings by colour, texture or both. eg Leukodema Papule Superficial elevated solid lesion, smaller 11 than 1 cm diameter. eg. Lichen planus. papule (skin lesions) Plaque Flat solid raised area, greater than 1 cm diameter. eg. Lichen planus, leukoplakia. Nodule Solid elevated mass of tissue, less than 1 cm diameter. Extends deeper. The over lining mucosa non-fixed, easily moved over the lesion. eg. Benign tumors as fibroma, lipoma. Vesicle Circumscribed fluid filled elevation in mucosa. Less than 1 cm diameter. Fluid, consist of lymph, serum Epithelial lining, thin, breakdown → ulcer. Common in viral infections eg. Herpes simplex, herpes zoster, chicken pox. Bulla Fluid filled elevation, greater than 1 cm diameter. eg. Pemphigus, pemphigoid, burns. Pustule Circumscribed elevation filled with purulent exudates resulting from infection. Less than 1 cm diameter. Creamy white or yellowish white in colour. eg. Herpes zoster Herpes labialis Secondary lesions Results from an alteration of the primary lesion either as a natural 12 course of the disease or as a result of manipulation E. g. bulla may rupture to give an ulcer. Erosion Denudation of epithelium above basal cell layer. Moist, slightly depressed. Results from broken vesicle or trauma. Healing with no scar. eg. Pemphigus. Ulcer Loss of epithelium, below basal cell layer. May heal with scar. Usually painful. eg. Traumatic ulcer Aphthous ulcer Fissure Linear cleft in the mucosa Affect lips and perioral tissues. When infected Pain, ulceration & inflammation eg. Angular cheilitis, Scar Permanent mark, cicatrix after wound heals. Any size and shape. Intraoral scar is lighter in colour than adjacent mucosa. eg. Major aphthous ulcer and M. m. pemphigoid Crust Results when blood, serum or purulent exudate dries on skin. Their appearance depends on the agent e.g: red when formed by blood Seen in erythema multiform Ulcerative and 13 Vesiculobullous lesions Burket’s classification for ulcerative and vesiculobullous lesions 2008 I-Patients with acute multiple lesions II-Patients with Recurring Oral Ulcers III-Patients with Chronic Multiple Lesions IV-Patients with Single Ulcers The patients with acute multiple lesions A- Herpes virus infection 1- Herpes simplex infection 2- Varicella zooster infection B- Coxsakie virus infection I-herpangina II- acute lymphnodular infection III- hand,foot and mouth diseases C- Erythema multiforme D- ANUG( acute necrotizing ulcerative gingivitis) Acute multiple lesions Acute multiple lesions 1-HSV lesions 2-VZV lesions 3-Coxsackievirus infection 4-ANUG and periodontitis 5- Erythema multiform Steven Johnson syndrome and Toxic Epidermal Necrolysis Human herpes virus(HHV) Herpesviridae family of virus contain different viruses that are pathogenic in humans Herpes simplex virus-1 (HSV-1) Herpes simplex virus-2(HSV-2) Varicella Zoster virus(VZV) Epstein-Barr virus(EBV) Hairy leukoplakia, infectious mononucleosis, Burket’s lymphoma, nasopharyngeal carcinoma) Cytomegalovirus (CMV) Human herpes virus (HHV-6, HHV-7, HHV-8) Herpes Simplex Virus infection There are two different types of herpes simplex virus HSV1 and HSV2 HSV1 is responsible for : Oral infection; as primary herpetic gingivostomatitis, recurrent intra-oral herpes and recurrent herpes labialis. Eye infection Dermatitis above the waist 14  HSV esophagitis Herpes encephalitis HSV2 is responsible for: Genital infection Infection in new born, due to contact of infant with vaginal lesions during delivery Dermatitis below the waist Herpes simplex virus infection (HSV-1) Structure of HSV virus 1- Genome. 2- Protein capsule. 