NEOPLASM

HARMAS YAZID YUSUF

DEPT OF ORAL AND MAXILLOFACIAL SURGERY

FACULTY OF DENTISTRY PADJADJARAN UNIVERSITY
HASAN SADIKIN HOSPITAL
BANDUNG - WEST JAVA - INDONESIA
 INTRODUCTION
Neoplasia literally means "new growth", and this tissue growth is called
NEOPLASM.
A neoplasm is an abnormal mass of tissue, the growth of which exceeds
and is uncoordinated with that of normal tissues, and persists in the same
excessive manner after cessation of the stimulus that evoked the change.

The key features of neoplasia that distinguishes it from other forms of cell
proliferation therefore are:
1] Excessive tissue growth
2] Lack of responsiveness to control mechanisms
3] Lack of dependence on the continued presence of the stimulus

There are several commonly used synonyms for neoplasms.

The term TUMOUR strictly speaking means tissue swelling or mass, but by
common usage has come to mean neoplasm.
CANCER is a lay term used to mean malignant neoplasm.
CHARACTERISTICS OF NEOPLASTIC CELLS

Neoplastic cells, particularly those of the malignant neoplasms differ in

many ways from normal cells.
Given that neoplasms represent uncontrolled growth of certain cells, it
clearly is important to attempt to understand those control mechanisms
that regulate cell growth, usually studied using cell cultures.

When normal cells are grown in vitro, they spread out to form a single
sheet (or monolayer) of cells. Growth ceases when the cells reach a
certain density and the cells remain quiescent but healthy. This process
is known as DENSITY-DEPENDENT INHIBITION or CONTACT
INHIBITION of growth.

In contrast, neoplastic cells, particularly malignant cells grow in

haphazard way, pile up into multiple layers, and are much less
responsive to cell density-dependent mechanisms of growth control.

These cells tend to grow until they exhaust the medium of nutrients, and
these characteristics may be induced by treatment with carcinogens
(neoplasm inducing agent; see later), the process being known as
neoplastic TRANSFORMATION.
Morphologically, transformed cells exhibit the
following characteristics:
1] May or may not resemble cells of origin (anaplasia and pleomorphism are common)
2] Increased nucleus to cytoplasmic ratio; nuclei enlarged, hyperchromatic and may be
multinucleated
3] High mitotic rate
4] Lacks orientation to adjacent cells
5] Decreased rough endoplasmic reticulum and increased free ribosomes

Besides morphological changes in neoplastic cells, transformed cells exhibit the

following characteristics:
1] Transplantability - will grow in tissue culture or in syngeneic host
2] Immortality - will divide and replicate indefinitely provided that nutrients required for
growth are present
3] Decreased sensitivity to density dependent inhibition of growth
4] Tumorigenicity - forms tumours in syngeneic host
5] Antigenic changes
6] Changes in karyotype - chromosomal damage or alterations in base pairs may be
basic to the induction of neoplasia; observed karyotypic changes are rarely
characteristics of any one tumour
7] Changes in Cell Biochemistry - neoplastic cells contain less cyclic adenosine
monophosphate (cAMP) and more cyclic guanosine monophosphate (cGMP) than
normal cell; absence of normal enzymes or the presence of abnormal ones can occur
CLASSIFICATION OF NEOPLASM

Neoplasms are named according to the features of differentiation that

can be recognised on histologic examination, and reflects the tissue of
origin.

Nomenclature and classification are important as they form the basis of

the language by which pathologists and clinicians discuss the nature and
significance of the lesion to one another.

Neoplasms are classified in several ways.

One way of classification is based on the tissue origin (Histogenetic) as
1] Mesenchymal or 2] Epithelial in origin.
Most are of one neoplastic cell type and fit into one or the other of these
two groups. A few types of neoplasm contain more than one neoplastic
cell type. When they are derived from the one embryonic germ layer,
they are called Mixed Neoplasm

TERATOMA is a neoplasm containing tissues derived from more than

one germ cell layer, and may contain any number of tissues of any type
including bone, skin, nervous tissue, muscle, hair and others.
Another classification is based on the growth
behaviour of neoplastic cells (Behavioral).
The terms Benign Neoplasm describes those which are relatively
inoffensive, and Malignant Neoplasm for those which are
aggressive and potentially life threatening.

Most often, the histogenetic and behavioral classification

schemes are used in naming neoplasms.
Benign neoplasms are named by adding the suffix "-oma" to a
prefix suggesting the tissue origin (e.g. benign neoplasm derived
from fibroblast is called fibroma).

