Diese Präsentation wurde erfolgreich gemeldet.
Die SlideShare-Präsentation wird heruntergeladen. ×

Premalignant condition of oral cavity.pptx

Anzeige
Anzeige
Anzeige
Anzeige
Anzeige
Anzeige
Anzeige
Anzeige
Anzeige
Anzeige
Anzeige
Anzeige
Nächste SlideShare
Benign Breast Diseases.pptx
Benign Breast Diseases.pptx
Wird geladen in …3
×

Hier ansehen

1 von 79 Anzeige
Anzeige

Weitere Verwandte Inhalte

Weitere von Pradeep Pande (20)

Aktuellste (20)

Anzeige

Premalignant condition of oral cavity.pptx

  1. 1. Tips on using my ppt. 1. You can freely download, edit, modify and put your name etc. 2. Don’t be concerned about number of slides. Half the slides are blanks except for the title. 3. First show the blank slides (eg. Aetiology ) > Ask students what they already know about ethology of today's topic. > Then show next slide which enumerates aetiologies. 4. At the end rerun the show – show blank> ask questions > show next slide. 5. This will be an ACTIVE LEARNING SESSION x three revisions. 6. Good for self study also. 7. See notes for bibliography.
  2. 2. Learning Objectives
  3. 3. Learning Objectives 1. Introduction & History 2. Relevant Anatomy, Physiology 3. Aetiology 4. Pathophysiology 5. Pathology 6. Classification 7. Clinical Features 8. Investigations 9. Management 10. Prevention 11. Guidelines 12. Take home messages
  4. 4. Introduction & History. •
  5. 5. Introduction & History. • Oral cavity cancer accounts for up to 30- 40% of all malignancies in India. • and is a significant worldwide health problem. • Most oral malignancies occur as squamous cell carcinomas (SCCs) • Despite remarkable advances in treatment modalities, the 5-year survival rate has not significantly improved over the past several decades and still hovers at about 50-60%.
  6. 6. Introduction & History. • Many oral SCCs develop from premalignant conditions of the oral cavity • Despite the general accessibility of the oral cavity during physical examination, many malignancies are not diagnosed until late stages of disease. • In order to prevent malignant transformation of these precursor lesions, multiple screening and detection techniques have been developed to address this problem.
  7. 7. Introduction & History. • The early detection of cancer is of critical importance because survival rates markedly improve when the oral lesion is identified at an early stage.
  8. 8. Premalignant conditions of Oral mucosa
  9. 9. Premalignant conditions of Oral mucosa Definition • Premalignant squamous lesions of the oral cavity are areas of altered epithelium that are at an increased risk for progression to squamous cell carcinoma (SCC). Not to be ignored, however, is the fact that up to 50% of oral SCCs cases arise from clinically normal mucosa.
  10. 10. Premalignant conditions of Oral mucosa 1. Leukoplakia 2. Erythroplakia 3. mixed erythroleukoplakia 4. palatal lesion of reverse cigar smoking 5. oral lichen planus 6. oral submucous fibrosis 7. discoid lupus erythematosus, Hereditary disorders 7.dyskeratosis congenital and 8. epidermolysis bullosa.
  11. 11. Premalignant conditions of Oral mucosa Other less-common conditions • xeroderma pigmentosum • dyskeratosis congenita, • epidermolysis bullosa • iron deficiency • late-stage syphilis
  12. 12. Aetiology
  13. 13. Aetiology • Idiopathic • Congenital/ Genetic • Nutritional Deficiency/excess • Traumatic • Infections /Infestation • Autoimmune • Neoplastic (Benign/Malignant) • Degenerative / lifestyle • Iatrogenic • Psychosomatic • Poisoning/ Toxins/ Drug induced
  14. 14. Aetiology • Idiopathic • Congenital/ Genetic • Nutritional Deficiency/excess • Traumatic • Infections /Infestation • Autoimmune • Neoplastic (Benign/Malignant) • Degenerative • Iatrogenic
  15. 15. Pathophysiology
  16. 16. Risk Factors and Pathophysiology 1. Tobacco 2. Alcohol 3. HPV 4. areca nut/betel quid 5. immune suppression HIV] infection 6. chronic sun exposure (specifically for cancer of the vermillion border of the lip), and nutritional deficiency. 7. poor oral hygiene.
  17. 17. Risk Factors and Pathophysiology • Industrial (metals [nickel, chromium], wood dust, textiles, furniture, leather • Chronic irritation (jagged teeth, luetic lesions, gastroesophageal reflux disease) • Asbestos • Diet (vitamin A deficiency) • Prior radiotherapy (to mucosa, salivary gland, thyroid, skin) • Iron deficiency (Plummer-Vinson syndrome) • Mutagen-induced chromosome fragility
  18. 18. Risk Factors and Pathophysiology • The use of tobacco has been well established as a significant risk for the development of oral squamous cell carcinoma (SCC) and premalignant lesions • Up to 80% of patients with oral SCC have used tobacco products • risk of developing malignancy is 5-9 times greater for smokers than nonsmokers. .