3- Envelope. Virus growth cycle Adsorption: HHV binds to receptors on the cell plasma membrane on keratinocytes and neurons Penetration: Virion enter the cytoplasm by endocytosis Virions uncoat and DNA enter the nucleus Replication occurs and thousands of viral copies are generated The nucleus swell (ballooning degeneration) Assembly: DNA packaged into the empty capsids on the nuclear membrane, acquire an envelope and released extracellulary The keratinocyte become lysed and undergoes necrosis. Adsorption Penetration Replication Assembly Released Pathogenesis: Virus has marked predilection to invade the epitheliial cells resulting in intra-epithelial vesicles. HSV -1 can cause primary or recurrent infections Acute herpetic gingivostomatitis (A) HSV 1 primary infection Primary (acute )herpetic gingivostomatitis Occurs in patients with no prior infection with HSV1. Transmission of the virus occurs by virus inoculation of the skin, mucosa and eye by infected secretion. Most of cases run a subclinical course or misdiagnosed as teething. Age uncommon before 6 months (because of the maternal antibodies usually (IgG) that can cross the placental barrier. common in children from 1-10 years , with higher 15 peak from 2-3 years. Adult onset primary HSV infection: The signs and symptoms are the same but more severe Clinical features Prodromal symptoms precede the local lesions by 1-3 days. It include fever, headache ,myalgia, malaise, loss of appetite, nausea and vomiting, submandibular and upper deep cervical lymph nodes enlargement. Clinical features Vesicles develop on the oral, gingival or even circum-oral tissues. They quickly rupture leaving ulcers which are: Shallow round Discrete, shallow ragged May coalesce to form larger ulcers with scalloped borders Few millimeters to 1 cm in size Very painful Surrounded by erythematous zone. Clinical picture … contd Clinical manifestations Oral pain leads to poor oral intake Patients may require hospitalization for hydration Pharyngitis cause swallowing difficulties and excessive salivation An important diagnostic criteria in primary herpetic gingivostomatitis is the appearance of generalized acute marginal gingivitis; without loss of inter dental papillae. Ocular herpes simplex virus type 1 infection from rubbing the eye with a saliva-contaminated finger in a patient with primary herpetic stomatitis. NB: HSV infection of the cornea is a major cause of blindness in the world. Herpetic whitlow Infection of the fingers of health professionals caused by HSV-1 or HSV-2 It was an occupational hazard in dentists before the wide spread use of gloves. Virus is inoculated into the fingers through a break in the skin ▪ Self limiting in the healthy children within 10-14 days ▪This is followed by life long immunity from this acute form of infection ▪In immunosuppressive patients the virus may be disseminated to CNS and may be fatal. 16 Fate Recurrent Herpes simplex virus infection Recurrent oral HSV infection Latency HSV travels along the sensory nerve axon and establishes chronic latency in a non-replicating state in the regional ganglion such as the trigeminal ganglion Extra neural latency : HSV remains latent in cells other than neurons such as the epithelium( may play a role in recurrent lesions of the lip). Recurrent Herpes simplex virus infection Reactivation of HSV leads to shedding of HSV in saliva and oral secretions( an important risk factor of transmission) 1. On the lip called: recurrent herpes labialis (RHL) 2. Intraorally called recurrent intraoral herpes(RIOH) Triggers for reactivation of HSV 8-10% of patients following dental treatment Fever Ultraviolet radiation Trauma Stress Sun light exposure Menstruation Recurrent herpes labialis Occurs in patients who have a previous herpes simplex infection and have serum antibody protection against another exogenous primary infection. Not associated with systemic signs and symptoms Clinical manifestations 1- Prodromal period: tingling or burning or soreness, accompained by edema at the site of the lesions. 2- A clusters of small vesicles (1-3mm) surrounded by erythema. These vesicles rupture, forming ulcers, covered by crust of purulent exudates. 