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Oral Pathology I …

Oral Pathology I
Third Year

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  • 1. Oral pathology 1 DR. Aiman A. Ali A 28 Hussain AL - hasan Vesiculo-Bollous Vesiculo-Bollous Diseases : Diseases Viral    Associated with immunologic defects Hereditary Viral infections of significance to clinical dentistry:      Herpes Simplex Virus (HSV) infection Varicella-Zoster infections Hand, Foot, and Mouth Disease Herpangina Measles (Rubeola) 1-HSV Infection pathogenesis: DNA virus. Two types HSV1 & HSV2. Transmitted by physical contact with an infected person. Virus travels through the trigeminal nerve to the t. ganglion . Virus becomes latent in the neural tissue. With reactivation it travels to the epithelial surface. Reactivation by exposure to sunlight [fever blister] or exposure to cold [cold blister] or other factors.        clinical features: A - clinical features - primary:  Primary herpetic gigivostomatitis  Usually affects children  Vesicular eruption may appear on the skin vermilion  In the oral cavity, lesions may appear on any part of the oral mucosa  Viremia symptoms: fever, arthralgia, malaise, headache and cervical lymphadenopathy  After 7 to 10 days the lesions heal without scar B - clinical features - secondary: • Usually on the lip and rarely on gingiva or palate • Prodromal symptoms • Within hours multiple fragile vesicles appear • Lesions ulcerate and coalesce • Lesions heal without scaring in 1 to 2 weeks • Rarely become secondarily infected • Recurrence vary from 1 per year to 1 per month
  • 2. C - clinical features - whitlow:  Typically occur in dental practitioners who don’t use gloves and had physical contact with infected individuals.  Either primary or secondary HSVI involving the fingers.  Recurrent lesions if occurred, would be expected on fingers.  Pain, redness, vesicles that break to become ulcers.  Duration vary from 4 to 6 weeks. Histopathology :  Vesicles are intraepithelial  Some virus-infected epithelial cells are seen  After several days these features disappear Differential diagnosis:  Primary HSV infection  Streptococcal pharyngitis  Erythema multiform  ANUG  Secondary HSV infection  Recurrent aphthous stomatitis  Virus culture, monoclonal antibodies or DNA hybridization Treatment : Time is very important. Acyclovir. • Oint 5% 5t. daily when symptoms first appear. • Tab 200 to 400 mg 5t daily is effective. Vidarabine or Idoxuridine are effective on ocular HS but not LHS. Primary HSV infection is best managed with supportive therapy [fluid, rest, oral lavage and antipyretics].     2-Varicella-Zoster Infection: Etiology & Pathogenesis: VZV is one of the herpes virus. Cause primary infection (varicella or chickenpox) and secondary disease (herpes zoster or shingles). After primary infection, virus remain latent in a sensory ganglia. Reactivation of latent VZV usually follows immunosuppressive status, drug administration, irritation or local trauma.    
  • 3. Clinical features : A- Clinical features-vericella : Common among children. Fever, chills, malaise and headache . Rash involves the trunk, head & neck including oral mucosa. It develops into vesicles pustular ulcerations. Lesions heal after several weeks. Secondary infection is common.       B- Clinical features-herpes zoster : • Involvement of 5th nerve result in unilateral oral, facial, and ocular lesions • Prodromal symptoms of pain or paresthesia maculo-papular rash vesiculo-bullae , Ulcerations heal after several weeks • Complications include: • Secondary infection • Post-herpetic neuralgia • Motor paralysis • Ocular inflammation * Hunt’s Syndrome: A special type of herpes zoster infection with involvement of the external ear and oral mucosa (facial and auditory nerves).  Histopathology : * Varicella-Zoster Infection:  The same as those seen in HSV.  Virus infected epithelial cells.  Homogenous nuclei .  In uncomplicated cases, epithelium regenerates with little or no scar. • Differential diagnosis: o HSV infection. Treatment : A -Varicella: • Supportive therapy. • In immunocompromised patients more substantial measures are indicated. B - Herpes zoster: • The same for HSV but in high dose . • Acyclovir 800 mg x 5 x 7 to 10 days. • Analgesics.  Corticosteroids are contraindicated.
