ORAL PATHOLOGY

1. ORAL PREMALIGNANCY
BY NGOGA ALAIN FABRICE AND KALIISA EDWARD
BDS
YEAR 3

2. ORAL PREMALIGNANCY
• Oral premalignancies are lesions which have a potential for malignant
change.
• Various oral mucosal lesions particularly red lesion ( erythroplasias)
and some white lesions (leukoplakias) have a potential for malignant
change.
• The risk of malignancy transformation is more common with
erythroplakias. The most common white lesions have the lowest risk
of malignant transformation.
• The best predictor of potential for malignant transformation is the
degree of dysplasia( abnormal growth) seen histologically. For this
reason, biopsy of red and white patches is mandatory.

3. • Dysplastic cells show histologically nuclear hyperchomatism, nuclear
pleomorphism and altered nuclear/cytoplasmic ratio, excess mitotic activity,
loss of polarity of cells, deep cell keratinization, disordered or loss of
differentiation.
• Surveys indicate that the risk of malignant change in
white lesions is higher in non-smokers.
• Surveys indicate also that malignant change in white lesions is more
frequent in women

4. PREMALIGNANT LESIONS AND CONDITIONS
1)Erythroplasia ('erythroplakia')
• Erythroplasias are red patches.
• Erythroplasia is uncommon in the mouth but carries the
highest malignant transformation.
• Lesions are often already malignant on first biopsy.
• Eurythroplastic lesions show severe epithelial dysplasia.
• The epithelium is atrophic and this, together with
inflammation, accounts for the red color seen clinically.

7. 2. Idiopathic Leukoplakia
• Leukoplakia is defined as a white patch which cannot be wiped
off the mucosa.
• If investigations fail to reveal any cause, it is called idiopathic leukoplakia.
• The most extensive follow-up studies on white patches suggest that idiopathic
leukoplakia now has the highest risk of developing cancer.
• The malignant transformation rate of leukoplakia is relatively low, around 1-2% in
5 years

8. • Even in smokers the vast majority of leukoplakias show no dysplasia
histologically and carry no risk of malignant transformation.
• Idiopathic leukoplakias are tough and adherent and form plaques
whose surface is raised above the surrounding mucosa.
• The most common sites are the posterior buccal mucosa, retromolar
region, floor of mouth and tongue.

10. SUBLINGUAL KERATOSIS
• The term sublingual keratosis is applied to white lesions on the
floor of mouth and ventral tongue.
• Malignant change was reported in an unusually high proportion of cases
(30%) in one series but this has not been widely confirmed.
• Probably the risk of malignant transformation is less than 10%
and possibly much lower.
• Clinical features
Sublingual keratosis is a white, soft plaque, usually with a finely
wrinkled surface, an irregular but well-defined outline and
sometimes bilateral with a butterfly shape.

11. • The plaque typically extends from the anterior floor of the mouth to
the undersurface of the tongue .

12. PIPE SMOKERS' KERATOSIS
• Palatal keratosis due to pipe smoking is benign.
• Any carcinomas related to pipe-smoking appear in
another site in the mouth and may not be preceded by keratosis.

13. SMOKELESS TOBACCO-RELATED KERATOSES
• Hyperkeratotic mucosal lesions can result from smoking or use
of smokeless tobacco ('topical tobacco' — snuff-dipping and
tobacco chewing).
• there is no characteristic hyperkeratotic lesion associated with the far more
common habit of cigarette smoking .
• The habit of snuff-dipping or tobacco-chewing may be maintained for
decades and gives rise to keratoses in the buccal or labial sulcus, where the
tobacco is held.

14. • Early changes are erythema and mild, whitish thickening.
• Long-term use gives rise to extensive white thickening and wrinkling
of the buccal mucosa.
• Malignant change can follow, but only after several decades of use.
• The main changes are thickening of the epithelium with plump
or squared-off rete ridges.
• There are varying degrees of hyperorthokeratosis or parakeratosis and
there may be subepithelial fibrosis in the area where the tobacco is
held.
• Dysplasia may eventually be seen.

15. Management
• Diagnosis is based on the history of snuff use and the white
lesion in the area where the tobacco is held.
• Biopsy is required to exclude dysplasia or early malignant change.
• in snuff-dippers carcinomas appear at a later age and are better
differentiated than in non-users.
• Snuff-dippers' lesions will resolve on stopping the habit even
after 25 years of use.

16. CHRONIC HYPERPLASTIC CANDIDOSIS (CANDIDAL LEUKOPLAKIA)
• Chronic oral candidosis produces a tough adherent plaque,
distinguishable only by biopsy from other leukoplakias.
• The most affected are Adults, typically males of middle age
or over.
• The usual sites are the dorsum of the tongue and the post-
commissural buccal mucosa.
• The plaque is variable in thickness and often rough or
irregular in texture, or nodular with an erythematous
background (speckled).

