Hyperkeratotic lesion

1. Case presentation
Dr.Bhavna Tyagi

2. Case History
A 40 year old male patient
reported with the chief
complaint of a brownish white
area in the right buccal
vestibule region since one year.

3. HISTORY OF PRESENT ILLNESS
• Patient was apparently normal one year back.
• Later he noticed brownish white patch in the
right buccal vestibule.

4. • Past medical history was non-
contributory.
• Personal history revealed habit of
tobacco placement in right buccal vestibule 8-
10 times per day since 10-15 years.

5. EXTRA ORAL EXAMINATION
• No changes were observed in the extra oral
examination.

6. INTRA ORAL EXAMINATION

7. On inspection
 Single brownish plaque
 With white edges
 Right posterior vestibule
extending on to the buccal
mucosa in relation to the lower
premolar .
 Showing hyperkeratotic
,wrinkled appearance .
Measured approximately 4cm x 2
cm in size.
On intraoral examination

8. • On palpation, inspectory findings with respect
to site, size, shape and extent were confirmed.
• Margins were irregular and non-tender on
palpation.

9. Provisional diagnosis
Tobbaco pouch keratosis

10. GROSSING
Single soft tissue
specimen, firm in
consistency ,0.9cmx
0.3cm ,greyish
white in colour
,received in 10%
formalin

11. HISTOPATHOLOGY
• H& E stained section showed parakeratinized
stratified squamous epithelium with broad
reteridges and connective tissue stroma.
• Epithelium showed dysplastic features which
include cellular and nuclear pleomorphism,
nuclear hyperchromatism and few keratin pearls
at some places, connective tissue stroma showed
collagen bundles with plump fibroblasts
interpersed.
• Overall H/P features are suggestive of
HYPERKERATOTIC LESION WITH MODERATE
DYSPLASIA

12. PHOTOMICROGRAPH AT 4X
Overlying epithelium
Connective tissue
stroma
Cross section of muscle

13. AT 10X
Collagen fiber
Broad rete ridge
PHOTOMICROGRAPH
AT 10X

14. AT
40X
keratin pearl

15. AT 40X
HYPERCHROMATIC
NUCLEI
NUCLEAR
PLEMORPHISM

16. • WHO:A white patch or plaque that cannot be
characterized clinically or pathologically as any
other disease.
• Axell T,1996 : ‘A predominentaly white lesion
of the oral mucosa that can’t be characterized
as any other definable lesion’.
(Rajendran R. Shafer's textbook of oral pathology. Elsevier India; 2009.)

17. • leukoplakia is a clinical term and the lesion has
no specific histology.
• May show atrophy or hyperplasia (acanthosis).
• May or may not demonstrate epithelial
dysplasia.
• It has a variable behavioural pattern but with
an assessable tendency to malignant
transformation.

18. Clinical types
• 2forms
Homogeneous Non-homogeneous leukoplakia
 Uniformly flat, thin
and exhibit shallow
cracks of the surface
keratin.
 The risk of malignant
transformation is
relatively low.
 carry a much higher risk of
malignant transformation.
 Non homogeneous varieties
include:
Speckled
Nodular
Verrucous
18

19. Homogeneous Leukoplakia
19
(Laskaris G. Pocket Atlas of Oral Diseases. Thieme; 2006)

20. Speckled leukoplakia
20

21. ETIOLOGY
The use of tobacco and Candida
infection are often mentioned as
etiologic factors for leukoplakias, and
both factors have been related to
prognosis.

22. Smoking
• Leukoplakias associated with a smoking habit
seem to have less malignant potential than
those not related to a smoking habit.
• The lesion disappears when the patient stops
smoking.
• There is one characteristic clinical finding that
indicates that a lesion is truly tobacco-
induced: fine white striae that, taken together,
imitate a fingerprint pattern in the mucosa
(Pindborg et al., 1980)

23. • The placement of tobacco quid, regardless of
the type, in direct contact with the oral
mucosa produces a thickened layer of keratin
on the oral epithelial surface that occurs
directly in the anatomic site where the
Smokeless tobacco is placed.

24. • Smokeless tobacco products include both snuff
and chewing tobacco.
• Snuff can be defined as a finely ground or
powdered tobacco that is sold in both dry and
moist forms.
• Snuff is not chewed; instead a small amount
(referred to as a "pinch") is placed and held in
the mucobuccal fold area between the cheek
and gingiva, or between the lower lip and
gingiva.

25. • Seen in young males, this lesion may be seen in
any individual who uses a smokeless tobacco
product.
• The lesion has a fairly characteristic clinical
appearance and is found at the preferred site
of tobacco placement.
• The lesion is a thin grayish white translucent
plaque that is soft on palpation.

