Malignant neoplasms of the oral cavity

Malignant Neoplasms of the Oral Cavity
Dr. Firas Kassab Page 1
Malignant
Neoplasms of
the Oral
Cavity
Dr. Firas Kassab

The oral cavity extends from the cutaneous vermilion junction of the lips to the
junction of the hard and soft palate above and to the line of the circumvallate
papillae below.
INCIDENCE
In 2010, there were an estimated 23,880 new cases of oral cavity cancer, leading to
5470 deaths.
BIOLOGIC CHARACTERISTICS
The natural history of oral cavity carcinoma depends on its anatomic site, histologic
type, and stage of the tumor.
STAGING EVALUATION
A physical examination should be performed to determine the location and extent of
the primary tumor and to assess for the possible presence and extent of nodal
involvement.
Computed tomography (CT) scanning will help to determine the extent of the tumor
(particularly, deep invasion), detect bone invasion (CT scanning plus panoramic x-
ray film [Panorex] view), and assess regional lymph nodes. For retromolar trigone
lesions, magnetic resonance imaging (MRI) is useful to assess muscle invasion and
chest radiograph will help to detect pulmonary metastases. The routine use of
positron emission tomography (PET) is not recommended.

PRIMARY THERAPY
For early disease (T1 to early T2 lesions), single-modality surgery or radiotherapy
can achieve excellent local control and survival rates in most oral cavity sites (85%
to 90%). The treatment choice is predicated on function and treatment side effects.
Moderately advanced (large T2 to early T3) lesions are more often treated with
radiotherapy alone or surgery plus irradiation. Moderate rates of local control (60%
to 80%) can be achieved.
LOCALLY ADVANCED DISEASE
For locally advanced disease (large T3 or T4 lesions), combined radiation plus
surgery is indicated in most sites because single-modality disease control is poor
(≤30%). Radiation alone or combined with concomitant chemotherapy likely results
in a lower probability of cure.
For locally recurrent cancers seen after the primary tumor has been treated with
surgery alone, salvage with surgery is appropriate, followed by postoperative
radiotherapy, radiation with or without chemotherapy, or palliative irradiation.
Locally recurrent cancers that occur after definitive irradiation alone or combined
with chemotherapy can be managed with surgical salvage, palliative chemotherapy,
or supportive care.
PALLIATION
Moderate-dose palliative irradiation can be given as 30 Gy in 10 fractions over 2
weeks or 20 Gy in 2 fractions with a 1-week interfraction interval.
The oral cavity consists of the lips, floor of the mouth, oral tongue (the anterior two-
thirds of the tongue), buccal mucosa, upper and lower gingiva, hard palate, and
retromolar trigone. ( Table ) shows the frequency of involvement of various
locations.2
After a general discussion of etiology and epidemiology, issues relative to
the various subsites will be presented separately. A discussion of preradiotherapy
and postradiotherapy dental care is included.
Distribution of Oral Cavity Cancer

Site Percentage
Lower lip 38
Tongue 22
Floor of mouth 17
Gingiva 6
Palate 6
Retromolar trigone 5
Upper lip 4
Buccal mucosa 2
Etiology and Epidemiology
Oral cavity cancer is predominately a disease of middle-aged men who use tobacco
and alcohol. Approximately 95% of carcinomas appear after age 45 years, with an
average age of 60 years. The use of tobacco in any form is associated with an
increased risk of oral cancer. Some evidence suggests that patients with oral cavity
cancer who continue to smoke during radiation therapy have poorer outcomes. The
risk of tobacco-related cancers of the upper aerodigestive tracts declines among
former smokers after 5 years, and after 10 years of abstention the risk may
approach that of nonsmokers. Although the effects of alcohol and tobacco in
inducing cancers of the upper aerodigestive tract seem to be additive, the risk of
alcohol consumption without tobacco use is unclear. Some studies indicate a slightly
increased risk with alcohol use in the absence of tobacco, whereas others show no
apparent increased risk.
Human papillomavirus (HPV) infection, marijuana smoking, betel quid use, and
drinking the beverage “mate” have also been implicated as causative factors in the
formation of squamous cell carcinomas of the upper aerodigestive tract. In recent

