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Oral cancer
Dr. Hani Al Sheikh Radhi
2016
Oncogenesis (Carcinogenesis): Progression from normal (healthy) cell to premalignant or
potentially malignant cell.
The process involves series of genetic steps; abnormal function of molecules regulating cell signaling,
growth, survival, angiogenesis and cell cycle control, over expression of oncogene and shutting down
of tumor suppressor genes.
Malignant transformation is a complicated process to be understood you must learn a few terms first.
 Dysplasia: Term used in pathology to refer to abnormalities of cell development. Increase
number of immature cells and decrease the number of mature cells [include: cells of unequal
size, abnormal shaped cells, hyper-chromatism (condition where part of the cell especially cell
nuclei stain more intensely than normal), increased number of cells which are currently
dividing]. According to the severity of the previously mentioned features dysplasia can be
classified into mild, moderate, and severe.
 Carcinoma in situ: The cells lost maturation and almost all the malignant changes occurred
(the tissue lost the original identity) but the cells are still contained within the basement
membrane; when these cells start the invasion beyond the basement membrane and start
invading the adjacent tissue it will change into invasive carcinoma.
 Apoptosis: programmed cell death.
 Angiogenesis: Growth of new blood vessels from pre-existing vessels. This mechanism will
provide nutrition for the growing mass.
 Metastases: Spread of tumor cells into different parts of the body. It is the process which is
often the most life threatening in cancer.
 Mutation: Changing the structure of a gene which cause an alteration in the genetic map of
the cell; which can lead to cancer.
 Oncology is the study and the science of new growths.
 Neoplasm refers to any new disease form of tissue growth.
 Cancer is the overall name applied to malignant growths.
Cancer development is a process of mutation within the cellular DNA influenced by many risk
factors.
What is cancer? Normal growth controlled by a fine balance between growth promoting and
growth inhibition, this mechanism is controlled by specific signals. When the body requires
new cell division (for example in wound healing) it will direct these signals in the specific
region, which required growth to stimulate or to initiate the cells to proliferate.
Oral cancer
Dr. Hani Al Sheikh Radhi
2016
In tumor this mechanism is defected and there will be
Continuous cell proliferation; tumor cell will initiate its own proliferating signals independently
from the body control.
The cell is no longer differentiated (it will be different from the surrounding original tissue),
and
There will be shut down of the programmed cell death mechanism (apoptosis).
Cancer arises from a single cell, [the whole tumor originate from one cell].
“Cancer is an abnormal growth of cells caused by multiple changes in gene
expression leading to a dysregulated balance of cell proliferation and cell death and
ultimately evolving into a population of cells that can invade tissues and
metastasize to distant sites, causing significant morbidity and, if untreated, death of
the host”
Features of malignant tumors: cells no longer depend on body control.
1- Normal cells will grow in mono-layer while cancer cells are able to grow into multi-layers
over and below each other).
2- Cancer cells are less adherent than normal cells.
3- Normal cells stop proliferation when they reach a certain size (mass) while tumor cells
keep proliferating.
Common related oral premalignant lesions
If a cancer can be detected early, before it has acquired all of the mutations necessary for invasion and
metastasis it may be possible to successfully treat the disease locally. It has been observed that certain
oral lesions, specifically leukoplakias and erythroleukoplakias, have the potential for malignant
transformation.
“Not all oral squamous cell carcinoma are preceded by leukoplakias, not all leukoplakias progress to
oral cancer”
1Leukoplakia: according to the WHO (World Health Organization) leukoplakia is defined as
“white patch or plaque that cannot be characterized clinically or pathologically as any other disease”.
It is diagnosed by exclusion [before the clinician inform the patient that he/she has leukoplakia he
must exclude other causes such as frictional keratosis, candidiasis, leukoedema, lichen palnus].
Malignant transformation rate of oral leukoplakia range between 3-6%. Floor of the mouth is the
highest risk site [leukoplakia discovered in this site usually demonstrate severe dysplasia, carcinoma in
situ, or invasive carcinoma]. Other high risk sites with leukoplakia are the tongue and lips.
