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Oral ulcersppt


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Oral ulcersppt

  1. 1. Or al ulcers
  2. 2. ULCER= defect or break in the continuity of the epithelial component of skin or mucosa, so that a depression or punched out area exists with exposure of the underlying .connective tissue
  3. 3. Important Causes of Oral :Mucosal Ulcers Vesiculo-Bullous Diseases: Infective • Primary and recurrent Herpes simplex. • Herpes zoster and chickenpox • Hand-foot-and - mouth disease • Herpangina
  4. 4. Non-infective Pemphigus vulgaris Mucous membrane pemphigoid Erythema multiforme Contact allergy
  5. 5. Ulceration Without Preceding Vesiculation (primary): Infective Cytomegalovirus-associated ulceration Some acute specific fevers Tuberculosis Syphilis
  6. 6. Non-infective Traumatic ulcers Aphthous stomatitis Behcet’s disease Reiter’s syndrome Lichen planus Acute necrotizing ulcerative gingivitis/stomatitis Some mucosal drug reactions Carcinoma
  7. 7. :I) Herpes Virus Infections Several herpes viruses cause human disease: Herpes simplex virus (HSV) 1 and 2 Varicella-Zoster virus Cytomegalovirus (causes oral ulcers in immunocompromised patients) Epstein-Barr virus Human herpes virus 6 (HHV6)
  8. 8. Herpes Simplex Virus Infection Primary Herpetic Stomatitis
  9. 9. :Clinical Features Incidence : Children 2-10 years old Non-immune adults Infection is unexpected below 6 months of age due to presence of maternal antibodies gained by the enfant during intrauterine life.
  10. 10. Prodrome Fever, headache, malaise, lymphadenitis, nausea and vomiting. These precede the appearance of oral vesicles by 1-2 days. The early lesions: vesicles 2-3 mm in diameter. Rupture of vesicles leaves circular, sharply defined, shallow ulcers with yellowish or grayish floors and red margins. The ulcers are painful and may interfere with eating.
  11. 11. The gingival margins: are frequently swollen and red, particularly in children. Sometimes labial and facial lesions appear without intraoral involvement. Oral lesions usually resolve within a week to ten days (Self-limiting).
  12. 12. :Pathology Intraepithelial vesicles. Ballooning degeneration. Multinucleated cells. Intranuclear inclusion bodies (lipschutz bodies) .
  13. 13. :Diagnosis 1-History: History of prodromal symptoms 1-2 days before oral lesions Negative history of recurrent herpes labialis Positive history of contact with a patient with primary or recurrent lesions.
  14. 14. 2-The clinical picture 3-Lab investigations: A smear showing virus-damaged cells A rising titre of antibodies reaching a peak after 2-3 weeks provides absolute but retrospective confirmation of the diagnosis.
  15. 15. Treatment Supportive measures sometimes are all that is needed . Acyclovir is a potent antiherpetic drug. It inhibits DNA replication in HSV-infected cells but has no effect on normal cells. Dose: adult: 200 mg 5 times/day (5 days) Children: 100 mg 5 times /day (5 days)
  16. 16. Recurrent Herpes Simplex :Lesions Due to reactivation of latent virus residing in cells after a previous primary attack (not a re-infection) A) Recurrent Herpes Labialis B) Recurrent Intra oral Herpes
  17. 17. :A) Recurrent Herpes Labialis Prodromal paraesthesia or burning sensations then erythema. Vesicles form after an hour or two usually in clusters along the mucocutaneous junction of the lips but can extend onto the adjacent skin.
  18. 18. The vesicles enlarge, coalesce and weep exudates. After two or three days they rupture and crust over Finally heal, usually without scarring. The whole cycle may take up to 10 days. Secondary bacterial infection may change the lesions into pustules
  19. 19. :B) Recurrent Intra oral Herpes Clusters of small vesicles that break into ulcers, 1-2 mm in diameter, appear mainly on keratinized oral mucosa (gingival, hard palate, …).
  20. 20. Treatment Treatment must start as soon as the premonitory sensations are felt. Acyclovir cream may be effective if applied at this time.
  21. 21. Chronic Herpes Simplex :Lesions It is a variant of recurrent herpes simplex lesion occurring in immunocompromised patients (AIDS, immunosuppressive therapy, leukaemia, lymphoma, …..) Lesions appear on skin or mucosal surfaces as an ordinary recurrent herpetic lesion but: remain for weeks or months and develop into large ulcers (up to several centimeters in diameter).
