Red lesion of oral mucosa

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Solitary Red Lesions Presented by Dr. Shrikant Sonune Guided by Dr Ashok Patil, Dr Shilpa Kandalgaonkar, Dr Mayur Chaudhary,

Transcript of Red lesion of oral mucosa

  1. 1. Presented by Dr. Shrikant Sonune Guided by Dr Ashok Patil, Dr Shilpa Kandalgaonkar, Dr Mayur Chaudhary, Dr Suyog Tupsakhare, Dr Mahesh Gabhane.
  2. 2. Introduction Factors affecting color of oral mucosa Normal variations Classification of red lesions Descriptions of all red lesions Summary
  3. 3. Specialized mucosa Lining mucosa Masticatory mucosa
  4. 4. Wide spectrum of pink colors varying from a dark pink(reddish) to a very pale pink(almost white) 1. Lining mucosa --- Reddish pink 2. Masticatory mucosa--Light pink Protective layer of keratin Dense sub epithelial connective tissue
  5. 5. Deep dusky red in color contrast to light red color of surrounding tissue. Painless red macular bands may present Richer blood supply Individual normal variation
  6. 6. Vascularity Thickness & degree of keratinization Presence of pigmentation Presence of inflammation
  7. 7. Duration Associated with pain Associated with habit Other systemic manifestations Any known cause
  8. 8. SOLITARY GENERALIZED RED TONGUE LESIONS
  9. 9. 1. Traumatic erythematous macules & erosions 2. Purpuric macules(early stage) 3. Inflammatory fibrous hyperplasia lesions 4. Nonpyogenic soft tissue odontogenic infections 5. Chemical or thermal erythematous macule 6. Nicotine Stomatitis
  10. 10. 8) Erythroplakia 9) Carcinoma in situ 10) Red macular Squamous cell carcinoma 11) Candidiasis (atrophic / erythematous, denture Stomatitis, angular Cheilitis) 12) Macular hemangioma & telangiectasia 13) Allergic macules 14) Vesiculobullous disease 15) Metastatic tumor of soft tissue
  11. 11. Vascular dilations from a. Inflammation (Erythema) b. Congenital defects(e.g. hemangioma) Extravasations of blood (e.g. trauma hemostatic disease or both) Atrophy or erosion of mucosa Marked increase in hemoglobin concentration of circulating blood
  12. 12. Inflammation (Erythema) Mechanical trauma Thermal trauma Chemical trauma Infections Ulcer with inflamed rim Congenital defects(e.g. hemangioma)
  13. 13. Erythematous macule Erosion The purpuric macule Granulomatous stage of inflammatory hyperplasia
  14. 14. Etiology --Produce by low grade, usually chronic physical insult Sharp margins of teeth & restorations Ill-fitting prosthesis Self inflected trauma Habits
  15. 15. Clinical feature (c/f) Erythematous macule are on Anterior & lateral border of tongue Cheek mucosa Lip mucosa Margins may or may not be sharply defined
  16. 16. Mild tenderness Digital pressure may cause blanching Regress quickly after removal of cause
  17. 17. H/P Inflamed lamina propria Slightly thinned or Eroded stratified Squamous epithelium
  18. 18. D/D Purpuric macule h/o trauma Purpuric macule of oral sex Macular hemangioma Atrophic Candidiasis Mononucleosis Herpangina (not transient)
  19. 19. Caused due to blunt trauma which is sufficient force to cause the extravasations of blood. Soon after the traumatic damage, lesion is red afterwards converts into blue color. Borders are poorly demarcated Blanching on pressure does not usually occur May also have secondary inflammatory component.
  20. 20. Slight extravasations of blood .
  21. 21. The purpuric macule due to oral sexual practices. Reddish Elliptical Purpuric macule Occurring on palatal mucosa near the junction of the hard & soft palate. Disappear within 2 to 3 days Judicial history with confidential setting revel the true identity.
  22. 22. D/D Traumatic Erythematous macule h/o Purpuric macule of oral sex trauma Macular hemangioma Atrophic Candidiasis Mononucleosis Herpangina
  23. 23. Traumatic origin Prolonged chronic physical stimulus can induce the production of granulation tissue
  24. 24. Mass of inflamed granulation tissue & clinically appears as soft & vary red. Reversible lesion up to this stage.