3- The area affected is the vermilion border, specially muco cutenous junction. Recurrent intraoral herpes or recurrent intraoral herpes simplex infection (RIH). Recurrent intraoral herpes: Clinical features: Multiple vesicles which are found on keratinized mucosa (tongue, palate and gingival) Small (1-5mm), usually found in clusters surrounded by erythema, tend to rupture forming multiple ulcers, that are painful. Fate: 17  Self limiting, healing without scar formation within 7-14 days. HSV in immunocompromized patients Such as : Those undergoing chemotherapy Organ transplantation as renal transplantation Patients acquired AIDS Patients with leukemia HSV in immunocompromized patients Clinically: Larger atypical appearing ulcers may be several centimeters in size. Diagnosis of HSV Diagnosis 1-History(short and acute onset& no previous episodes) 2-Clinical examination 3-Special investigations 1- HSV isolation : Isolation by tissue culture is the gold standard test for identification of the virus. 2-Polymerase chain reaction(PCR) PCR from swabs to detect HSV antigen 3-Rising antibody titer Laboratory diagnosis 4-Cytology: ▪ cytological smear from unruptured vesicles can be obtained from the base of the lesions ▪ and placed on microscopic slide and stained with Giemsa stain (Tzank preparation) or papanicolaou stain ▪ and searched for multinucleated giant cell or intranuclear inclusion. Herpes simplex 1 viruses. A, Pseudogiant cells 4-Cytology: ❑ Inclusion body ( Lipschutz bodies). : Virus induced masses seen in the nucleus or cytoplasm of infected cells by light microscope multinucleated Giant cells ( fusion of infected and normal cells ). ❑ Ballooning degeneration Management Primary HSV infection In healthy children and adults; supportive measures e.g.Pain control , liquid diet, topical anesthesia and antiseptic mouth wash e g. chlorhexidine Acyclovir family of drugs15mg/kg body weight 5 times daily. It reduces duration of fever, viral shedding and infectivity and inhibits viral replication 18  12 years 200 mg 5 times / day for 5 days. Recurrent HSV It can often be suppressed by reducing trigger factors such as sun screen. It is self limiting Topical antiviral 5% acyclovir cream (zovirax) Should be applied 3-6 times a day initiated early at the first prodrome or sign of a lesion. It can reduce shedding, infectivity, pain, size and duration of the lesion HSV in immunocompromized patients Should be treated with systemic antiviral to prevent dissemination to other sites Acyclovir dose in 400mg 5 times daily. Varicella zoster virus infection Varicella zoster virus infection Varicella zoster (VZV) is a herpes virus (DNA virus), and like HSV causes both a primary and a secondary infection and remains latent in nerve tissue. VZV is responsible for two major clinical infections in man; chickenpox (Varicella) and herpes zoster (shingles). Clinical manifestations Chicken pox ( primary VZV infection ) It is a childhood disease characterized by mild systemic symptoms (low grade fever and malaise) and generalized intensely pruritic skin vesicle (trunk & face). Vesicles turn cloudy and pustular, burst and crusts. Crust fall off after 1-2 weeks Orally: minor acute ulceration. After the primary infection healed, VZV becomes latent in the dorsal root ganglia of spinal nerves or extramedullary ganglia of the cranial nerves. VZV which becomes activated in some individuals produces herpes Zoster infection (HZI) commonly called Shingles The incidence increased with age and degree of immunosuppression Herpes Zoster Virus Infection (Shingle) Herpes Zoster Virus (Shingles) Usually seen in adults and old age (rare in children). Patients at high risk group are 1. HIV patients 2. leukemia, lymphomas 19 3. Irradiation 4. Immunosuppressive drugs patients. Clinical manifestation Starts with a prodrome of deep, aching or burning shooting pain along the affected nerve, usually unilateral. There is little or no fever Commonly involves the sensory branches of trigeminal nerve herpes zoster virus (shingle) After 2-4 days, unilateral vesicles, on an erythematous base appear along the course of the affected nerve; these vesicles appear in clusters giving the clinical picture of single dermatome involvement (dermatomic distribution). Vesicles crust in one week and Healing takes place after 3-4 weeks herpes zoster virus (shingle) Diagnostic problem Occasionally, HZI may occur without the appearance of dermatomal lesions. This is called zoster sine eruption or zoster sine herpes Diagnosis depends here on increased antibody titer of the virus. herpes