Download Oral Cancer Genetics: From Diagnosis to Treatment Natalie Kaweckyj, LDARF, CDA, CDPMA,

Oral Cancer Genetics:
From Diagnosis to Treatment
Natalie Kaweckyj, LDARF, CDA, CDPMA,
COA, COMSA, CPFDA, CRFDA, MADAA, BA
Continuing Education Units: 5 hours
Online Course: www.dentalcare.com/en-US/dental-education/continuing-education/ce72/ce72.aspx
Disclaimer: Participants must always be aware of the hazards of using limited knowledge in integrating new techniques or
procedures into their practice. Only sound evidence-based dentistry should be used in patient therapy.
This continuing education course will teach the dental professional to recognize signs and symptoms
of cancer, the effects various cancer treatments have on the oral cavity, and how you can ease patient
discomfort.
Conflict of Interest Disclosure Statement
• The author reports no conflicts of interest associated with this work.
ADAA
This course is part of the home-study library of the American Dental Assistants
Association. To learn more about the ADAA and to receive a FREE e-membership
visit: www.dentalassistant.org
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The Procter & Gamble Company is an ADA CERP Recognized Provider.
ADA CERP is a service of the American Dental Association to assist dental professionals in identifying
quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses
or instructors, nor does it imply acceptance of credit hours by boards of dentistry.
Concerns or complaints about a CE provider may be directed to the
provider or to ADA CERP at: http://www.ada.org/cerp
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Approved PACE Program Provider
The Procter & Gamble Company is designated as an Approved PACE Program Provider
by the Academy of General Dentistry. The formal continuing education programs of this
program provider are accepted by AGD for Fellowship, Mastership, and Membership
Maintenance Credit. Approval does not imply acceptance by a state or provincial board
of dentistry or AGD endorsement. The current term of approval extends from 8/1/2013 to
7/31/2017. Provider ID# 211886
Overview
Understanding oral cancer genetics will help dental professionals care for their patients immediately following
diagnosis, as well as during and after cancer treatment. This course will teach the dental assistant to
recognize signs and symptoms of cancer, the effects various cancer treatments have on the oral cavity, and
the best techniques to ease patient discomfort.
Learning Objectives
Upon completion of this course, the dental professional should be able to:
• List the characteristics associated with oral cancer risk factors.
• Summarize the basics of tumor formation.
• Understand the basics of cancer genetics and development.
• Recognize the signs and symptoms of oral cancer.
• Identify areas most common to oral cancer formation.
• Describe the various treatment modalities.
• Understand how oncogenes and tumor suppressor cells work.
• Describe the staging of oral carcinomas.
• Explain metastasis.
• Recognize the six classes of chemotherapy drugs and their effects on cells.
• Distinguish the difference between benign and malignant tumors.
• Explain the treatment considerations necessary in treating dental patients with oral complications.
• Differentiate between the types of supplemental fluoride according to existing oral restorations.
• Explain the home delivery procedures of supplemental fluoride application.
Course Contents
•Glossary
• Introduction to Oral Cancer Genetics
• Risk Factors
Gender
Ethnicity
Age
Tobacco
Alcohol
Diet
Oral Hygiene
Lifestyle
Lowered Immunity
• Tumor Formation
• Signs and Symptoms
•Diagnosis
• Cancer Genetics
• Cancer Development
•Metastasis
• Treatment Options
Surgery
Chemotherapy
IMRT Radiation
Radiation Therapy
•Prognosis
•Research
• Dental Considerations for the Diagnosed
Patient
Prior to Treatment
After Treatment
Supplemental Fluoride
•Conclusion
• Appendix A
• Appendix B
• Course Test Preview
• References
• About the Author
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Glossary
adenopathy – Any disease of the glands,
especially of the lymphatic glands.
erythema – A red area of variable shape and size
reflecting inflammation, thinness, and irregularity of
the epithelium and lack of keratinization.
allele – One of two genes containing inheritable
characteristics.
erythroplakias – Red lesions of the mucous
membranes.
angiogenesis – The process that stimulates the
formation of blood vessels.
etiology – The cause of the disease.
apoptosis – Programmed death of cells.
extracellular matrix – The material outside of
the cell.
asymptomatic – Without symptoms.
fixation – A non-mobile lesion occurring as a result
of abnormally dividing cells invading to deeper areas
and onto muscle and bone.
basement membrane – A thin layer of delicate
non-cellular material of a fine filamentous
structure underlying the epithelium.
benign – Not recurrent or progressive; non
malignant.
free radicals – Molecules that have split and now
have an odd number of electrons; often repaired with
antioxidants found in fruits and vegetables.
carcinogenic – Cancer causing.
hematogenous – Originating in the blood.
carcinoma – A new growth or malignant tumor
that occurs in epithelial tissue; etiology is
unknown.
heterozygosity – Possessing different alleles.
immunosuppression – Prevention of the activation
of the immune responses.
centromeric – Region of the chromosome that
connects the chromatids during cell division.
chromatid – One of two potential chromosomes
formed by DNA replication.
induration – Hardness, primarily as a result of
an increase in the number of epithelial cells from
an inflammatory reaction that has spread into the
surrounding tissue.
chronicity – Failure to heal.
innocuous – Innocent
clone – Group of cells descended from a single
cell.
integrin – The receptor on cell surfaces that links
with proteins and chemical mediators for cell-to-cell
communication.
differentiation – The acquiring of individual
characteristics.
Kaposi's Sarcoma – A vascular malignancy
that is often first apparent in the skin or mucous
membranes; the most common AIDS-related
tumor; etiology is unknown but thought to involve
immunosuppression.
DNA – Deoxyribonucleic acid; carrier of genetic
information.
down-regulate – To inhibit or suppress the
normal response of a gene.
keratin – An extremely tough, but fibrous protein
substance that may be hard or soft.
dysplastic – Abnormal development of tissue.
keratinization – The process of keratin formation.
epithelial – A type of tissue cell that forms the
outer layer of skin and lines the inner cavities
of the body; arranged in one to few layers and
devoid of blood vessels.
lateral borders of the tongue – Sides of the tongue.
leukoplakia – A white patch on the mucosal surface.
