Lect.1.mouth cavity


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mouth cavity disease

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Lect.1.mouth cavity

  1. 1. ULCERATIVE LESIONS OF THE ORAL CAVITY SMS 2044 Pathophysiology of Gastrointestinal System
  2. 2. ORAL CAVITY <ul><li>LIPS </li></ul><ul><li>TEETH </li></ul><ul><li>GINGIVA </li></ul><ul><li>ORAL MUCOUS MEMBRANES </li></ul><ul><li>PALATE </li></ul><ul><li>TONGUE </li></ul><ul><li>ORAL LYMPHOID TISSUES </li></ul>
  3. 3. Acute: small, recent onset, short duration, recurrent <ul><li>Trauma </li></ul><ul><li>Recurrent Aphthous Stomatitis </li></ul><ul><li>Herpesvirus Infection </li></ul><ul><li>Herpangina </li></ul>
  4. 4. Trauma: <ul><li>Cheek Biting </li></ul>
  5. 5. Trauma: <ul><li>Ill-Fitting dentures </li></ul>
  6. 6. Trauma: <ul><li>Chemical Burns </li></ul>
  7. 7. Trauma: <ul><li>Abrasions from Teeth </li></ul>
  8. 8. Recurrent Aphthous Stomatitis(RAS) <ul><li>Most common ulcerative lesion of oral cavity </li></ul><ul><li>Recurrent, painful ulcers </li></ul><ul><li>Confined to soft mucosa </li></ul><ul><li>Subdivided into three types: </li></ul><ul><ul><li>Minor aphthae </li></ul></ul><ul><ul><li>Major aphthae </li></ul></ul><ul><ul><li>Herpetiform aphthae </li></ul></ul>
  9. 9. INFLAMMATORY and ULCERATIVE LESIONS Aphthous Ulcers (Canker Sores): These lesions are extremely common, small (usually less than 5 mm in diameter), painful, shallow ulcers. Characteristically, they take the form of rounded, superficial erosions, often covered with a gray-white exudate and having an erythematous rim.
  10. 10. <ul><li>They appear singly or in groups on the no keratinized oral mucosa, particularly the soft palate, buccolabial mucosa, floor of the mouth, and lateral borders of the tongue. </li></ul><ul><li>The sores are self-limited and usually resolve within a few weeks, but they may recur in the same or a different location in the oral cavity. </li></ul><ul><li>Frequent episodes-four times or more per year-earn the moniker of recurrent </li></ul><ul><li>aphthous stomatitis . </li></ul>
  11. 11. <ul><li>Causes </li></ul><ul><li>The life often apparently triggered by stress, fever, ingestion of certain foods, and activation of inflammatory bowel disease. </li></ul><ul><li>In patients who are not immunosuppressed or do not have known viral infection such as with herpesvirus, an autoimmune basis is suspected. </li></ul>
  12. 12. Recurrent Aphthous Stomatitis(RAS) <ul><li>Minor aphthae: </li></ul><ul><ul><li>Less than 1 cm </li></ul></ul><ul><ul><li>Heal completely in 7-10 days without scarring </li></ul></ul><ul><ul><li>Painful </li></ul></ul><ul><ul><li>Prodromal stage </li></ul></ul><ul><ul><li>Shallow and round to oval </li></ul></ul><ul><ul><li>Gray to yellow membrane </li></ul></ul><ul><ul><li>Clusters of up to 5 ulcers </li></ul></ul><ul><ul><li>Steroids </li></ul></ul>
  13. 13. Recurrent Aphthous Stomatitis (RAS) <ul><li>Minor apthae </li></ul>
  14. 14. Recurrent Aphthous Stomatitis (RAS) <ul><li>Major Aphthae </li></ul><ul><ul><li>Uncommon </li></ul></ul><ul><ul><li>Irregular, deep ulcers </li></ul></ul><ul><ul><li>1-3 cm in size </li></ul></ul><ul><ul><li>Raised borders </li></ul></ul><ul><ul><li>Heal in 4-6 weeks </li></ul></ul><ul><ul><li>Extensive scarring and distortion </li></ul></ul><ul><ul><li>BIOPSY!! </li></ul></ul><ul><ul><li>Steroids </li></ul></ul>
  15. 15. Recurrent Aphthous Stomatitis (RAS) <ul><li>Major apthae </li></ul>
  16. 16. Recurrent Aphthous Stomatitis (RAS) <ul><li>Herpetiform Aphthae </li></ul><ul><ul><li>Uncommon </li></ul></ul><ul><ul><li>Crops of up to 150 very small (<3mm) ulcers </li></ul></ul><ul><ul><li>Heal completely in 7-10 days </li></ul></ul><ul><ul><li>COMPLETELY UNRELATED TO HERPESVIRUS </li></ul></ul>
  17. 17. Recurrent Aphthous Stomatitis (RAS) <ul><li>Herpetiform aphthae </li></ul>
  18. 18. RAS Treat…. <ul><li>A number of different treatments exist for apthous ulcers including: analgesics, anesthetics agents, antiseptics. </li></ul><ul><li>anti-inflammatory agents, steroids, sucralfate, tetracycline suspension, and silver nitrate. </li></ul><ul><li>Amlexanox paste has been found to speed healing and alleviate pain. </li></ul><ul><li>Vitamin B 12 has been found to be effective in treating recurrent aphthous ulcers, regardless of whether there is a vitamin deficiency present </li></ul>
