case presentation 5 TOBACCO POUCH KERATOSIS.pptx

case presentation on tobacco pouch keratosis

1. CASE PRESENTATION Dr. Nitha Willy Second Year PG Department Of Oral Medicine And Radiology

2. BIOGRAPHIC DATA Name : Shibu Jose Age : 42 Sex :M Occupation : Driver Address : Meenacheril , Thattekkad O P No :164257 Phone no: 9495077648

3. CHIEF COMPLAINT Patient complaints of bleeding gums while brushing since last one month.

4. HISTORY OF PRESENTING ILLNESS Patient has noticed bleeding gums while brushing since last one month. Patient has no bleeding from any other sites and also no bleeding noticed other than while brushing. Patient also experiences bad breath since one month. History reveals yellowish deposits on tooth since once year.

5. MEDICAL HISTORY No history of previous serious illness childhood diseases hospitalization/operations injuries to head and neck

6. DRUG ALLERGY No allergy to medications No allergic reactions in general

7. CNS: No abnormalities reported GIT: No abnormalities reported Respiratory system: No abnormalities reported CVS: No abnormalities reported Endocrine system: No abnormalities reported Genitourinary system: No abnormalities reported REVIEW OF SYSTEMS

8. PAST DENTAL VISIT Previous visit for scaling tooth before two years.

9. PERSONAL HISTORY Marital status: married Sleep and appetite: Normal Bowel and bladder movements: Regular Diet: Mixed Oral hygiene: Brushes once daily using toothpaste and toothbrush No parafunctional habits

10. Patient revealed a habit history of using one packet of “KUBER” (refined tobacco product: 20 gm per packet) since five years two times only during long night drives. Patient divides this packet into two and keeps half of product above the upper front tooth region for almost one hour and then spits off and again places the Kuber for next one hour and spits off.

11. FAMILY HISTORY No history of genetic or hereditary or infectious diseases.

12. GENERAL PHYSICAL EXAMINATION Patient was conscious, co-operative and well oriented with person, place, time. Gait: steady gait Built: moderately built Nourishment: moderately nourished Temperature: 37 ͦ C Pulse rate:72 beats/minute

13. Respiratory rate: 16 breaths/minute Blood pressure: 110/80 mm Hg No Pallor, No Icterus, No Cyanosis, No Clubbing, No Edema and No Lymphadenopathy Height: 5 ft 8 in Weight: 85 kg

14. LOCAL EXAMINATION OF HEAD AND NEC K EXTRA ORAL EXAMINATION Head : Mesencephalic Hair : No abnormalities detected Face :Apparently symmetrical Skin : no abnormalities detected Eyes : no abnormalities detected

15. Ears : no abnormalities detected Nose: no abnormalities detected Lips :competent Finger and nails: normal TMJ : Mouth Opening Within Normal Limits, No Deviation, No Clicking, No Crepitus Muscles of mastication : non-tender Lymph nodes : not palpable Cranial nerve examination: no abnormalities

16. INTRA ORAL EXAMINATION SOFT TISSUE EXAMINATION Labial mucosa: no abnormalities detected Labial vestibule: Right labial vestibule shows corrugated greyish white keratotic area. Buccal mucosa: no abnormalities detected Buccal vestibule: no abnormalities detected. Gingiva : in the lower anterior and posterior tooth region, gingiva has smooth and shiny appearance and with bright red color , marginal gingiva rolled out, interdental papilla is blunted, consistency is soft.

17. Bleeding on probing: present along the marginal gingiva of lower anterior and posterior tooth Periodontal pocket: absent Tongue: no abnormalities detected Floor of mouth: no abnormalities detected Frenal attachment : mucosal attachment of frenum Palate: no abnormalities detected Oropharynx: no abnormalities detected Salivary gland orifices: no abnormalities detected

18. Number of teeth : 28 Carious teeth : 17, 26, 27, 36, 37, 46, 47 Missing teeth :18, 28, 28, 48 Root stump: 0 Restored tooth: 0 HARD TISSUE EXAMINATION

19. Fractured tooth: 0 Mobility : 0 Attrition : generalised Calculus : +++ Stains: ++ Tenderness on percussion : absent

20. ON INSPECTION A greyish-white corrugated keratotic area seen on right upper labial vestibule with diffuse borders. Antero-posteriorly extending from labial frenum to 1 cm posteriorly corresponding to mesial aspect of 13. Supero -inferiorly extending from mucogingival junction irt to mesial aspect of 11 to mesial aspect of 13 to labial mucosa.