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library – A large set of clones that collectively
contain all the donor’s DNA.
during and following treatment, the patient
experiences xerostomia, changes in salivary flow
and perhaps difficulty in maintaining proper oral
hygiene.
localized – Restricted to a limited area.
lymphadenopathy – Disease process affecting
the lymph nodes resulting in the hardening and
enlargement of the nodes.
squamous cell – A flat, scaly, epithelial cell.
stage – Period in the course of a disease such as
cancer; the higher the number of the stage, the
more advanced the disease.
lymphoma – A usually malignant lymphoma
neoplasm.
stomatoxic – Toxicity to the oral cavity.
malignant – Cancerous growths resisting
treatment.
telomerase – An enzyme present in cancer cells
that allows them to divide indefinitely.
melanoma – A malignant tumor of the skin.
transformation – Changing of shape or form.
metabolites – Byproducts of metabolism.
trismus – A contraction of the jaw muscles as a
result of oral infection, trauma, or inflammation of
the salivary glands.
metalloproteinases – A protease bound to metal.
metastasis – Movement of cancerous cells from
one part of the body to another.
tubulin – A protein present in cells.
mutations – Permanent variation in genetic
structure.
tumor – A spontaneous new growth of tissue
forming a mass.
myeloma – A tumor originating in the cells of the
bone marrow.
tumor suppressor genes – Genes that suppress
the growth of a tumor.
neoplasm – A new and abnormal formation of
tissue (tumor) that grows at the expense of the
healthy organism.
ulceration – Loss of skin surface with a gray to
yellow center surrounded by a red halo, resulting
from the destruction of epithelial integrity owing to
discrepancy in cell maturation, loss of intracellular
attachments, and disruption of the basement
membrane; formation of a sore (ulcer).
oncogenes – Genes that have the ability to
induce cell malignancy.
oropharynx – The central portion of the pharynx
lying between the soft palate and the upper
portion of the epiglottis.
up-regulate – To increase or excite the normal
response of a gene.
ventral surface of the tongue – Under side of
the tongue.
p53 – A protein produced by a tumor-suppressor
that is believed to play an important role in the
birth and death of cells.
Introduction to Oral Cancer Genetics
Oral cancer can develop in any part of the oral
cavity or oral pharynx, but the most common sites
are the floor of the mouth, lips, soft palate, and
tongue. Mouth cancer is considered anything
from the last molar forward to the lips, including
the part of the tongue seen in the mirror, the hard
palate and the inside of the cheeks. Anything
behind the last molar is a different area called
the oropharynx, which includes the tonsils, soft
protease – A class of enzymes that break down
amino acid proteins.
proto-oncogenes – Normal cell genes before
they become oncogenes.
radiation-induced caries – Carious lesions that
develop in reaction to head and neck radiation;
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Figure 1. Oral Pharynx.
palate and the base of the tongue. Cancers of
the hard palate are not common in the United
States. The most recent estimates in 2013 from
the American Cancer Society show that each year
over 36,000 people will be diagnosed with oral or
oropharyngeal cancer and over 6,850 people will
die from these cancers.
Many of these malignant conditions could be
arrested if detected earlier. The dental profession
has a unique opportunity during patient
assessment to detect oral cancer while it is still
asymptomatic, innocuous, and unsuspected. It
is estimated that 5-10% of routine dental patients
have some unusual findings, from something
as harmless as mandibular or maxillary tori to
something as serious as a malignant neoplasm.
Oral squamous cell carcinoma accounts for 90%
of all primary oral malignancies. It is possible for
the oral cavity to be the site for tumor metastasis
from other locations, such as the breast, lung,
and gastrointestinal tract.
Oral cancer is more common than cancers of the
brain, liver, bone, stomach, cervix and ovaries;
it is even more common than leukemia. When
oral cancer is detected early, the cure rate can
be as high as 96% depending on the location
of the cancer. Unfortunately, by the time a
medical or dental diagnosis is made, about
two-thirds of oral cancers are advanced lesions
with evidence of invasion and metastasis. This
leads to high morbidity and mortality in spite of
advances in surgical techniques, radiotherapy and
chemotherapy. Little has changed in the last 40
years and approximately half of the people who
develop oral cancer die because of the disease.
Oral cancer is particularly dangerous because
it has a high chance of producing secondary
tumors, usually in the lymph nodes of the neck.
This increased risk factor can last up to a decade
after the first episode of tumor invasion.
Cancer of the three major salivary glands
(parotid, submaxillary, and sublingual) is
considered a separate form of oral cancer, as are
cancers of the jaw and the muscles of the face.
Therefore, it is important to identify the area the
cancer originated from, even if it has spread to
other areas of the head. The origin is the factor
that determines the type of cancer.
Risk Factors
Oral cancer affects men twice as often as women.
It is more common among African-Americans
than Caucasians, and seen more often in those
of lower socioeconomic status. The average age
at onset is 62 years old. Most patients are over
40 years old, but it is also important to remember
Annually, oral cancer kills more people than
female cervical cancer and costs society more
than 2 billion in treatment costs and lost wages.
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Tobacco
Oral cancer is a multi-step process of accumulated
genetic mutations caused by a combination of diet,
alcohol and tobacco use, oral hygiene, lifestyle,
lowered immunity, and genetic susceptibility.
The use of tobacco in all of its forms (cigarettes,
cigars, pipes, marijuana, and chewing tobacco)
is a well-established risk factor for not only oral
cancer, but other cancers as well. In oral cancer,
it is considered the number one risk factor. Even
children who use chewing tobacco, often to
emulate famous baseball players, have developed
oral cancer. A strong association has been noted
between development of oral premalignancy in
the form of erythroplakias and the use of chewing
tobacco combined with alcohol consumption. Pipe
smokers have a greater incidence of developing
lip cancer. The more tobacco that is used for a
longer period of time, the higher the risk for oral
cancer. Likewise, when tobacco usage is stopped,
the risk declines to almost normal over a 10-20
year period.
that oral cancer can strike at any time. The exact
causes for those affected at a younger age are
not known at this time. There are some probable
links to young males who use chewing tobacco.
Other researchers believe that the underlying
link is viral based, given that the amount of time
these individuals have been exposed to known
causative agents, such as tobacco, is short.
Gender
From a gender perspective, oral cancer had
affected six males for every female for decades.
The ratio is now two males for every one
female. Published studies do not draw concrete
conclusions as to why females have closed the
gap, but many believe that lifestyle changes
in which the number of women smokers has
increased over the last twenty years plays a
significant role.
Ethnicity
From a racial and an ethnic perspective, oral
cancer occurs twice as frequently in the African
American population as it does in the Caucasian
population. Among African American men,
the oral cavity is the fourth most frequent site
of cancer. Survival statistics for an African
American individual over a five-year period are
about 40%, while for a Caucasian individual it is
approximately 60%. Researchers are unlikely
to find a genetic reason for this anytime soon.
Published statistics do not take into consideration
socio-economic factors such as availability of
proper health and dental care, education, income
levels, and the increased use of both tobacco and
alcohol by different ethnic populations.
Alcohol
Excessive alcohol use also can increase the risk
of developing oral cancer. One theory suggests
that alcohol generates metabolites that are
carcinogenic to humans; the major metabolite of
ethanol is acetaldehyde, a known carcinogen.
Acetaldehyde may be produced both systemically
and by the oral microflora. Alcohol may also act
as a solvent for tobacco, making it easier for the
carcinogens to infiltrate the oral mucosa. The
use of both alcohol and tobacco simultaneously
generates a greater risk for oral cancer than using
either substance alone. It is estimated that the
combination of both smoking and drinking causes
approximately 75% of all oral and pharyngeal
cancers in the United States. As with tobacco,
lowering the frequency of alcohol usage gradually
lowers the risk of cancer to that of non-drinkers
who don’t smoke.
