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CASE PRESENTATION
PRESENTED BY
Dr. URVASHI TOMAR
MDS IST YEAR
DEMOGRAPHIC DETAILS
• NAME: Munnalal Soni
• AGE/SEX: 50/M
• ADDRESS: Sagar , M.P
CHIEF COMPLAINT
• Patient complains of ulcers and burning
sensation in mouth since 15 days.
HISTORY OF PRESENT ILLNESS
• Patient was apparently alright 2 years back
then he noticed ulcers on the palate which
gradually progressed to current condition.
• Patient developed burning sensation since15
days which brought him to the hospital.
• PAST DENTAL HISTORY – Not relevant
• PAST MEDICAL HISTORY – Not significant
• PAST SURGICAL DATA- Not significant
• FAMILY HISTORY – Not significant
• PERSONAL HISTORY/HABITS: smoked and smokeless
tobacco
General physical examination
• BUILT- Moderate
• GAIT- Normal
• MENTAL STATUS - No abnormality detected
• VITAL SIGNS :
• TEMPERATURE - Afebrile
• PULSE- 70 per min
• BLOOD PRESSURE – 120/80 mm of Hg
• RESPIRATORY RATE - 17 per min
Extra oral examination
• NECK LYMPH NODES - Not palpable
Intra oral examination
• INSPECTION:
• Lesion extending from
right buccal mucosa,
palate to the left buccal
mucosa and left alveolar
ridge in relation to 35
and 36.
• Papillary growth seen
on the palate and left
alveolar ridge in relation
to 35 and 36.
Left alveolar ridge
Right buccal mucosa
Intra oral examination
PALPATION
• All inspectory findings were confirmed.
• The lesion was firm in consistency with leathery texture.
• Induration was absent.
• Lesion was non scrapable.
• Lesion was non tender.
Provisional diagnosis
Proliferative verrucous leukoplakia
Differential diagnosis
• Hypertrophic candidiasis
• Verrucous carcinoma
• Plaque type lichen planus
Macroscopic details
• Received 3 soft tissue – one circular in shape (ovoid), firm in
consistency measuring approximately 0.5 X 0.3cm, other two irregular
in shape, soft in consistency, brownish in colour.
146/011/HP/PDA
Microscopic details
H&E STAINED SECTION 10X
H&E STAINED SECTION 40X
H&E STAINED SECTION 100X
H&E STAINED SECTION 100X
Histopathological findings
• Orthokeratinized stratified squamous epithelium showing nuclear and
cellular pleomorphism upto two third of epithelium.
• Keratin pearl formation also seen in superficial layer of epithelium .
• Alteration in N:C ratio alongwith abnormal mitosis.
• Minimal connective tissue seen showing loosely arranged fibrocellular
stroma.
• Suggestive of Severe Dysplasia/Proliferative Verrucous
leukoplakia.
DISCUSSION
• Proliferative verrucous leukoplakia (PVL) is a rare condition first
described by Hansen et al, 1985.
• Proliferative verrucous leukoplakia begins as a simple slow-growing,
persistent hyperkeratosis that tends to spread and become multifocal
and, in time develops exophytic, wart-like, or erythroplakic areas that
become carcinomas.
• Cabay et al, 2007 defined PVL as a distinct clinical form of oral
leukoplakia which in turn is defined by its progressive clinical course,
changing clinical and histopathologic features, and potential to develop
into cancer.
• The buccal mucosa and tongue are the most common sites associated
with PVL, with palatal mucosa, alveolar mucosa, gingiva, floor of mouth,
and lip showing a lower incidence.
• PVL most often manifests as a flat white keratotic lesion with a grainy or
verrucous surface. In some cases, there is an erythematous
component.
• As the lesion progresses, it may exhibit horizontal and vertical growth,
eventually taking on a more exophytic granular or verruciform
appearance.
• PVL may progress to multiple oral foci of VC or SCC over time in spite
of numerous treatment interventions, suggesting that PVL is associated
with diffuse submicroscopic changes of the oral mucosa, sometimes
described as ‘field cancerization’.