zoster virus (shingle) Oral manifestation Trigeminal nerve(v) may be affected with involvement of one or more of it’ branches. Oral and facial lesions results from HZ of the second and third divisions of the trigeminal nerve but involvement of first is more common. herpes zoster virus (shingle) Ophthalmic division involvement Ophthalmic → skin covering forehead, upper eyelids, cornea Corneal involvement may lead to blindness. herpes zoster virus (shingle) Maxillary division The involvement of maxillary division gives rise to unilateral lesions which involve:Upper lip, hard and soft palate, vestibule of upper jaw, and skin of cheek and sides of nose. herpes zoster virus 20 (shingle) Maxillary → skin→ cheek, side of the nose → oral → soft and hard palate, vestibule of upper jaw. herpes zoster virus (shingle) Maxillary division The lesion are in form of vesicles which rupture to leave erosions and ulcerations The ulcers are: painful, unilateral, small, shallow, rounded with erythematous base. Herpes zoster Oral lesions → unilaterally grouped vesicles on buccal mucosa, tongue, palate & gingiva. Usually the lesions extend to involve the skin overlying the affected quadrant. herpes zoster virus (shingle) Mandibular division Mandibular → lower face oral → lower lip, tongue, buccal mucosa, vestibular of lower jaw herpes zoster virus (shingle) The lesion are in form of vesicles which rupture to leave erosions and ulcerations The ulcers are: painful, unilateral, small, shallow, rounded with erythematous base. herpes zoster virus (shingle) Complications Post herpetic neuralgia (uncommon in the oral cavity). Ramsy Hunt syndrome herpes zoster virus (shingle) Post herpetic neuralgia Means neuralgic pain may persist after the rash has resolved for 30-120 days(some experience pain for years). It is due to inflammation and fibrosis of the affected nerve. It usually affects the elderly patients 21 Ramsay- Hunt Syndrome Special form of HZ affecting the facial nerve via infection of the geniculate ganglion. (sens.& mot.) Clinical pictures: Headache, malaise, fever, pain localized in the ear or radiate to the jaw or to the neck. Herpetic oticus: Eruption of small crops of vesicles (unilateral) appear on the external ear Unilateral facial palsy , vertigo and deafness may accompany herpetic oticus. Oral manifestations in Ramsay Hunt syndrome: 1- Unilateral localized oral pain affecting two thirds of the tongue, soft palate followed by vesicular lesions. 2- Vesicular lesions that soon rupture and give rise to oral ulceration. 3- Xerostomia may occur due to disturbance in the secretion of the parotid gland. 4-Loss of taste sensation in the anterior two thirds of the tongue. Diagnosis 1- History: prodromal pain 2- Clinical examination:, unilateral dermatomic distribution. 3-Special investigation: Laboratory investigations Viral isolation using tissue culture is the best way. Differentiate between HZI and HSV infection. Polymerase chain reaction PCR cytological smear from the base of the vesicles. Treatment of VZV Supportive care and hydration for Mild cases in young healthy individuals. Sedatives as ibuprofen (not aspirin). Oral lesions by 0.2% chlorhexidine mouth wash to avoid secondary infection 5% Acyclovir ointment for skin and eye lesion Self limiting In HZ topical anesthesia are not effective since the pain arise from the sensory nerve. For immunocompromized patients Rapid treatment is needed to prevent dissemination Acyclovir accelerates healing, decrease pain, 800 mg 5 times daily for 10 days. it should be started within 72 hours of the disease onset, they also reduce the risk for post herpetic neuralgia Treatment of post herpetic neuralgia 22  Corticosteroids and antiviral therapy together in an attempt to reduce postherpetic neuralgia. Vaccination for prevention of VZV infection has been shown to reduce varicella outbreaks and for adults causes increase in antibody titer and reduces incidence and severity of HZI and postherpetic neuralgia A- Herpes virus infection 1- Herpes simplex infection 2- Varicella zooster infection B- Coxsakie virus infection I-herpangina