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![Information
Herpes zoster (HZ) results from the involvement of
second and third branch.
Primary infection remains latent in the neurons of sensory
ganglion, especially dorsal roots of ganglion of the spinal
nerves and extramedullar ganglion of the cranial nerves.
(trigeminal nerve) V1-upper eyelid, forehead & scalp
V2-midface & upper lip [i/o hard palate & buccal gingiva]
V3-lower lip & face [i/o mandibular gingiva & tongue]](https://image.slidesharecdn.com/priya-20seminar-20on-20ulcerative-2cvesicular-20and-20bullous-20lesions-140507115114-phpapp01/75/Priya-seminar-on-ulcerative-vesicular-and-bullous-lesions-28-2048.jpg)
![Two types
Erythema multiforme may occur once or recur.
A] Mild, self-limited rash -erythema multiforme minor
B] Severe, life-threatening form -erythema multiforme
major (Or erythema multiforme majus)-Steven’s
Johnson Syndrome](https://image.slidesharecdn.com/priya-20seminar-20on-20ulcerative-2cvesicular-20and-20bullous-20lesions-140507115114-phpapp01/75/Priya-seminar-on-ulcerative-vesicular-and-bullous-lesions-58-2048.jpg)
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Priya seminar on ulcerative,vesicular and bullous lesions
This document discusses various vesiculobullous and ulcerative lesions that can occur in the oral cavity. It begins by defining vesicles, bullae, erosions, and ulcers. It then examines the causes of acute multiple oral lesions which can include viral infections like herpes simplex virus or coxsackievirus. It also discusses recurrent lesions like recurrent aphthous stomatitis. Chronic multiple lesions may be caused by conditions like pemphigus. Single ulcer lesions can result from fungal infections. The document then examines specific conditions in more detail like herpes infections, lichen planus, and pemphigus. It provides information on diagnosis and treatment of these oral conditions.
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Priya seminar on ulcerative,vesicular and bullous lesions
- 2. Introduction Classification Infectious Causes Of Oral Ulcerations Vesiculobullous lesions Ulcerative lesions
- 3. Vesicle: circumscribed collection offree fluid up to 0.5 cm in diameter Bulla: circumscribed collection of free fluid greater than 0.5 cm in diameter
- 4. Erosion: a focalloss of epidermis which does not include the dermoepidermal juction. Heals without scar. Ulcer: focal loss of epidermis and dermis. Heals with scar.
- 6. THE PATIENT WITHACUTE MULTIPLE LESIONS H SV Infections Primary HSV Infections Coxsackievirus Infections Varicella-Zoster Virus Infection Erythema Multiforme Contact Allergic Stomatitis Oral Ulcers Secondary to Cancer Chemotherapy Acute Necrotizing Ulcerative Gingivitis THE PATIENT WITH RECURRING ORAL ULCERS Recurrent Aphthous Stomatitis Behçet’s Syndrome Recurrent HSV infection
- 7. CONTD… THE PATIENT WITHCHRONIC MULTIPLE LESIONS Pemphigus Subepithelial Bullous Dermatoses HSV Infection in Immunosuppressed Patients THE PATIENT WITH SINGLE ULCERS Histoplasmosis Blastomycosis Mucormycosis
- 8. I. VESICULAR LESION A.Nonfebrile Lesion Recurrent herpes labialis Recurrent herpes stomatitis Reiter’s syndrome Contact stomatitis Impetigo Dyskeratosis congenita B. Febrile Lesion Hrpetic gingivostomatitis Herpangina Hand-foot and mouth disease Chicken pox Herpes zoster Smallpox II.BULLOUS LESION Pemphigus Familial benign chronic pemphigus Bullous pemphigoid Benign mucous membrane pemphigoid Epidermolysis bullosa Dermatitis hepetiformis Erythema multiforme Stevens-johnson’s syndrome