• The etiology of PVL is unknown as tobacco does not appear to play a
major role, nor does the coexistence of Candida species, and the role of
human papillomavirus (HPV), subtype 16, as a cofactor in PVL is only
questionable.
• Studies investigating the role of HPV in PVL have not yielded
indisputable link between HPV and PVL as a few studies have found no
significant difference between PVL and oral leukoplakia for risk of HPV
infection.
• Viral studies
• Proliferative verrucous leukoplakia is of uncertain etiology.
An association with human papillomavirus (HPV) infection
has been suggested (Eversole, 2000) and Palefsky et al
(1995) studying nine lesions from seven.
• Genetic studies
Aberrations in the cell cycle regulatory genes p16INK4a
and p14ARF, with homozygous deletion, loss of
heterozygosity, and mutation appear to be frequent
findings in 20 PVL cases (Kresty et al, 2008).
REFERENCES
• Proliferative verrucous leukoplakia: a concise update J Bagan1, C Scully2, Y
Jimenez3, M Martorell1 Oral Diseases (2010) 16, 328–332.
• Proliferative verrucous leukoplakia and its progression to oral carcinoma: a
review of the literature Robert J. Cabay1, Thomas H. Morton Jr2, Joel B.
Epstein3 J Oral Pathol Med (2007) 36: 255–61
• Molecular biology of squamous cell carcinoma of the head and neck B Perez-
Ordoñez, M Beauchemin and R C K Jordan J. Clin. Pathol. 2006;59;445-453
• A Genetic Explanation of Slaughter’s Concept of Field Cancerization: Evidence
and Clinical Implications1 Boudewijn J. M. Braakhuis,2 Maarten P. Tabor, J.
Alain Kummer, C. Rene´ Leemans, and Ruud H. Brakenhoff CANCER
RESEARCH 63, 1727–1730, April 15, 2003
• Verrucous Hyperplasia of the Oral Mucosa M. SHEAR, Dsc (DENT), MDS,
FRCPATH* AND J. J. PINDBORG, DDS, DR ODONT, Dsc (DENT), Frcpatht

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case proliferative leukoplakia .ppt

  • 1. CASE PRESENTATION PRESENTED BY Dr. URVASHI TOMAR MDS IST YEAR
  • 2. DEMOGRAPHIC DETAILS • NAME: Munnalal Soni • AGE/SEX: 50/M • ADDRESS: Sagar , M.P
  • 3. CHIEF COMPLAINT • Patient complains of ulcers and burning sensation in mouth since 15 days.
  • 4. HISTORY OF PRESENT ILLNESS • Patient was apparently alright 2 years back then he noticed ulcers on the palate which gradually progressed to current condition. • Patient developed burning sensation since15 days which brought him to the hospital.
  • 5. • PAST DENTAL HISTORY – Not relevant • PAST MEDICAL HISTORY – Not significant • PAST SURGICAL DATA- Not significant • FAMILY HISTORY – Not significant • PERSONAL HISTORY/HABITS: smoked and smokeless tobacco
  • 6. General physical examination • BUILT- Moderate • GAIT- Normal • MENTAL STATUS - No abnormality detected • VITAL SIGNS : • TEMPERATURE - Afebrile • PULSE- 70 per min • BLOOD PRESSURE – 120/80 mm of Hg • RESPIRATORY RATE - 17 per min
  • 7. Extra oral examination • NECK LYMPH NODES - Not palpable
  • 8. Intra oral examination • INSPECTION: • Lesion extending from right buccal mucosa, palate to the left buccal mucosa and left alveolar ridge in relation to 35 and 36. • Papillary growth seen on the palate and left alveolar ridge in relation to 35 and 36.
  • 10. Intra oral examination PALPATION • All inspectory findings were confirmed. • The lesion was firm in consistency with leathery texture. • Induration was absent. • Lesion was non scrapable. • Lesion was non tender.