  19. 19. Herpesvirus Infection <ul><li>HSV-1 and/or HSV-2 </li></ul><ul><ul><li>Primary Infection </li></ul></ul><ul><ul><li>Secondary Infection </li></ul></ul><ul><li>Varicella zoster virus (HHV-3) </li></ul>
  20. 20. Herpesvirus Infection <ul><li>Primary Infection </li></ul><ul><ul><li>Herpetic gingivostomatitis </li></ul></ul><ul><ul><li>Younger patients </li></ul></ul><ul><ul><li>Often asymptomatic </li></ul></ul><ul><ul><li>May be associated with fever, chills, malaise </li></ul></ul><ul><ul><li>Vesicles-ulcers-crusting </li></ul></ul><ul><ul><li>Anywhere in the oral cavity </li></ul></ul>
  21. 21. Herpesvirus Infection <ul><li>Primary Infection </li></ul>
  22. 22. Herpesvirus Infection <ul><li>Primary Infection </li></ul>
  23. 23. Herpesvirus Infection <ul><li>Secondary Infection </li></ul><ul><ul><li>Reactivation of latent virus </li></ul></ul><ul><ul><li>Not associated with systemic symptoms </li></ul></ul><ul><ul><li>Small vesicles </li></ul></ul><ul><ul><li>Occur only on the hard palate and gingiva </li></ul></ul><ul><ul><li>Prodromal signs ( prodrome is an early symptom) </li></ul></ul>
  24. 24. Herpesvirus Infection <ul><li>Secondary infection </li></ul>
  25. 25. Herpesvirus Infection <ul><li>Varicella zoster virus (HHV-3) </li></ul><ul><ul><li>Latent infection </li></ul></ul><ul><ul><li>Oral ulcers </li></ul></ul><ul><ul><li>Dermatomal distribution </li></ul></ul>
  26. 26. Herpesvirus Infection <ul><li>Varicella zoster virus </li></ul>
  27. 27. Herpesvirus Infection <ul><li>Varicella zoster virus </li></ul>
  28. 28. Herpes virus Infection <ul><li>Herpetic stomatitis is an extremely common infection caused by herpes simplex virus (HSV) type 1 . </li></ul><ul><li>The pathogen is transmitted from person to person, most often by kissing; by middle life over three fourths of the population have been infected. </li></ul><ul><li>In most adults, the primary infection is asymptomatic, but the virus persists in a dormant state within ganglia about the mouth (e.g., trigeminal). </li></ul><ul><li>With reactivation (fever, sun or cold exposure, respiratory tract infection, trauma), solitary or multiple small (less than 5 mm in diameter) vesicles containing clear fluid appear. </li></ul>
  29. 29. Herpes V……. Inf…. <ul><li>They occur most often on the lips or about the nasal orifices and are well known as &quot;cold sores&quot; or &quot; fever blisters.&quot; </li></ul><ul><li>They soon rupture, leaving shallow, painful ulcers that heal within a few weeks, but recurrences are common. </li></ul>
  30. 30. <ul><li>Histologically, the vesicles begin as an intraepithelial focus of intercellular and intracellular edema. </li></ul><ul><li>The infected cells become ballooned and develop intranuclear acidophilic viral inclusions. </li></ul><ul><li>Sometimes adjacent cells fuse to form giant cells or polykaryons. </li></ul><ul><li>Necrosis of the infected cells and the focal collections of edema fluid account for the intraepithelial vesicles seen clinically. </li></ul>
  31. 31. Cont………. <ul><li>Identification of the inclusion-bearing cells or polykaryons in smears of blister fluid constitutes the diagnostic Tzanck test for HSV infection; antiviral agents may accelerate healing. </li></ul><ul><li>In the worst case, viremia may seed the brain (encephalitis) or produce disseminated visceral lesions. </li></ul>
  32. 32. Herpesvirus pharyngitis. A, Herpesvirus blister in mucosa. B, High-power view of cells from blister , showing glassy intranuclear herpes simplex inclusion body <ul><li>HSV type 1 may localize in many other sites, including the conjunctivae (keratoconjunctivitis) and the esophagus when a nasogastric tube is introduced through an infected oral cavity. </li></ul><ul><li>HSV type 2 (the agent of herpes genitalis), on the other hand, is transmitted sexually and produces vesicles on the genital mucous membranes and external genitalia that have the same histologic characteristics as those that occur about the mouth. </li></ul>
  33. 33. This is a photomicrograph of infected cells, with inclusion bodies in both the nucleus and the cytoplasm.