Benign neoplasms derived from glandular epithelia are called

Adenomas. This term refers to both those with a solid lobular
pattern of growth and those with recognisable tubules, ducts or
acini. Because the term adenoma is nonspecific, the tissue of
origin is usually shown (e.g. adenoma of sweat gland, adenoma
of thyroid gland, or adenoma of adrenal cortex).
Also, many modifying terms are applied to the names
of neoplasm of epithelial origin.
For example, cystadenoma describes an adenoma in
which the glandular spaces are cystic; papillary
adenoma is one in which branching finger-like
processes of neoplastic tissue extend into the lumen;
ductular adenoma is one derived from ducts.
Papillary neoplastic masses growing at a surface are
known as polyps or papillomas.
Another classification is based on the growth
behaviour of neoplastic cells (Behavioral). Con’t
Malignant neoplasms of mesenchymal origin are called sarcoma. As in
their benign equivalent, a prefix is used to suggest the tissue of origin (e.g.
malignant neoplasm of fibroblast is called fibrosarcoma). Malignant
neoplasms of epithelial cells are called carcinoma.

Then, only those that form recognisable ducts, tubules or acini are called
adenocarcinoma. Those that form solid pattern are called simply as
carcinoma (e.g. those forming stratified squamous epithelium is called
squamous cell carcinoma). Again, if the tissue of origin is recognisable, it
is included in the name (e.g. adenocarcinoma of sweat gland;
adenocarcinoma of adrenal cortex). Some neoplasms fail to mimic their
tissue of origin sufficiently for it to be recognised. In such a case, the
neoplasm is said to be poorly differentiated sarcoma or carcinoma as the
case may be.

Despite these rules for classifying and naming neoplasms, inconsistencies

persist. Neoplasms do not always fall neatly into one or the other category,
but a spectrum between completely benign and highly malignant exists
and errors are bound to occur in trying to predict the future behaviour of a
neoplasm.
FEATURES OF NEOPLASTIC CELL DIFFERENTIATION

The differentiation of neoplastic cells refers to the degree to which

they resemble morphologically and functionally the tissue from which
they originate. Again, there is great variability in the degree of
differentiation.
Benign tumours usually are well differentiated and resemble the
tissue of origin, both cytological and architecturally.
Malignant tumours on the other hand vary greatly in the degree to
which they differentiate. But generally they exhibit some degree of
ANAPLASIA.
Anaplasia is failure of cells to differentiate or loss of differentiation,
and is one of the most important morphologic features of malignancy.
Anaplasia should not be thought of as dedifferentiation, which would
imply that cells already differentiated revert to a more primitive form.
It is not generally accepted that this can occur.
Anaplastic cells usually exhibit pleomorphism. Their
nuclei are often large, hyperchromatic or vesicular,
have an abnormal shape and may contain one or
more prominent nucleoli. The nuclear to cytoplasmic
ratio are usually abnormal.

Besides these cytological features, the cells in

malignant neoplasms often do not grow in well-
differentiated architectural patterns, making it difficult
to or impossible to classify such neoplasms.
Well-differentiated neoplasms may retain the
functional characteristics of the parent tissue.
Thus, glandular adenomas may secrete mucus and
endocrine adenomas may secrete hormones.

Functional activity is in fact the basis on which the

origin of many neoplasms may be recognised (e.g.
melanomas produce melanin, osteosarcomas
produce osteoid, and adenocarcinoma of thyroid
produce colloid).
The idea that neoplastic cells divide at a more rapid rate than normal tissue
is not true. Frequently, the cell cycle time for neoplastic cells is longer than
that of the normal germinal cells from which they are derived.

The actual growth rate of neoplasm like that of the normal tissue is decided
by the:
1] length of the mitotic cycle,
2] the growth fraction (or proportion of cells in mitosis) and
3] the rate of loss of cells from the neoplasms (i.e. through necrosis and
apoptosis).

What is important is the relative proportion of neoplastic cells in mitosis,

and this decides the rate of growth of neoplastic tissue. In many cells, full
differentiation precludes further mitotic division.
Thus, the degree of differentiation decides the growth fraction of
neoplasms. Therefore, well-differentiated neoplasms (i.e. benign
neoplasms) contain high proportion of cells unable to divide and so grow
slowly. Conversely, poorly differentiated neoplasms (i.e. malignant
neoplasms) often contain many cells in the growth fraction and usually
grow rapidly.
SPREAD OF TUMOURS: INVASION AND
METASTASIS

Benign tumours are generally noninvasive, are localised, clearly

demarcated from the surrounding tissue and are often but not invariably
separated from it by a capsule or rim of normal connective tissue. The
latter may be derived from compressed pre-existing stroma or may be
part of the stroma of neoplasm. Benign neoplasm usually grows by
expansion.