  19. 19. Risk Factors and Pathophysiology • Alcohol use has also been implicated as a risk factor for the development of oral SCC and premalignant lesions. • moderate to heavy drinkers have a 3-9 times greater risk of developing cancer. • heavy use of alcohol and tobacco combined may convey a risk greater than 100 times the general population.
  20. 20. Risk Factors and Pathophysiology • The role of human papillomavirus(HPV) in the development of oral premalignant disorders and SCC continues to undergo investigation. • HPV types 16 and 18 may be found in approximately 22% and 14% of oropharyngeal tumors • a recent study demonstrated HPV DNA in 17.6% of oral leukoplakic lesions and 19.7% of oral lichen planus samples. [
  21. 21. Risk Factors and Pathophysiology • Despite the association between tobacco and alcohol and the development of persistent oral lesions, a definitive etiology is seldom identified in many of these lesions. • the lack of distinctive histopathologic features in many of the potentially malignant disorders supports the multifactorial pathogenesis of these lesions.
  22. 22. Classification
  23. 23. Classification • The World Health Organization classifies oral precancerous/potentially malignant disorders into 2 general groups, as follows: 1. A precancerous lesion 2. A precancerous condition
  24. 24. Classification • A precancerous lesion is “a morphologically altered tissue in which oral cancer is more likely to occur than its apparently normal counterpart 1. leukoplakia, 2. erythroplakia, 3. the palatal lesions of reverse smokers.
  25. 25. Classification • A precancerous condition is “a generalized state associated with significantly increased risk of cancer- 1. submucous fibrosis 2. lichen planus, 3. epidermolysis bullosa, 4. discoid lupus erythematous.
  26. 26. Clinical Features •
  27. 27. Clinical Features • Demography • Symptoms • Signs • Prognosis • Complications
  28. 28. Demography
  29. 29. Demography • prevalence rate ranges between 1% and 5%. • Most affected patients are middle-aged or elderly men. • buccal mucosa, lower gingiva, tongue and floor of mouth, with the remaining cases distributed throughout the remainder of the oral cavity. • oral cancer is one of the most common malignancies in Southeast Asia, accounting for up to 30-40% of all malignancies in India.
  30. 30. Demography • increase in the incidence of tongue cancer in young individuals (< 40 years old), from 3% in 1973 to approximately 6% in 1993, • many of the affected individuals are without traditional risk factors. • traditional male predominance is less overt in young individuals with oral SCC • This trend is thought to be a reflection of the general acceptance of social habits such as smoking and drinking by both sexes.
  31. 31. Demography • Overall, the rates of oral squamous dysplasia and subsequent squamous cell carcinoma (SCC) are decreasing, closely paralleling the reduction in cigarette smoking.
  32. 32. Leukoplakia • Leukoplakia is defined by the World Health Organization as a white lesion of the oral mucosa that cannot be scraped off and cannot be attributed to another definable lesion • The precise definition of leukoplakia continues to undergo refinement in an attempt to distinguish benign from premalignant lesions, • leukoplakia remains a clinical diagnosis of exclusion.
  33. 33. Leukoplakia Leukoplakia is subdivided into 1. homogeneous leukoplakia 1. nonhomogeneous leukoplakia ( erythroleukoplakia ) 2. proliferative verrucous leukoplakia (PVL).
  34. 34. Leukoplakia Nonhomogeneous leukoplakia is subdivided into speckled and nodular types, 1. Speckled leukoplakia consists of flecks of white on an erythematous base. 2. Nodular leukoplakia consists of small surface excrescences, often on a red background.
  35. 35. Leukoplakia • Leukoplakia occurs most often in middle- aged and older men and arises most frequently on the buccal mucosa, alveolar mucosa, and lower lip. • lesions arising on the floor of mouth lateral tongue and lower lip are the most likely to harbor dysplasia or progress to malignancy. • The rate of progression to malignancy has been reported to be between 3.6% and 17.5%,
  36. 36. Leukoplakia •
  37. 37. Leukoplakia • 19.9% of leukoplakic lesions may demonstrate some degree of dysplasia, • 3.1% showing frank carcinoma.
  38. 38. Leukoplakia • Risk factors for malignant transformation of oral leukoplakia 1. advanced age 2. female sex 3. lesions of more than 200 mm2 4. nonhomogeneous lesions 5. higher-grade dysplasia.
  39. 39. Erythroplakia • Erythroplakia is a clinical term used to describe a fiery red patch that cannot be clinically or pathologically distinguished as any other definable disease. • Similar to leukoplakia, the erythroplakic lesion is considered as a diagnosis of exclusion because numerous other disease entities must be excluded before erythroplakia is considered as the diagnosis.