Age
Age is frequently named as a risk factor for oral
cancer since most cases occur in those over the
age of 40. The average age of those diagnosed
with oral cancer is 62. The ages of the diagnosed
patients may indicate a time component in the
biochemical or biophysical processes of aging
cells that allows malignant transformation. New
trends, inevitably emerge, and recently there
has been an increase in the number of patients
in their 20’s and 30’s who have developed oral
cancer, especially cancer of the tongue, without
any apparent risk factors such as tobacco and
alcohol use or immunosuppression.
Diet
Research suggests that diets lacking fruit and
vegetables could contribute to oral cancer, as well
as other forms of cancer. Fruits and vegetables
contain beneficial antioxidants that trap harmful
molecules called free radicals. Antioxidants can
help prevent cancer causing genetic mutations.
Natural carotenoid compounds, dietary selenium,
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folate, and vitamins A, C, & E reportedly
offer protection against cancer development.
Consumption of Cantonese salted fish from
early childhood on into adulthood has been
associated with oral cancer formation in some
Asian countries. Betel nut chewing in Indian
populations is strongly associated with tooth loss
and oral cancer, due to prolonged irritation of the
tissues.
Cancer of the lip is one oral cancer that has
declined over the past few decades, most likely
due to society’s increased awareness of the
damaging effects of prolonged exposure to
sunlight and the increased use of sunscreen
products.
Lowered Immunity
Infections such as syphilis can lead to cancer
over time due to poor healing mouth sores that
are repeatedly irritated. The constant attempt to
heal affected tissue leads to chronic cell division
and a greater chance for cancer to develop.
Lowered immunity from AIDS or transplant antirejection drugs will increase the risk for many
cancers, including those of the aero-digestive
tract (the area from the nose and mouth to the
lungs and stomach).
Oral Hygiene
Each teaspoon of saliva contains about 1 billion
bacteria, which are making waste products that
cling to the teeth in the form of plaque. This
sticky white film can easily be removed with
proper daily brushing and flossing techniques. If
plaque isn’t removed, it will calcify over time and
cause irritation to the teeth and gums. Plaque
itself is not shown to cause oral cancer, but it aids
other irritants like tobacco and alcohol to stick in
the mouth, irritate the tissues, and stimulate the
cells to divide. The more cells that divide, the
more chance one of them will become cancerous.
The common thread of many risk factors is
irritation which can lead to a lot of cell division.
Tumor Formation
Some viruses are suspected in the development
of oral cancer. Viruses can get into the cells of
the oral cavity and change the genes in them to
form a cancer cell. This process is known as
“oncogene activation.” The Human Papilloma
Virus (HPV), particularly the HPV-16 and the
HPV-18 strains, and the Herpes Viruses are now
considered contributors to some oral cancers.
The HPV-16 and the HPV-18 strains are the
causative agents in cervical cancer, accounting
for 70% of all cervical cancers. DNA from
HPV and particular herpes viruses (including
the Epstein-Barr, cytomegalovirus, and herpes
simplex) has been discovered in biopsies from
the oral cavity. Each year, more than 2,370
women and 9,350 men are diagnosed with HPV
associated oropharyngeal cancer. Studies have
shown a dramatic increase of 225% when looking
at cases of HPV associated oropharyngeal
cancer from 1988 to 2004. As with many other
types of oral cancer, oropharyngeal cancer is 2
times more likely in men than women. Genes
encoded within these viruses are involved in the
initiation of the multiple steps needed for a normal
cell to become malignant. Two genes, Rb and
p53 regulate normal cell division. Rb has the
role of separating transcription factors needed for
progression through the cell cycle, preventing the
normal cells from dividing until it has separated
enough transcription factors. Rb is a tumor
suppressor gene that segregates a protein called
E2F. When normal cells are infected with HPV,
Ill fitting dental appliances such as partials and
dentures irritate the gingiva and trap debris.
Continued irritation can lead to lesions and
eventually develop into oral cancer.
Lifestyle
The decision to smoke or drink is certainly a
lifestyle risk factor. Those who do not smoke
or drink alcohol have a lower risk of developing
oral cancer than those who choose to indulge.
Ultraviolet radiation is another lifestyle risk.
Figure 2. Oral Fibroma caused by an ill-fitting denture.
Image courtesy of dentalcare.com
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the E7 gene from HPV binds to Rb, releasing
E2F and other proteins, signaling the start of
the cell cycle. This cycle continues as long as
E7 remains attached to Rb. Uncontrolled cell
division is a sign of malignancy.
function is affected. Early oral cancer symptoms
can be painless, hidden, and not bothersome.
Oral precancer and cancer exhibit a wide range
of clinically detectable alterations that may range
from an early, subtle change in surface texture,
color, or elasticity to a more obvious lesion.
Changes in the oral epithelial cells often present
as white, or red/white patches called leukoplakia
or as velvety, red patches called erythroplakia.
These changes represent cellular alterations that
result from genomic changes within the surface
epithelial cell population, including changes in
DNA content, loss of heterozygosity, and genetic
alterations in a cascade fashion that lead to the
formation of invasive squamous cell carcinoma.
The other gene that HPV attacks is the p53 gene,
responsible for repair of damaged DNA and
apoptosis in the event that repair is impossible.
In malignant cells, p53 is often nonfunctional or
missing entirely. The viral E6 protein binds to
p53 making it nonfunctional. Damaged DNA is
then replicated continually since the nonfunctional
or missing p53 does not initiate apoptosis. E6
protein also activates telomerase, an enzyme that
synthesizes the telomere repeat sequences. The
activation of this enzyme ensures the repeated
cell cycle that continually produces more viral
cells, leading to malignancy.
The most common intraoral sites for squamous
cell cancer are the lateral borders and ventral
surfaces of the tongue, floor of the mouth, and
the oropharynx. Any of the signs and symptoms
that persist for longer than two weeks after
removal of potentially irritating factors and/
or application of therapeutic measures should
be considered a cancer until proven benign by
biopsy and microscopic evaluation.
Scientists have linked a new virus (human herpes
virus-8) with AIDS-related Kaposi's Sarcoma,
another cancer that prefers the head and neck
region. Oral lesions are present in about half of
the Kaposi’s Sarcoma cases, with the hard palate
and the gingival areas being the most commonly
affected areas. This new virus has been found
in all forms of Kaposi’s Sarcoma, insinuating that
it might be involved in sarcoma development. A
direct role has not yet been identified.
One of the greatest dangers of oral cancers,
especially in the early stages, is that it can go
unnoticed. Unfortunately, and all too often,
the earliest symptoms are noticed when body
Other cancers found less frequently in the oral
cavity include carcinomas of salivary gland
origin, lymphomas, melanoma, and bone and
soft tissue sarcomas. Cancers that begin in
other parts of the body may metastasize to or
exhibit manifestations in the oral cavity. The
most common metastases are from tumors in the
lung, breast, colon, and kidney. Manifestations of
leukemia, lymphomas, and multiple myeloma may
also be present within the oral cavity.