Malignant neoplasms, in contrast, usually exhibit local invasiveness or

infiltration, meaning they extend into and may cause considerable
destruction of surrounding tissue. Malignant neoplasms also have the
potential to metastasize or spread to distant sites not directly adjacent
with the primary mass. Neoplasms that metastasize are unequivocally
malignant.
Metastasis may occur by via the following routes:
1] Lymphatics
2] Blood vessels
3] Coelomic spaces
4] Epithelial cavities
 METASTASIS CONT’
The processes by which tumour cells spread from one site to
another include the following:
1] Embolism
2] Vascular invasion
3] Exfoliation and implantation
4] Transplantation

The mechanism that account for the ability of malignant cells to

invade tissues is poorly understood.
Several theories have been proposed.
1. Mechanical pressure resulting from rapid growth results in neoplastic cells
being forced into the surrounding tissue.
2. Neoplastic cells produce enzymes that can degrade adjacent tissues, and
this includes lysosomal hydrolases, collagenase and plasminogen
activator.
3. Recent information suggests that motility of neoplastic cells may be an
important factor in invasiveness.
However, no single mechanism could fully explain the invasive feature of
malignant neoplasms and conflicting evidences exist.
 METASTASIS CONT’

The understanding of tumour metastasis by mere

appreciation of the mechanisms and the routes taken by
neoplastic cells is certainly an oversimplification of the
process.

For tumour tissues to successfully form metastases, it

must complete the following steps:
1] Release from site of origin
2] Transportation
3] Lodgment in distant site
4] Growth and survival

Metastasis therefore is a selective process and only

those cells able to satisfy all these steps can produce
metastasis.
METASTASIS CONT’
Metastasis is defined as the formation of secondary tumor foci at
a site discontinuous from the primary tumor.
Metastases can form following invasion and penetration into
adjacent tissues followed by dissemination of cells in the
lymphatics, blood vasculature, coelomic cavities, or epithelial
cavities.
Metastatic cells arise within a population of
neoplastic/tumorigenic cells as a result of genomic instability.
This subset of cells has accumulated mutations in addition to
those that have already rendered the cells tumorigenic.
Metastasis-competent cells have evolved so that they detach and migrate
away from the primary tumor.
During transport, cells travel individually or as emboli composed of tumor cells
(homotypic) or of tumor cells and host cells (heterotypic).
At the secondary site, cells or emboli arrest either because of physical
limitations (i.e., too large to traverse a lumen) or by binding to specific
molecules in particular organs or tissues.
Once there, tumor cells then proliferate either in the vasculature or in the
surrounding tissue after extravasation.
To form macroscopic, clinically detectable metastases (on the order of mm),
cells recruit a vascular supply  angiogenesis.
To form clinically important metastases, cells must complete every step of this
complex cascade and proliferate at the secondary site
EFFECTS OF TUMOURS ON HOST

Neoplasms cause harm to the host in several ways as follows:

1] Functional tumours - some tumours retain their functional ability and secrete
substances that may cause disease in the host (e.g. functional tumour of
parathyroid produce hyperparathyroidism)
2] Effusion - some tumours produce secretory products or cell debris that may
cause altered blood flow or decreased lymphatic drainage, or obstruction of ducts
3] Paraneoplastic syndromes - cells which become neoplastic may make altered
products or because of gene deregulation may make products characteristics of
other cells and cause clinical abnormalities in the host.
4] Cancer cachexia - wasting occurs out of proportion to biomass of neoplasm;
inappetence may be due to liberation of toxic products, or to pain.
5] Production of onco-fetal antigens - many tumours bear new antigens not found
on normal host cells. These antigens are known by several names as tumour
specific antigens (TSA), tumour specific transplantation antigen (TSTA), or tumour
associated transplantation antigens (TATA). Some of these transplantation
antigens sensitizes the host's immune system and cause an immune reaction to
the neoplastic tissue mass. Some are immunosuppressive and favor growth of
neoplasm.
EFFECTS OF TUMOURS ON HOST
CONT’

Obviously, malignant neoplasm because of their invasive nature

and ability to metastasize will cause more harm to the host than
benign tumours.

However, benign tumours can have devastating effects as follows:

1] Pressure effects - any space occupying lesion can lead to dysfunction of an

organ (e.g. benign neoplasm of the brain cause local destruction of neuropil and
can produce severe illness and eventually death of the animal)
2] Obstruction - benign neoplasm may compress hollow organs (e.g. compression
of bile ducts lead to massive destruction of liver tissue).
3] Ulceration, haemorrhage, infarction - some may cause massive blood loss that
leads to death following ulceration, perforation or rupture of the organ; or necrotic
neoplastic cells, or tumour emboli may lodge at arteries and cause infarction or
congestion in an organ
4] Hormone production
5] Malignant transformation - some benign neoplasm may progress to form
malignant neoplasm
AETIOLOGY OF NEOPLASIA

The exact aetiology of most spontaneous neoplasm is unknown.