  25. 25. H/P Granulomatous tissue Covering epithelium is usually intact
  26. 26. 1. Pyogenic granuloma 2. Hormonal tumor 3. Epulis fissuratum 4. Papillary hyperplasia 5. PGCG 6. Peripheral fibroma with calcification
  27. 27. Excisional biopsy Elimination of irritant (priority depends on clinical judgment)
  28. 28. Caustic drugs or hot foods or beverages Depends on duration & intensity of stimuli Stimuli may produce coagulative necrosis of superficial tissues that appears white After scraping off that white layer it may produce clinically appreciable red lesion
  29. 29. Ulceration & properly stripping off mucosa Tender to painful May blanch on pressure Size & shape varies depend on stimuli.
  30. 30. D/d Erythema from mechanical trauma Purpuric macule Erythroplakia Atrophic Candidiasis
  31. 31. Other names Leukokeratosis nicotina palati, Smokers palate, Nicotine palatinus
  32. 32. Conventional smokers Is seen primarily on the palate of pipe smokers. Also seen in bidi smoker Does not having premalignant nature It develops in response to heat rather than tobacco.
  33. 33. Appears red in initial stage In later keratotic stage minor salivary duct orifices appear red Men , 4-5 decade
  34. 34. H/p Hyperkeratosis Acanthosis Squamous metaplasia Chronic inflammation of subepithelial connective tissue Inflammatory exudate within duct
  35. 35. D/d Lesions associated with reverse smoking Denture Stomatitis Atrophic Candidiasis
  36. 36. Erythroplakia Commonly seen on buccal mucosa , floor of mouth, tongue Definition Persistent velvety red patch that can not be identified as any other specific red lesion such as inflammatory Erythema or those produce by blood vessel anomalies or infection.
  37. 37. It appear red because Absences of surface keratin layer Connective tissue papillae, containing enlarge capillaries, project close to the surface.
  38. 38. C/F- Velvety red or granular red macules. Varies greatly in size Borders may be well defined Painless Drying of the mucosa will intensify the red colour
  39. 39. Types Homogenous erythroplakia Erythroplakia interspread with patches of Leukoplakia Speckled erythroplakia
  40. 40. The lesion may have an irregular, red granular surface interspersed with white or yellow foci, which may be described as granular erythroplakia. There may be numerous, small irregular foci of leukoplakia dispersed in the erythroplakic patch, and this has been called speckled leukoplakia.
  41. 41. Oral erythroplakia is soft to palpation and does not become indurated or hard until an invasive carcinoma develops.
  42. 42. Histopathologically erythroplakia almost always show dysplasia, carcinoma in situ or invasive squamous cell carcinoma. Epithelium is frequently atrophic with lack of keratin production. The connective tissue demonstrates chronic inflammation.
  43. 43. If the lesion persist for more than 21 days after all local trauma & infections foci have been eliminated, biopsy is mandatory.
  44. 44. D/D- Traumatic Erythema Atrophic Candidiasis Purpuric macules
  45. 45. Malignant epithelial neoplasm exhibiting Squamous differentiation as characterized by formation of keratin & / or presence of intercellular bridges (pinborg JJ 1997)
  46. 46. Annually, nearly 30,000 new cases of oral and oropharyngeal cancer are expected to occur in men and women in the United Sates. The ratio of cases in men and women is now about 2 to 1.
  47. 47. Tobacco, Typically mixed with areca (betel) nut, Slaked lime, All forms of tobacco smoking Reverse smoking Alcohol Poor nutritional status HPV 16 & 18 has some role in the development of OSCC. Ultraviolet (UV) light
  48. 48. A compromised immune system Chronic irritation
  49. 49. The first is loss of cell cycle control through increased proliferation and reduced apoptosis. The second stage is increased tumor cell motility, leading to invasion and metastasis.