  40. 40. Erythroplakia • red macule or patch with a soft, velvety texture most often occurring on the floor of mouth, lateral tongue, retromolar pad, and soft palate. •
  41. 41. Erythroplakia
  42. 42. Erythroplakia • Although far less common than leukoplakia, erythroplakia is a worrisome clinical condition that often harbors dysplasia. • 51% of erythroplakic lesions have been shown to demonstrate invasive squamous cell carcinoma (SCC), with 40% demonstrating carcinoma in situ, and 9% exhibiting mild-moderate dysplasia.
  43. 43. Erythroleukoplakia
  44. 44. Proliferative verrucous leukoplakia • Proliferative verrucous leukoplakia (PVL) is a unique form of aggressive continuum of leukoplakia and erythroplakia. • Most patients with PVL are women, and many do not have a history of tobacco use. • irregular white patch or plaque with a varying surface • characterized by resistance to treatment, recurrence, multifocal proliferation, and a progression to carcinoma in up to 87% of patients.
  45. 45. Proliferative verrucous leukoplakia
  46. 46. Palatal lesion of reverse smokers • The palatal lesion of reverse smokers is unique to individuals who place the lit end of a cigarette inside the mouth. • red, white, melanotic patch or papule. • Up to 84% of palatal lesions have been demonstrated to harbor dysplasia upon histologic analysis
  47. 47. Oral submucous fibrosis • Oral submucous fibrosis (OSF) is a chronic progressive condition found predominantly in people of Asian decent. • OSF is considered to be the result of the use of the Areca nut product with resultant disruption of the extracellular matrix. • The disease often manifests with diffuse involvement of the oral cavity, pharynx, and upper esophagus that appears clinically as whitish mucosa lacking elasticity.
  48. 48. Oral submucous fibrosis • Epithelial dysplasia has been described in 7- 26% of OSF tissues, and long-term studies suggest a malignant transformation rate in approximately 7% of these lesions. • class I cytology (ie, characteristics indicative of benign atypical cytologic changes)
  49. 49. Lichen planus, discoid lupus erythematous, and epidermolysis bullosa • Although classified as potentially malignant conditions, the data regarding progression to malignancy for these conditions is controversial. Because of the difficulty in classifying and clinically distinguishing the varied lesions associated with these conditions, the potential for malignant transformation remains unclear.
  50. 50. Work-up and the Early Detection of Oral Cancer
  51. 51. Work-up and the Early Detection of Oral Cancer • Oral examination • Supravital staining • Oral cytology • Chemiluminescent light • Tissue autofluorescence
  52. 52. Supravital staining • Toluidine blue (TB) is an acidophilic dye designed to stain acidic cellular components such as DNA and RNA • dysplastic tissue contains quantitatively more DNA and RNA than nondysplastic tissue. • 1% solution is placed on the oral mucosa and removed after 1-2 minutes with 2% acetic acid. The clinician then examines the oral mucosa for areas of increased cellular staining.
  53. 53. Supravital staining • TB staining may provide better demarcation of lesion margins, may guide biopsy site selection, and may be valuable in the identification and visualization of lesions in high-risk patients. • cells undergoing inflammatory changes and benign hyperplasia may also retain dye leading to false-positive results. • Overall, the sensitivity of TB staining ranges from 0.78 to 1.00, and the specificity ranges from 0.31 to 1.00.
  54. 54. Oral cytology • a stiff brush to the oral mucosa with enough pressure to induce pinpoint bleeding, which ensures a full-thickness or trans-epithelial tissue sample. • cytomorphometry, DNA cytometry, and immunocytochemical analysis. • The use of oral cytology in the detection of dysplastic lesions shows considerable promise but has been limited thus far by variable false-positive and false-negative results.
  55. 55. Chemiluminescent light • a diffuse chemiluminescent light source to visualize abnormal oral mucosa not visible under normal incandescent light. • Under illumination, normal epithelium absorbs the light (appearing light blue) while abnormal tissue reflects the light (appearing white, with sharper, distinct margins). • toluidine blue stain to aid in further lesion assessment.
  56. 56. Tissue autofluorescence • exposure of epithelial tissue to specific wavelengths of light that results in the excitation of cellular fluorophores and emission of energy in the form of fluorescence. • With the disruption of normal tissue morphology in dysplastic lesions, tissue fluorescence is scattered and absorbed, resulting in characteristic alterations in color that can be visually interpreted.