Figure 3. Leukoplakia.
Figure 4. Erythroplakia.
Signs and Symptoms
Image courtesy of dentalcare.com
Image courtesy of dentalcare.com
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Table 1. Common Signs of Oral Cancer.
Figure 5. Squamous Cell Carcinoma.
Figure 6. Squamous Cell Carcinoma.
Diagnosis
hidden beneath the tongue. These deviations
are often discovered during a routine head and
neck examination, whether the patient is in for
their recare visit or for some restorative work.
The American Dental Association stresses the
importance of doing routine head and neck
exams and oral cancer evaluations on each
Image courtesy of dentalcare.com
Image courtesy of dentalcare.com
The diagnostic phase of patient management
begins with an assessment of the medical history
and its possible impact and overall management
of any oral disease or condition. Many times
patients are not even aware they have a lesion
or lump in the oral cavity, especially if it is
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and every patient. The screening takes just 90
seconds and can make the difference between life
and death for the individual. Although there is no
definitive set of steps for an oral cancer screening,
there are several areas that should be routinely
checked. Dental practitioners would be wise to
check the following areas: sides and underside
of the tongue, lips and cheek, floor of the mouth,
palate, tonsils, and finally the neck.
Unfortunately, in the recent past, the number of
oral cancers diagnosed at an early stage had not
increased, possibly reflecting the lack of effective
professional and public education. This trend is
beginning to improve as more practitioners are
doing regular screenings and diagnostic aids are
improving. Early detection reduces morbidity and
decreases mortality.
lesion is brushed gently with the OralCDx® brush,
then smeared over a glass microscope slide,
fixed, and then sent to a laboratory that scans the
slide. Results from the lab are usually available
within 24 hours. Should positive results be
returned through this system, the brush biopsy
must be followed by a conventional biopsy
procedure. Recent research has shown that
brush biopsies such as OralCDx® result in a high
number of false positive results. One researcher
reports that of 152 positive results from a brush
biopsy there were only 12 cases that were truly
dysplastic. Scalpel and punch biopsies are
used for highly suspicious lesions, whereas
the OralCDx® is used for lesions of uncertainty.
Early-stage oral cancers mimic many benign
conditions seen more frequently. This is when
the OralCDx® is best used.
Ideally, a pathologist must test any observed
suspicious mucosal abnormality obtained by
using a scalpel, punch biopsy, or brush biopsy for
evaluation. One of the simplest tools for obtaining
a sample of oral epithelial cells is the OralCDx®
Brush. The OralCDx® is a brush biopsy followed
by a computer-assisted analysis. The suspected
Chemoluminescent lights are also available
under the name of ViziLite® and VELscope®.
VELscope® will fluoresce differently when normal
tissues and the suspected tissue is exposed
to certain wavelengths of light. Precancerous
tissues become “excited” under exposure to this
wavelength. ViziLite® first involves washing the
Figure 7. Oral Cancer Screening.
Courtesy of sixstepscreening.org
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Figure 8a. OralCDx® brush biopsy on a patient’s
tongue.
Figure 8b. Specimen obtained from the OralCDx®
brush biopsy is sent to a laboratory for testing.
Copyright© Image Courtesy of OralCDx®
Copyright© Image Courtesy of OralCDx®
Figure 9. Velscope®.
Copyright © Image courtesy of LED Dental Inc.
mouth with acetic acid followed by using blue
phenothiazine dye to mark the lesions. The
wavelength of the illumination is absorbed by
normal tissues and reflected back by abnormal
tissues, making them easier to identify.
Figure 10. Velscope® being used for an oral cancer
screening.
Copyright© Image Courtesy of OralCDx®
Cancer Genetics
Toulidine blue, a selective binding stain on
malignant cells, is a useful supplement to a
clinical examination and biopsy. Use of this stain
is economical, simplistic and noninvasive with
accurate results. Additionally, the use of this stain
can assist in determining the most appropriate
biopsy sites and to surgically delineate margins
or malignant areas. One of the disadvantages of
using this stain includes the risk of obtaining false
negative reactions and the patient is not followed
up adequately, resulting in a tissue biopsy.
Cells of the mouth divide quickly during
development in the womb and throughout
infancy. This rapid division slows down greatly
as an individual ages so that it is just sufficient
to replace cells that are dead or injured. The
division of cells in the mouth and elsewhere is
under very tight control, regulated by genes in
the cells. When this control is lost, the cells
begin to divide in a haphazard way, and grow
to form a swelling of abnormal cells–a tumor. A
benign tumor grows only within its local area,
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Table 2. The oncogenes identified thus far as possible participants in oral cancer include:
not spreading to distant organs. It is not cancer.
A malignant tumor can spread to another area
of the body and it is a cancer. Cancers of the
mouth tend to grow to large sizes locally before
they metastasize, but any cancer can spread at
any time.
works by recognizing damage to a cell’s DNA
and preventing continued cell growth and division
until the damage is repaired. If unable to repair,
p53 causes the cell to experience apoptosis. p53
is also the gatekeeper of genome transcription
and regulator of the angiogenesis inhibitor
thrombospondin-1.
Proto-oncogenes
Scientists now understand that multiple mutations
in specific classes of genes contribute to cancer
of the head and neck. The two classes most fully
characterized to date are proto-oncogenes and
tumor suppressor genes. Proto-oncogenes code
proteins that stimulate cell division. Altered forms
of these genes called oncogenes can cause
stimulatory proteins to be overactive, resulting in
a cell dividing more rapidly than normal.
Appendix A lists the oral cancer genes and
unique genes found in the Cancer Genome
Anatomy Project so far. Appendix B lists the
genes involved in oral cancer genetics that have
been reported in literature to be up-regulated.
Oral cancer results in many chromosomal
changes. Chromosomal changes include
recurrent chromosomal loss of 9, 13, 18, and
4; chromosomal deletions of 3p, 7q, 8p, 11q,
and 17p; and chromosomal breakpoints in the
centromeric regions of 1, 3, 14, and15 on bands
1p22, 11q13, and 19p13. With ongoing research,
more will be learned about the genetics of oral
cancers.
Tumor Suppressor Cells
Tumor suppressor genes code proteins that
inhibit cell division. When these genes mutate,
the corresponding protein is no longer produced
correctly (in form, amount, or at time needed)
and cell division may occur when it should
not. Inactivated tumor suppressor genes that
are suspected in oral cancer include Rb, p16
(MTS1 or CDKN2), E-cadherin, doc-1 and p53.
E-cadherin is responsible for cell-cell adhesion
and differentiation while doc-1 is induced by
TNF-α and results in the inhibition of apoptosis
and is deleted in oral cancer. p53 is already
involved in approximately 60% of all human
cancers.
Cancer Development
The stages of oral cancer development are
similar to the stages of many other cancers.