years, oral cancers have increased among relatively young females who have never
consumed alcohol or smoked. The reason for this is unclear.
Smokeless tobacco (snuff) can promote carcinomas of the buccal gingival sulcus,
which are diagnosed most often in older Caucasian women living in the southeastern
United States. Carcinoma of the buccal mucosa is also associated with chewing
tobacco. It is commonly seen in the southeastern United States, with a male to
female ratio of 3 or 4 to 1. Leukoplakia is seen with oral carcinoma in approximately
15% of cases.
Persons with a “Scotch-Irish” complexion (red hair and blue eyes) and/or prolonged
exposure to sunlight are most susceptible to lip carcinoma. In one series, 82% were
previous or present tobacco smokers. Pipe smoking is an alleged risk factor, but this
has not been substantiated by most studies. Lip cancer is often associated with poor
dental hygiene or edentulous patients. Lip trauma and a history of alcohol abuse are
also related factors. Most cases appear after age 40 years, but approximately 10%
occur before age 40 years and a few before age 30 years. This disease is uncommon
in blacks.
Oral Care
A complete dental examination should be performed on all patients, whether dentate
or edentulous, before irradiating any portion of the mandible or maxilla. The
radiation oncologist should inform the patient’s dentist of the anticipated radiation
treatment plan, including dose and location of the radiotherapy (RT) fields. To make
appropriate pretherapy recommendations, the dentist should be familiar with
possible postradiotherapy complications, such as caries and osteoradionecrosis.
There is a lifelong risk of impaired healing that can lead to osteoradionecrosis,
especially when teeth are extracted from hypovascularized and hypocellular bone.
Therefore, one objective of the pretherapy oral evaluation is to determine whether
teeth in the proposed irradiated area can be reasonably maintained in a healthy
state for the remainder of the patient’s life.

Medical, dental, and psychosocial issues that affect a person’s future dental health
should be assessed at the pretherapy evaluation. The patient’s compliance,
motivation for daily oral hygiene procedures, dental awareness, and access to dental
care are predictors of dental health. A panoramic radiograph, intraoral radiographs,
and hard and soft tissue examinations should be performed to identify high-risk
dental factors such as deep caries, nonrestorable teeth, root tips, bony pathology,
endodontically treated teeth, periapical and pulpal pathology, and nonfunctional
teeth. Teeth exhibiting periodontal disease should be evaluated to determine their
long-term prognosis. Some prognostic factors for poor periodontal health include
probing depths more than 6 mm, gingival recession, furcation involvement, and
mobility. Because of the numerous reported cases of progression of gingival
recession and periodontal disease after RT, it may be difficult to assess the longevity
of each tooth.
To reduce the future risk of osteoradionecrosis, teeth with high-risk dental factors
should be removed before the patient receives doses of more than 55 Gy. Whether
extraction of teeth with moderate disease is indicated remains controversial. If the
patient has poor resistance to dental disease or an unwillingness to perform routine
dental care or fluoride applications, pretherapy extraction of moderately diseased
teeth may be justified. A healing time of 14 to 21 days is recommended after
extraction, before initiating radiation therapy. Extraction should be accomplished as
atraumatically as possible, with alveoloplasty to remove sharp, bony projections. The
dentist should coordinate dental appointments with the radiation oncologist to
minimize the delay in cancer therapy. However, extraction of healthy teeth does not
reduce the risk of osteoradionecrosis and should be avoided.
Denture adjustments, smoothing edges of sharp teeth, dental cleaning, and oral
hygiene instruction can be accomplished at the pretherapy dental visit. Ill-fitting
dentures that irritate mucosal surfaces should be worn with caution during
radiotherapy. Daily disinfection of dental prostheses is recommended.
Impressions for custom fluoride trays can be made before or within the first 2 weeks
of radiation therapy. Patients who receive radiotherapy to major salivary glands are
at lifelong risk for rampant caries. Daily use of 0.4% stannous fluoride or 1.1%

sodium fluoride gel for 5 minutes, in custom trays, is imperative as long as natural
teeth remain. Patients should be advised to refrain from rinsing, eating, or drinking
for 30 minutes after fluoride application. The dentist and radiation oncologist should
consistently promote proper oral hygiene and use of fluoride throughout the
posttreatment years.
Clinical practice guidelines for the treatment of cancer therapy-induced oral
mucositis have been published. Radiation–induced mucositis cannot be prevented;
however, excellent oral hygiene can reduce the risk of oral infections. Supersoft
toothbrushes and mild toothpastes are available for patients to facilitate proper oral
hygiene during and after RT.
Consultation with the radiation oncologist is required before postirradiation
extraction of teeth or invasive procedures that involve the exposure of irradiated
bone. Preextraction and postextraction hyperbaric oxygen therapy may be indicated
to promote healing of extraction or surgical sites.
Patients should be closely monitored for possible late effects of radiotherapy to
oropharyngeal regions. Trismus, xerostomia, caries, and oral candidiasis can persist
or occur at any time after treatment is completed.
first-echelon nodes in the oral cavity
Two or three submental nodes lie on the mylohyoid muscle in the submental
triangle. This triangle is bounded by the anterior bellies of the digastric muscles and
the hyoid bone.
Six or more submandibular nodes lie on the anterior surface of the submandibular
gland or between the gland and the lower jaw adjacent to the facial artery.
The nodes on the surface of the gland are preglandular nodes; those adjacent to the
facial artery are facial nodes.
They extend upward along the course of the facial artery and are subdivided into
prevascular and retrovascular nodes, depending on their relationship to the facial
artery. With the exception of one or two at the lower border of the jaw, the facial
nodes are small and inconstant.