- 9. i. Herpes Viruses Herpessimplex Varicella Zoster Cytomegalovirus Epstein-Barr Virus ii. Lichen Planus iii. Lichenoid Drug Reaction iv. Erythema Multiforme Steven's Johnson Syndrome v. Pemphigus vi. Benign Mucous Membrane Pemphigoid i.Traumatic Ulcers ii. Recurrent Apthous Stomatitis iii. Radiation and Chemotherapy-Induced ulcers iv. Mucositis v. Odontogenic Infection Ulcers vi. Squamous Cell Carcinoma vii. Syphilis
- 10. I. acute multiplelesions: Causes: Viral infection. Primary herpetic gingivostomatitis. Herpengina. Hand, foot and mouth disease. Herpes Zoster. Bacterial infection: Acute Necrotizing Ulcerative Gingivitis (ANUG). Immunological. Erythema Multiforme. Contact Allergic Stomatitis. Oral Ulcers Secondary To Cancer Chemotherapy. II. Recurrent Oral Lesions: Recurrent Aphthous Stomatitis. Behcet’s Disease. Recurrent herpes simplex
- 12. Herpes simplex Primaryherpetic gingivostomatitis Recurrent herpes labialis Recurrent intraoral herpes Varicella zoster Chickenpox Shingles Coxsackievirus Herpangina Hand foot and mouth disease
- 13. Information about virus HSV-1: causes oral and pharyngeal infection, meningoencephalitis and dermatitis above the waist HSV2 : most genital infections above the waist Transmitted directly by contact with body fluids Average incubation time is 7 days Following resolution, virus becomes dormant until reactivation
- 15. Herpetic gingivostomatitis Primary infection Etiology •Herpes simplex virus (HSV) • Over 95% of oral primary herpes due to HSV-1 • Physical contact is mode of transmission
- 16. Clinical Presentation 88%of population experience subclinical infection or mild transient symptoms mostly in 0.5 and 5 years of age. Incubation period of up to 2 weeks Vesicles -> ulcers ->crusting in 7-14 days General features Fever, anorexia, lymphadenopathy, headache
- 17. Contd…. Both keratinizedand nonkeratinized mucosa affected mucocutaneous junction of lips, hard palate, and attached gingiva Tingling, Itching, burning at site of lesion just prior to vesicular eruption Coalescing, grouped, pinhead-sized vesicles that ulcerate Ulcers:1-5mm in size yellow, fibrinous base with scalloped borders and erythematous halo Fiery red Gingiva with edema, intense erythema. painful and difficulty in swallowing.
- 18. Diagnosis Obtain fluidfrom unruptured vesicle as it is most likely to contain virus PCR – much better than cultures Culture Smear – multinucleated giant cells Serology ELISA testing for antibodies to HSV Western Blot – very accurate, but very time consuming
- 19. Differential Diagnosis • Herpangina– site- posterior -soft palate, faucial pillars, phryngitis, occurs in summer & children • Hand-foot-and-mouth disease- systemic viral disease symptoms of fever, malaise Multiple pinpoint vesicles & ulers at hard palate, gingiva, tongue, hand & foot
- 20. • Varicella-chicken pox unilateralpainful grouped vesicles, ends at midline, trigeminal course • Herpes zoster (shingles) h/o recurrence • Erythema multiforme no gingival lesions, skin-bull’s eye or target appearance
- 21. 1. Symptomatic andsupportive Antipyretics, analgesics, hydration 2. Antiviral Acyclovir-(zorivax) topical-5% cream/ointment for 1 week 800mg 5 times/day for 1 week Pencyclovir-(denavir) topical-1%cream 2 hrly for 4 days Docosanol-(Abreva) 10%cream qid until healed 3. Anesthetic- Dyclonine hydrochloride 0.5% topical anesthetic
- 22. Etiology- Reactivation ofHSV Triggers- Fever, menstruation UV radiation Trauma, stress
- 23. Clinical Presentation Prodromeof tingling, burning, or pain at site of recurrence Multiple, grouped, fragile vesicles that ulcerate and coalesce Most common on vermilion border of lips or adjacent skin Intraoral recurrences on hard palate or attached gingiva Immunocompromised patients- any oral site, more severe (herpetic geometric glossitis).