21. ON PALPATION Non tender Non scrappable No induration

22. CASE SUMMARY A 42 year old male patient reported to our department with chief complaint of bleeding gums while brushing since last one month. History reveals bad breath since one month and yellowish deposits on tooth since once year. On examination, an incidental finding of a greyish-white corrugated keratotic area seen on right upper labial vestibule with diffuse borders. Antero-posteriorly extending from labial frenum to 1 cm posteriorly corresponding to mesial aspect of 13. Supero -inferiorly extending from mucogingival junction irt to mesial aspect of 11 to mesial aspect of 13 to labial mucosa. On palpation, it was non tender, non scarppable , non indurated.

23. PROVISIONAL DIAGNOSIS CHRONIC GENERALISED GINGIVITIS TOBACCO POUCH KERATOSIS IN RELATION TO RIGHT LABIAL VESTIBULE - DEGREE 2

24. CRITERIA FOR RECOGNIZING AND DIAGNOSING THE CONDITION AS TOBACCO POUCH KERATOSIS External appearance: Greyish-white corrugated area seen Age: 30- 50 years Location of lesion: mucosa which is in direct contact with snuff or chewing tobacco Presence of precipitating factor: Quid with both areca nut and tobacco products (gutkha)

25. DIFFERENTIAL DIAGNOSIS FRICTIONAL KERATOSIS ORAL LEUKOPLAKIA

26. FRICTIONAL KERATOSIS : Constant irritation of the oral mucosa from activities such as chewing or rubbing. Sites: buccal mucosa, tongue, and lips Clinical appearance may vary, there may be formation of a distinguishing white keratotic linea alba along the occlusal plane. These lesions typically resolve upon cessation of the irritative behavior and have not been reported to have malignant potential

27. ORAL LEUKOPLAKIA is characterized by the presence of a white patch or plaque that cannot be scraped off or explained by another disease. There is a male predominance and the peak incidence is in adults over the age of 50. The patches or plaques may be entirely white or have intralesional red speckles. Common sites include the soft palate, lateral and ventral tongue, or the floor of the mouth. It is the most common premalignant oral mucosal lesion and is associated with alcohol and tobacco use.

28. TREATMENT PLAN Habit counselling Oral Prophylaxis Tab Lycaplus : 0-0-1 * 30 days (Beta Carotene 30mg + Lycopene 10000iu + Zinc 27.5 mg + Manganese 2 mg + Copper 2 mg+ Selenium 200mg)

29. DISCUSSION

30. Potentially Premalignant Oral Epithelial Lesions Oral White Lesions Tobacco Pouch Keratosis Antioxidant with Lycopene

31. POTENTIALLY PREMALIGNANT ORAL EPITHELIAL LESIONS

32. Potentially Malignant Disorders is defined by WHO 2005 as the risk of malignancy being present in a lesion or condition either at time of initial diagnosis or at a future date.

33. ETIOLOGY A. Extrinsic Factors Tobacco in any form (smoking or chewing) Alcohol regardless of beverage type and drinking pattern – synergistic action along with tobacco Virus infection – HPV, EBV, HBV, HIV, HSV. Bacterial infection – treponema pallidum. Fungal infection – candidiasis. Electro-galvanic reaction between unlike restorative metals. Ultraviolet radiation from sunlight -associated with lip lesions. Chronic inflammation or irritation from sharp teeth or chronic cheek-bite

34. B. Intrinsic Factors 1. Genetic (5% are hereditary). 2. Immunosuppression – organ transplant HIV. 3. Malnutrition – iron ( anemia ), vitamin A, B, C deficiency.

35. Average age of population affected with PMDs is 50-69yrs, Most common sites for PMDs in India are buccal mucosa followed by tongue, palate and floor of the mouth. PMDs have traditionally shown a predilection for males.

36. CLASSIFICATION OF ORAL POTENTIALLY MALIGNANT DISORDERS 1.High Risk Erythroplakia . Leukoplakia . Oral Submucous Fibrosis Erosive Lichen Planus. 2. Life-style Related Smokeless Tobacco Keratosis. Reverse Smoker’s Palate. Actinic Cheilitis. 3. Infections Hyperplastic Candidiasis. Viral (HPV, HIV, EBV, HBV, HSV). Tertiary Syphilis. 4. Immunodeficiency Solid Organ Transplantation. Graft Versus Host Disease. Chronic Cutaneous Lupus Erythematous. 5. Inherited Disorders Xeroderma Pigmentosum. Dyskeratosis Congenita. Epidermolysis Bullosa. Bloom Syndrome. Fanconi’s Anemia .