Once an actual diagnosis has been made, the
degree of development and invasiveness is
also determined. This determination aids in
the treatment planning and prognosis for the
patient. Although it is true that individuals who
are diagnosed with cancer in advanced stages
have a poorer prognosis of both cure and
survival; it does not automatically mean that these
individuals will have a poorer outcome.
p53
There has been much interest in p53 since it
was discovered that the gene can stop tumor
formation when functioning properly. p53 is
located on the short arm of chromosome 17. It
Stages of Development
The following stages are used to describe cancer
of the lip and oral cavity.
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Table 3. Stages of cancer of the lip and oral cavity:
TNM Method of Staging
Another technique of staging oral carcinomas
is referred to as the TNM method. With this
technique, T describes the tumor, N describes
the lymph nodes, and M describes the distant
metastasis.
of adhesion cell molecule, is found to be partly or
entirely missing in malignant cells. Without these
molecules, the tumor is free to detach and travel
to another site. Research has shown that saliva
provides a good environment for metastasis.
Hyaluronic acid, a molecule that binds to surfaces
of the cell, is found in abundance in saliva and
makes it easier for cells to move around, aiding in
the escape from cell adhesion.
Metastasis
Although the spread of oral cancer to regional
neck lymph nodes is common and indicates
an advanced tumor, metastases to other organ
systems below the clavicle are rare. If a tumor
should metastasize below the clavicle, the
lung is the most common site. Metastases
from oral cancers occur primarily through the
lymphatic system, while distant metastases are
hematogenous. The ability of malignant cells to
metastasize varies among patients and depends
on certain cell surface molecules and extracellular
matrix interactions.
Another type of molecule called an integrin
is needed to anchor the normal cell to the
extracellular matrix. Without being anchored,
a normal cell cannot reproduce and will
eventually die. A nuclear protein called
E-CDK2 regulates the cell cycle. Cancer cells
do not need to be anchored to the extracellular
matrix in order to reproduce. The cell cycle
regulator E-CDK2 remains active and allows
for continued proliferation. The exact reason
for this integrin remaining active in malignant
cells is uncertain, although researchers feel that
oncogenes may be a key factor. Once a cancer
cell has detached from both its neighbors and
the extracellular matrix, it must find a way into
the blood or lymphatic system for transport. In
order to enter the bloodstream, the malignant
In order for a tumor to metastasize, the malignant
cells must first break free from adjacent cells
and the extracellular matrix. Cells are normally
held close together with cell-cell adhesion
molecules, allowing for interactions between the
proteins on the cell surface. Cadherins, a type
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Table 4. TNM method of staging.
cell must penetrate the basement membrane of
the epithelial cells by releasing enzymes called
metalloproteinases, which dissolve the basement
membranes and extracellular matrices. Only
certain cells of the malignant tumor are able
to metastasize, and not all cancer cells have
metastatic properties.
cancer treatment is dependent upon the type
and the stage of cancer. It may include surgery,
chemotherapy, radiation, hormones, and/or
immunotherapy. Some cancers respond to a
single mode of treatment, whereas others require
multi-modality treatment strategies.
The ultimate goal of the treatment is to remove
totally or destroy the malignant cells from the
body. Unfortunately, treatments available today
are not able to target only the cancer cells,
and normal healthy cells must sometimes be
destroyed in the process of treating the cancer.
This can result in significant psychological stress
Treatment Options
Treatment for oral cancer is different than other
cancer. It is critical to get prompt diagnosis and
proper treatment for a mouth cancer condition.
It can make the difference between successful
surgery and life and death. The choice for
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and physical morbidity or death. The goals of
multi-disciplinary care are to cure the disease
and prevent and assuage the side effects of
treatment. Treatment does not stop at ridding
the individual of cancer, but goes on to include
the management of side effects of the treatment,
and plan for reconstruction and rehabilitation.
The dental profession plays a major role in the
management of oral complications associated
with cancer therapy and the prevention in some
of the systemic problems that may occur.
clothing, cosmetics, or prostheses. Consequently,
some individuals experience depression,
withdrawal, anger, and/or stigmatization. Surgical
procedures for oral cancer result in long-term
disability. These problems may be short-term if
reconstructive surgery by an oral surgeon and
rehabilitation are possible.
Chemotherapy
Chemotherapy is often used as an adjunct to
another treatment option. Chemotherapy is the
use of certain chemicals to interfere with cancer
cell proliferation, eventually leading to apoptosis.
There are six classes of chemotherapy drugs and
each one affects the cell’s chemistry differently,
depending on location of the cancer and the
stage in which the cells are in the cell cycle.
Choice of treatment for oral cancer is dependent
on the stage of the disease at the time of
diagnosis. A small lesion of less than 1 cm may
only require surgery or radiation therapy. Larger
cancers, especially those that have spread to
the lymph nodes in the neck, generally require
surgery and radiation. Chemotherapy is not a
curative treatment for oral squamous cell cancer,
but it may be used as an adjunct before surgery
or radiation therapy to reduce the size of the
tumor, or as a palliative treatment for recurrent
and advanced tumors.
Depending on the drug chosen, current
chemotherapy will affect malignant cells in one of
three ways:
1. Damage to the DNA of the cancer cells so
they can no longer proliferate. This is done by
altering the DNA structure in the nucleus of the
cell, thus preventing replication.
2. During the S phase of the cell cycle, the
chemo agent inhibits the synthesis of new
DNA strands so that no replication is possible.
This occurs when the drugs block the
formation of nucleotides that are necessary for
new DNA to be produced.
3. Stop the mitotic processes of the cell so
that the cancer cell cannot divide into two
cells. The formation of the mitotic spindles
is necessary to move the original DNA to the
opposite sides of the cell so the cell can divide
into two daughter cells.
Surgery
Surgery is preferred as the main treatment when
oral cancer is not sensitive to radiation therapy,
when lymph nodes, salivary glands, or bone are
involved, or when there is a recurrence of a tumor
in a site that has already received a therapeutic
dose of radiation. The disadvantage of surgery
is the sacrifice of important, functional oral
structures.
Acute physical complications after head and
neck surgery may include any of the following:
airway obstruction, fistula formation, necrosis
in the surgical site, impairment of the senses
(hearing, vision, smell, taste), impairment of
swallowing and speech, and compromised
nutritional status. Long-term complications
include speech impairment, malnutrition from the
inability to swallow foods, drooling, malocclusion,
temporomandibular disorders, facial deformity,
and chronic pain in the shoulder muscles.
The six classes of chemotherapy agents are
alkylating agents, antimetabolites, antitumor
antibiotics, nitrosoureas, vinca alkaloids, and
steroid hormones.
Chemotherapy is an effective way of killing
malignant cells, but in the course of treatment
normal cells are also killed. Once treatment has
been completed, the non-cancerous cells will
return to their normal function or be replaced by
new healthy cells.