  34. 34. Herpangina <ul><li>NOT caused by Herpesvirus </li></ul><ul><li>Coxsackie A virus </li></ul><ul><li>Children < 10 years of age </li></ul><ul><li>Common in summer and fall </li></ul><ul><li>Often subclinical presentation </li></ul><ul><li>Headache/Abdominal pain 48hrs prior to papulovesicular lesions on tonsils and uvula. </li></ul><ul><li>Sore throat </li></ul>
  35. 35. Herpangina
  36. 36. Chronic: longer duration, well circumscribed, raised borders, indurated base with crater <ul><li>Trauma </li></ul><ul><li>Infection </li></ul><ul><li>Neoplasm </li></ul><ul><li>Necrotizing sialometaplasia </li></ul>
  37. 37. Trauma: <ul><li>Ill-Fitting dentures </li></ul>
  38. 38. Infection <ul><li>Rare </li></ul><ul><li>HIV/AIDS patients </li></ul><ul><li>Bacterial </li></ul><ul><li>Deep mycotic infection </li></ul><ul><li>Candida </li></ul>
  39. 39. Infection <ul><li>Bacterial </li></ul><ul><ul><li>Usually secondary infection </li></ul></ul><ul><ul><li>Primary infection: syphilis, tuberculous, or actinomycosis </li></ul></ul>
  40. 40. Infection <ul><li>Bacterial-Syphilis </li></ul>
  41. 41. Infection <ul><li>Bacterial-Syphilis </li></ul>
  42. 42. Infection <ul><li>Mycotic </li></ul><ul><ul><li>Blastomycosis </li></ul></ul><ul><ul><li>Histoplasmosis </li></ul></ul>
  43. 43. Infection <ul><li>Histoplasmosis; Histoplasmosis is common among AIDS patients because of their depressed immune system </li></ul>
  44. 44. Infection <ul><li>Candida </li></ul><ul><ul><li>Candida albicans </li></ul></ul><ul><ul><li>Most common </li></ul></ul><ul><ul><li>Normal flora </li></ul></ul><ul><ul><li>Predisposing factors </li></ul></ul><ul><ul><li>White creamy patches </li></ul></ul><ul><ul><li>KOH prep </li></ul></ul><ul><ul><li>Nystatin oral suspension </li></ul></ul>
  45. 45. Fungal Infection <ul><li>Candida albicans is a normal inhabitant of the oral cavity found in 30% to 40% of the population; it causes disease only when there is some impairment of the usual protective mechanisms. </li></ul><ul><li>Oral candidiasis (thrush, moniliasis) is a common fungal infection among persons rendered vulnerable by diabetes mellitus, anemia, antibiotic or glucocorticoid therapy, immunodeficiency, or debilitating illnesses such as disseminated cancer. </li></ul><ul><li>Patients with the acquired immunodeficiency syndrome (AIDS) are at particular risk. </li></ul><ul><li>Typically, oral candidiasis takes the form of an adherent white, curd like, circumscribed plaque anywhere within the oral cavity. </li></ul><ul><li>The pseudomembrane can be scraped off to reveal an underlying granular erythematous inflammatory base . </li></ul>
  46. 46. Infection <ul><li>Candida </li></ul>
  47. 47. <ul><li>Oral candidiasis (&quot;thrush&quot;). A white plaque like membrane coats the gingival mucosa of the left lower jaw in an edentulous young patient. </li></ul><ul><li>This pseudomembrane is composed of a layer of candidal </li></ul><ul><li>In the particularly vulnerable host , candidiasis may spread into the esophagus, especially when a nasogastric tube has been introduced, or it may produce widespread visceral lesions when the fungus gains entry into the bloodstream. </li></ul><ul><li>Disseminated candidiasis is a life-threatening infection that must be treated aggressively. </li></ul><ul><li>For poorly understood reasons, local candidal lesions may appear in the vagina, not only in predisposed persons but also in apparently healthy young women, particularly ones who are pregnant or using oral contraceptives or using broad-spectrum antibiotics. </li></ul>
  48. 48. <ul><li>Histologically, the pseudomembrane is composed of a myriad of fungal organisms superficially attached to the underlying mucosa. </li></ul><ul><li>In milder infections there is minimal ulceration, but in severe cases the entire mucosa may be denuded. </li></ul><ul><li>The fungi can be identified within these pseudomembranes as chains of tubular cells producing pseudohyphae from which bud ovoid yeast forms, typically 2 to 4 μm in greatest diameter. </li></ul>