  • 4. 3- Hand foot & mouth disease: Pthogenesis: Coxsackie virus: • CV type A • CV type B • A16, and occasionally A5, A9, A10, B2 and B5 cause HFM disease • HFM is a highly contagious infection • Virus transmission: through airborne spread or oral-fecal contamination  clinical features: • Affect children under the age 5 years • Resolve spontaneously after 1 to 2 weeks • Signs and symptoms of viremia (low grade) • Oral lesions: multiple vesicles ulcers covered by yellow membrane surround by erythema • Occur anywhere of the oral cavity • Hand and feet lesions are maculopapular with or shortly after the oral lesions vesicles ulcers Histopathology : Vesicles are intraepithelial The vesicle cavity filled with proteinaceous debris and inflammatory cells   Diffretial Diagnosis : 1- Primary HSV infection and varicella: • Milder symptoms • Cutaneous distribution • Virus culture or detection of antibodies 2- Aphthous stomatitis. Treatment : Symptomatic therapy 4- Herpangina: Etiology & Pathogenesis  Coxsackie type A (A1-6, A8, A10, A22, B3 and possibly others)  Transmission through contaminated saliva
  • 5. clinical features: * Common in summer and in children * Pain, malaise, fever, dysphasia and sore throat * Oral vesicular eruption on the soft palate, faucial pillars and tonsils * Pharyngitis * Lesions last less than 1 week Differential diagnosis: HSV infection, HFM and varicella • Clinically • Short duration Streptococcal Pharyngitis • Vesicular eruption • Summer presentation • Mild symptoms Aphthous stomatitis • Systemic symptoms    Treatment is usually not required 5-Measles (Rubeola) : pathogenesis:  Highly contagious.  Measles virus (DNA paramyxovirus). clinical fetures:  Commonly affect children in winter and spring  incubation period of 7 to 10 days  Fever, malaise, conjunctivitis and cough  After 2 days small macules with white necrotic center (Koplik’s spots) appear in the buccal mucosa.  After 2 days skin rash appear initially on the head and neck followed by the trunk and then the extremities. histopathology: Warthin-Frankeldey giant cells are seen in lymphoid tissue. Infected epithelial cells which become necrotic.  
  • 6. Diagnosis: M. Rubeola But, Rubella (German  Usually made on: M.) • Clinical signs and symptoms. • Prodromal symptoms. • Koplik’s spots. • If necessary, serologic test for antibodies to measles virus. Treatment:  Supportive treatment: • Bed rest • Fluids • Adequate diet • Analgesics Differential diagnosis between : M. Rubeola : • Paramyxovirus Family • Contagious • (sever) Fever respiratory symptoms and rash • Koplik's spots • Does not cause develop-mental abnormalities in the fetus • • • • • Rubella (German M.) : Togavirus Family Contagious (mild) Fever, respiratory symptoms and rash no Koplik's spots Cause developmental abnormalities in the fetus
  • 7. ‫محاضرة جديدة‬ Vesiculo-Bollous Diseases Associated with immunologic defects: 1. Pemphigus Vulgaris 2- Pemphigus vegetans 3. Cicatricial pemphigoid 4. Bullous pemphigoid 5. Dermatitis herpetiformis 6. Linear IgA Disease Pemphigus antibody + Activate epithelial intracellular protolytic enzyme Desmosome-tonofilament complex 1- Pemphigus Vulgaris Etiology  Reactive IgG against epithelial desmosome-tonofilament complexes  Loss of cell-to-cell adherence (acantholysis) * Clinically:  Mucocutaneuos disease.  Skin lesions appear after OL in a period of 1 year.  Ulcers preceded by bullae.  60% of cases the first appearance in the oral cavity.  More common in the 4th and 5th decade.  Nikolsky sign is positive. * Histopathologically:  Acantholysis  Tzanck cells [free-floating rounded or spherical SSC]  Basal layer remains attached to the basement membrane  Bulla or vesicle are filled with fluid, Tzanck cells and neutrophils • Immunofluorescence: Immunofluorescence Direct Target antigen Indirect Acantholysis