There may be consequential psychological
problems associated with surgery because the
results of the treatment are often visible and
can be devastating and humiliating. Physical
impairments cannot be completely disguised by
There are many side effects associated with
chemotherapy that can bring discomfort
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Table 5. Six Classes of Chemotherapy Agents.
and inconvenience. Most side effects are
manageable, and are treatable if they do become
problematic. Some common side effects
include hair loss, mouth sores, gastrointestinal
problems (nausea, constipation, diarrhea, loss
of appetite), low blood cell counts, sore throat,
rashes, fatigue and infertility (temporary and
permanent). One very important side effect is the
effect chemotherapy has on bone marrow and the
maturing red and white blood cells and platelets
found there. The strong drug agents affect the
quickly dividing marrow cells in the same way
as the malignant cells. Decreased output of
healthy red blood cells can lead to anemia, while
a decreased output of white blood cells and
platelets can lead to a compromised immune
system and clotting and healing ability.
IMRT Radiation
IMRT is a state of the art cancer treatment
that delivers high doses of radiation directly
to the cancer cells in a precise, targeted way,
while sparing more of the surrounding healthy
tissue. This has important advantages in oral
cancer as it allows the beam to hit the target
area while missing the surrounding structures
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such as the salivary glands and sinuses. IMRT
uses computer-generated images for planning
and then delivers a tightly focused beam to
the cancerous tumor. Clinicians “paint” the
tumor with the radiation beam, which conforms
closely to the shape of the tumor. IMRT can be
used to treat tumors that in the past have been
considered untreatable given their close proximity
to critical organs and structures. A powerful
computer program optimizes a treatment plan
based on tumor size, shape, location, and dose
requirements from the physician. A medical
linear accelerator, equipped with a special device
called a multi-leaf collimator that shapes the
radiation beam, delivers the radiation according
to instructions. The equipment can be rotated
to access the tumor from the most favorable
vantage point. IMRT is currently being used to
treat other tumors of the head and neck, brain,
liver, lung, pancreas, prostate, and uterus.
area, xerostomia, infection, radiation-induced
caries, trismus, alteration of taste, possible hair
loss, and fatigue.
Osteoradionecrosis is a condition that affects bone
healing and can occur in individuals who receive
high doses of radiation during cancer therapy.
This can occur after dental surgery or extraction
of teeth. High doses of radiation can decrease
the bone’s blood supply, resulting in the decrease
of oxygen to the area and eventual necrosis of
bone tissue. The mandible is the most often
affected area. Symptoms of osteoradionecrosis
may occur months to years after radiation therapy
with common symptoms including mouth pain,
swelling of the jaw and trismus. Treatment
of osteoradionecrosis can vary from antibiotic
therapy, local debridement, and in more severe
cases removal of affected bone.
Prognosis
Prognosis is highly variable and dependant upon
the stage and the location of the disease when
first diagnosed. The more advanced stages will
result in a lower survival rate. The survival rates
for carcinomas of the base of the tongue (distal to
the circumvallate papillae) are very low compared
with those carcinomas on the oral portion of the
tongue. The American Cancer Society reported in
2013 that the 5-year survival rate for stage I cancer
of the lip is 96% whereas the 5-year survival rate
for stage I cancer of the oropharynx and tonsil is
only 56%. The public often does not comprehend
the severity of oral cancer, perhaps because it
associates diseases in the mouth with dental care
that is not life threatening.
Radiation Therapy
Radiation therapy, also known as radiotherapy,
is used in treating localized solid tumors,
such as those in the head and neck. Before
starting treatment, a CAT scan is done and
measurements and markings are made on it in
preparation of treating the tumor. A porous mesh
mask is made for the patient to immobilize the
head during treatment, and to prevent irradiation
of healthy areas. The total dose of radiation is
prescribed by a radiation oncologist and broken
down into smaller doses to be given over a period
of days. Most patients tolerate these smaller
doses without an adverse effect on the maximum
benefit. The treatment course is usually 2-8
weeks, allowing for normal tissues to repair after
each exposure and minimizing permanent injury.
Research is being conducted to increase the
effectiveness of current techniques.
Research
Ongoing research is being done in several areas
of oral cancer at many university hospitals, medical
centers and other institutions nationwide. Each
year more is learned about the deadly disease.
Current research is being done in the areas of
DNA changes, gene therapy, new chemotherapy
agents and radiotherapy methods, tumor growth
factors, and vaccines.
Recent radiotherapy research has focused on the
use of radiolabeled antibodies to deliver doses of
radiation directly to the cancer site. Some tumor
cells contain specific antigens that trigger the
body’s immune system so that it produces tumor
specific antibodies. Benefits of this approach
include minimizing the risk to healthy tissues.
Safe, but effective dosages and identification of
appropriate radioactive substances are still being
worked out. Side effects of radiation therapy
include irritation of the tissue in the treatment
Research in DNA Changes
Work is being done with the p53 gene and Human
Papilloma Virus (HPV) DNA. Tests are being
formed to detect p53 alterations, allowing for early
detection of oral and oropharyngeal tumors. Tests
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are also being conducted for detection of HPV
DNA in cells for earlier diagnosis of other forms of
cancer.
vaccine, but less effective in individuals who had
already been exposed. This vaccine is not used
in treating existing HPV infections, genital warts,
precancers or cancers.
Gene Therapy
Research in reversing DNA changes in oral
cancer as a treatment is being conducted.
Clinical trials involving p53 and its replacement
with a normal gene to restore normal function
to the cells currently are being conducted.
Gene therapies to disrupt HPV replication also
are being developed. Another type of therapy
involves new genes being added to cancer genes
to make them more susceptible to a particular
type of drug in treating the particular type of
cancer.
Dental Considerations for the
Diagnosed Patient
It can be challenging caring for a patient who
is undergoing cancer treatments or will be
in the near future. Patient education is an
essential part of the pretreatment assessment
and should include a discussion of possible oral
complications.
Tumor Growth Factors
New drugs that recognize cells with too many
Epithelial Growth Factors receptors are now
being tested in clinical trials. These drugs also
may boost the patient’s immune system.
Prior to Treatment
A thorough exam of the hard and soft tissues:
• Reduces the risk and severity of oral
complications.
• Allows for immediate identification and
treatment of existing infections and other
problems.
• Increases the probability that the patient will
successfully complete the prescribed course of
treatment.
• Reduces the likelihood of oral pain.
• Minimizes oral infections that could lead to
potentially fatal systemic infections.
• Minimizes complications that compromise
nutrition.
• Preserves or improves oral health by
improving the quality of life and decreasing the
cost of care in the future.
• Establishes a baseline for comparison post
treatment.
Vaccines
Vaccines are being investigated as a way to
treat cancer patients by helping to boost their
immune systems to recognize and attack cancer
cells. Vaccines against the Human Papilloma
Virus (HPV) have been developed. The vaccine,
Gardasil®, is made up of proteins from the
outer coat of the virus and does not contain
any infectious material. Gardasil® protects
against four types of HPV, attributing to 75% of
the cervical cancer cases and 90% of genital
warts. This vaccine, recently approved for use
in females and males aged 9-26 years, is given
through a series of three shots over a period of
six-months. Studies have found Gardasil® to be
almost 100% effective in preventing diseases
caused by the four types of HPV covered by the
The following measures should also be taken into
consideration:
• Identify and treat existing infections, carious
lesions and other compromised teeth.