Lymphatics of the oral cavity
Upper deep jugular nodes located along the upper internal jugular vein, between
the levels of the digastric and omohyoid muscles.
Malignancies of the lips and anterior floor of the mouth as well as adjacent
gingiva and buccal mucosa tend to metastasize to submandibular lymph nodes
first.
Tumors situated more posteriorly in the oral cavity usually metastasize initially to
the upper deep jugular lymph nodes.
As multiple cervical nodes become involved with metastatic disease, spread to
the middle and lower deep jugular nodes occur.

Lips
The lips begin at the
junction of the vermilion
border with the skin and
form the anterior
boundary of the oral
vestibule.
The lip includes only the
vermilion surface, or that
portion of the lip that comes into contact with the opposing lip.
Numerous anastomoses from the lymphatic vessels of the two lip halves are
present near the midline and account for bilateral metastases from tumors that
are close to or cross the midline.
The upper-lip lymphatics drain to preauricular, infraparotid, submandibular, and
submental lymph nodes.
In contrast to the lower lip, only a few of the upper-lip cutaneous lymph trunks
drain to contralateral nodes. No crossing of the midline has been documented for
the mucosal lymphatics of the upper lip.
Pathology and Patterns of Spread
The most common neoplasms are moderately to well differentiated squamouscell

carcinomas; approximately 5% are poorly differentiated.26 Basal cell carcinomas
usually arise on the skin above or below the lip and invade the vermilion border,
but rarely arise from the vermilion border. Squamous cell carcinomas start on the
vermilion of the lower lip, and less commonly on the upper lip. The commissure
is rarely the site of origin. Leukoplakia is a common problem on the lower lip and
may precede carcinoma by many years.
Early lesions can initially invade adjacent skin and the orbicularis oris muscle.
Advanced lesions can invade the adjacent commissures of the lip and buccal
mucosa, the skin and wet mucosa of the lip, the adjacent mandible, and
eventually the mental nerve. The incidence of perineural invasion is
approximately 2%. Lymph node involvement at presentation occurs in
approximately 5% to 10% of patients. An additional 5% to 10% of patients with
a clinically negative neck subsequently develop lymph node metastases. The risk
of lymph node involvement increases with depth of invasion, poor differentiation,
larger lesions, invasion of the commissure, and recurrence after prior treatment.
Hendricks and colleagues28 from the Mayo Clinic reported the following incidence
of positive cervical lymph nodes by T stage: T1, 2%; T2, 9%; and T3, 30%. The
overall incidence of adenopathy was 19% when the commissure was involved.
Clinical Manifestations and Staging
Carcinoma of the lip usually presents as a slowly enlarging exophytic lesion with
an elevated border. Occasionally, there is minor bleeding. Erythema of the
adjacent skin may suggest dermal lymphatic invasion. Anesthesia or paresthesia
of the skin indicates perineural invasion.
The American Joint Committee on Cancer (AJCC) staging for lip cancer applies to
lesions arising from the vermilion surface
Oral Cavity Primary Tumor Staging
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor

Tis Carcinoma in situ
T1 Tumor 2 cm or less in greatest dimension
T2 Tumor more than 2 cm but not more than 4 cm in greatest dimension
T3 Tumor more than 4 cm in greatest dimension
T4 (lip) Tumor invades through cortical bone, inferior alveolar nerve, floor of
mouth, or skin of face (i.e., chin or nose)
T4 (oral cavity) Tumor invades through cortical bone into deep (extrinsic)
muscle of tongue (genioglossus, hyoglossus, palatoglossus, and styloglossus
muscles), maxillary sinus, or skin of face
T4b Tumor involves masticator space, pterygoid plate, or skull base and/or
encases internal carotid artery
Early lip cancers rarely require diagnostic imaging. Locally advanced, deeply
infiltrating, or recurrent carcinomas may benefit from a computed tomography
(CT) scan or panoramic x-ray film to evaluate possible bony invasion and regional
nodal spread.
Treatment
Early Lesions (<2 cm)
The majority of these lesions can be surgically excised with primary closure as an
outpatient procedure. Surgery is satisfactory if the lip commissure does not need
to be resected and if the resulting aperture of the oral cavity permits the
insertion of dentures. Postoperative irradiation is recommended for positive
margins or perineural invasion.
Tumors that should be treated with radiotherapy include those involving a
commissure in order to obtain better cosmesis and improved local control. The
uncommon, poorly differentiated lesions are also preferably treated by irradiation
to cover a more generous treatment volume and the first-echelon lymph nodes.
An algorithm for treatment planning is shown in