Epidemiological data has led to association of certain agents
with certain cancer types. Animal experimentation has confirmed
their carcinogenicity. Other studies have suggested an infectious
aetiology that has been confirmed for some spontaneous
tumours.

Substances that cause neoplasia are called CARCINOGENS or

ONCOGENS. More specifically, carcinogens may be defined as
any substance or agent which produces, in exposed individuals,
an incidence of neoplasia greater than that observed in those
which are unexposed.
CARCINOGENS
Classes of carcinogens include the following:

1] Direct-reacting carcinogen - reactive moieties that require no

activation by biologic processes
2] Procarcinogen - agents that must be metabolised in the animal
body to the "proximate or ultimate" carcinogen.
3] Initiator - may be direct-reacting or procarcinogens or may not
be carcinogenic per se but are capable of initiating a change in
the cell which will lead to transformation
4] Promoter (Co-carcinogen) - agents which when applied after
initiation promotes the development of tumours
5] Complete carcinogen - act as both initiator and promoter

Known carcinogens fall into three major categories: 1] Physical

agents, 2] Chemicals, and 3] Viruses.
CARCINOGENS CONT’

Physical agents
Ionising radiation has some mutational effects on
cells that possibly lead to neoplastic transformation
(e.g. High incidence of neoplasia in survivors of
atomic bomb explosions). Ultraviolet light cause
mutational effect and damage DNA in cells (e.g. skin
cancer).
Trauma such as burns acts as "co-carcinogen" by
increasing the mitotic rate (reparative hyperplasia).
Solid state (e.g. bone pins may cause osteosarcoma)
produces neoplasia probably due to chronic irritation.
Chemical carcinogens

Many chemical carcinogens are procarcinogens and must

undergo cellular metabolism to produce the ultimate or
proximate carcinogen.

For example, aflatoxin and polycyclic hydrocarbons are

metabolised to epoxides that are the true carcinogens.
Types of chemical carcinogens include naturally occurring
substances (e.g. aflatoxin, nitrosamines, betel nut, cycasin) and
man-made chemicals (e.g. polycyclic aromatic hydrocarbons,
azo dyes, saccharine, polyvinyl chloride)
Oncogenic viruses

Both DNA and RNA viruses cause tumours.

Oncogenic DNA viruses include adenovirus,
herpesvirus, papovavirus, and poxvirus.
All oncogenic RNA viruses belong to the retrovirus,
so named because they possess an enzyme called
reverse transcriptase or more correctly RNA-
dependent DNA polymerase.
This enzyme is capable of forming DNA using an
RNA template, a feat which mammalian cells cannot
normally accomplish.
THEORIES IN CARCINOGENESIS

At present, there is no generally accepted, unified

idea of the biologic mechanisms which underlie the
development of neoplastic disease. Whatever the
fundamental cellular changes in carcinogenesis are,
certain observations can be made about the process.
Carcinogenesis usually is a multi-step process, dose
dependent and cumulative.

In an attempt to explain the mechanisms involved,

several theories have been proposed and will be
considered here.
THEORIES IN CARCINOGENESIS CONT’

Somatic mutation theory

This theory explains that damage to DNA leads to

transformation that is heritable and is passed from
one cell generation to the next.

Evidences for this theory include the finding that most

carcinogens are mutagens, radiation act this way,
some tumours are hereditary and therefore genome
can code for malignancy, and oncogenic virus insert
their genome before they can cause transformation.

Of all the theories, this theory is widely accepted.

THEORIES IN CARCINOGENESIS CONT’

Oncogene theory

It has been proposed that all cells (somatic and germ cells)
contain latent oncogene from oncogenic viruses which are
activated by a variety of external insults to produce transforming
substances.

Supporting evidence includes the finding that oncogene

sequences can be found in nearly all cells from all creatures.

It suffered from the basic unexplained fact that tumours induced

by oncogenic viruses contain specific antigens in neoplastic cell
surfaces while those produced by chemicals do not have this
antigen.
THEORIES IN CARCINOGENESIS CONT’

Epigenetic theory

This theory considers that all cells contain the complete genome capable
of producing the characteristics of a malignant cell. Derepression of
genes through alterations of cytoplasmic proteins leads to differentiation
to a fetal cell type.

Supporting evidences include the findings that even the most malignant
feature (invasion and metastasis) do occur in normal cells (e.g.
trophoblast extension, leucocyte migration); not all carcinogens are
mutagens but can bind to proteins as well as DNA and RNA;
Derepression of normal genes results to expression of fetal products
(onco-fetal antigens); and transformation proceeds in stages not as an all
or none phenomenon as expected for a genetic mutation.