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the clinical presentation can be associated with how serious the leukoplakia. Main clinical
presentations include:
Thin homogenous leukoplakia
Thick leukoplakia
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Verrucous Leukoplakia: papillary exophytic projections.
Speckled Leukoplakia: Mixed Red and white lesion.
The risk from high to low, speckled, verrucous, thick and the least serious thin leukoplakia [that
doesn’t mean thin leukoplakia cannot be sinister].
Speckled Leukoplakia ; this is
the worst type of leukoplakia
which is speckled and the worst
site which is floor of the mouth
Thick leukoplakia extending
from the lateral borders of the
tongue to the floor of the
mouth,
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Dr. Hani Al Sheikh Radhi
Thin Homogenous Leukoplakia,
consider the least sinister type
of leukoplakia
Verrucous Leukoplakia, in this
case it was diagnosed as
invasive carcinoma.
Management of Leukoplakia
Exclude any other conditions.
Establish Leukoplakia.
Identify the degree of dysplasia or malignancy by doing a biopsy and histopathological examination.
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Dr. Hani Al Sheikh Radhi
2016
The management will depend on the degree of dysplasia, the site, and the clinical appearance.
Lesions exhibit carcinoma in situ or early invasive carcinoma must be excised with normal margins
to allow better histopathological investigation.
Lesions with low to moderate dysplasia in high risk sites (floor of the mouth, tongue) and lesions
with severe dysplasia at low risk sites are the most debatable. Shall we excise with margin? Or just
excise the lesion by itself? That answer will depend on the surgeon’s clinical decision, by estimating
how serious the condition and according to the surgeon experience.
Treatment options
Surgical excision, cryosurgery, CO2 Laser, systemic and local application of vitamins and other
medications.
Surgical Excision: Traditional method Recurrence rate 15-30%, usually recurrence noted adjacent to
the excised lesions, especially at high risk sites. One of the problems includes inability to excise
widespread or diffuse lesions without causing morbidity and esthetic problems.
Cryosurgery: destroy and remove soft tissue by therapeutic freezing. Liquid nitrogen is the most
commonly used material in cryosurgery. Main disadvantages are lack of depth control [we cannot
know how much we can remove from the tissue], the other problem will that cryosurgery will
destroy the tissue so we cannot have a proper biopsy to detect the lesion, Nowadays replaced by
CO2 laser.
CO2 Laser: Can be used either to evaporate the entire lesion [not recommended because we will
not have enough tissue for examination], the other is to excise the lesion and it can provide tissue
sample. CO2 laser has the advantage of obtaining biopsy (specimen) with less morbidity than scalpel
technique and provide adequate hemostasis especially when we excise large lesions. Healing is
better with CO2 laser than scalpel. The only drawback of CO2 laser is that the specimen margins
may be cauterized and therefor lateral spread of dysplasia or malignancy cannot be assessed.
Nonsurgical Therapies: Vitamin A, Retinoid, Vitamin E, and Bleomycin (glycopeptide antibiotic,
destroy DNA used in treatment of Hodgkin’s lymphoma, squamous cell carcinoma.
2Erythroplakia: a premalignant considered uncommon compared leukoplakia.
 Appears mainly on soft palate, buccal mucosa, and floor of the mouth.
 WHO definition “ the term erythroplakia is used analogously to leukoplakia to designate lesions of
the oral mucosa that present as red areas and cannot diagnosed as any other definable lesion”.
 Almost all erythroplakias demonstrate epithelial dysplasia, carcinoma in situ, invasive carcinoma.
 Erythroplakia is diagnosed by exclusion and biopsy, conditions that may resemble eythroplakia
can include candidal infections, histoplasmosis, TB, lichen planus, systemic lupus erythromatosis,
pemphigus, pemphigoid, hemangioma, Kaposi sarcoma….etc.
 Oral squamous mucosal lesions appear red why? Due to atrophy of the mucosa and dilation of
sub-epithelial capillaries.
 Erythroplakia can appear smooth, granular, and nodular, with well-defined margins.