• Stabilize or eliminate potential sites of
infection.
• In adults, extract teeth that may pose a future
problem or are non-restorable to prevent later
extraction-induced osteonecrosis.
• In children, consider extracting highly mobile
primary teeth and teeth that are expected to
exfoliate during the course of treatment.
• Perform oral surgery at least 2 weeks before
any radiation therapy begins.
• Oral surgery should be performed at least
7 to 10 days before the patient receives
myelosuppressive chemotherapy.
New Chemotherapy and Radiotherapy
Methods
New drugs are being developed that are
more effective against advanced oral cancer.
Intraarterial chemotherapy (injection of drugs into
the arteries feeding the cancer) is being tested
in conjunction with radiation therapy. Advances
in intralesional chemotherapy are being made.
New methods are also being developed in
radiotherapy that will reduce side effects and
tissue/organ destruction.
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Supplemental Fluoride
Supplemental fluoride is often prescribed during
cancer treatment as a fluoride gel delivered via
custom trays. Fluoride rinses are not adequate
to prevent demineralization. Several days prior
to the start of radiation therapy, a daily regime
of a 5-minute application using 1.1% neutral pH
sodium fluoride gel or 0.4% stannous fluoride
should be started. Whether stannous or sodium
fluoride is used, the patient should always use
unflavored fluoride. Flavored fluorides can be
irritating to already inflamed and possibly painful
oral tissues. For patients with porcelain crowns,
composite, or glass ionomer restorations, a
neutral pH fluoride should be used to prevent
damage to the restorations. When using a tray
to deliver the fluoride application, the following
instructions should be given to the patient:
• Remove orthodontic bands and brackets if
highly stomatoxic chemotherapy is planned or
if the appliances will be in the radiation field.
• Prescribe an individualized oral hygiene
regime to minimize oral complications.
• Patients undergoing head and neck radiation
therapy should be instructed in the use of
supplemental fluoride.
• If a removable prosthetic appliance is worn,
make sure it is well adapted to the tissues
and that the patient is able to wear and clean
it daily. Instruct the patient to leave the
appliance out at night.
After Treatment
Continued patient education is needed during and
after cancer treatment. Instruction in adequate
nutrition and avoiding alcohol and tobacco can
prevent or decrease oral complications. Detailed
instructions should be provided for the patient on
specific oral health care practices such as how
and when to brush and floss, how to recognize
signs of oral complications, and other instructions
appropriate for the individual. Instructions may
include:
• Place a thin ribbon of fluoride in each tray.
• Place the trays on the teeth and leave in place
for 5 minutes. If the gel overflows the tray, too
much is being used and the amount should be
reduced.
• After 5 minutes, remove the trays and spit out
any excess gel. Do not rinse.
• Do not eat or drink for 30 minutes.
• Clean the trays with a toothbrush and allow
to air dry. Trays can be cleaned weekly in
a denture cleaner following manufacturer’s
instructions.
• Brush teeth, gums, and tongue gently with an
extra-soft toothbrush and fluoride toothpaste
after every meal and before bed. Bristles may
be softened on the brush with warm water
• Floss teeth gently every day; It is
recommended that if gums are sore or
bleeding, to avoid those areas and floss the
other teeth.
• Avoid alcohol-containing mouth rinses, spicy
or acidic foods, toothpicks, tobacco products
and alcoholic beverages.
• Avoid candy, gum, and soda unless they are
sugar-free.
• Rinse the mouth with a baking soda-salt
solution followed by a plain water rinse several
times a day (Use 1/4 teaspoon of baking soda
and 1/8 teaspoon of salt in 8 ounces of warm
water).
• Exercise the jaw muscles three times a day to
prevent and treat jaw stiffness; Open as far as
possible without causing pain and close the
mouth; repeat 20 times.
• Follow instructions for using fluoride gel.
• Keep all appointments recommended by the
dentist.
For those patients reluctant to use a fluoride tray,
a high-potency fluoride gel should be brushed on
the teeth following daily brushing and flossing.
Either 1.1% neutral pH sodium or 0.4% stannous
Figure 11. Fluoride Tray and Toothbrush.
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patients who have undergone blood/platelet
transfusion therapies and marrow transplantation.
Patients who have completed radiation therapy to
the head and neck and whose oral complications
have decreased should be evaluates every 4 to 8
weeks for the first six months. Time intervals can
be changed depending upon the patient’s dental
needs. It is, however, important to remember that
oral complications may continue or appear long
after radiation therapy has ended.
Conclusion
Figure 12. Supplemental Fluoride - Toothbrush
Application.
Continued research is needed in the fight against
all cancers. Basic research has already paid
off in many ways. Researchers know which
specific classes of genes are involved in cancer
development, that environmental factors can
trigger genetic mutations and that cancer cells
can become out of control and proliferate without
restraint. The general populace needs further
education about changing lifestyle factors.
Quitting all forms of tobacco use, stopping
excessive use of alcohol, making sure dental
appliances fit appropriately, and eating a diet
rich in fruits and vegetables are all things people
can do now to reduce their risk of developing the
disease. Medical and dental professionals can
save more lives by consistently performing simple
head and neck exams on all patients, and by
discussing with them the early warning signs of
oral cancer.
fluoride gel is recommended, based on the type
of dental restorations present in the mouth.
When using the brush-on method of application
the following instructions should be given to the
patient:
• After brushing with fluoride toothpaste, rinse
as usual.
• Place a thin ribbon of fluoride gel on the
toothbrush.
• Brush for 2 to 3 minutes by the clock.
• Spit out any excess gel at the end of the timed
period. Do not rinse.
• Do not eat or drink for 30 minutes.
• Rinse toothbrush well and allow to air dry.
Patients with radiation-induced salivary gland
dysfunction must continue lifelong daily fluoride
application to help preserve the dentition.
Head and neck exams should become the
standard protocol for each new patient entering
a practice, as well as for patients returning for
routine care. The importance of a tobacco-free
lifestyle should be addressed with patients who
use. Various modalities should be incorporated
into their care, whether it is prescribing a nicotine
patch or a referral to a tobacco cessation clinic at
a dental school or medical center.
Once all complications of chemotherapy
have been resolved, patients may be able to
resume their normal dental care schedules.
However, if the patient’s immunity continues
to be compromised, the patient’s hematologic
status needs to be determined before any
dental treatment or surgery is initiated. This
is particularly important to remember for those
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Appendix A.
Appendix B.
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Course Test Preview
To receive Continuing Education credit for this course, you must complete the online test. Please go to:
www.dentalcare.com/en-US/dental-education/continuing-education/ce72/ce72-test.aspx
1.
One of the most common intraoral sites for squamous cell carcinoma is the ______________.
2.
The diagnostic phase of patient management begins with an assessment of the ___________.
3.
If oral cancer is detected early, the cure rate can be as high as ________.
4.
The ____________ is the factor that determines the type of cancer.
5.