II- acute lymphnodular infection III- hand,foot and mouth diseases C- Erythema multiforme D- ANUG( acute necrotizing ulcerative gingivitis) Acute multiple lesions Coxsackie virus infection oCoxsackie virus are RNA enteroviruses separated into group A and B. oThere are about 23 types of coxsackie virus A & 6 types of coxsackie B. oCVA is important to dentist because it can induce infection in the mouth and oropharyngeal region: Herpangina Hand ,foot and mouth disease. Acute lymphonodular pharyngitis. Herpangina The word herpangina derives from herpes(vesicular eruption) and angina meaning inflammation of the throat. CVA (1-10,16,22) are the most common viruses isolated from the disease. Clinical features Children under 10 are usually affected Patients develop fever, headache, and myalgia that usually lasts from 1-3 days. Usually occur in epidemics(widely spread in certain period) in summer. Oral manifestations First oral symptoms are sore throat and pain on swallowing. There may be erythema of the oropharynx, soft palate, and tonsillar pillars Small vesicles form but rapidly break down to 2-4 mm ulcers Herpangina is clinically distinguished from primary HSV by the following: It occurs in epidemics 23 Tends to be milder with smaller lesions than HSV lesions primarily affect the posterior part of the oral cavity and pharynx while HSV affects primarily the anterior part. Generalized acute gingivitis doesn’t occur in it. A smear doesn’t show any giant cells or ballooning degeneration of the nucleus in Herpangina. Treatment: Self limiting disease, treatment is supportive including proper hydration and topical anesthesia when eating or swallowing is difficult. Acute lymphonodular pharyngitis Caused by Coxsackie A 10 Patient present with sore throat. The development of diffuse small Yellow-white nodules in the oropharynx is more commonly encountered than vesiculation and ulceration. The disease is self limiting. Hand foot and mouth disease Caused by Coxsackie A 16 in majority of cases. Characterized by low grade fever, sore mouth and throat.(children) Lesions begins as erythematous macules that become vesicles that rapidly break down to ulcers Skin lesions on palms of hands & sole of feet. Oral lesions are more extensive than those caused by Herpangina. Lesions of hard palate, tongue & buccal mucosa are common. Treatment is supportive. Acute necrotizing ulcerative gingivitis ANUG Definition These are acute ulcerative-inflammatory condition of the gingiva and periodontium(ANUP), that are associated with polymicrobial infection. Risk group AIDS, smoking, stress, poor oral hygiene, local trauma. diabetes could also be a risk factor ANUG Clinical findings May or may not be associated with fever, with submandibular lymphadenopathy ANUG 24 Oral manifestation NUG has a rapid and acute onset. Excessive salivation, metallic taste Extremely painful and erythematous gingiva with punched out interdental papillae and formation of ulcers covered by necrotic membrane in M.G. There is accompanying foul odor and gingival bleeding ANUG Erythema Multiforme Erythema multiforme Definition: EM is an acute self limiting inflammatory Mucocutaneous Disease involving skin , oral mucous membrane and may involve other m.m. as genitalia. It causes several types of skin lesions, so the name multiform. EM may occur once or recur however it is catagerized with acute multiple lesions Classification Minor : less than 10% skin involvement with or without minimal MM involvement. Major : skin, oral mucosa and other mucous membrane involvement. Fulminant : Steven Johnson syndrome, and Toxic epidermal necrolysis(TEN or Lyell’s disease) NB: Recent data suggest that EM is etiopathogenetically distinct from SJC & TEN. Etiology : It is a hypersensitivity reaction The most initiating factors are: 1-Drug reaction to NSAIDS or anticonvulsants 2-Infection particularly HSV infection (other viral, fungal, bacterial or protozoal Micro organisms have been reported). Recurrent EM has been shown in 65-70% related to HSV infection Etiology : It might be type III hypersensitivity reaction OR It is postulated that HSV