37. Greater than normal risk for malignant phenotype are associated with Red and white intermixed lesions, or presence of multiple lesions. Proliferative verrucous surface appearance, or presence of nodule, erosion, ulceration, or presence of candidiasis. Non-smoker (passive smokers have greater risk), or those with no habits Lesion not regressed after habit cessation, or after the causative initiating factor is removed, or continuation of habit after initial diagnosis.

38. Duration of the lesion before initial diagnosis (long duration poor prognosis). Lesion size greater than 200mm High-risk anatomic site – floor of mouth, lateral posterior border tongue, lip. Young age at diagnosis (30-35yrs). Female gender (for unknown reason 47% of women show malignant transformation).

39. Diagnostic aids in detection of potentially malignant disorders 1. Clinical Methods a. Conventional Oral Examination (COE). b. Vital Staining. 2. Optical Methods a. Vizilite . b. MicroLux DL. c. VELscope . d. Fluorescence Spectroscopy.

40. 3. Imaging Methods a. Computed Tomography (CT). b. Magnetic Resonance Imaging (MRI). c. Positron Emission Tomography (PET). d. Thalium-201 (201Tl) Scintigraphy. e. Photoactive Imaging. f. Optical Coherence Tomography (OCT). g. Narrow Band Imaging (NBI). h. Nano Diagnostic Methods.

41. 4. Histopathological Methods a. Scalpel Biopsy. b. OralCDx Brush Test®. c. Cytology. d. Laser Capture Micro Dissection. 5. Molecular Methods a. Immuno Histochemistry. b. Flow Cytometry. c. Polymerase Chain Reaction (PCR). d. Blotting Techniques. e. Spectral Karyotyping. f. AgNOR . g. Fluorescent In-situ Hybridization (FISH). h. DNA Microarray. i . Comparative Genomic Hybridization.

42. 6. Salivary Diagnostic Methods a. Protein Electrophoresis. b. Sialochemistry .

43. ORAL WHITE LESIONS

44. White lesions of the oral mucosa obtain their characteristic appearance from the scattering of light through an altered mucosal surface. Such alterations may be the result of a: thickened layer of keratin (hyperkeratosis) thickening of spinous layer of the epithelium (acanthosis) intracellular edema of epithelial cells reduced vascularity of subjacent connective tissue.

45. CLASSIFICATION OF WHITE LESIONS : 1. HEREDITARY/DEVELOPMENTAL : - Leukoedema - White spongy nevus - Hereditary benign intraepithelial dyskeratosis - Pachyonychia congenita - Dyskeratosis congenita

46. 2. REACTIVE : - Frictional keratosis - Morsicatio buccarum - Nicotine stomatitis - Tobacco pouch keratosis - Chemical burn

47. 3. IMMUNOLOGIC : - Lichen planus - Lichenoid mucositis - Discoid lupus erythematosus - Graft-versus- host disease

48. 4. Bacterial/Viral/Fungal : - Candidiasis - Mucous patches in secondary syphilis - Oral hairy leukoplakia 5. Systemic disease : - Uremic stomatitis 6. Potentially malignant disorders : - Leukoplakia - Actinic cheilitis 7. Neoplastic : - Squamous cell carcinoma

49. TOBACCO POUCH KERATOSIS

50. Tobacco pouch keratosis is a ‟white keratotic oral mucosal changes „‟ resulting from chronic use of smokeless tobacco [ST] . Tobacco pouch keratosis also referred as ‟spit tobacco keratosis” and formerly referred as ‟tobacco chewers white lesion”. It is a condition that results from spit tobacco being habitually placed in the muco-buccal fold in the mandibular anterior or buccal regions. It is only seen where the mucosa is in direct contact with snuff or chewing tobacco and it is also called as snuff dippers keratosis and smokeless tobacco keratosis

51. Smokeless tobacco keratosis, or snuff dipper’s keratosis , is a benign lesion characterized by the formation of white, gray, or pale macules or papules in the oral mucosa, often accompanied by wrinkling or rugae in response to use of smokeless tobacco products.

52. The Axéll , Mörnstad , and Sundström system has four degrees: DEGREE 1 : superficial lesion with color similar to that of the surrounding mucosa with slight wrinkling and no obvious thickening DEGREE 2 : superficial whitish or reddish lesion with moderate wrinkling and no obvious thickening DEGREE 3 : red or white lesion with intervening furrows of normal mucosal color, obvious thickening, and wrinkling DEGREE 4 : marked white-yellowish to brown and heavily wrinkled lesion with intervening deep and reddened furrows and heavy thickening.