  50. 50. Carcinoma of the Lips: Carcinomas of the lower lip are far more common than upper lip lesions. Pipe smoking, uv light exposure. The growth rate is slower for lower lip Favorable prognosis Account for 25% to 30% of all oral cancers
  51. 51. Lesions arise on the vermilion surface Appear as a chronic non healing ulcer (Exophytic ,verrucous type may present) Deep invasion -- later in the course of the disease. Metastasis to local submental or Submandibular lymph nodes is uncommon
  52. 52. One of the most common intraoral malignancy. Predilection for men (6-8th decade) However, lesions may uncommonly be found in the very young.
  53. 53. Exhibit a particularly aggressive behavior. Lingual carcinoma is typically asymptomatic. As deep invasion occurs, pain or dysphagia may be a prominent patient complaint.
  54. 54. Appear in one of four ways: indurated, nonhealing ulcer, a red lesion, a white lesion, a red-and-white lesion.
  55. 55. The neoplasm may occasionally have a prominent exophytic, as well as endophytic, growth pattern
  56. 56. The most common location of cancer of the tongue is the posterior-lateral border. Specific reason is due to chronic irritation because of tooth Approximately 1/4th of tongue cancers occur in the posterior one third or base of the tongue.
  57. 57. Metastases from tongue cancer are relatively common. The first nodes to become involved are the submandibular lymph node. Uncommonly, distant metastatic deposits may be seen in the lung or the liver.
  58. 58. Second most common intraoral location of squamous cell carcinomas. Predominantly in older men,
  59. 59. Painless, nonhealing, indurated ulcer. It may also appear as a white or red patch. May widely infiltrate the soft tissues of the floor of the mouth, Decreased mobility of the tongue. Metastasis to Submandibular lymph nodes is common
  60. 60. Predominantly in Men Clinical appearance varies from a white patch to a nonhealing ulcer to an exophytic lesion.
  61. 61. It is slow growing Usually well differentiated, Rarely metastasizes, Has a favorable prognosis
  62. 62. Palatal squamous cell carcinomas generally present as asymptomatic red or white plaques or as ulcerated and keratotic masses
  63. 63. 1. Well differentiated: It consists of sheets and nests of cells of squamous epithelium. Cells are large and show distinct cell membrane but intercellular bridges or tonofibrils are not seen. Pleomorphic nuclei and becomes hyperchromatic.
  64. 64. Mitotic figures are seen but not numerous. Individual cell keratinization and formation of numerous keratin pearl. Group of cells invades underlying connective tissue.
  65. 65. Shape of cells and their arrangement may be altered. The growth rate of individual cells is more rapid and this is reflected in the greater numbers of mitotic figures. Keratin pearl formation may or may not be seen.
  66. 66. More pleomorphic cells. Loss of keratinization and keratin pearl. Loss of individual cell differentiation. Increase mitotic figures.
  67. 67. D/D- Inflammatory hyperplasia Papilloma Erythroplakia Leukoplakia
  68. 68. Coxsackie virus A4 -cause a majority of cases of Herpangina, Types A1 to A10, A16 to A22 Herpangina may be seen more than once in the same patient. Herpangina frequently occurs in epidemics The majority of cases affect young children adolescents.
  69. 69. Clinical Manifestations. After a 2- to 10-day incubation period, The infection begins with generalized symptoms of fever, chills, and anorexia.
  70. 70. The fever and other symptoms are generally milder than those experienced with primary HSV infection. The patient complains of sore throat, dysphagia, and occasionally sore mouth.
  71. 71. Lesions start as punctate macules, which quickly evolve into papules and vesicles involving the posterior pharynx, tonsils, faucial pillars, and soft palate. Lesions are found less frequently on the buccal mucosa, tongue, and hard palate.
  72. 72. Within 24 to 48 hours, the vesicles rupture, forming small 1 to 2 mm ulcers. The disease is usually mild and heals without treatment in 1 week.
  73. 73. Definition Infectious mononucleosis is an acute, self-limited infectious disease that primarily affects children. Etiology EpsteinBarr virus transmitted through saliva transfer, Cytomegalovirus (CMV) CMV is the major cause of non-Epstein-Barr virus infectious mononucleosis in the general population.