- 24. On lips- RecurrentHerpes Labialis “cold sores” or fever blisters lips and extend to skin around the mouth Unilateral and recur two or three times a year Tingling, pain and/or itching in the perioral area appears 6-24 hours before the appearance of a lesion Erythematous areas →papules→ vesicles →ulcers → crust → normal within 2 weeks.
- 25. Diagnosis History and examination. Polymerasechain reaction (PCR) Differential diagnosis: Aphthous ulcers - not unilateral non-keratinised mucosa. Chickenpox, impetigo Lip cancer. Primary oral chancre of syphilis.
- 26. COMPARISION- ref byWood & Goaz 3rd edi RAU IRHS Age- any Nonkeratinized mucosa Erythematous macule or papule with central blanching followed by necrosis and ulceration Large shallow ulcers 5mm – 3cm in dia. Mostly single,1 or 2 may be widely distributed Adult or old age group Keratinized mucosa Clusters of small discrete vesicles No erythematous halo Vesicle rupture small(1-2mm)multiple round ulcers in clusters in small localized area
- 27. Treatment Analgesic & antipyretic- Paracetamol - 500mg-1gm tds Ibuprofen- 200-600mg tds Choline salicylate gel Lidocaine gel Topical antiviral agents: Aciclovir 5% cream Penciclovir 1% cream 4-5 days. Oral antiviral agents: Indicated in severe episodes. Laser treatment Laser therapy decreases pain and reduces the number of recurrences
- 28. Information Herpes zoster(HZ) results from the involvement of second and third branch. Primary infection remains latent in the neurons of sensory ganglion, especially dorsal roots of ganglion of the spinal nerves and extramedullar ganglion of the cranial nerves. (trigeminal nerve) V1-upper eyelid, forehead & scalp V2-midface & upper lip [i/o hard palate & buccal gingiva] V3-lower lip & face [i/o mandibular gingiva & tongue]
- 29.
- 30. Etiology- Varicella-zoster virus(VZV)- Human Herpes Virus III (HHVIII) Primary VZV (varicella /chickenpox): a childhood exanthem Secondary VZV (recurrent): (herpes zoster/shingles) infection Spread by respiratory droplets and less commonly by direct contact
- 31. Clinical Presentation Varicella (chickenpox)- primaryinfection 1st or 2nd decade of life Fever, headaches, malaise, and a rash Buccal mucosa & hard palate with short-lived vesicles Shallow, defined like aphthous ulcers Skin with widespread vesicular eruption ’’dewdrop like’’ Vesicles -> pustules -> rupture (ulcers) -> crust - >healing by 2-3 wks
- 32. secondary infection Herpes zoster(shingles)- Unilateral, dermatomal, grouped vesicular eruption of skin and/or oral mucosa-”zosteriform” Vesicles may coalesce prior to ulceration and crusting. Oral lesions typically occur after skin involvement Prodromal symptoms- Pain, paresthesia, burning, tingling Postherpetic pain may be severe.
- 33. Maculopapular rash-> vesicles-> pustules -> ulcerations -> crust -> heals by 2-4 wks -> scarring & hypopigmentation
- 34. Secondary infection (Shingles) Triggeredby immune suppression. Common in- o Elder persons, o Immunocompromised o HIV positive individuals, o malignant blood dyscrasias, o Malignant tumours, o Pt. Undergoing radiotherapy.