antigen incite a T cell mediated delayed type hypersensitivity reaction (type IV hypersensitivity reaction) destroying the epithelial cells NB :the destruction of epithelium is not by the action of the virus but by the cytotoxic T cell and cytotoxins NB: HSV is not cultured from the lesion Type III – Hypersenstivity Reaction (Immune Complex) Mechanism Ag activates sensitized T-cell to release factors (cytokines) that 25 stimulate other leucoytes Mediators Activ.T Helper cells, activate macrophages Type IV Delayed type hypersensitivity reaction (Stomatitis venenata) Clinical manifestations 1-EM is seen most frequently in children(20%) and young adults(20-40 years), and is rare after age 50. 2- There may be a prodrome of fever, malaise, headache, sore throat, rhinorrhea and cough 3- Skin lesion appear rapidly over a few days and begin as red macules that become papular 4- The most common sites of involvement are the extremities, face, and neck 5- The skin lesions may take several forms hence the term multiform The classical skin lesion is called target or iris lesion that consists of central bulla or pale area or necrosis surrounded by edema and concentric rings of erythema which is pathognomonic sign of EM (ie it’s presence indicates that it is erythema without any doubt). Genital and occular sites may be affected. Target or Iris lesion Oral findings: The oral findings range from mild erythema and erosion to painful ulceration When severe, ulcers may be large &bleeding causing difficulty in eating, drinking and swallowing and drools blood-tinged saliva. The most common affected site orally is the lips(bloody crusted lip), buccal mucosa, tongue and labial mucosa The gingiva is rarely affected It must be differentiated from other causes of acute multiple lesions especially primary herpes simplex infection. Oral lesions Vesiculobullous lesions on an erythematous base, when rupture give rise to deep, irregular bleeding ulcer. Bloody crusted lip ERYTEMA MULTIFORME Characterestic features Acute disease May be with prodrome of fever Most common on face,neck AND extremeties Skin lesions are maculopapular, iris lesion Lesions are large and diffuse Em heals within weeks 26  Rare gingival involvement usually associated with HSV or specific drugs Diagnosis 1- History rapid onset 2- Clinical examination bloody crusted lip 3-Target lesion on the skin if present. 4-Histopathological finding are helpful only in excluding other possible diseases. Laboratory findings There are no specific laboratory tests Diagnosis made mainly primarily by clinical findings Histopathologically: Subepithelial bulla formation and lymphocytic infiltration, dilatation of capillaries with areas of edema in superficial connective tissue Management Mild EM: Systemic or topical analgesics for pain and supportive care since the disease is self limiting and resolves within few weeks Topical steroids may also help resolve lesions More severe cases are usually managed with systemic corticosteroids In recurrent EM Cases suspected of being HSV associated should be treated with antiviral medications Treatment with acyclovir at the first sign of recurrent EM disease controls disease in 50% of cases. Steven Johnson Syndrome(SJS) and Toxic Epidermal Necrolysis (TENS) Fulminant Forms The more severe form=Stevens Johnson syndrome occurs when the generalized vesicles involve the skin, mouth, eyes and genitals (Mucocutaneous Occular Syndrome) Most severe form = Toxic epidermal necrolysis (TEN) It involves skin, mucous membrane of mouth ,throat, nasal passage, trachea, conjunctiva , genitalia and anus. Severe ulcerative lesions resembling burn with hot steam. Death may occur as a result of loss of body fluid, electrolyte imbalance and secondary infection. 27 Differences than EM They are more severe and tend to be on chest rather than extremities More likely associated with medication and rarely HSV More commonly incited by drugs which include antibacterial sulfonamides, anticonvulsants, and NSAIDs. Treatment Because of the severity of the condition, treatment is generally with high doses of systemic corticosteroid 28