  22. 22. :Treatment Systemically administered acyclovir, doubling the dose; i.e. 400 mg 5 times/day, till healing takes place.
  23. 23. :Herpetic Cross-infections Both primary and secondary herpetic infections are contagious. Herpetic whitlow, which is an infection of fingers after manipulation of herpetic lesions, is a hazard to dental surgeons and their assistants. Herpetic whitlows, in turn, can infect patients In immunodeficient patients such infections can be dangerous but acyclovir has dramatically improved the prognosis in such cases . Mothers applying antiherpetic drugs to children’s lesions should wear gloves.
  24. 24. Herpetic whitlows
  25. 25. :Varicella –Zoster infection A) Chicken Pox B) Herpes Zoster (1) H Zoster of Trigeminal Area (2) Ramsay Hunt Syndrome
  26. 26. :A) Chicken Pox A childhood disease characterized by: Mild systemic symptoms. Generalized pruritic eruption of maculopapular lesions that rapidly develop into vesicles on erythematous base. Oral vesicles that rapidly rupture giving ulcers.
  27. 27. B)Herpes zoster :(1)The trigeminal area      Recurrence of VZV infection occurs typically in the elderly Pain precedes the rash (prodrome) Facial rash accompanies the stomatitis Lesions are localized to one side (absolutely unilateral), within the distribution of any of the divisions of the trigeminal nerve Malaise can be severe
  28. 28. Sometimes pain occurs without rash or oral lesions, (herpes sine eruption) which leads to problems in diagnosis.
  29. 29. Herpes Zoster of maxillary nerve
  30. 30. Herpes Zoster of mandibular nerve
  31. 31. Pathology The varicella zoster virus produces similar epithelial lesions to those of herpes simplex, in addition to inflammation of the related posterior root ganglion.
  32. 32. Complications Sometimes followed by post-herpetic neuralgia, particularly in the elderly. Can be life-threatening in immunocompromised patients. Secondary infection may cause suppuration and scarring of the skin. When the ophthalmic division is involved, blindness due to corneal scarring may occur
  33. 33. Treatment Oral acyclovir (800 mg five times daily, usually for 7 days) as early as possible. Intravenous acyclovir :In immunodeficient patients. Analgesics. The addition of prednisolone (corticosteroids) may accelerate relief of pain and healing and prevent postherpetic neuralgia in elderly patients.
  34. 34. :Ramsay Hunt Syndrome) 2(
  35. 35. Complications Permanent facial paralysis. Deafness
  36. 36. :Management Corticosteroids or ACTH are given in addition to antiviral drugs (acyclovir) to avoid permanent fibrosis of the facial nerve.
  37. 37. Hand-foot-and-mouth Disease Common mild viral infection Causes minor epidemics among school children Characterized by ulceration of the mouth and a vesicular rash on the extremities. Caused by strains of Coxsackie A virus. The incubation period is 3-10 days.
  38. 38. Clinical Features Small scattered oral ulcers usually with little pain. Intact vesicles are rarely seen Gingivitis is not a feature. Regional lymph nodes are not usually enlarged and systemic upset is mild or absent. The skin rash consists of vesicles, sometimes deep-seated, or occasionally bullae, mainly seen around the base of fingers or toes, but any part of the limbs may be affected.
  39. 39. Hand-foot-and-mouth Disease
  40. 40. Treatment No specific treatment available or needed.
  41. 41. Herpangina    Coxsackie virus A infection (usually A4). Children 3-10 years are mostly affected (but other ages are possible). Frequently occurs in epidemics.
  42. 42. Clinical Features     Incubation period: 2-10 days Prodrome: fever, chills, anorexia, sore throat, dysphagia Lesions (soft palate, tonsils, pharynx): macules → papules and vesicles → small (12 mm) ulcers. Ulcers heal without treatment in about 7 days.
  43. 43. Herpangina
  44. 44. Tuberculosis Ulcer on the mid-dorsum or tip of the tongue; the lip or other parts of the mouth are infrequently affected. The ulcer is typically angular with overhanging edges and a pale floor, but can be ragged and irregular. Ulcer is painless in its early stages regional lymph nodes are usually unaffected.
  45. 45. Pathology Typical tuberculous granulomas are seen in the floor of the ulcers.
  46. 46. Management Diagnosis Biopsy Chest radiography . Specimen of sputum. Mycobacterial infection is confirmed by culture or PCR.