- 35. Complication of HZinfection Postherpetic neuralgia (PHN) Paresthesia of ant 2/3rd of tongue persist for months and year. Neuralgic pain is frequently associated with sensory loss. Ramsay Hunt syndrome HZ inf of Facial ns Blindness Encephalitis Pneumonia, Myocarditis Hepatitis
- 36. Diagnosis Clinical pictureusually all that is needed Direct fluorescent antibody test-highly sensitive Cytology PCR Differential diagnosis Pulpitis Primary herpes simplex/acute herpetic gingivostomatitis Recurrent intraoral herpes simplex Pemphigus vulgaris Mucous membrane pemphigoid
- 37. Treatment Prevent orlessen severity of infection with vaccination Supportive care (Antipyretics, analgesics, hydration) Antiviral- Valacyclovir-1000mg -3 times/day for 7 days Acyclovir- 800mg -5 times/day for 7 days Famciclovir -500mg -3 times/day for 7 days Postherpetic neuralgia- Gabapentine & 5% lidocaine patch
- 38. Etiology By β-herpesvirus Primary infection-infectious mononucleosis like disease Common in immunocompromized /HIV patients Causes pneumonia within 4 months after hematopoetic stem cell transplantation CMV within endothelium causes vascular inflammation, vascular occlusion and end-organ damage. Transmission-direct contact and transfer of infected WBCs through blood transfusions CMV is associated with Guillain-Barre syndrome, polyradiculopathy and myopathy with AIDS
- 39. Clinical presentation General Fever Lymphadenopathy Spleenomegaly Meningoencephalitis Myocarditis Thrombocytopenia Oral manifestations- Gingivitis and gingival hyperplasia Single large necrotic ulcer Painful Sustain weeks or months Any site Coinfected with HSV and VZV
- 40. Lab diagnosis Bloodculture using”shell vials” PCR-CMV DNA Biopsy Differential diagnosis Sq cell carcinoma Benign or malignant salivary gland tumors Traumatic ulcer Ulcerative granuloma
- 41. Treatment Topicalanaesthetics Systemic analgesic Soft diet Hydration Antivirals- o ganciclovir-i.v. 10mg/kg/day to prevent blindness o valganciclovir o cidofovir o α interferon
- 42. Coxsackievirus infection Ribonucleicacid (RNA) enteroviruses Type-A-24 types Type-B-6 types These viruses cause hepatitis, meningitis, myocarditis, pericarditis, and acute respiratory disease. Group A coxsackieviruses: herpangina, handfoot-and-mouth disease, and acute lymphonodular pharyngitis.
- 43. Hand-Foot-and-Mouth Disease Etiology • coxsackievirusA10 or A16, which may occur in mild epidemic proportion, chiefly in Children Age- 6months-5yrs • Incubation period <1 week
- 44. Clinical Presentation General features low-grade fever,anorexia Nonpruritic macules, papules, and vesicles, particularly on the extensor surfaces of the hands and feet. Severe cases- central nervous system, myocarditis and pulmonary edema Common in children
- 45. Oral manifestations Symptoms-Soremouth and throat, red and edematous tongue more extensive herpangina Erythematous macules→ vesicles→ ulcers Site- hard palate, tongue, and buccal mucosa . Oral mucosal lesions with focal herpes simplex–like appearance, Short course -3 to 7 days
- 46. Diagnosis • Concomitant oraland cutaneous lesions • Skin lesions- hands, feet and buttocks. • Antibody-titer increase measured between acute and recovery Phases Differential Diagnosis • Herpangina • Herpes simplex infection • Acute lymphonodular pharyngitis
- 47. Treatment Self limitingdisease Symptomatic treatment only Prognosis Excellent
- 48. Herpangina apthous pharyngitis/vesicular pharyngitis Etiology Most often by members of coxsackievirus group A (7, 9, 10,and 16) or group B (1–5) Occasionally due to echovirus 9 or 17 Mostly in summer Age- 3 to 10 yrs