 Erythroplakia has the highest risk of malignant transformation compared to all other premalignant
and potentially malignant oral mucosal lesions.
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Dr. Hani Al Sheikh Radhi
2016
Management
Because of the high incidence of significant epithelial dysplasia, carcinoma in situ or early
invasive carcinoma at the time of diagnosis. Surgical intervention is necessary, complete
excision of the lesion with clear margins down to the submucosal level. This will provide good
specimen for investigation and decrease risk of recurrence.
General management protocol for suspected
premalignant conditions
(1) Eliminate risk factors- tobacco,alcohol
(2) Clinical photographic records.
(3) Base line haematology- full blood count,serum ferritin, B12, folate
(4) Candidal swab
(5) Incisional biopsy and dysplasia characterization.
(6) Careful clinical follow-up and consider repeat biopsy for mild dysplasias
(7) Laser excision for moderate/severe dysplasias.
(8) Long-term clinical follow up
(9) Monitor oral mucosa for field changes.
Cancer Risk Factors
Cancer is a multifactorial condition. DNA mutation occurs spontaneously, especially
via damage by oxidation or free radicals. The rate of DNA mutation increases by
various cancer risk factors.
Life style Factors: Tobacco, Alcohol, and Betel quid chewing (it is a combination of certain plants that
used in India). This risk factor is usually age related (i.e. people age 50 and more), because the effect is
accumulative depending on how long the patient had been exposed to the previous factors. Younger
age groups are being more involved nowadays may be due to associating of other factors. [viruses
such as Human Pailloma Virus & Epistin Barr Virus can induce early malignancy]. Tobacco generates
carcinogen [cancer causing chemicals], such as TSNAs (Tobacco specific nitrosamines) they destroy
anti-oxidant enzymes. Alcohol carcinogenesis process: alcohol metabolized by certain enzymes into
“Acetaldehyde” which is a carcinogen.
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2016
Tobacco and alcohol have synergistic effect (each one increase the carcinogenesis properties of the
other).
Virus Infection:
Human papilloma virus (HPV): More than 100 types of human papilloma virus are known. HPV-16 &
HPV-18 have been the most common types associated with oral cancer. It is less associated with
alcohol and smoking but more related to marijuana and oral sex. Generally they have better prognosis
than cancer associated with smoking and alcohol.
Herpes virus: Herpes simplex virus nucleic acid had been extracted from oral cancer, and herpes
simplex associated cancer is usually associated with smoking.
Dietary Factors: Eating fruits and vegetables is believed to reduce the risk of oral cancer. Studies have
shown that Mediterranean (Especially Greece and Italy) diet particularly associated with reduced
cancer risk. The main components of their diet [fresh fruits and vegetables, reduced red meat, white
meat and fish being a major component, increased consumption of unprocessed olive oil, and
increased consumption of dietary fibers]. The whole idea of diet is to increase the anti-oxidants level
within the body, to decrease the oxidation risk of DNA.
Social and Economic status: Deprived people from low socio-economic class is associated with
increased risk of oral cancer. That can be due to the bad living environment, stressful life; they have
much bad lifestyle factors, and a bad diet.
Environment: Ionizing radiation from natural or therapeutic sources or nuclear accident (such as
Chernobyl accident or Iraq war) may contribute to oral cancer.
Occupation: Workers in leather and metal producing factories without taking the proper precautions
can be a risk.
Genetic Factors: Inheritance of oral cancer specifically and Cancer generally extremely low and may
contribute to no more than 1-3% of cancer.
Anatomical Knowledge in Cervical lymph nodes
Cervical Lymph Node Levels: Before we start discussing how to manage oral cancer you need
to have a knowledge about the lymph nodes that drain the oral cavity; lymphatic drainage through
lymph nodes within the neck considered the main route of metastases.
The lymphatic system of the neck is divided into three systems:
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Waldeyer’s internal ring. This ring includes the adenoids, the tubal and lingual tonsils, the
palatine tonsils and aggregates of the lymphoid tissue on the posterior pharyngeal wall. Tumors
from this area have a high tendency for lymphatic spread.