This theory is widely accepted.

FACTORS INFLUENCING CARCINOGENESIS
The factors that influence carcinogenesis include the following:

1] Environment/Geographic factors - related to exposure of animals to carcinogens

(e.g. high incidence of sunlight associated with skin cancer )
2] Sex - the presence (or absence) of susceptible tissues and sex hormones
influences carcinogenesis (e.g. mammary tumours are rare in male )
3] Hormones - prolonged hormonal stimulation may predispose the target tissue to
undergo transformation or susceptible to carcinogenesis (e.g. cyclic hormonal
stimulation of mammary gland predisposes to cancer)
4] Hereditary factors
5] Nutrition - related to dietary exposures (e.g. in man, low fibre diet predisposes to
colonic carcinoma; exposure to aflatoxin in diet may lead to liver tumours)
6] Age - tumours increases with increasing age, and may be related to the
accumulation of somatic mutations or epigenetic events; altered cellular metabolism
with age; long latency of carcinogenesis; and decreased immune competence with
age.
7] Immunity - The role played by the immune system in tumour rejection and/or
enhancement is still an area of debate. While the immune system may modulate the
onset and development of tumours .
While tumour cells, in process of transformation, acquire a
different surface antigen that normally provokes an immune
reaction, this does not usually happen for some still unknown
phenomena.
This could be explained by known immunologic phenomena as
follows:
[a] Blocking antibodies coat the tumour cells and prevent T cell
recognition;
[b] Soluble tumour antigens blocks the specific receptors
required for immune recognition;
[c] Tumour cell surface antigens may be poorly immunogenic
[d] Tumour cell secretions may be immunosuppressive
[e] Tumour cell secretions may induct T-cell suppressor system
(T-suppressor cells modulate immune reactivities)
HEAD AND NECK CANCER
INTRODUCTION

The management of cancers of the head and neck has conventionally been the
province of surgeons and radiotherapists. In the past fifteen years, medical
oncologists have been increasingly involved in patients with these neoplasms.

Multimodality management of head and neck cancer patients is now the modus
operandi in most medical centers. Head and neck tumors should not only be the
concern of head and neck surgeons, radiotherapists and oncologists, but also all
primary care physicians and dentists.

Practitioners familiar with these tumors can often recognize the symptoms and
signs of early disease. The establishment of a diagnosis of head and neck
cancer at an early stage significantly improves the prospect of curative therapy.
MUCOSAL TUMORS

INCIDENCE AND EPIDEMIOLOGY

Squamous cancers of the upper aerodigestive tract constitute approximately

6% of new cancer cases in men and 2% of women.
At all sites except the salivary glands there is a significant preponderance of
cases in men. Oral and pharyngeal cancer is more common in white males at
every site, but the incidence of laryngeal cancer is somewhat higher in black
males.
The geographic distribution pattern for head and neck cancer shows
considerable variation and is site-dependent. For example, cancers of the
nasal cavity and paranasal sinuses are slightly more common in the South
than in the rest of the United States. Nasopharyngeal cancer is a very
common disease in the Chinese, with age-specific incidence rates in males
from Kwangtung Province (Cantonese) 40 times that of U.S. Caucasian males.
ETIOLOGY AND PATHOGENESIS

The overwhelming majority of head and neck cancers have been related to prolonged exposure
to environmental factors. While many associations between risk factors and various head and neck
cancers are firm, others remain questionable.
Sunlight - Lip cancer, skin cancer
Tobacco - Tobacco contains many carcinogens
Risk is a function of the degree of exposure and the inherent susceptibility of the site. Tobacco chewing is
uncommon in the United States. However, it is common practice in some parts of the world, such as
Ceylon, Bombay, other parts of India and portions of Southeast Asia, which have some of the highest
incidence rates in the world of oral and pharyngeal cancer. Oral cavity cancer is the commonest form
of cancer in Bombay. A mixture called pan (betel, nut and leaf, lime, catechu, tobacco and other
additives) is very popular in India. It is chewed into a quid and buccal mucosa cancer usually
develops at the site where the quid is kept and has most frequent contact.
Further evidence of the importance of type of exposure and site of cancer is the high incidence of cancer
of the hard palate in populations that practice reverse smoking, i.e., where the burning end of the
cigarette is kept in the mouth during smoking, in parts of India, Sardinia, Venezuela and Panama.
Hard palate cancer is otherwise uncommon in most of the world.
Cancer of the lip associated with pipe smoking.
Cigarette smoking, the most popular form of tobacco use in this country clearly plays a causative role in
tongue, pharyngeal, laryngeal, esophageal and lung cancer.
ETIOLOGY AND PATHOGENESIS con’t