- 49. Clinical Presentation Incubationperiod of 5 to 9 days Acute onset Mostly in young children & summer Subclinical Site- posterior oral cavity, tonsillar pillars, soft palate General feature- fever, chills, headache, anorexia, prostration, a bdominal pain, vomiting, sore throat, dysphagia macules-papules-vesicles short-lived -> ulcers Ulcers- Small,1-2mm,gray base and inflamed periphery Self-limiting, <2 weeks
- 50. Diagnosis • Other viralillnesses to be ruled out or separated • Course, time of year, location of lesions, contact with known infected individual Differential Diagnosis • Hand-foot-and-mouth disease • Varicella • Acute herpetic gingivostomatitis
- 51. Comparing with HSVinfection Herpangina HSV infections 1. occurs in epidemic 2. Milder 3. site- pharynx and posterior portions of the oral mucosa 4. does not cause a generalized acute gingivitis 5. Smaller 1. do not. 2. Painful 3. anterior portion of the mouth. 1. Causes acute generalized gingivitis 2. Larger than herpangina
- 52. Treatment • Soft diet •Hydration • Antipyretics • Chlorhexidine rinses Prognosis • Excellent
- 53. Acute Necrotizing UlcerativeGingivitis “Vincent’s infection”/“trench mouth” necrosis of the gingiva Etiology Fusiform bacillus and spirochetes and bacteroides intermedius. Local factors- Poor oral hygiene Pre-existing marginal gingivitis Faulty dental restorations Periodontal pockets Traumatized gingiva Smoking Emotional stress Systemic- Nutritional deficiency Debilitating disease-HIV, anemia, leukemia Marked malnutrition
- 54. Clinical features Age- 16 and 30 yrs ,low socio-economic group Sudden onset, tenderness, profuse salivation, metallic taste, spontaneous bleeding from gums, loss of taste sensation, fetid odor. Teeth- extruded, sensitive to tender, woody sensation, difficulty in chewing food. Necrotic punched out-crater like ulcerations on interdental and marginal gingiva. Gingiva covered by gray pseudomembranous slough, painful & raw on removing. Severe form- noma, a large necrotic ulcer.
- 55. Diagnosis Characteristic blunted,necrotizing interdental papillae with punched out crater appearance Only on gingiva Free cortisol in urine Differential diagnosis Leukemia Immunosuppression related conditions Primary herpetic gingivostomatitis Pemphigus vulgaris Erosive lichen planus
- 56. Treatment Local Debridgement, ultrasonicscaling, Rinses of chlorhexidine 3% hydrogen peroxide+saline- 12 times a day Topical povidone iodine Systemic antibiotics- Penicillin-500mg qid for 5 days Tetracycline-250-500mg 6 hrly Metronidazole-200-400mg tds 15mg/kg body wt 6 hrly I.V. Eliminating predisposing factors Maintainance of oral hygiene Prognosis Excellent
- 57. It is anacute, self limited, inflammatory mucocutaneous disease of the skin and oral mucous membranes that causes a variety of skin lesions— hence the name “multiforme.” The oral lesions, typically inflammation accompanied by rapidly rupturing vesicles and bullae.
- 58. Two types Erythema multiformemay occur once or recur. A] Mild, self-limited rash -erythema multiforme minor B] Severe, life-threatening form -erythema multiforme major (Or erythema multiforme majus)-Steven’s Johnson Syndrome
- 59. Etiology Infection withherpes simplex, Mycoplasma pneumoniae or other organisms Drug consumption, Sulfonamides, Antibiotics, Analgesics, Barbiturates Radiation therapy.
- 60. Clinical Presentation Acuteonset of multiple, painful, shallow ulcers and erosions with irregular margins Early mucosal lesions are macular, erythematous, and occasionally bullous. May affect oral mucosa and skin. Mostly in young adults Target or iris skin lesions may be noted over extremities. Genital and ocular lesions may occur. Usually self-limiting; 2- to 4-week course
- 61. Intraoral EM lesions Lips most commonly affected with eroded, crusted, and hemorrhagic lesions (Stevens- Johnson syndrome) Erythematous- vesiculobullous eruptions- erosions Circumoral crusting Recurrence is common.