Oral Cancer is dangerous because it has a __________ chance of producing __________
tumors.
a.lip
b. dorsal surface of the tongue
c.vestibule
d.oropharynx
a.
b.
c.
d.
patient’s chief complaint
medical history
physician’s recommendations
dentist’s findings
a.96%
b.82%
c.75%
d.58%
a.location
b.origin
c.cell-type
d.tissue-type
a.
b.
c.
d.
low / primary
low / secondary
high / primary
high / secondary
6.
____________ recognizes damage to the cell’s DNA.
7.
Oral cancer affects men ________ times as often as women.
8.
A benign tumor can ____________ and is ____________.
a. TNF-α
b.p53
c.E-cadherin
d.Rb
a.six
b.four
c.two
d.three
a.
b.
c.
d.
spread / not cancerous
not spread / not cancerous
spread / cancerous
not spread / cancerous
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9.
The choice for cancer treatment is dependent upon the type and ___________ of the cancer.
a.location
b.movement
c.prognosis
d.stage
10. Plant alkaloids work by _______________.
a.
b.
c.
d.
binding to steroids
interrupting the DNA
preventing RNA synthesis
preventing cell division
11. Squamous cell carcinoma accounts for ______ percent of all __________ oral malignancies.
a.
b.
c.
d.
50
50
90
90
/
/
/
/
primary
secondary
primary
secondary
12. The disadvantage of ____________ is the sacrifice of important functional oral structures.
a.chemotherapy
b. IMRT Therapy
c. radiation therapy
d.surgery
13. A malignant tumor can ____________ and is ____________.
a.
b.
c.
d.
spread / not cancerous
not spread / not cancerous
spread / cancerous
not spread / cancerous
14. _______________, a class of chemotherapy agents can be used in treating melanomas by
crossing the blood-brain barrier.
a.
b.
c.
d.
Antitumor antibiotics
Nitrosoureas agents
Plant alkaloids
Steroid hormones
15. ____________ is considered the gatekeeper of the genome.
a.E-cadherin
b. p- 53
c.HPV
d. TNF-α
16. Tumor suppressor cells code ____________ that ____________ cell division.
a.
b.
c.
d.
enzymes / activate
enzymes / inhibit
proteins / activate
proteins / inhibit
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17. _______________, a class of chemotherapy agents can be useful in treating leukemia.
a.Nitrosoureas
b.Antimetabolites
c. Antitumor antibiotics
d. Steroid hormones
18. _______________ is often used as an adjunct to another treatment option.
a.Chemotherapy
b. IMRT therapy
c. Radiation therapy
d.Surgery
19. The number one risk factor in oral cancer is _______________.
a.alcohol
b.tobacco
c.age
d. poor diet
20. Alkylating agents work by _______________.
a.
b.
c.
d.
blocking cell growth
invading the DNA
preventing RNA synthesis
preventing cell division
21. One advantage of IMRT radiation therapy is _______________.
a.
b.
c.
d.
small targeted area
low dose of radiation
large targeted area
high dose of radiation
22. Side effects of radiation therapy include _______________.
a.energy
b. caries-free dentition
c.xerostomia
d. increased immunity
23. Oral cancer occurs ________ times as often in Africans Americans than Caucasians.
a.six
b.four
c.two
d.three
24. Antimetabolites work by _______________.
a.
b.
c.
d.
interrupting DNA
interrupting RNA
blocking transmission
allowing transmission
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25. For patients with resin restorations or porcelain crowns, a ____________ fluoride should be
prescribed.
a.
b.
c.
d.
0.4%
0.4%
1.1%
1.1%
neutral pH
stannous
neutral pH
stannous
26. The OralCDx® Brush Biopsy can help diagnose __________ oral cancer.
a.Early-stage
b.Mid-stage
c.End-stage
d. all stages of
27. Tray fluoride should be left on for __________ minutes.
a. 2 to 3
b.4
c.5
d.30
28. There are __________ classes of chemotherapy agents available.
a.three
b.four
c.six
d.eight
29. Chemotherapy is a curative treatment for oral squamous cell carcinoma.
a.False
b.True
c. Depends on tumor location.
d. Depends on tumor size.
30. __________ malignant oral cancers may mimic benign conditions.
a.
b.
c.
d.
Stage
Stage
Stage
Stage
4
3
2
1
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References
1. Alfano MC, Horowitz AM. Professional and community efforts to prevent morbidity and mortality
from oral cancer. J Am Dent Assoc. 2001 Nov;132 Suppl:24S-29S.
2. American Association Oral Maxillofacial Surgeons. Head, Neck and Oral Cancer. 2007.
3. American Cancer Society. Cancer Facts & Figures 2013.
4. American Dental Assistants Association. Early detection of oral cancer with brush biopsy. The
Dental Assistant Journal, May- June, 2001.
5. ADA Council on Scientific Affairs. Statement on human papillomavirus and squamous cell cancers
of the oropharynx. 2013.
6. Bhoopathi V, Kabani S, Mascarenhas AK. Low positive predictive value of the oral brush biopsy in
detecting dysplastic oral lesions. Cancer. 2009 Mar 1;115(5):1036-1040.
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Crest + Oral-B at dentalcare.com Continuing Education Course, Revised July 16, 2014
About the Author
Natalie Kaweckyj, LDARF, CDA, CDPMA, COA, COMSA, CPFDA, CRFDA, MADAA, BA
Natalie currently resides in Minneapolis, MN, where she is the Clinic Coordinator
and Compliance Analyst for a nonprofit pediatric dental clinic. She is a Licensed
Dental Assistant in Restorative Functions (LDARF), Certified Dental Assistant (CDA),
Certified Dental Practice Management Administrator (CDPMA), Certified Orthodontic
Assistant (COA), Certified Oral & Maxillofacial Surgery Assistant (COMSA), Certified
Preventive Functions Dental Assistant (CPFDA), and a Master of the American Dental
Assistants Association. She holds several expanded function certificates, including
the administration of nitrous oxide/oxygen analgesia. Ms. Kaweckyj graduated from the American
Dental Association-accredited dental assisting program at ConCorde Career Institute and has received
a Bachelor of Arts in Biology and Psychology from Metropolitan State University. She is currently
writing her dissertation for her master’s in Public Health. She has worked clinically, administratively and
academically. Ms. Kaweckyj is currently serving as on several ADAA Councils after having served on the
ADAA Board of Trustees 2002–2012. She served as ADAA President in 2010-2011. She is the current
Business Secretary and legislative chairman for the Minnesota Dental Assistants Association (MnDAA)
and a three time past president of MnDAA. She also is a Past President of the Minnesota Educators of
Dental Assistants (MEDA) and still an active member. In addition to her association duties, Natalie is very
involved with the Minnesota state board of dentistry as well as with state legislature in the expansion of
the dental assisting profession. She is a freelance writer and lecturer and is always working on some
project. She has authored many other courses for the ADAA.
Email: [email protected]
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Crest + Oral-B at dentalcare.com Continuing Education Course, Revised July 16, 2014