Alcohol
Synergistic with tobacco
Ethanol per se, not a carcinogen, other factors implicated
Nutritional Deficiencies - Specific role not established, but an area of increasing study and
investigation
Occupational Factors - e.g., nickel workers, wood workers implicated in paranasal sinus cancer
Epstein-Barr Virus (EBV) - Possible etiological role in nasopharyngeal carcinoma
Genetic Factors - An area of increasing study and interest. Certainly, some families have high
incidence of cancer but genetic link not completely understood. However, some head and neck
neoplasms have had recent chromosomal identification, e.g., retinoblastoma linked to q14 band of
chromosome 13, medullary carcinoma of thyroid to chromosome 10, neurofibromatosis to
chromosome 22.
Poor Oral Hygiene - Oral cavity, especially floor of mouth cancer, tongue, and alveolar ridge
neoplasms.
Radiation - Ionizing radiation which was used in past to treat such benign conditions as acne,
tonsillar and adenoid hypertrophy, enlarged thymus in newborn and chronic sialoadenitis has led
to increased risk of thyroid cancer, parotid neoplasms, malignant degeneration of papillomas and
possibly other upper aerodigestive tract neoplasms
PATHOLOGY ULCERATIVE OR EXOPHYTIC

Histology
Majority are squamous cell carcinoma (> 90%)
Adenocarcinoma
Verrucous carcinoma
Others
Modes of Spread
Epidermoid carcinomas of the head and neck usually remain localized and
tend to progressively invade adjacent tissues.
Extension into regional lymph nodes are more likely in lesions with:
Large size
Sites with abundant lymphatic drainage
Hematogenous metastases-less common-seen in more aggressive tumors,
and tumors present for some time
Symptoms and Signs - Reflect the anatomic location, the
degree of advancement and growth characteristics

An obvious lesion
Bleeding
Malodorous breath/Halitosis
Odynophagia
Otalgia - local or referred
Trismus to muscles of mastication
Nasal stuffiness, unilateral nasal obstruction, postnasal drip, headache and epistaxis should
not be attributed to sinusitis without careful investigation
Nasal speech
"Hot potato" voice
Poorly fitting dentures
Loosening of teeth
Dysphagia
Hoarseness
Cranial nerve palsies
Cervical adenopathy - in patient with known head and neck primary malignancy,
approximately 85% are metastatic
DIAGNOSIS

Most head and neck cancers are treatable and curable when discovered early.
However, many cancers of the head and neck are large and extensive when
diagnosed.

History
Occupational risks and social habits
Symptoms and signs
Physical Examination
Head and Neck Examination - both inspection and palpation especially oral cavity,
base of the tongue, and palate
General Physical Examination - distant metastases, coexisting medical problems
Radiographic and Laboratory Studies
Chest roentgenogram, complete blood count and platelet count, prothrombin
time, partial thromboplastin time, urinalysis and electrocardiogram
Radionuclide scanning utility is dependent upon the likelihood of metastatic
disease
DIAGNOSIS CONT’

Biopsy - histologic confirmation of the diagnosis is mandatory before

proceeding with any definite therapy

Superficial lesions - punch biopsy - ideal for readily accessible lesions of the
skin or mucosa
Deeper lesions
Needle biopsy
Fine needle aspiration with cytology
Large bore needle
Incisional biopsy - violates capsule and potentially seeds tumor. Useful when
all diagnostic modalities have failed to establish a diagnosis and excisional
biopsy of the mass is not technically feasible.
Excisional biopsy - removal of a suspected tumor mass in its entirety. Rarely
indicated in squamous cell carcinomas of the upper aerodigestive tract.
Evaluation of the Neck Mass - any neck mass in an adult that persists more
than four to six weeks should be considered potentially malignant until proven
otherwise, especially in patient with a history of smoking, drinking or neck
radiation.
The proper evaluation of this particular patient does not consist of immediate
open neck biopsy, but begins with a complete physical examination with an
emphasis on the head and neck. Appropriate blood studies and radiographs
should be carried out. If complete examination of the head and neck does not
reveal a primary lesion, then the patient should undergo endoscopy under
general anesthesia.
He/she should have nasopharyngoscopy, direct laryngoscopy, bronchoscopy,
and esophagoscopy performed. In most instances, a primary lesion will be
identified at the time of endoscopy and appropriate biopsies can be taken. A
treatment plan can then be outlined based on the information obtained at
endoscopy.
In a small percentage of patients, no primary lesion will be grossly evident.
Selected random biopsies should be performed of the nasopharynx, pyriform
sinus, base of tongue, and tonsillar fossa, as these areas have been identified
in previous studies as the most common sites for occult head and neck
primaries.
With this careful systematic evaluation, the primary tumor will be identified in
almost all cases. However, in a small percentage of cases, no primary lesion
will be found. If this is the case, then exploration of the neck with biopsy of the
mass is indicated.
The patient should be prepared for a neck dissection which is indicated if
frozen section analysis reveals squamous carcinoma. In the case of
adenocarcinoma or lymphoma, then a neck dissection is not performed and
further diagnostic work-up and definitive therapy should be pursued.
STAGING /TNM
The most commonly accepted staging in the
United States is that of the American Joint
Committee for Cancer Staging/AJCC and End
Results Reporting.
UICC
SPECIFIC AND SUPPORTIVE MANAGEMENT