  • 12. Differential diagnosis • Hypertrophic candidiasis • Verrucous carcinoma • Plaque type lichen planus
  • 13. Macroscopic details • Received 3 soft tissue – one circular in shape (ovoid), firm in consistency measuring approximately 0.5 X 0.3cm, other two irregular in shape, soft in consistency, brownish in colour. 146/011/HP/PDA
  • 18. Histopathological findings • Orthokeratinized stratified squamous epithelium showing nuclear and cellular pleomorphism upto two third of epithelium. • Keratin pearl formation also seen in superficial layer of epithelium . • Alteration in N:C ratio alongwith abnormal mitosis. • Minimal connective tissue seen showing loosely arranged fibrocellular stroma. • Suggestive of Severe Dysplasia/Proliferative Verrucous leukoplakia.
  • 19. DISCUSSION • Proliferative verrucous leukoplakia (PVL) is a rare condition first described by Hansen et al, 1985. • Proliferative verrucous leukoplakia begins as a simple slow-growing, persistent hyperkeratosis that tends to spread and become multifocal and, in time develops exophytic, wart-like, or erythroplakic areas that become carcinomas. • Cabay et al, 2007 defined PVL as a distinct clinical form of oral leukoplakia which in turn is defined by its progressive clinical course, changing clinical and histopathologic features, and potential to develop into cancer.
  • 20. • The buccal mucosa and tongue are the most common sites associated with PVL, with palatal mucosa, alveolar mucosa, gingiva, floor of mouth, and lip showing a lower incidence. • PVL most often manifests as a flat white keratotic lesion with a grainy or verrucous surface. In some cases, there is an erythematous component. • As the lesion progresses, it may exhibit horizontal and vertical growth, eventually taking on a more exophytic granular or verruciform appearance. • PVL may progress to multiple oral foci of VC or SCC over time in spite of numerous treatment interventions, suggesting that PVL is associated with diffuse submicroscopic changes of the oral mucosa, sometimes described as ‘field cancerization’.
  • 21. • The etiology of PVL is unknown as tobacco does not appear to play a major role, nor does the coexistence of Candida species, and the role of human papillomavirus (HPV), subtype 16, as a cofactor in PVL is only questionable. • Studies investigating the role of HPV in PVL have not yielded indisputable link between HPV and PVL as a few studies have found no significant difference between PVL and oral leukoplakia for risk of HPV infection.
  • 22. • Viral studies • Proliferative verrucous leukoplakia is of uncertain etiology. An association with human papillomavirus (HPV) infection has been suggested (Eversole, 2000) and Palefsky et al (1995) studying nine lesions from seven.
  • 23. • Genetic studies Aberrations in the cell cycle regulatory genes p16INK4a and p14ARF, with homozygous deletion, loss of heterozygosity, and mutation appear to be frequent findings in 20 PVL cases (Kresty et al, 2008).
  • 24. REFERENCES • Proliferative verrucous leukoplakia: a concise update J Bagan1, C Scully2, Y Jimenez3, M Martorell1 Oral Diseases (2010) 16, 328–332. • Proliferative verrucous leukoplakia and its progression to oral carcinoma: a review of the literature Robert J. Cabay1, Thomas H. Morton Jr2, Joel B. Epstein3 J Oral Pathol Med (2007) 36: 255–61 • Molecular biology of squamous cell carcinoma of the head and neck B Perez- Ordoñez, M Beauchemin and R C K Jordan J. Clin. Pathol. 2006;59;445-453 • A Genetic Explanation of Slaughter’s Concept of Field Cancerization: Evidence and Clinical Implications1 Boudewijn J. M. Braakhuis,2 Maarten P. Tabor, J. Alain Kummer, C. Rene´ Leemans, and Ruud H. Brakenhoff CANCER RESEARCH 63, 1727–1730, April 15, 2003 • Verrucous Hyperplasia of the Oral Mucosa M. SHEAR, Dsc (DENT), MDS, FRCPATH* AND J. J. PINDBORG, DDS, DR ODONT, Dsc (DENT), Frcpatht