  47. 47. Treatment Oral lesions clear up rapidly if vigorous multi-drug chemotherapy is given for the pulmonary infection. No local treatment is needed.
  48. 48. Syphilis Primary Syphilis: An oral chancre appears 3-4 weeks after infection on the lip, tip of the tongue or rarely, other oral sites. It consists initially of a firm nodule about a centimeter across. The surface breaks down after a few days, leaving a rounded ulcer with raised indurated edges. A chancre is typically painless but regional lymph nodes are enlarged, rubbery and discrete. Serological reactions are negative at first. Treponema pallidum can be demonstrated by darkground illumination of a smear from the chancre. Oral chancres are highly infective. After eight or nine weeks the chancre heals, often without scarring
  49. 49. Secondary Syphilis: Develops 1-4 months after infection. Mild fever with malaise, headache, sore throat and generalized lymphadenopathy, soon followed by a rash and stomatitis. The rash consists of asymptomatic pinkish (coppery) macules, symmetrically distributed and starting on the trunk. It may last for a few hours or weeks Oral lesions, which rarely appear without the rash, mainly affect the tonsils, lateral borders of the tongue and lips. They are usually flat ulcers covered by grayish membrane and may be irregularly linear (snail track ulcers) or coalesce to form well-defined rounded areas (mucous patches). Discharge from the ulcers contains many spirochaetes and saliva is highly infective. Serological reactions are positive and diagnostic at this stage.
  50. 50. Tertiary Syphilis: Develops in many patients about three or more years after infection. A characteristic lesion is the gumma. Clinically, a gumma, which may affect the palate, tongue or tonsils can vary from one to several inches in diameter. It begins as a swelling, sometimes with a yellowish centre which undergoes necrosis, leaving a painless deep ulcer. The ulcer is rounded, with soft, punched-out edges. The floor is depressed and pale. It eventually heals with severe scarring which may distort the soft palate or tongue, perforate the hard palate or destroy the uvula.
  51. 51. Minor aphthous ulcer
  52. 52. Major aphthous ulcer
  53. 53. Herpetiform ulcers
  54. 54. Clinical Picture Lesions are confined to oral mucosa ( no extraoral manifestations). Prodrome: burning sensation (2-48 hours) with the appearance of localized erythema Ulceration: single or multiple ulcers appear within few hours. Ulcers are surrounded by erythema and painful. No tissue tags surround the ulcers.
  55. 55. Healing: in minor form it takes 7-14 days, in major ulcers it may take several months. No scar formation occurs except in major form. Healing is characterized by disappearance of the surrounding erythema.
  56. 56. Diagnosis and Management Check-list for Diagnosis of Recurrent Aphthae: History Examination Special investigations
  57. 57. Treatment In cases with underlying systemic disease : remedy the cause For minor aphthae: treatment is related to the severity.
  58. 58. In mild cases: Protective topical treatment as orabase Topical anaesthetic Non-steroidal anti-inflammatory Benzydamine hydrochloride mouth wash. In more severe cases: Potent topical steroid asTriamcinolone dental paste
  59. 59. Treatment of major aphthae. Effective treatments include Systemic or intralesional steroids, Azathioprine, Cyclosporine Colchicines and Dapsone.
  60. 60. Tetracycline mouth rinses. For herpetiform aphthae particularly . Chlorhexidine. A 0.2% solution has also been used as a mouth rinse for aphthae.
  61. 61. Behcet's Disease Behcet's syndrome was originally defined as a triad of oral aphthae, genital ulceration and uveitis. However, it is a multisystem disorder with varied manifestations. Patients are usually young adult males between 20 and 40 years old.
  62. 62. Patients suffer one of four patterns of disease: Mucocutaneous (oral and genital ulceration) Arthritic (joint involvement with or without mucocutaneous involvement) Neurological (with or without other features) Ocular (with or without other features). The oral aphthae of Behcet's disease are not distinguishable from common aphthae. They are the most consistently found feature and frequently the first manifestation.
  63. 63. Diagnosis Pathergy Test: The test is positive if there is an exaggerated response to a sterile needle puncture of the skin, where such puncture is followed by pustule formation.