General Consideration of Specific Therapy for Various Stages of Disease -

Choice of treatment should be based on the histopathology of the tumor, the
staging classification of the tumor, the general physical status of the patient
and the psychosocial condition of the patient at the time of diagnosis.

These considerations will determine whether treatment should be directed at

cure or palliation or simply support. Any treatment employed may affect
respiration, deglutition, phonation and aesthetic appearance. It is important
that the patient be an informed and active participant in treatment decisions
throughout the course of therapy. The patient's ultimate decision should be
respected at all times. By the same token, the patient should be made aware
of the consequences of failing to pursue active treatment.
 The principles of therapy of head and neck cancer
directed at cure of the disease should try to meet
three objectives:
1. To eradicate the neoplasm completely
2. To give the patient the best functional result by careful
planning of the radiation fields or appropriate
reconstructive techniques for surgical defects
3. To leave the patient with as good a cosmetic result as
possible
Principles of Palliation Therapy.

In cancers which are deemed unresectable because of local

extension or deemed incurable because of diffuse metastatic
spread, treatment can be directed toward palliation.

Palliative treatment may be employed to:

1. Control local advancement of tumor
2. Provide relief from pain, e.g., the use of radiotherapy for bone
metastasis can be quite helpful in relieving the extreme pain
incurred from such metastases
3. Provide relief from obstruction, e.g., a patient with a far
advanced laryngeal tumor may benefit greatly from a
tracheostomy to prevent suffocation
4. To control bleeding
 Concern for the patient's quality of life should guide the
treatment decisions.
The choice of treatment modalities will depend on:
1. The size of the tumor and the location of the lesion
2. The gross characteristics of the tumors, i.e., exophytic or
infiltrative
3. Histopathologic differentiation of the tumor
4. Presence of local bone and muscle involvement
5. Presence or absence of nodal disease
6. The general medical condition of the patient
7. Socio-economic condition and occupation of the patient
8. The experience of the surgeon, radiotherapist and oncologist in
treating head and neck tumors
The tools at the disposal of the radiotherapist, the
surgeon, and the medical oncologist differ greatly.

Only a thorough understanding of the nature of the

biologic process as well as the capabilities and
limitations of each treatment modality will allow
selection of the most appropriate therapy for any
individual patient.
Radiation Therapy

Megavoltage therapy. Despite the tremendous advance in

technological equipment available to the radiation therapist,
including computerized dosimeters, the proper treatment of
lesions with minimal side effects requires an experienced and
sophisticated therapist who understands both the nature of these
tumors as well as the capabilities and limitations of his
equipment.
External Beam
Interstitial
Surgery

Gross removal of the primary tumor in its entirety

Removal of all involved lymph nodes dependent on the histopathology of the
tumor, the location of the tumor, the propensity for the tumor to metastasize,
and general status of the patient
Classical radical neck dissection-En bloc resection of lymphatics and soft
tissue contained in superficial layer of deep cervical fascia to deep layer of
deep cervical facia from the trapezius to the clavicle to the midline to
mandible. Weakness of the shoulder because of the sacrifice of cranial nerve
XI. The carotid artery and remaining cranial nerves are spared.
Modified (conservation) neck dissection-resection of lymphatics and soft tissue
within the limits defined above but with preservation of the sternocleidomastoid
muscle, strap muscles, internal jugular vein, and cranial nerve XI. This is a
technically difficult procedure and should be attempted only by experienced
head and neck surgeons.
 Restoration of physiologic function and
reconstruction of all significant physiological
and cosmetic defects dependent on:
1. Location of the tumor
2. Extent of resection
3. Reconstructive methods employed
4. Patient's motivation and ability to adapt
Chemotherapy

Head and neck tumors frequently respond to chemotherapeutic

agents. However, these drugs are used primarily for palliation or
as adjuvant therapy in conjunction with surgery and radiation and
have not replaced other modalities.