  74. 74. The oral manifestations are early and common, and consist of palatal petechiae, uvular edema, tonsillar exudate, gingivitis, rarely ulcers
  75. 75. Generalized lymphadenopathy, hepatosplenomegaly, maculopapular skin rash, sore throat are common. Prodromal symptoms such as anorexia, malaise, headache, fatigue, and later fever occur before the clinical manifestations.
  76. 76. Differential diagnosis Fellatio, Thrombocytopenic purpura,
  77. 77. Caused by Nonpyogenic bacteria Prepyogenic Postpyogenic state
  78. 78. It is the infection with yeast like fungus Candida albicans Earlier termed moniliasis Types ACUTE CHRONIC Psuedomembranous Hyperplastic Atrophic Mucocutaneous Atrophic Candidiasis
  79. 79. clinical type Appearance Erythematous Red Atrophic Red Hyperplastic White, red raised Mixed Red/ white keratotic / white necrotic Mucocutaneous Lip/ angles Psuedomembranous White lesion
  80. 80. ACUTE ATROPHIC
  81. 81. Acute atrophic Candidiasis/Antibiotic sore mouth Painful mucosa due to broad spectrum antibiotics Angular Cheilitis- Erythema, fissuring of angles of mouth
  82. 82. D/D- Chemical burn Drug reactions Syphilitic mucous patches Necrotic ulcers Traumatic ulcer Contact allergy
  83. 83. CHRONIC ATROPHIC
  84. 84. Due to denture cuts off the underlying mucosa from the protective action of saliva. The erythema is sharply limited to the area of mucosa occluded by a well-fitting upper denture or even an orthodontic plate.
  85. 85. Hyphae proliferates in denture mucosal interface Gram staining shows gram +ve hyphae.
  86. 86. It is red colored unraised area usually present on buccal mucosa. It is usually capillary type, Also occur as port wine stain on skin.
  87. 87. History of long duration It is non tender Even no inflammatory component Absence of recurrent traumatic episode
  88. 88. References- Text book of oral and maxillofacial pathology- Neville Differential diagnosis of oral lesions by- Wood and Goaz, Fifth Edition Shafers textbook of oral pathology 6th edition . Textbook of oral medicine Burkait 10th edition .
  89. 89. 1. Traumatic erythematous macules & erosions 2. Purpuric macules(early stage) 3. Inflammatory fibrous hyperplasia lesions 4. Nonpyogenic soft tissue odontogenic infections 5. Chemical or thermal erythematous macule 6. Nicotine Stomatitis 7. Erythroplakia 8. Carcinoma in situ 9. Red macular Squamous cell carcinoma 10. Candidiasis (atrophic / erythematous, denture Stomatitis, angular Cheilitis)
  90. 90. 16. Actinomycosis 17. Anemia (solitary red patch) 18. Amyloidosis 19. Angiosarcoma 23. Blastomycosis 24. Candidiasis endocrinopathy syndrome 25. Crohns disease
  91. 91. 25. Coccidiodimycosis 26. Dermatitis herpetiformis 27. Erysipelas 28. Exfoliative Cheilitis 29. Gonococcal infection 30. Graft versus host disease (GVHD) 31. Herpangina
  92. 92. 32. Histoplasmosis 33. Hyperemic oral tonsils 34. Larva migrans 35. Lichen planus 36. Lupus erythematous 37. Ludwigs angina 38. Lymphonodular pharyngitis 39. Multinucleate cell angiohistiocytoma
  93. 93. 40. Mycosis fungoides 41. Non- Hodgkin's lymphoma 42. Peripheral Ameloblastoma 43. Plasma cell gingivitis 44. Psoriasis 45. Sarcoidosis 46. Secondary syphilis 47. Self mutilation 48. Subacute necrotizing sialadenitis 49. Tuberculosis 50. Tumoral calcinosis
  94. 94. Thank you
  95. 95. Increase Vascularity Decrease thickness of epithelium Decrease keratinization Inflammation Mechanical trauma Increase Hb content extravasations of blood Connective tissue papillae, containing enlarge capillaries, project close to the surface.
  96. 96. Blood supply Thick cortical plate Gravity Food lodgment
  97. 97. Dysplasia involving full vertical & horizontal thickness of epithelium along with basilar hyperplasia