  64. 64. Diagnostic criteria for Behcet's disease Major Criteria Recurrent oral aphthae Genital ulceration Eye lesions (uveitis, retinal vasculitiz ) Skin lesions(Erythema nodosum, subcutaneous thrombophlebitis, hyperirritability of the skin +ve pathergy test)
  65. 65. Minor Criteria Arthralgia or arthritis Gastrointestinal lesions Vascular lesions (mainly thrombotic) Central nervous system involvement
  66. 66. Treatment No specific treatment, but oral lesions can be controlled by: Topical or intralesional corticosteroids Topical anaesthesia to alleviate pain Systemic corticosteroids in resistant cases (40-60 mg prednisone/day). Combination of steroid and immunosuppressive drugs (e.g. azathioprine).
  67. 67. Reiter’s Syndrome A triad of urethritis, arthritis and conjunctivitis. Oral manifestations: Painless circinate white lesions that may ulcerate giving aphthous-like ulcers. Geographic tongue like lesions Purpuric rash in palate
  68. 68. Treatment Oral lesions are self limiting
  69. 69. Erythema Multiforme This is an acute inflammatory mucocutaneous disease but among dental patients oral lesions are the most prominent or the only ones present
  70. 70. Aetiology Infections, particularly herpetic can be triggering factors. Drugs, particularly sulphonamides and barbiturates. In most patients no precipitating cause can be found.
  71. 71. The histological appearance Intraepithelial or subepithelial vesicle or bulla formation due to widespread necrosis of keratinocytes Infiltration by inflammatory cells which also involve the corium and may have a perivascular distribution.
  72. 72. Clinical Picture Erythema Multiforme Major-Stevens Johnson Syndrome Erythema Multiforme Minor
  73. 73. Typical cases show at least some target (or iris) lesions. A typical target lesion is less than 3 cm in diameter, rounded, and has three zones: a central area of dusky erythema or purpura, a middlepaler zone of oedema and an outer ring of erythema with a well-defined edge. Atypical target lesions have only two of the zones The kobner phenomenon
  74. 74. Localized vesiculobullous form This form is intermediate in severity. The skin lesions present as erythematous macules or plaques, often with a central bulla and a marginal ring of vesicles. Mucous membranes are quite often involved.
  75. 75. Erythema Multiforme Major:Stevens Johnson Syndrome Stevens-Johnson Syndrome, Toxic epidermal necrolysis
  76. 76. The onset is usually sudden There may be a prodromal systemic illness of 1-13 days before the eruption appears. Numerous organs are affected, changes were found with the following frequency: mouth 100% eyes, skin, male genitalia, anal mucous membrane, bronchitis and pneumonitis.
  77. 77. :Management Systemic corticosteroids Antibiotics are usually also given in severe cases
  78. 78. :Pemphigus Vulgaris Pemphigus is an uncommon autoimmune disease causing vesicles or bullae on skin and mucous membranes. It is usually fatal if untreated
  79. 79. :Clinical Features Females aged 40-60 years are predominantly affected. Lesions often first appear in the mouth but spread widely on the skin. Vesicles are fragile . Residual erosions often have ragged edges and are superficial, painful and tender. Positive Nikolsky's sign. Oral lesions show lack of inflammatory signs unless secondary infection occurs. Extension of lesions to the vermilion border may lead to the formation of a crusted lesion.
  80. 80. :Pathology Intra epithelial vesicles and bullae are formed. Lesions result from the destruction of desmosomal junction between prickle cells and basal cells due to the presence of autoantibodies against desmoglein 3 which is an attachment molecule in desmosomes.
  81. 81. Management Diagnosis is confirmed by direct immunofluorescence and by the demonstration of circulating autoantibodies. 60-100 mg/day of predisolone alone or in addition to azathioprine (1-1.5 mg/kg daily). Azathioprine is given to allow doses of the conrticosteroid to be lowered and reduce their side-effects. Intralesional steroid application may help.
  82. 82. Mucous Membrane (Cicatricial) :Pemphigoid Mucous membrane pemphiogoid is an uncommon chronic disease causing bullae and painful erosions. Skin involvement is uncommon and often trivial. In stead, mucous membranes all over the body are affected. The term cicatricial pemphigoid is sometimes used for this group of disease, but particularly applies to ocular involvement where scarring is prominent and impairs sight.
  83. 83. :Desquamative Gingivitis The term desquamative gingivitis is a clinical description, not a diagnosis. It is used for conditions in which the gingivae appear red or raw. Usually the whole of the attached gingival of varying numbers of teeth is affected
  84. 84. :Oral Reactions to Drugs Many drugs can occasionally cause oral reactions. They are varied in type but frequently lichenoid or ulcerative. The mechanisms of reactions to drugs are often obscure