Waldeyer’s external ring. This set of nodes mainly drains the superficial tissues of the head and
neck. In the head, the nodes are mainly located around the skull base and are the occipital, postauricular, parotid and buccal nodes. In the neck, the main nodes completing the Waldeyer’s
external ring are the superficial cervical, submandibular, submental and anterior cervical nodes.
These nodes drain tissues from the scalp, eyelids, face, nasal sinuses and oral cavity.
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The deep lymph node system. This consists of the upper, middle and lower cervical nodal groups
that are situated along the internal jugular vein, the spinal accessory group that accompanies the
XI nerve in the posterior triangle, and the nodes in the midline of the neck.
Neck is divided into six surgical levels based on anatomical structure area. The head and neck area
drains into more than 300 nodes within the neck. Understanding levels will help clinicians to tailor
the proper treatment plan.
Level I: Include submental and submandibular lymph nodes.
Level II: Upper jugular lymph nodes surrounding jugular vein and adjacent spinal accessory nerve.
Level III: Middle jugular lymph nodes surrounding internal jugular vein.
Level IV: Lower jugular lymph nodes.
Level V: All the nodes in the posterior triangle, posterior to the sternocleidomastoid muscle.
Level VI: Anterior triangle includes pretracheal, paratracheal, prelaryngeal lymph nodes.
These are the surgical Levels of the Neck, Notice that
almost each level is subdivided into A & B, to cover
precisely the anatomical relation of the nodes with their
source of drainage.
These are the anatomical triangles of the
neck, which can be less helpful during
surgery.
Physical Examination of Oral Squamous cell
carcinoma
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Complete evaluation of the head and neck.
Thorough examination of the oral cavity. Size, appearance, texture, colour, fixation to bone and
adjacent structures.
Inspection and palpation of all mucosal surfaces.
Cranial nerves examination [specifically V, VII, X, XI, and XII].
o Explore tongue mobility for hypoglossal nerve.
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Dr. Hani Al Sheikh Radhi
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o Facial nerve and spinal accessory must be evaluated because these structures can be involved
by Oral Squamous Cell Carcinoma.
Area of erythroplakia, leukoplakia, ulcerations, and masses especially fixed or firm masses.
Palpation of the neck is critical because of the cervical nodal metastases is the single most reliable
prognostic factor in patients with Oral SCC. Check number, size, and site of the involved lymph
nodes.
Early stage oral cancer usually involves level I, II, and III. In patient with cervical metastases at the
time of the diagnosis 5 year survival rate is reduced by 50%. Cervical node metastases are noted in
about 30% of patients who have Oral SCC.
Presence of trismus can indicate pterygomaxillary space involvement. Decreased mobility of the
tongue can be a sign of involvement of tongue deep muscles.
Perineural invasion [tumor invades nerves and sometimes metastases occur through nerve fibers]
can occur in 27-53% of patients with Oral SCC. Evaluated by checking sensation of the cheeks, lips,
chin, palate, and alveolar gingivae.
Accurate measurements of primary lesion before biopsy is very important because that will help the
surgeon to determine the T stage: tumor size (will be discussed later), other important factor
edema post biopsy can alter the true size of the tumor.
Complete evaluation of all anatomical locations within the oral cavity must be performed by visual
examination and palpation to detect any mucosal abnormalities.
Examination of the oral cavity: remove all dental appliances, use of dental mirror for indirect
evaluation of nasopharynx and hypopharynx. Bimanual palpation to assess any involvement of
structures such as deep muscles of the tongue, floor of the mouth, buccal mucosa, salivary
structures, or bony mandibular structures. Assessment of the lateral tongue done by anterior and
lateral traction of the tongue with cotton gauze.
Radiographic Examination and Evaluation
Evaluation of deep tissue involvement and the presence of positive cervical lymphadenopathy will
require several imaging modalities to assess the depth of involvement, spread, and estimate the
CLINICAL Margins.
Plain Radiograph:
 OPG (ORTHOPANTOMOGRAM): To establish jaw bone or teeth involvement.