  49. 49. Acquired Immunodeficiency Syndrome (AIDS) <ul><li>AIDS and less advanced forms of human immunodeficiency virus (HIV) infection are often associated with lesions in the oral cavity. </li></ul><ul><li>They may take the form of candidiasis, herpetic vesicles, or some other microbial infection (producing gingivitis or glossitis). </li></ul><ul><li>particular interest are the intraoral lesions of Kaposi sarcoma and hairy leukoplakia. </li></ul><ul><li>Kaposi sarcoma, is a multifocal, systemic disease that eventually evolves into highly vascular tumor nodules. </li></ul>
  50. 50. <ul><li>Although Kaposi sarcoma may occur in the absence of HIV infection, it affects about 25% of AIDS patients, particularly homosexual or bisexual males. </li></ul><ul><li>More than 50% of those afflicted develop intraoral purpuric discolorations, raised, </li></ul><ul><li>nodular masses. </li></ul>
  51. 51. <ul><li>The peri-venular infiltrate of Kaposi sarcoma shows a mixture of  spindle cells, inflammatory cells </li></ul><ul><li>KS lesions contain tumor cells   with a characteristic abnormal elongated shape </li></ul><ul><li>The tumor is highly vascular , containing abnormally dense and irregular blood vessels, which leak red blood cells into the surrounding tissue and give the tumor its dark color. </li></ul>
  52. 52. Hairy leukoplakia <ul><li>is an uncommon lesion seen virtually only in persons infected with HIV. </li></ul><ul><li>It constitutes white confluent patches, anywhere on the oral mucosa, that have a &quot; hairy &quot; or corrugated surface resulting from marked epithelial thickening. </li></ul><ul><li>It is caused by Epstein-Barr virus infection of epithelial cells. Occasionally, the development of hairy leukoplakia calls. </li></ul>
  53. 53. LEUKOPLAKIA <ul><li>As generally used, the term leukoplakia refers to a whitish, well-defined mucosal patch or plaque caused by epidermal thickening or hyperkeratosis. </li></ul><ul><li>The term is not applied to other white lesions, such as those caused by candidiasis, lichen planus, or many other disorders. </li></ul><ul><li>The plaques are more frequent among older men and are most often on the vermilion border of the lower lip, buccal mucosa, and the hard and soft palates and less frequently on the floor of the mouth and other intraoral sites. </li></ul><ul><li>They appear as localized, sometimes multifocal or even diffuse, smooth or roughened, leathery, white, discrete areas of mucosal thickening. </li></ul>
  54. 54. <ul><li>On microscopic evaluation they vary from banal hyperkeratosis without underlying epithelial dysplasia to mild to severe dysplasia bordering on carcinoma in situ. </li></ul><ul><li>Histologic evaluation, lesions are of unknown cause except that there is a strong association with the use of tobacco, particularly pipe smoking and smokeless tobacco (pouches, snuff, chewing). </li></ul><ul><li>Less strongly implicated are chronic friction, as from ill-fitting dentures or jagged teeth; alcohol abuse; and irritant foods. </li></ul><ul><li>More recently, human papillomavirus antigen has been identified in some tobacco-related lesions, raising the possibility that the virus and tobacco act in concert in the induction of these lesions. </li></ul>
  55. 56. <ul><li>Oral leukoplakia is an important finding because 3% to 6% (depending somewhat on location) undergo transformation to squamous cell carcinoma. </li></ul><ul><li>The transformation rate is greatest with lip and tongue lesions and lowest with those on the floor of the mouth. </li></ul><ul><li>Those lesions that display significant dysplasia on microscopic examination have a greater probability of cancerous transformation. </li></ul>A, Leukoplakia of the tongue in a smoker. Microscopically, this lesion showed severe dysplasia with transformation to squamous cell carcinoma in the posterior elevated portion (arrow). .
