7- Oral Epithelial Tumors II

Dr. Tahani Abualteen

Oral Epithelial Tumors, Melanocytic Nevi, and Melanoma (II)

Sequamous cell carcinoma (SCC):

Clinical presentation:

Clinical presentation of oral Sequamous cell carcinoma can take many forms

Early diagnosis is the most important factor influencing prognosis

Clinicians must be suspicious of any lesion for which no cause can be found or which does not respond as expected when possible causes are eliminated

Early lesions are usually asymptomatic and have many forms of presentation, most commonly:

1. Leukoplakia "White patch"2. Small exophytic mass which in early stages shows no ulceration or Erythema3. Small indolent "inactive" ulcer4. Eryethroplakia "Red patch"

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Suspicious clinical features for early carcinoma:

1. Persistent ulceration2. Induration

** Induration = rubbery hardness caused by invasion of the carcinoma resulting in loss of normal elasticity of oral mucosa

3. Fixation to underlying structures

** Fixation is caused by the carcinoma infiltrating through and binding together different natural tissue planes

4. Destruction of underlying bone in alveolar mucosa lesions5. Enlarged reactive regional lymph nodes

Carcinoma of vermilion border of lip is clearly visible and may be noticed at an early stage as a slightly raised swelling, or crusty lesion resembling delayed healing of herpes labialis

Advanced or late lesions may present as:

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Leukoplakia


1. Broad-based, exophytic mass with rough, nodular, warty, hemorrhagic, or necrotic surface2. Deeply destructive, crater-like ulcer with raised, rolled everted edges3. Infiltration of musculature may result in functional disturbances (particularly if tumor

involves the tongue or floor of mouth) including impaired speech and difficulty in swallowing

4. Radiographic evidence of bone destruction 5. Mobility of teeth 6. Altered sensation over distribution of mental nerve in the mandible 7. Pathologic fracture of mandible8. Metastatic spread to regional lymph nodes9. Pain may be a feature

It is important to note that the size of surface lesion does not indicate extent of underlying invasion

Pathology:

Considerable variation in the histological appearance of oral Sequamous cell carcinoma Cytologically, malignant Sequamous epithelium shows variable degrees of differentiation (e.g.

well differentiated, moderately differentiated, and poorly differentiated) and keratinization varies with degree of differentiation

Well differentiated tumors (low grade):

- Neoplastic epithelium is obviously Sequamous in type- Neoplastic epithelium consists of masses of prickle cells

with a limiting layer of basal cells around them- Intercellular bridges are recognizable - Keratin pearls are often found within the masses of

infiltrating cells, each pearl consisting of a central area of keratin surrounded by prickle cells

- Nuclear and cellular pleomorphism is not prominent- Relatively few mitotic figures

Moderately differentiated tumors:

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- Neoplastic epithelium is still readily identified as Sequamous in type- Less keratinization- More pleomorphism of cells and nuclei- Abundant and atypical mitotic figures

Poorly differentiated tumors (high grade):

Cells are so abnormal and may be hardly recognized as epithelial cells ** In such cases we might need immunohistochemistry to identify the type of cell by demonstrating the cytokeratin which characterize epithelial cells (cells stained brown are epithelial cells positive for cytokeratin)

- Keratinization usually absent- Prominent pleomorphism of cells and nuclei - Abundant and atypical mitotic figures

It must be appreciated that the assessment of grade of carcinoma is entirely subjective and a degree of overlap between different grades is inevitable

There's variable lymphocytic and plasma cell infiltration in the stroma supporting a malignant epithelium, this probably represents an immune reaction by host's immune system to tumor antigens as well as a response to tumor necrosis and ulceration

Most oral Sequamous cell carcinomas are extremely locally destructive

Invasion & metastasis:

All carcinomas show invasion and destruction of local tissues and it is this that accounts for Induration and fixation detected clinically

Pattern of infiltration (invasion) of adjacent tissues by neoplastic epithelium is variable:

oIn some tumors, invasive front consists of broad groups or sheets of malignant cells

oIn other tumors, invasive front consists of small separate islands of carcinoma, narrow strands

or even individual malignant cells Pattern of infiltration (invasion) affects prognosis:

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Poorly differentiated SCC stained for cytokeratin

** Brown stain epithelial cells positive for cytokeratin


o Cohesive invasive fronts (consists of broad groups or sheets of malignant cells) Better

prognosis

o Non- Cohesive invasive front (consists of separate islands of carcinoma or even

individual malignant cells) poorer prognosis

Variable patterns of local infiltration (invasion) and destruction, e.g.:

o Lymph vessels: Lymphatic permeation

o Blood vessels: Vascular invasion

o Muscles: Sarcolemmal spread

o Nerves: perineural spread

o Bones: bone invasion as a result of local spread, and the extent of invasion may be greater

clinically than that seen on radiographs

In edentulous patients, bone invasion occurs through the alveolar crest In dentate patients, bone invasion occurs through the PDL

Variable patterns of metastatic spread to the regional lymph nodes:

o The frequency of metastasis increases with the size of the

primary tumoro Cervical lymph nodes are divided into 5 groups

o Tumors tend to metastasize initially to the nodes in the

superior drainage groups (levels I and II), with progressive involvement of the more inferior groups in the chain, metastatic disease spreads

o Metastatic spread to regional lymph nodes in the neck

may be:

Intra-capsular (tumor confined within capsule of node) Extra-capsular (tumor destroys & replaces the nodal lymphoid tissue and infiltrates

through the capsule into the adjacent tissue of the neck), this results in :- Fixation of the node seen clinically- Poorer prognosis

o Late in the clinical course of the disease metastasis to distant sites occurs

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Cohesive invasive front Non-cohesive invasive front


Blood-borne metastasis Risk of distant metastases increases with increasing involvement of nodal metastases

in the neck

Verrucous Carcinoma:

Uncommon pathological variety of well differentiated (low grade) Sequamous cell carcinoma

Clinical features:- Presents as slowly growing, thick white warty plaque

of heaped up folds of tissue with deep cleft-like spaces in between

- In the mouth, the most common location is mandibular buccal sulcus and adjacent buccal mucosa

- Mainly affects the elderly - Particularly seen in tobacco chewers and snuff

dippers- Prognosis is good & doesn’t metastasize - However, some cases transform into a regular

Sequamous cell carcinoma with metastasis

Histopathological Features:

- Very well differentiated, heavily keratinized Sequamous cell carcinoma with little or no cytological atypia

- Although it is an exophytic tumor, it also has a slowly pushing cohesive invasive front causing local destruction BUT NO metastasis

- Mitoses are rare

Diagnosis of Verrucous carcinoma is difficult and strict criteria must be adopted

Verrucous carcinoma must be differentiated from:

- Well differentiated Sequamous cell carcinoma with a papillary surface- Luekoplakic lesions with warty surfaces (Verrucous Leukoplakias or Verrucous

hyperplasias)

Carcinoma-In-Situ

A term used to describe severe epithelial dysplasia in which the whole, or almost the whole thickness of epithelium is involved BUT basement membrane is intact and there is NO invasion of lamina propria

Usually presents clinically as leukoplakia or Erythroplakia It is a premalignant lesion In some patients it may progress to invasive carcinoma, but

in others it may remain static or even regress Field cancerization:

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http://www.usc.edu/hsc/dental/opfs/SC/08bb.html


- It is common to find histological changes of dysplasia, including carcinoma-in-situ, in the epithelium surrounding an invasive carcinoma, even though this may appear clinically healthy

- This suggests that in some patients there may be a field of premalignant change involving a wide area of mucosa “field cancerization”

- It is probable that some carcinomas which are thought to be recurrent tumors, may be actually new primary lesions arising in such a field change

Precancerous (or premalignant) lesions or conditions:

1. Premalignant lesion a morphologically altered tissue in which cancer is more likely to occur than in its normal counterpart, that is the lesion itself undergoes malignant transformation

The following may be considered premalignant lesions:

- Leukoplakia (homogenous & non-homogeneous: nodular, speckled or Verrucous) - Erythroplakia- Candidal leukoplakia (chronic hyperplastic candidosis) - Carcinoma in situ

2. Premalignant condition a generalized disorder associated with a significantly increased risk of cancer developing somewhere in the mouth

The following may be considered premalignant conditions:

- Oral Submucous fibrosis- Lichen planus (atrophic/erosive)- Actinic keratosis (or actinic cheilitis for cancer of the lip)- Other conditions associated with oral epithelial atrophy, e.g. Sideropenic dysphagia

** However, it must be remembered that relatively few oral SCCs are preceded by a recognizable premalignant lesion or condition

Basal cell carcinoma (rodent ulcer):

Common neoplasm of skin, especially face Clinical features:

Affects old people with chronic exposure to UV radiation Occasionally presents on lips, particularly upper lip However, many may be skin tumors spreading to involve vermilion

border Typically presents as a slow growing nodule that

eventually ulcerates Multiple basal cell carcinomas arising at younger

age and on non-sun-exposed sites are a feature of nevoid basal cell carcinoma syndrome

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Nevus cells

Intra-mucosal nevus


Histologically consists of malignant basaloid cells arranged in various patterns, invading adjacent tissues

Melanocytic Nevi and Melanoma:

Melanocytes are dendritic cells of neuro-ectodermal origin They are located mainly in the basal layer of epidermis and some mucous membranes They are widely distributed and present in large numbers in oral mucosa of clinically pigmented and

non-pigmented races, the difference being of activity and not number Their function is to produce melanin which they pass to adjacent keratinocytes Acquired Melanocytic Nevi (moles) :

Clinical features:

- Nevus (from Latin naevus = birthmark) any developmental blemish on skin or mucosa

- Acquired Melanocytic nevi are very common, particularly on skin of head and neck

- They are considered hamartomatous lesions formed by proliferation of Melanocytes with variable melanin pigment production

- Most present in childhood and adolescence - The average person may develop 20-30 nevi- Malignant change can rarely occur in nevi - Melanocytic nevi are rare in the oral mucosa- Most reported intraoral nevi present in adult life as

slightly elevated, pigmented lesions on the hard palate or buccal mucosa

Histopathological features:

- There are different stages in the natural history of Melanocytic nevi based on location of nevus cells relative to epithelium:

Intra-mucosal (intra-dermal) Most oral nevi are of this type Junctional nevus Compound nevus

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Nevus cells Nevus cells

Junctional nevus Compound nevus


Malignant melanoma:

Excessive exposure to UV light is the most important predisposing factor for malignant melanoma of the skin, hence many tumors arise in head and neck area

Skin lesions may present as pigmented plaques or nodular lesions and may be preceded by melanoma in situ characterized by horizontal spread within epithelium

Vertical spread into dermis characterizes invasive melanoma and prognosis depends mainly on depth of invasion at time of diagnosis

Clinical Features (ABCD):

- Asymmetry (uncontrolled growth pattern) - Border irregularity (uneven edges) - Colour variation (2 or more shades) - Diameter greater than 6 mm (greater than 1/4 inch)

Oral malignant melanoma:

- Rare- Slightly more common in males than females- > 70% involve posterior maxillary alveolar

ridge and hard palate- Oral melanomas present as dark brown or bluish

black slightly raised lesions with an uneven nodular or papillary surface

- Some lesions don’t produce melanin “a-melanotic lesions” and these tend to appear reddish

- Growth may be rapid with extensive destruction of bone and loosening of teeth

- Most are advanced & extensively invasive at presentation, with both regional lymph node and blood-borne metastases common

- But, in about a third of cases, there is history of previous pigmentation in the area

- Prognosis is very poor in most of the cases

Histopathological features:

- Highly Pleomorphic neoplasms- Variable melanin production, but there may be no

melanin (a-melanotic melanoma)- Immunohistochemical studies using specific markers for

malignant Melanocytes (S-100 & HMB-45) are useful

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- Ultra-structural examination to identify immature melanosomes can be used

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7- Oral Epithelial Tumors II

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