 Chest x-ray: Screening for bronchial caner or metastatic lung cancer.
 Occipitomental View (OM): Assess maxillary sinus or orbital involvement.
 Occlusal and periapical view: Augment the OPG for better screening
Plain films are not useful for routine screening because they fail to show early
cortical involvement.
CT scan: CT scans alone or usually with intravenous contrast (iodine based) are the most common
imaging modality. CT scan is very good in demonstrating hard tissue structures; however, MRI is a
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Dr. Hani Al Sheikh Radhi
2016
better investigation modality for soft tissue involvement. MRI: Superior in defining soft tissue
details. Ultrasound: Ultrasound has limited success in the evaluation of oral cancer, but it can easily
evaluate neck masses and nodal involvement. Ultrasound has the advantage of being available and
inexpensive made it a good diagnostic tool for examining tneck involvement before obtaining more
advanced imaging of the neck.
PET Scan (Positron emission tomography): It is a form of nuclear medicine that has been used to
differentiate between malignant disease recurrent tumor and to identify nodal metastasis. FDGPET: [FDG (Fluro-Deoxy Glucose)] is the most commonly used form of PET scans, depends on the
difference of metabolism of this type of glucose between normal and malignant tissue. [Malignant
tissue and cells uptake (consume) of FDG is much greater than normal cells] the PET will examine
the areas within the body that will show higher uptake rate, which will suggest tumor. The main
draw backs of PET that it is expensive and it doesn’t shows anatomical landmarks; so new machines
developed which correlate CT scans with PET scan, the CT will give the anatomical landmarks while
the PET will examine the area for tumor involvement, the new machine had been named CT/FDGPET.
Diagnostic Methods
A variety of approaches have been used to obtain diagnostic tissue samples of suspicious oral
lesions, and several are discussed in this lecture.
Despite the growing number of adjuncts available to assist in the clinical evaluation of lesions with
uncertain biologic potential, surgical biopsy remains by far the most popular means of obtaining a
final tissue diagnosis.
Punch Biopsy: A punch biopsy is a soft tissue sampling instrument having a circular cutting
edge of varying diameter. It is most frequently used by dermatologists to sample skin lesions
but can be used on mucosal surfaces as well. For study purposes, an advantage of the punch
instrument is its ability to provide reproducibly sized epithelial samples of lesion or control
tissues.
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2016
Punch biopsy technique, rarely
used in oral cavity, it can be
used when we want to have
multiple biopsies within the
same size especially for
researches and studies.
Scalpel Biopsy (Gold standard): is the most commonly and most successful used method. We have
two types either Excisional (remove the whole lesion) or Incisional (remove part of the lesion).
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Excisional biopsy is most often reserved for clinically benign or, at worst, precancerous
mucosal lesions that are less than 2 cm in diameter.
Most suspicious lesions of the oral cavity are diagnosed through an incisional biopsy, where
a portion of the abnormal surface tissue is removed for histopathologic interpretation.
The desirable and undesirable
biopsies. The desirable although
narrow but it is deep, containing part
of the normal tissue.
The upper incision is excisional biopsy including
the whole lesion within the biopsy, while below
notice that we removed only part of the lesion
with large part of the clinically normal tissue.
Fine Needle Aspiration (FNA): Fine-needle aspiration (FNA) cytology is a valuable tool in the
diagnosis of superficial masses of the head and neck region. Rarely helpful for oral cavity squamous
cell carcinoma, it is best used for lesions with cystic cavities which allow aspiration of fluids and cells
for cytology diagnosis.
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Diagnostic Adjuncts
Cytology: Oral exfoliative cytology (remove superficial layer of cells) has been an adjunct to oral
diagnosis. It has been primarily used to provide rapid and inexpensive identification of superficial
infectious agents, such as fungi. It showed to be inefficient method in the diagnosis of malignant
and pre-malignant lesions as we mentioned to obtain proper diagnosis, we need good amount of
tissue, including normal tissue. Brush Biopsy (Brush Cytology): investigating persistent oral
epithelial lesions not considered suspicious for carcinoma.