  56. 57. Cont……… <ul><li>The treatment of leukoplakia mainly involves avoidance of predisposing factors — tobacco cessation, smoking, quitting betel chewing , abstinence from alcohol — and avoidance of chronic irritants, e.g., the sharp edges of teeth. </li></ul>
  57. 58. Neoplasm <ul><li>Squamous cell carcinoma (SCC) </li></ul><ul><ul><li>Most common </li></ul></ul><ul><ul><li>Irregular ulcers with raised margins </li></ul></ul><ul><ul><li>May be exophytic, infiltrative or verrucoid </li></ul></ul><ul><ul><li>Mimic benign lesions grossly </li></ul></ul>
  58. 59. CANCERS OF THE ORAL CAVITY AND TONGUE <ul><li>The overwhelming preponderance of oral cavity cancers are squamous cell carcinomas </li></ul><ul><li>Although they represent only about 3% of all cancers in the United States, they are disproportionately important. Almost all are readily accessible to biopsy and early identification. </li></ul><ul><li>These cancers tend to occur later in life and are rare before age 40. </li></ul><ul><li>The various influences thought to be important in development of these cancers are summarized in Table. </li></ul>
  59. 60. RISK FACTORS FOR ORAL CANCER Factor Comments Leukoplakia, erythroplasia May including tobacco, long-term alcohol use and other chronic irritants Tobacco use Best-established influence, particularly pipe smoking and smokeless tobacco Human papillomavirus types 16, 18, and 33 Identified by molecular probes in one half to one third of cases; early involvement in carcinogenesis is hypothesized Alcohol abuse Less strong influence than tobacco Protracted irritation Weakly associated
  60. 61. MORPHOLOGY <ul><li>The three predominant sites of origin of oral cavity carcinomas are </li></ul><ul><li>(1) vermilion border of the lateral margins of the lower lip, </li></ul><ul><li>(2) floor of the mouth, </li></ul><ul><li>and (3) lateral borders of the mobile tongue. </li></ul><ul><li>Early lesions appear as pearly white to gray, circumscribed thickenings of the mucosa closely resembling leukoplakic patches. </li></ul><ul><li>They then may grow in an exophytic fashion to produce readily visible and palpable nodular and eventually fungating lesions, </li></ul><ul><li>or they may assume an endophytic , invasive pattern with central necrosis to create a cancerous ulcer. </li></ul>
  61. 62. <ul><li>The squamous cell carcinomas are usually moderately to well-differentiated keratinizing tumors . </li></ul><ul><li>Before the lesions become advanced it may be possible to identify epithelial atypia , dysplasia, or carcinoma in situ in the margins, suggesting origin from leukoplakia or erythroplasia. </li></ul><ul><li>In about 50% of cases of tongue cancer, and in more than 60% of those with cancer of the floor of the mouth. </li></ul>
  62. 63. Clinical Features <ul><li>These lesions may cause local pain or difficulty in chewing, but many are relatively asymptomatic and so the lesion (very familiar to the exploring tongue) is ignored. </li></ul><ul><li>The overall 5-year survival rates after surgery and adjuvant radiation and chemotherapy are about 40% for cancers of the base of the tongue, pharynx, and floor of the mouth without lymph node metastasis, compared with under 20% for those with lymph node metastasis. </li></ul><ul><li>When these cancers are discovered at an early stage, 5-year survival can exceed 90%. </li></ul>Oral squamous cell carcinoma. Invasive tumor islands show formation of keratin pearls.
  63. 64. <ul><li>Squamous cell carcinoma </li></ul>carcinoma S=normal s c.
  64. 65. Squamous cell carcinoma (arrow) invasion to the skeletal muscle (arrowhead). The carcinoma cells have enlarged, hyperchromatic and pleomorphic
  65. 66. <ul><li>Squamous cell carcinoma </li></ul>Squamous cell carcinoma (arrow) invasion to the skeletal muscle (M).