26. • All smokeless tobacco products (STP) contain
nicotine, a potent addictive substance.
• The major group of carcinogens in STP includes
non-volatile tobacco-specific nitrosamines
(TSNA) and N-nitroamino acids Snuff dipper’s
lesion

27. STP can irritate the mucosa of the mouth and
esophagus
Promote nicotine absorption by the oral mucosa
into the bloodstream, since their pH raising action
dramatically increases the proportion of
unprotonated nicotine
Ray CS, Gupta PC. Bidis and smokeless tobacco. Current science 2009; 96(10) : 1324-
34

28. • Stretching of the mucosa often reveals a
distinct “pouch” caused by flaccidity in
chronically stretched tissues in the area of
tobacco placement.
• The most frequent sites of involvement
include the mucobuccal fold area in the incisor
and molar regions.

29. Candida infection
• The association between Candida infection and
the risk for malignant development originates
from findings of an association between Candida
infection and non homogeneous leukoplakias.
• The catalytic transformation in vitro of the
carcinogenic nitrosamine , N –nitrosobenzyl –
methylamine by the strains of C . Albicans
demonstrated to be selectively associated with
leukoplakia
(Jepsen and Winther, 1965; Renstrup, 1970; Bánóczy and Sugar, 1972)

30. Other factors
• Use of Alcohol.
• The possible implication of human papilloma
virus (HPV) in the etiology and potential for
malignant transformation of oral pre-
malignant lesions has been studied
extensively (Nielsen et al., 1996; Praetorius, 1997; Miller and Johnstone,
2001).
• HPV was 2-3 times higher in pre-cancerous
oral mucosa and 4-5 times higher in oral
squamous cell carcinomas than in normal oral
epithelium.

31. • Serum levels of vitamin A, B12, C
,betacarotene and folic acid were significantly
decreased in patients with oral leukoplakia.

32. 32
Parakeratotic
keratin layer
Histopathological picture showing :
Increase basal
cell layer
Loss of adhesion
between cells
Nuclear and
cellular
Pleomorphism

34. • The distinction- is purely clinical, based on
surface colour and morphological (thickness)
characteristics.
• Mixed white and red plaques - higher risk status
-denoted as ‘erythroleukoplakia’.
• Proliferative verrucous leukoplakia (PVL)
presents with multiple, simultaneous
leukoplakias-covers a wide area-fits with the
proposed terminology of ‘potentially malignant
disorder’
34

35. Disorders that need exclusion to
diagnose leukoplakia
35
• White sponge nevus: Noted in early life, family
history, large areas involved,genital mucosa
may be affected.
• Frictional keratosis: History of trauma, mostly
along the occlusal plane, an etiological cause
apparent, mostly reversible on removing the
cause.
• Chemical injury Known history, site of lesion
corresponds to chemical injury, painful,
resolves rapidly.

36. • Discoid lupus erythematosus: Circumscribed
lesion with central erythema, white lines
radiating.
• Lichen planus (plaque type): Other forms of
lichen planus (reticular) found in association.
• Hairy leukoplakia: Bilateral tongue keratosis
36

37. Schematic representation of the steps
in diagnosis of oral
leukoplakia
37

38. Treatment results of oral leukoplakia:
[modified from Miller et al.]
• Type of treatment
Surgical (incl. CO2)
Non-surgical
Chemo-prevention
Observation only
38

39. • Response rate (in case of non-surgical
treatment or observation without treatment):
No response (stable disease).
Partial response (>50% reduction in size, but
not complete).
Complete response.
Progressive disease (>25% increase in size or
the appearance of a new lesion).
39

40. Recurrence: Leukoplakia at the same subsite,
irrespective of time interval.
New primary :Leukoplakia at a distinctly
different subsite.
Malignant transformation.
Malignant event in the head-and-neck region,
outside the oral cavity.
Malignant event outside the head-and-neck
region.
40

41. Conclusion
Oral cancer continues to be a deadly disease for more
than 50% of the cases diagnosed every year. This is due to
the fact that most of these cases are diagnosed when they
have already progressed to the advanced stage. Detection
of oral cancer in its initiation phase is important as there is
a direct correlation between survival and the stage of the
disease at the time of diagnosis.
Also early detection provides the patient with the best
opportunity for successful management and positive cure
and is crucial to improve the patient’s survival rate.
Having cancer is in itself tragic, having it at a younger age
is disastrous

42. • Reibel J. Prognosis of oral pre-malignant lesions: significance of
clinical, histopathological, and molecular biological characteristics.
Critical Reviews in Oral Biology & Medicine. 2003 Jan 1;14(1):47-62.
• Warnakulasuriya S, Johnson N, Van der Waal I. Nomenclature and
classification of potentially malignant disorders of the oral mucosa.
Journal of oral pathology & medicine. 2007 Nov 1;36(10):575-80.
• Cawson RA, Binnie WH, Eveson JW. Colour Atlas of Oral Disease
Clinical and Pathological Correlation’s.
• Rajendran R. Shafer's textbook of oral pathology. Elsevier India; 2009.
• Ray CS, Gupta PC. Bidis and smokeless tobacco. Current science 2009;
96(10) : 1324-34
References