Toluidine Blue: dye designed to stain acidic cellular components, such as DNA and RNA. Its use in
the detection of precancerous/cancerous tissue is based on the fact that dysplastic tissue contains
quantitatively more DNA and RNA than non-dysplastic tissue. TB staining may provide better
demarcation of lesion margins, guide biopsy site selection, and is thought to be valuable in
identification and visualization of lesions in high-risk patients. Drawbacks; the main drawback that it
can give misdiagnosis in inflammation, hyperactive, and bengin hyperplasia.
Optical Detection of oral cancer: optical technologies provide information on the physiologic
condition of the tissue at a molecular level. Early research in optical diagnostics suggested
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Dr. Hani Al Sheikh Radhi
that alterations in light-tissue interactions can be used to differentiate normal from
malignant tissue.
Oral Cancer Prognostic Factors & Treatment
Options
TNM staging: Staging method based on tumor size (T), Nodal status (N), and Metastases (M).
Developed in 1950, and it is only applied to carcinoma. The TNM staging system is applied to
various carcinomas each TNM has different evaluation of each anatomical site.
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Purpose of TNM staging
Aid clinician in planning of treatment.
Give some indication about prognosis.
Assist in evaluation of treatment results.
Facilitate the exchange of information between clinicians.
The components of TNM usually assessed by physical examination and imaging techniques to
delineate each of its components.
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Invasion of adjacent structures (Ex: T4a Invasion of larynx, intrinsic muscles of the tongue, medial
pterygoid plate, hard palate, or mandible.)
Histologic grading, tumor staging, and clinical behavior
1- Tumor size and staging: T refers to the primary lesion and is graded on greatest dimension and
presence of adjacent tissue infiltration. N refers to regional lymph node involvement and is graded
on the presence of nodes, greatest dimension, and side of involvement in relation to the primary
tumor. M grades distant metastasis and is based simply on its presence (M1) or absence (M0).
2- tumor volume: can be done easily depending on CT and MRI scans, but the role of these
measurements in prognosis requires further studying because sometimes we have small
volume tumor but with aggressive biological behavior which may be related to bad
prognosis, on the other hand we may have large exophytic growth, well differentiated which
may shows good prognosis. Tumor thickness can be more helpful than diameter, however,
until now defining tumor thickness between clinicians and pathologist is not established yet
[some commented on tumor thickness post-surgery resected specimen, some depended on
the maximum point of measurements, while others believe that the invasion front is more
relevant to calculate tumor depth].
3- Tumor behavior: tumor behavior can vary even within the same type of malignancy and
especially with squamous cell carcinoma the behavior can vary.
- Age of the patient: the younger the patient more agrressive tumor.
- Gender: males are prone to more aggressive tumors.
- Race: Africans and some tribes may have more aggressive tumors
- Degree of differentiation: the less differentiated cells the more aggressive tumor.
- Vascular and Perineural Invasion: Both parameters have been noted to be signs of
aggressive tumor behavior. Those parameters can alter treatment options
significantly especially for T1/T2 tumors, because when vascular and perinueral
invasion present the prognosis will be very poor.
4- site of the tumor: Tongue tumors used to have the worst prognosis, but nowadays the outcomes
are improving after the introduction of elective neck dissection [removal of lymph nodes in patients
with N0].
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Buccal sites now considered to have the worst prognosis. They usually have more aggressive biology
with tendency for local recurrence, and that is exacerbated by involvement of stensons’s duct or
muscular invasion.
5- Surgical Margins: Determining the surgical margin is a challenging procedure; the surgeon must
cut into about 1.5 cm of healthy tissue during surgery to reduce the risk of recurrence and ensure
removal of the clinical tumor. Unclear margin on histopathological examination post-resection
considered as a poor prognostic sign and one of the criteria for post – operative radiotherapy.
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Frozen Section Biopsy: is intra-operation biopsy. The surgeon will cut until he/she feels
that they reach clear margin surgically, the biopsy will be sent for examination during the
surgery to ensure that margins are not only clear surgically but histopathologically as
well.