  • 8.   Direct Indirect Immunofluorescence:  Appear in 80% of Pemphigus Vulgaris patients.  To assess the severity of the lesion. * Differential diagnosis:  Pemphigoid (bullous or cicatricial)  Erythema multiform  Bullous lichen planus  Dermatitis herpetiformis  Paraneoplastic pemphigus syndrome  In small lesions, aphthous stomatitis 2- Pemphigus vegetans:  Skin, vermilion and oral mucosa  Histopathologically: epithelial hyperplasia with intraepithelial abscess formation  Abundant eosinophils * Treatment:  High dose of corticosteroids.  Immunosuppressant agents to reduce complications of SAIDs as (osteoporosis, hyperglycemia, hypertension).  When SAIDs are contraindicated Gold therapy is recommended. 3- Cicatricial Pemphigoid : * Etiology:  Benign mucous membrane pemphigoid, ocular pemphigus, childhood pemphigoid, and mucosal pemphigoid  Idiopathic autoimmune disease  Deposit of IG and complement components along the basement zone  Usually no circulating antibodies * Clinical features: More common among adult women. Chronic lesions appear as vesiculo-bullous eruptions involve oral mucosa, which heal with scaring. When affects gingiva exclusively is referred to as gingivosis or desquamative gingivitis. Other sites: conjunctiva, larynx, genitalia, and esophagus. Skin lesions are uncommon. Nikolsky’s sign is positive.       * Histopathology:  Sub-basal clefting with clear cut separation at the basement membrane.
  • 9. No evidence of acantholysis. Variable infiltration with lymphocytes, plasma cells and occasionally eosino- and neutrophils.  Blood vessels often are dilated.   * Immunofluorescence:  Direct IF of intact oral mucosa demonstrate linear pattern of IgG fluorescence.  Occasionally IgA may detected.  Complement components are commonly found.  Indirect IF studies are usually negative. * Differential diagnosis:  Pemphigus vulgaris.  Erosive lichen planus. * Treatment:  Topical corticosteroids (betamethasone dexamethasone…etc).  In severe cases systemic SAIDs with immunosuppressive agents. 4- Bullous pemphigoid * Etiology:  Similar to cicatricial pemphigoid.  There are circulating autoantibodies to basement membrane zone antigen.  Degeneration of basement membrane attachment complexes.  Separation occur at the lamina lucida plane. * Clinical features:  Very common in the 7th and 8th decades.
  • 10.  Lesions affect the skin. * Histopathology:  Normal MS: the same of CP  Ultrastructurally: the basement membrane is cleaved at the level of lamina lucida * Immunopathology:  There is a detectable level of circulating antibodies in 70% of cases.  However, no correlation with the level of clinical disease.  IF findings corresponding to those in CP. * Treatment:  Systemic corticosteroids. 5- Dermatitis herpetiformis * Etiology:  Unknown cause.  Deposits of IgA in the skin and mucosa.  No circulating autoantibodies in the patient’s serum . *Clinical features:  Chronic disease typically seen in young adults.  Cutaneous disease, rarely appear in the oral cavity.  Symmetrical aggregated vesicular lesions of the skin with face and scalp involvement.  Periods of exacerbation and remission.  Iodide component exacerbate some cases.  Orally lesions appear as superficial ulcers with fibrinous base preceded by vesicles. * Histopathology:  Accumulation of neutrophils and eosinophils producing dermal micro- abscess  Connective tissue become necrotic and the overlying epithelium separate  Formation of subepithelial vesicle * Immunopathology:  Immunofluorescent staining is positive at the epidermal-dermal junction.  Almost IgA alone or in combination with IgG or IgM. * Treatment:  It dose not respond to SAIDs.  Sulfapyridine is the treatment of choice. 6 -Linear IgA Disease (Read it from the book) Hereditary: Epidermolysis Bullosa
  • 11. (Read it from the book)