  66. 67. <ul><li>Squamous cell carcinoma </li></ul>
  67. 68. Necrotizing Sialometaplasia <ul><li>Inflammatory condition </li></ul><ul><li>Ischemia to minor salivary glands </li></ul><ul><li>Deep ulcers of the hard palate </li></ul><ul><li>Resolves in 6 weeks </li></ul>
  68. 69. Sialometaplasia
  69. 70. Sialometaplasia
  70. 71. Generalized: broad classification encompassing a wide variety of causative agents or conditions <ul><li>Contact stomatitis </li></ul><ul><li>Radiation mucositis </li></ul><ul><li>Cancer chemotherapy </li></ul>
  71. 72. Dermatologic Disorders: cutaneous and oral manifestations <ul><li>Erythema multiforme </li></ul><ul><li>Lichen planus </li></ul><ul><li>Benign mucous membrane pemphigoid </li></ul><ul><li>Bullous pemphigoid </li></ul><ul><li>Pemphigus vulgaris </li></ul>
  72. 73. Dermatologic Disorders <ul><li>Erythema multiforme </li></ul><ul><ul><li>Rapidly progressive </li></ul></ul><ul><ul><li>Antigen-antibody complex deposition in vessels of the dermis </li></ul></ul><ul><ul><li>Target lesions of the skin </li></ul></ul><ul><ul><li>Diffuse ulceration, crusting of lips, tongue, buccal mucosa </li></ul></ul><ul><ul><li>Self-limited, heal without scarring </li></ul></ul>
  73. 74. Dermatologic Disorders <ul><li>Erythema multiforme </li></ul>
  74. 75. Dermatologic Disorders <ul><li>Lichen planus </li></ul><ul><ul><li>Chronic disease of skin and mucous membranes </li></ul></ul><ul><ul><li>Destruction of basal cell layer by activated lymphocytes </li></ul></ul><ul><ul><li>Reticular: fine, lacy appearance on buccal mucosa (Wickman’s striae) </li></ul></ul><ul><ul><li>Hypertrophic: resembles leukoplakia </li></ul></ul><ul><ul><li>Atrophic or erosive: painful </li></ul></ul>
  75. 76. Dermatologic Disorders <ul><li>Lichen planus </li></ul>
  76. 77. Dermatologic Disorders <ul><li>Lichen planus </li></ul>
  77. 78. Dermatologic Disorders <ul><li>Lichen planus </li></ul>
  78. 79. Dermatologic Disorders <ul><li>Benign mucous membrane pemphigoid </li></ul><ul><ul><li>Tense subepithelial bullae of skin and mucous membranes </li></ul></ul><ul><ul><li>Rupture, large erosions, heal without scarring </li></ul></ul><ul><ul><li>Sloughing (Nikolsky sign) </li></ul></ul><ul><li>Bullous pemphigoid </li></ul><ul><ul><li>Cutaneous lesions more common </li></ul></ul><ul><li>Both show subepithelial clefting with dissolution of the basement membrane </li></ul><ul><ul><li>IgG in basement membrane </li></ul></ul>
  79. 80. Dermatologic Disorders <ul><li>Benign mucous membrane pemphigoid </li></ul>
  80. 81. Dermatologic Disorders <ul><li>Benign mucous membrane pemphigoid </li></ul>
  81. 82. Dermatologic Disorders <ul><li>Pemphigus vulgaris </li></ul><ul><ul><li>Severe, potentially fatal </li></ul></ul><ul><ul><li>Cause; Autoimmune response  by secretion antibodies create a reaction that cause skin cells to separate. </li></ul></ul><ul><ul><li>Intraepithelial bullae, Intraepithelial clefting </li></ul></ul><ul><ul><li>and acantholysis bcz Loss of intracellular bridges betwn cells. </li></ul></ul><ul><ul><li>Nikolsky’s sign (top layers of the skin slip away from the lower layers when slightly rubbed) </li></ul></ul><ul><ul><li>Oozing or Draining skin, </li></ul></ul>
  82. 83. Dermatologic Disorders <ul><li>Pemphigus vulgaris </li></ul>
  83. 84. Dermatologic Disorders <ul><li>Pemphigus vulgaris </li></ul><ul><li>suprabasal separation of the epithelial cells </li></ul><ul><li>intraepithelial vesicle </li></ul>