Ablative Surgical Treatment for Malignant Tumors of the
Oral Cavity
Key Points
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Most common malignant tumors of the oral cavity are Squamous Cell Carcinoma (SCC).
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Treatments of oral cancer are multidisciplinary and consider the need for adjunctive therapy,
reconstruction, and rehabilitation of the patient in addition to ablative surgery.
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Surgical management of lesions inside the oral cavity is affected by the size and the location
of the tumor.
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Three dimensional excision with cuff of normal tissue at the peripheral and deep margins of
the specimen.
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Bone resection for invasion of the mandibular bone can be performed either by rim
resection or by segmental resection. Rim resection is recommended when the depth of soft tissue
invasion from pre-op scanning is less than 5mm. Segmental resection is necessary if extensive
invasion of soft tissue is close to the mandible or within the mandible itself.
A: Rim resection (marginal)
mandibulectomy. B: Segmental
Mandibulectomy.
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Surgical management of the neck varies according to the tumor stage. Treatment of N0 tumors
is controversial. “WAIT-AND –SEE” strategy is more accepted in T1 tumor (depending on the
site usually) than in large lesions. Thick T2 N0 of the tongue usually warrants the use of
elective neck dissection (selective neck dissection).
Neck Management
We mentioned before that neck and nodal involvement can be the most important prognostic
factor during the management of head and neck cancer.
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30-40% of patients presented with OSCC usually have nodal involvement.
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Occult metastasis: Undetectable infiltration of tumor cells into the nodal lymphatic system.
That cannot be diagnosed by our available conventional modalities. That opened the way for what
is called N0-STAGE management by “elective neck dissection”.
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Sentinel lymph node biopsy (SLN biopsy): It is a procedure developed in surgical oncology.
The concept is based on the fact that the efferent lymphatic channels draining the primary tumor
lead directly to the first (sentinel) lymph node in a regional chain. The sentinel lymph node is the
most likely to include metastatic disease. When patient present with OSCC without any clinical
involvement of lymph nodes the surgeon may decide to obtain (SLNB), by removing only the first
most suspicious lymph node for histopathological assessment; if the result were negative (the
node is not infiltrated with cancerous cells) this may suggest that the rest of the chain is clear and
further surgery is indicated. Problems with SLNB, skipping of lymph nodes, lymphatics anatomy is
not predictable.
Lymph nodes drainage in
relation to oral sites
Different functional anatomy of
lymphatic drainage from
different oral sites; notice the
complicated pattern of
drainage which made it difficult
to predict the exact pathway of
drainage.
Neck Dissection
Classification of Neck Dissection
1- Radical Neck Dissection (RND): Include removal of all ipsilateral (on the same side of the tumor)
cervical lymph nodes extending from the inferior borders of the mandible, to the clavicles including
levels I – V. Including the removal of three important non-lymphatic structures: the internal jugular
vein (IJV), Sternocleidomastoid SCM, and the spinal accessory nerve (SAN).
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2- Modified Radical Neck Dissection (MRND): Refers to removal of the same lymph nodes
level I-V as the radical neck dissection but with preservation of (SAN), or (IJV), or (SCM).
According to the preserved non-lymphatic structures (MRND) can be further subdivided into
three types:
TYPE I: Preserve the spinal accessory nerve (SAN)
TYPE II: Preserve the (SAN) and the Sternocleidomastoid Muscle (SCM)
Type III: Preserve the (SAN), (SCM), and the internal Jugular vein (IJV) with removal of only
lymph nodes from level I-V.
3- Selective Neck Dissection (SND): Refers to the preservation of one or more lymph nodes group
normally removed in (RND). The majority of oral cancer will primarly involve nodes from level I-III.
SND used with oral cancer is named SND(I-III)[i.e. Selective neck dissection from level I to level III:
previously known as supra-omohyoid selective neck dissection]. Nowadays it is recommended to
include level IV when the cancer involves the tongue because about 16% of tongue tumors may skip
into level IV, so SND (I-IV).