17. • Unlike thrush, the plaque cannot be wiped off, but fragments
can be detached by firm scraping.
• Gram or periodic acid-Schiff(PAS) staining shows candidal hyphae embedded in
clumps of detached epithelial cells.
• Like thrush, the plaque of chronic candidosis is parakeratotic,
but more coherent because it is not widely infiltrated by
inflammatory exudate .
• PAS stain clearly shows the hyphae growing (as in thrush) through the full thickness
of the keratin to the prickle cell layer where the inflammatory cells tend to be more
concentrated.
• Electron microscopy shows Candida albicans to be an
intracellular parasite growing within the epithelial cytoplasm

18. • Induction of epithelial proliferation by Candida albicans
infection has been demonstrated experimentally.
• in candida plaques there is often rete hyperplasia with rounded
downgrowths and acanthosis.
Management
• After confirmation of the diagnosis by histology, treatment
should be with a systemic antifungal drug such as fluconazole.
• Stopping the patient from smoking and elimination of candidal infection
from under an upper denture are important.
• Any iron deficiency should also be treated.

20. LICHEN PLANUS
• Lichen planus is a common chronic inflammatory disease of
skin and mucous membranes. It mainly affects patients of middle
age or over.
• The potential of lichen planus to undergo malignant change is
controversial.

22. LUPUS ERYTHEMATOSUS
• Lupus erythematosus is an uncommon connective tissue disease
• There is a small risk of malignant change in cutaneous lupus,
especially in lesions of the lower lip.

23. DYSKERATOSIS CONGENITA
• Dyskeratosis congenita is a rare heritable recessive or dominant
trait.
• The main features are dysplastic white or red lesions of
the oral mucosa, cutaneous pigmentation, dystrophies of the
nails and haematological abnormalities.
• Many patients may also be immunodeficient or have other
abnormalities.
• Causes of death include cancers of the mouth or other sites,
bleeding (gastrointestinal or cerebral) but in 50% from infections,
which are frequently opportunistic

24. ORAL SUBMUCOUS FIBROSIS
• Affected areas of the oral mucosa such as the palate or buccal mucosa appear
almost white.
• The pallor is due to the underlying fibrosis and ischaemia
rather than a superficial plaque.
• the mucosa is typically smooth, thin and atrophic.
• Erythroplasia and leukoplakia may be associated and the epithelium may
show dysplasia on biopsy.
• Surveys suggest that oral submucous fibrosis undergoes
malignant transformation in 4.5-7.6% of cases.
• Contributes to the high incidence of oral cancer in the Indian
subcontinent and in Asian immigrant populations in other countries.

25. SYPHILITIC LEUKOPLAKIA
• Leukoplakia of the dorsum of the tongue is a characteristic
complication of tertiary syphilis.
• The lesion has an irregular outline and surface.
• Cracks, small erosions or nodules may prove on histology to be foci of invasive
carcinoma.
• Carcinoma developing near the centre of the dorsum of the tongue is typically a sequel to
syphilitic leukoplakia.
• In addition to hyperkeratosis and acanthosis, often with dysplasia,
the characteristic late syphilitic chronic inflammatory changes, with plasma cells
predominating, may be seen.
• Giant cells and rarely, granulomas may be present and endarteritis of small arteries
is particularly characteristic.

26. • Management
• The diagnosis is confirmed mainly by the serological findings.
• even if positive, biopsy is still essential, as minute areas of malignant
change may be found, and the management is affected accordingly.
• The presence of syphilitic endarteritis, may be a contraindication to
radiotherapy.
• Antibiotic treatment of syphilis does not cure the leukoplakia.

28. • EARLY CARCINOMA
• An early carcinoma produces surface keratin and
appears as a white patch
• It should not be interpreted as malignant change in a leukoplakia.

29. • MANAGEMENT OF DYSPLASTIC LESIONS
• The prognosis in oral carcinoma is good only when the diagnosis is
made early and the tumour is small.
• The best predictor of malignant potential is the presence of
dysplasia on biopsy

30. Principles of management of dysplastic lesions
• Stop any associated habits, e.g. smoking
• Treat candidal infection and/or iron deficiency if present
• Biopsy to assess dysplasia
• Assess risk of premalignant change on clinical and histological
findings
• Consider ablation of individual lesions
• Maintain observation for signs of malignant change

31. Options for management of premalignant lesions
• Observation for early detection of carcinoma
• Surgical excision with grafting, if required
• Cryotherapy
• Laser excision or vaporisation
• Topical chemotherapy
• Retinoids