- 62. Diagnosis Appearance Rapidonset Multiple site involvement in half of the cases Biopsy results often helpful, but not always diagnostic Differential Diagnosis Acute herpetic gingivostomatitis Erythema multiforme rarely affects the gingiva Pemphigus vulgaris Major apthous ulcers Erosive lichen planus Mucous membrane (cicatricial) pemphigoid
- 63. Treatment Mild (minor) form: symptomatic/supportivetreatment- adequate hydration, liquid diet, analgesics, topical corticosteroid Severe (major) form: systemic corticosteroids, parenteral fluid replacement, antipyretics viral infection or trigger exists-systemic antiviral drugs Prognosis Generally excellent Recurrences common
- 64. Stevens-Johnson Syndrome Etiology • Acomplex mucocutaneous disease affecting two or more mucosal sites simultaneously • Most Common Trigger: Recurrent Herpes Simplex Infection, Infection with Mycoplasma, Medications • Sometimes referred to as “erythema multiforme major”
- 65. Clinical Presentation GENERAL Eye(conjunctival), Genital, Cutaneous, Iris or target lesions are characteristic on skin.
- 66. Oral Lesions Labialvermilion and anterior portion of oral cavity Early phase is macular followed by erosion, sloughing, and painful ulceration Lip ulcers- crusted and hemorrhagic. Pseudomembrane; foul-smelling Vesicle→ painful erosions → grayish- white /hemorrhagic pseudomembranes. Posterior oral cavity and oropharyngeal involvement - odynophagia, sialorrhea, drooling
- 67. Differential Diagnosis Pemphigusvulgaris Paraneoplastic pemphigus Bullous pemphigoid Acute herpetic gingivostomatitis Stomatitis medicamentosa
- 68. Prognosis Good; self-limiting usually Recurrences common Treatment Hydration - Oral rinses - Topical steroids– - hydrocortisone-wycort 2.5% ointment - Orabase 0.5% - Triemcinolone-kenolog cream o.1% - Betamethasone-valisone cream 0.1% Systemic corticosteroid – Tab.cortin 100 mg 6 hrly Tab.wysolon 60 mg in div doses Antiviral -Acyclovir, famciclovir, valacyclovir May require admission to hospital burn unit
- 69. Plasma cell gingivitis Etiology- Hypersensitivity reaction to cinnamon, mint in toothpaste, chewing gums etc. Clinical presentation Young women, Sore/burning mouth Marked erosions and erythema with or without ulceration Oropharynx involvement- hoarseness, dysphagia,mild airway obstruction Reddene,velvety marginal and attached gingiva Maxillary and mandibular sulcus and buccal mucosa Persistent upto 3 yrs
- 70. Differential diagnosis- Erosivelichen planus Mucous membrane pemphigoid, Pemphigus vulgaris Pregnancy induced gingivitis Chronic candidiasis Treatment- Self limiting - Topical steroids– - hydrocortisone-wycort 2.5% ointment - Orabase 0.5% - Triemcinolone-kenolog cream o.1% - Betamethasone-valisone cream 0.1% Intralesional triemcinolone injection
- 71. 1- Filaments. 2- Desmosome. 3-Hemidesmosome. 4- Basal cell layer NORMAL CELL ATTACHMENTS
- 72. Desquamation The wordcomes from the Latin "desquamare" meaning "to scrape off the scales of a fish." The shedding of the outer layers of the skin, there is desquamation.
- 73. Bullous Diseases Pemphigusis a potentially life-threatening disease that causes blisters and erosions of the skin and mucous membranes. These epithelial lesions are a result of autoantibodies that react with desmosomal glycoproteins that are present on the cell surface of the keratinocyte. The immune reaction against these glycoproteins causes a loss of cell-to-cell adhesion, resulting in the formation of intraepithelial bullae.