4- Extended Neck Dissection: Refers to removal of additional lymph node groups, or additional nonlymphatic structure or both, that is not normally included within the RND (for example; medistinal
nodes or non-lymphatic structure such as carotid artery or hypoglossal nerve).
In the presence of metastases in level (I) through (III) the risk of disease in level (IV) increases from
3% to 17% but the risk of level (V) involvement remains less than 3%, so it is logical to dissect only
level (I) through (III) in oral cancer with clinically N0 neck and level (I) through (IV) if there is a
clinically evident nodal disease in level (I) through (III).
Radiotherapy post- surgery is recommended when neck stage is N2 or above, or when extracapsular
spread (ECS) is present.
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2016
SND not recommended in the presence of large lymph node, and SND is contraindicated when we
have nodal fixation or large ECS and history of surgery and radiotherapy.
The incidence of occult
metastases in N0 neck,
according to the distribution of
the major nodal groups within
the neck
Access Surgery for Oral Cancer
Maxillary Approaches
1- Weber-Fergusson Maxillectomy Incision
2- Mid-face degloving.
3- Posterior maxillary approach (Weber-Fergusson + Lip splitting Mandibulotomy)
Mandibular Approaches
1- Transoral approach.
2- Lip Splitting Mandibulotomy
3- Pull through (transcervical approach)
Radiation
Cell death can be divided into two general types: 1- Reproductive cell death; which results from
damage to the cellular genetic materials. 2- Apoptosis; programmed cell death. Radiation can
cause either type and also slows cellular division.
Aims of Radiotherapy
Oral cancer
Dr. Hani Al Sheikh Radhi
2016
Radical Radiotherapy: It is radiotherapy given at high doses with curative intent. The dose
will be the highest delivered without functional consequences. That means avoiding catastrophic
squeal (such as blindness) and limiting the incidence of major complications (such as
osteoradionecrosis) to low levels, commonly around 5% or less, and limiting other conditions as
far as possible (such as dryness of the mouth and problems with swallowing). For most epithelial
tumors, higher doses result in better rate of local control but higher doses also create greater
morbidity.
Palliative Radiotherapy: control of symptoms in situations which canecr is incurable or the
patient is not fit enough to withstand the intensity of radical treatment. The dose given is
balanced between the need to control symptoms and reduce morbidity.
Tissue tolerance to Radiotherapy
Mucositis: develops about 3 weeks after the start of radiotherapy, the intensity of this condition
depends on the total dose of radiotherapy delivered. Patient usually unable to eat or swallow,
Mucositis heals within about 2-4 weeks of completing radiotherapy. The principles of
pathophysiology of mucositis, production of free-radicals caused by chemo or radiotherapy which
damage cell DNA.
Dry mouth (xerostomia): the effect of radiotherapy on salivary function may be appearnt within
the 1st week of treatment, as treatment continues saliva become stickier leading to difficulties in
swallowing and it is a common cause of nausea because of the collection of the sticky secretions in
the oropharynx and hypopharynx. In practice it is difficult to shield the parotid and submandibular
gland with conventional radiotherapy.
Skin: Erythema normally develops in the 3rd week of the treatment. Healing take place 7-10 days
post treatment.
Osteoradionecrosis: (ORN) is a debilitating late complication of radiation therapy. ORN is a
chronic side effect that develops slowly and tends not to heal spontaneously. Biologically the
process is characterized by inadequate repair and repopulation and by a reduction in the vascular
potential of the tissues. This hypovascularity with attendant hypoxia reduce cellular activity.
Treatment of osteoradionecrosis relies on a combination of conservative measures (antibiotics,
Oral cancer
Dr. Hani Al Sheikh Radhi
2016
debridement, and irrigation) and surgical resection (sequestrectomy, marginal mandibulectomy,
or segmental mandibulectomy with or without reconstruction) formation and wound healing.
Using hyperbaric oxygen (HBO) chamber may be helpful. Theory that osteoradionecrosis is a result
of hypoxia, hypocellularity, and hypovascularity, HBO seems like an attractive option. It increases
oxygen supply in hypoxic tissue, stimulating fibroblast proliferation and angiogenesis.