Some drugs with proven activity in head and neck cancers:

Methotrexate
Bleomycin
Hydroxyurea
Cisplatin
5-Fluorouracil
Supportive Measures

Treat underlying medical condition

Supplemental nutrition
Rehabilitation

It often involves relearning such basic skills as swallowing and

talking.
Laryngectomy
Esophageal speech
Electrical vibratory device
Pharyngotracheal fistula
Palatal and Orbital Resection Prostheses
Allow swallowing and normal sounding speech
Camouflage of large nasal and orbital defects
Radical Neck Dissection-may need a physical therapist for
shoulder weakness
Follow-up

Monitor the patient's response to therapy

To detect recurrence or second primary
Every two months in the first year
Every three months the second and third year
At least every six months in the fourth and fifth years
Yearly thereafter
SALIVARY GLAND TUMORS

The salivary glands are divided into the major glands (parotid,
submandibular and sublingual) and minor glands (found in the
submucosa of the nose, sinuses, mouth and upper aerodigestive
tract).

Tumors arise in both the major and minor glands, but are more
frequent in the former. The most common site for a salivary
tumor is the parotid gland and fortunately 70-80% are benign.
Occurring less frequently than parotid lesions, submandibular
and sublingual tumors are malignant in approximately 50% of
cases. Minor salivary gland tumors are unusual and
approximately 60% are malignant.
TYPES OF TUMORS

Benign
Benign Mixed Tumor (Pleomorphic adenoma) - The most common tumor of the parotid gland
Warthin's Tumor (papillary cystadenoma lymphomatosum) - Occurs most frequently in the "tail" of
the parotid gland of white, middle aged males. Appear "hot" on Tc99 scan. Bilateral lesions not
uncommon.

Malignant
Adenoid Cystic Carcinoma - Very lethal even when treated early. Although five-year survivals are
quite good, 20 year survival is very poor-15% or less depending on site of origin. Most patients die
of pulmonary metastases. This tumor also has a proclivity for perineural spread.
Mucoepidermoid Carcinoma - Graded into high grade (very malignant and lethal) to low grade
(very curable with surgery alone). The most common parotid tumor seen in childhood. Generally
metastatic to lymph nodes.
Acinic Cell Carcinoma - Low grade malignancy
Squamous Cell Carcinoma - Very aggressive tumor. Must rule out metastasis from a skin lesion to
parotid lymph nodes. Primary parotid lesions tend to metastasize to cervical lymph nodes.
DIAGNOSIS

It is generally difficult to reliably differentiate benign from malignant lesions on

the basis of history and physical examination. Facial paralysis and pain are
almost exclusively associated with malignant lesions. A several year history of
a slowly enlarging, lobulated mass is suggestive of a benign mixed tumor.
Computerized axial tomography may be helpful, but is unreliable in accurately
differentiating benign from malignant lesions.
Thin needle aspiration is frequently accurate in diagnosing the lesions, but
generally does not change the therapy which is surgical removal. Except for
readily accessible, minor salivary gland lesions, open, incisional biopsy is to
be condemned as this may lead to "seeding" or spread of the tumor,
particularly the benign mixed tumor.
 TREATMENT

Parotid Lesion - Complete excision of the tumor with a margin of surrounding normal
salivary gland. Since the vast majority of lesions occur in the superficial lobe (lateral to the
facial nerve) then the primary operation is a superficial parotidectomy with facial nerve
dissection. This is potentially curative for all benign lesions and is generally the only
surgery necessary for many malignant lesions. If a branch of the facial nerve is involved by
a malignancy (particularly the adenoid cystic carcinoma) then that branch and perhaps all
of the parotid gland and the facial nerve may need to be removed. A neck dissection is
frequently indicated in squamous and high grade mucoepidermoid carcinomas.

Submandibular and Sublingual Glands - Complete excisions of the gland and tumor. If a
malignancy is discovered, then a neck dissection and perhaps excision of the floor of
mouth may be indicated depending on the tumor type.

Minor Salivary Glands - The operation depends on the location of the involved gland, but
complete excision with a margin of normal tissue is essential. In the case of adenoidcystic
carcinomas, surrounding nerves must be sampled for possible invasion and excised if
involved.
RADIATION THERAPY

Although not curative, most malignant salivary gland

tumors respond to radiation therapy and it is usually
incorporated into the treatment plan of the more
ominous lesions (adenoid cystic carcinoma,
adenocarcinoma, high grade mucoepidermoid
carcinomas and squamous cell carcinomas).
Radiation is used as the primary treatment for
malignancies in patients who are poor surgical
candidates. Radiation of benign lesions is not the
accepted therapy in most circumstances.
It is easy to kill cancer
cells, but the challenge is
keeping the patient alive
at the same time…..!
 TERIMA KASIH ATAS
PERHATIANNYA
SEMOGA BERMANFAAT