  57. 57. Tissue autofluorescence • Under excitation with the VELscope device, normal mucosa emits a pale green light, whereas abnormal mucosa appears dark. • The initial evidence suggests that the VELscope may be useful as both an adjuvant method of margin determination during surgical procedures as well as a screening technique to identify premalignant lesions not visualized during conventional examination.
  58. 58. Microscopic Findings Squamous epithelial dysplasia 1. Abnormal architecture 2. Cytologic atypia.
  59. 59. Microscopic Findings Abnormal architecture- 1. loss of cellular organization or stratification, 2. basal cell layer hyperplasia 3. and loss of polarity, 4. dyskeratosis (single-cell keratinization) 5. keratin pearls deep within the epithelium 6. drop-shaped rete ridges
  60. 60. Microscopic Findings Cytologic atypia- 1. nuclear enlargement, 2. increased nuclear-to-cytoplasmic ratio 3. variations in cellular and nuclear size and shape 4. prominent nucleoli 5. nuclear hyperchromasia, 6. increased mitotic activity 7. atypical mitotic figures.
  61. 61. Microscopic Findings grading schemes for dysplasia- 1. mild, 2. moderate, 3. severe 4. carcinoma in situ,
  62. 62. Prognosis
  63. 63. Prognosis • Homogeneous leukoplakia transforms to malignancy in only about 6% of cases. • Nonhomogeneous leukoplakia and erythroplakia, although less common, have a much higher rate of dysplasia, with at least 85% of cases showing severe dysplasia or frank squamous cell carcinoma • Proliferative verrucous leukoplakia (PVL), in contrast, is a slowly progressive, multifocal disease that eventually progresses to SCC in almost all cases.
  64. 64. Investigations • Laboratory Studies – Routine – Special • Imaging Studies • Tissue diagnosis – Cytology • FNAC – Histology – Germ line Testing and Molecular Analysis • Diagnostic Laparotomy.
  65. 65. Differential Diagnosis
  66. 66. Differential Diagnosis • Candidiasis • Lichen planus • Radiation atypia • Reactive atypia
  67. 67. Management
  68. 68. Management • Despite recognition of the premalignant nature of oral dysplastic lesions, few, if any, therapies to prevent cancer progression are effective.
  69. 69. Management • The treatment of leukoplakia consists of excisional biopsy, when feasible, • Multifocal advanced disease represents approximately 10-15% of all oral premalignant lesions and is rarely controlled adequately with local therapy. • Surgical excision can be used to remove grossly evident disease
  70. 70. Management • ionizing irradiation does not prevent the progress of carcinogenesis. Ionizing irradiation makes a sick mucosa sicker and cannot be used again when the need may be urgent.
  71. 71. Prevention
  72. 72. Prevention • Diet richer in vegetables and fruits • Avoid Tobacco • Avoid alcohol consumption. • Self examination. • Good oral hygiene.
  73. 73. cancer-prevention tips. • Don't use tobacco • Avoid Alcohol • Eat a healthy diet. ... • Maintain a healthy weight and be physically active. ... • Protect yourself from the sun. ... • Get vaccinated. ... • Avoid risky behaviors. ... • Get regular medical care. • .
  74. 74. Early Detection • Dental practitioners and dental care professionals should remain vigilant for signs of potentially malignant disorders and oral cancer while performing routine oral examinations. • The mnemonic RULE – Red – Ulcerated – Lump – Extending for 3 or more weeks. • Biopsy
  75. 75. Chemoprevention Agents • Retinoids and vitamin A (beta carotene) • Vitamin E • Biochemoprevention • Selenium • Cyclooxygenase-2 (COX-2) inhibitors • Tyrosine kinase inhibitors (TKIs) • ONYX-015 • Protease inhibitors (PIs)
  76. 76. Chemoprevention Agents Under Investigation • EKB-569 - Family of drugs called EGFR inhibitors • Pioglitazone - Peroxisome proliferator– activated receptor inhibitor • Ad5CMV - Targets the TP53 gene • Polyphenols of pomegranate juice • Curcumin analogs • Erlotinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor
  77. 77. Get this ppt in mobile 1. Download Microsoft PowerPoint from play store. 2. Open Google assistant 3. Open Google lens. 4. Scan qr code from next slide.
  78. 78. Get this ppt in mobile
  79. 79. Get my ppt collection • https://www.slideshare.net/drpradeeppande/ edit_my_uploads • https://www.dropbox.com/sh/x600md3cvj8 5woy/AACVMHuQtvHvl_K8ehc3ltkEa?dl =0 • https://www.facebook.com/doctorpradeeppa nde/?ref=pages_you_manage

Hinweis der Redaktion

  • drpradeeppande@gmail.com
    7697305442
  • https://emedicine.medscape.com/article/1491418-overview#a8
    https://emedicine.medscape.com/article/1840467-overview#a9
    https://emedicine.medscape.com/article/855712-overview#a2
  • https://emedicine.medscape.com/article/1491418-overview#a8
    https://emedicine.medscape.com/article/1840467-overview#a9

×