53. Squamous epithelium is hyperkeratinized and acanthotic (Thickened spinous layer with or without intracellular vacuolization or “edema” of glycogen-rich superficial layer.) Characteristic of smokeless tobacco induced lesion is parakeratic chevrons seen as pointed projections above or within superficial epithelial layer

54. Smokeless tobacco is a method of intra oral application and represents a nonhomogenous group of compounds. The term smokeless tobacco also known as dip , plug , chew or spit tobacco , refers to both chewing tobacco (coarse cut ) and snuff ( fine cut ). The average consumption in regular users of snuff is about 10-15 g per day.

55. TOBACCO forms are 1. Smoke 2. Smokeless Smoke: Cigar, Beedi, Hookah, Reverse smoke. Smokeless: Paan, Paan Masala, Mawa , Khaini

56. SMOKELESS TOBACCO PRODUCTS Smokeless tobacco exists in two major forms: SNUFF CHEWING TOBACCO

57. Snuff may be MOIST DRY Moist snuff is usually taken orally. This product is sold in small round cans, in which the snuff is loosely packed, or in small, tea-bag-like sachets. Dry snuff, which is less commonly used, is usually inhaled through the nose.

58. Chewing tobacco is coarser than snuff and exists in three forms: looseleaf (sold in a soft package or pouch) plug (sold in a small block) twist (dried tobacco leaves that are twisted into strands).

59. Chewing tobacco is usually placed in the buccal vestibule. It is referred to as a “chaw” or “quid” of chewing tobacco. The quid may be retained in the mouth for hours, and the user expectorates the saliva that mixes with the tobacco extract. Quid are classified into three basic categories: 1.Quid with areca nut without tobacco products (pan or betel quid) 2.Quid with tobacco products without areca nut (chewing tobacco, moist and dry snuff) 3. Quid with both areca nut and tobacco products (gutkha)

60. The chemical carcinogens in smokeless tobacco include polynuclear aromatic hydrocarbons (usually benzo[a]pyrene) polonium 210 N-nitrosamines radium-226 lead-210.

61. The carcinogenic TSNAs(Tobacco-specific nitrosamines) : N‟- nitrosonornicotine (NNN) 4-(N-methyl-N- nitrosamino )-1-(3-pyridyl)-1-butanone (NNK) N- nitrosoanabasine (NAB) VOLATILE NITROSAMINES : N- nitrosodimethylamine N- nitrosodiethylamine have been detected in the saliva of chewers of BQ with tobacco

62. Types And Ingredients Of Smokeless Tobacco Products

63. EFFECT OF SMOKELESS TOBACCO ON TEETH STAINING OF TEETH The stains bind and penetrate the enamel, dentin, root surfaces causing a brown to black discolouration . Artificial dentures, prosthesis are also discoloured by prolonged tobacco chewing. ABRASION OR TOOTH WEAR (due to coarse abrasives in tobacco products) INCREASED INCIDENCE OF DENTAL CARIES (due to the high content of sweetening and flavouring agents in tobacco products)

64. Other oral effects include staining of composite restorations and teeth, halitosis, and reduction of taste and smell acuity.

65. EFFECTS OF SLT ON GINGIVA AND PERIODONTAL TISSUES Increased gingival recession (Gingival recession and attachment loss are generally seen in the area adjacent to where the SLT is held) with exposure of tooth root surface, periodontal pocket formation, plaque and calculus accumulation which leads to periodontitis. Acute Necrotizing Ulcerative Gingivitis (ANUG), gingivitis, and periodontitis are found

66. SMOKELESS TOBACCO AND SYSTEMIC DISEASE One of the important systemic effects of ST is nicotine dependence or addiction Oral ST causes a duration-dependent increase in oxidative stress . ST is a risk factor for osteoporosis and also associated with cataract , cardiovascular diseases, and immediate increase in blood pressure and heart rate .

67. The five major steps recommended for tobacco cessation activity in the dental office are popularly known as “5 As” ASK ADVISE ASSESS ASSIST ARRANGE

68. Antioxidants can decrease oxidative stress induced carcinogenesis by a direct scavenging of ROS and/or by inhibiting cell proliferation secondary to the protein phosphorylation. Lycopene is an effective antioxidant and free radical scavenger . Lycopene, because of its high number of conjugated double bonds, exhibits higher singlet oxygen quenching ability . Lycopene have anti-cell-proliferative, anticarcinogenic and antiatherogenic activities. ANTIOXIDANT WITH LYCOPENE