- 74. Nikolsky’s sign: A positive Nikolsky's sign signifies a separation of epithelial cells either from one another or from the basement membrane which epithelium usually adhered. The Nikolsky’s sign +ve in pemphigus and epidermolysis bullosa. Pemphigus- pencil twist easily rips the spinous cells apart because they possess defective desmosomes Pemphigoid-the hemidesmosomes are defective. Within minutes, a blister will form, which is absolutely indicative, of a vesiculobullous disease
- 75. Bullous Diseases: PemphigusVulgaris Pemphigus Vegetans, Pemphigus Foliaceus, Pemphigus Erythematosus, Paraneoplastic Pemphigus Drug Related Pemphigus.
- 76. Pemphigus Vulgaris -Potentially fatal disease. - It is a rare autoimmune mucocutaneous disorder, characterized by blistering of the skin and mucous membrane. - 80% of Pemphigus cases. - first site of attack- oral mucosa Paraneoplastic pemphigus- pv asso. With neoplasm like lymphoma Associated ds- thymoma, myasthenia gravis, autoimmune ds High mortality rates previously Age: middle-age and elderly Sex: Females predominantly
- 77. Oral manifestations Bullaon a noninflamed base->rapidly breaks - >shallow irregular ulcers. A thin layer of epithelium peels away in an irregular pattern, leaving a denuded base. The edges of the lesion continue to extend peripherally over a period of weeks and involves large portions of the oral mucosa. Sites- buccal mucosa, palate and gingiva highly variable ranges from small blisters or erosions to widespread destruction of the oral epithelium
- 78. Rupture occurs withindays leaving a broad areas of desquamation associated with erythema. +ve Nikolsky’s sign.
- 79. DIFFRENTIAL DIAGNOSIS: Pemphegoid– blistrs doesn’t shift laterally Erythema multiforme young adults, acute ds, erosive-crusty changes, -ve Nikolsky’s sign Bullous lichen plannus
- 80. TREATMENT: systemiccorticosteroids, 1 to 2 mg/kg/d Azathioprine or cyclophosphamide added to reduce the complications of long-term corticosteroid Prednisone is used initially Advanced cases- prednisolone plus azathioprine methotrexate and cyclophosphamide mycophenolate, effective when resistant to other drugs adjuvants. Topical with systemic steroid therapy, prednisone tablets to dissolve slowly in the mouth before swallowing or by using potent topical steroid creams.
- 81. Pemphigus vegetens 1-9%of pemphigus cases Neumann type- early lesion same as PV Hallopeau type- pustules like verrucous hyperkeratotic vegetation Oral lesions- lace like ulcers with purulent surface, erythematous base, granular or cobblestone appearance Asso with inflammatory bowel ds. Diagnosis- Histopathology or the newer techniques of molecular biology. Treatment same as PV
- 82. Ulcerations Ulcer- Focus ofnecrotic tissue on surface and a destroyed overlying epithelium Margins-junction between normal epithelium and ulcer Edges-junction between margin and floor Floor-exposed surface within the ulcer (see) Base-on which the ulcer rest (felt)
- 83. Edges Undermined-tuberculous Punchedout-gumma/syphilis Sloping-healing,traumatic Raised, pearly white or beaded-rodent ulcer Rolled out/everted-malignant
- 85. Classification of ulcers Infective:- HSV Infections Primary HSV Infections Coxsackievirus Infections Varicella-Zoster Virus Infection 2. Traumatic: Mechanical: causes, dxtic criteria, hist Chemical: chemicals, aspirin burn Thermal: palate Factitious: biting, nails Radiation: immediate & delayed Eosinophilic 3. Idiopathic: Recurrent Aphthous Stomatitis (RAS) Minor Major Herpetiform 4. Vesiculobullous diseases 5. Neoplastic: SCC & others
- 86. TRAUMATIC ULCERS: Clinical features Mostly single, painful ulcer smooth red or whitish-yellow surface thin erythematous halo. soft on palpation spontaneously or after removal of cause heal without scarring within 6–10 days tongue, lip, and buccal mucosa
- 87. Mechanical Lip tongue, cheekbiting hard food Pins, nails Faulty restorations Prosthesis
- 88.
- 89.
- 90.
- 91. Diagnosis- based onthe history and clinical features. if an ulcer persists over 10–12 days a biopsy must be taken to rule out cancer. Differential diagnosis Apthous ulcer Sq cell carcinoma Chancre(primary syphilis)
- 92. 1. Removing causativefactors 2. Good hygiene of oral cavity 3. Antiseptic for 7-10 days 4. Analgetics if it is necessary 5. Topical steroids may be used for a short time.
- 93. Recurrent Aphthous Stomatitis Etiology Unknown 20% population Triggers- Varies from case to case Psychological-Stress,anxiety Hormonal-pregnancy,menstruation, Dietary- deficieny of iron, folic acid, vit C, vit B12 etc. Allergy Trauma
- 94. COMPARISION- ref byWood & Goaz 3rd edi RAU IRHS Age- any Nonkeratinized mucosa Erythematous macule or papule with central blanching followed by necrosis and ulceration Large shallow ulcers 5mm – 3cm in dia. Mostly single,1 or 2 may be widely distributed Adult or old age group Keratinized mucosa Clusters of small discrete vesicles No erythematous halo Vesicle rupture small(1-2mm)multiple round ulcers in clusters in small localized area
- 95. Minor aphthous ulcer -< 1cm in diameter - Located on freely mobile oral mucosa - Appears as a well-delineated white lesion with an erythematous halo - Prodrome of burning or tingling in area prior to ulcer’s appearance - Resolve in 7-10 days - Never scars
- 96. Major aphthous ulcer -> 1cm in diameter - Involves freely mobile mucosa, tongue, and palate - interfere with speech and eating - - Last much longer – 6 weeks or more - Typically scar upon healing
- 97. Herpetiform ulcers - Small,1-3mm Crops /multiple ulcers - site-mobile oral mucosa, tongue, and palate - Last 1-2 weeks - herpetiform- resemble those of HSV, but no vesicular phase
- 98. Differential diagnosis Intraoral recurrent herpes simplex- Keratinized mucosa Herpangina-posterior region Mild pharyngitis Hand-foot-mouth ds HSVin immunocompromized patients- large, longer duration. Raised border, small satelite ulcer
- 99. COMPARISION- ref byWood & Goaz 3rd edi RAU IRHS Age- any Nonkeratinized mucosa Erythematous macule or papule with central blanching followed by necrosis and ulceration Large shallow ulcers 5mm – 3cm in dia. Mostly single,1 or 2 may be widely distributed Adult or old age group Keratinized mucosa Clusters of small discrete vesicles No erythematous halo Vesicle rupture small(1-2mm)multiple round ulcers in clusters in small localized area
- 100. Treatment - Topical tetracyclinesolution for 5-7 days - Topical steroids –hydrocortisone-wycort 2.5% ointment - Orabase 0.5% - Triemcinolone-kenolog cream o.1% - Betamethasone-valisone cream 0.1% - Flucocinolone- flucort ointment 0.25%
- 101. Behcet’s disease Aetiology: HLA-B51 Clinical presentation Young adult males RAS in oral cavity, eye and Genitalia Uveitis, conjunctivitis, retinitis E. nodosum, pustular & macular lesions, Subcutaneous thrombophlebitis Arthralgia GIT lesions Thrombotic vascular lesions CNS lesions
- 102. Diagnosis Occurs threetimes/year Occular, genital,cutaneous problems Differential diagnosis Erythema multiforme Reiter’s syndrome Crohn’s disease Treatment Systemic corticosteroids Immunosupressive drugs- interferon(alferon)- 2ml inj , TNFα inhibitors Prognosis manageable