Moderately Advanced Lesions (2 to 4 cm)
The length of the lower lip is approximately 7 cm. Removal of more than half of
the lower lip with simple closure produces a poor cosmetic and functional result
so that a reconstructive procedure is usually necessary. In these cases,
irradiation has the advantage of a better functional and cosmetic result.
Traditionally, the reconstructed lip may look normal in a photograph but may lack
sensory and motor innervation as well as elasticity. However, there have been
recent improvements in the functional and cosmetic results of various
reconstructive surgical procedures.
Locally Advanced Lesions (> 4 cm)
Large lesions are managed by resection and postoperative irradiation. Erythema
of the skin adjacent to the lesion may indicate dermal lymphatic involvement;
wide-field irradiation is recommended followed by consideration of surgical
resection depending on the response to radiation therapy. Management by

definitive radiotherapy and concomitant chemotherapy is generally preferred in
patients who are not surgical candidates.
T4 Lesions
Cancers that present with bone or nerve involvement are usually treated with a
combination of surgery and EBRT. There are limited data pertaining to the local
control rates after RT or surgery alone, ranging from 0% to 74% ; therefore,
combined treatment is usually recommended.
The postoperative EBRT portals should include the primary site as well as the
regional lymphatics (levels IA, IB, and II). The low neck is usually treated to
doses sufficient for subclinical disease, and doses are frequently higher in
patients with positive nodes. The total dose ranges from 60 to 70 Gy, at 2 Gy per
once-daily fraction to the primary site, depending on the pathologic findings.
Higher doses with altered fractionation schemes (e.g., 74.4 Gy at 1.2 Gy per
fraction twice daily), as well as concomitant chemotherapy, should be considered
in patients with positive margins or other high-risk factors such as extracapsular
extension
Irradiation Techniques
EBRT is usually delivered with either orthovoltage x-rays or electron beam. The
electron beam energy depends on the tumor thickness. Lead shields are placed
behind the lip to limit the dose to the oral cavity and mandible. Orthovoltage
fractionation schedules range from 40 to 45 Gy in 3 to 4 weeks for smaller
lesions, and 50 to 55 Gy in 4 to 6 weeks for moderately advanced lesions. The
dose is increased 10% to 15% for electron beam RT to account for differences in
the relative biological effectiveness. Orthovoltage x-rays are preferred, if
available, because the maximum dose is at the surface and there is less beam
constriction compared with electron beam.

An appositional field with a margin of 1 to 1.5 cm is sufficient for most small to
moderately advanced lesions if orthovoltage irradiation is used. The field borders
are determined by bimanual palpation. Because of beam constriction, 2- to 2.5-
cm margins are necessary if an electron beam is employed. A lead shield is used
to collimate the beam at the skin/lip surface.
Brachytherapy may be used as the sole treatment or in conjunction with EBRT.
Implantation is usually performed under local anesthesia using Ir sources and a
single-plane plastic tube technique. The sources are arranged horizontally 10 to
12 mm apart with crossing sources on the lateral aspects of the implant. Three to
five horizontal sources are used depending on the size of the lesion. The
advantage of the plastic tube technique is that the volume of the implant is more
easily adapted to the extent of the tumor and the commissure is readily included,
if necessary. Alternatively, cesium needles mounted in a nylon bar may be
employed .
The sources are spaced 1 cm apart and the dose is specified 0.5 cm from the
plane of the implant. A gauze roll is placed between the lip and gum to increase
the distance between the radioactive sources and the alveolar ridge. The
recommended dose is 60 to 70 Gy at a dose rate of 0.4 to 0.5 Gy per hour for an
implant alone. Large infiltrative lesions may be first treated with EBRT, 30 Gy at
2.5 Gy per fraction to shrink the tumor, followed by an interstitial brachytherapy

boost to deliver an additional 35 to 40 Gy. Treatment of lip cancer with high-
dose-rate interstitial needles is advocated by some.
T3 and T4 Tumors
Low-volume T3 cancers may be treated with primary irradiation, preferably
combining EBRT to the primary lesion and neck followed by a brachytherapy boost.
EBRT is administered with parallel opposed fields, including the lip lesion and the
level I and II lymph nodes .
A cork is placed in the mouth to displace the maxilla and upper lip and reduce the
volume of normal tissue included in the fields. A separate anterior field is used to
treat the level III and IV lymph nodes with a tapered midline block over the larynx.
The supraclavicular lymph nodes are at low risk and are not included in the fields.
Both sides of the neck are treated with irradiation because it is unlikely that T3 and
T4 primary lesions would be well lateralized.

The junction between the parallel opposed fields and the low-neck field is at the
thyroid notch. The dose fractionation schedule used varies from 38.4 Gy at 1.6 Gy
twice daily to 50 Gy at 2 Gy per fraction once daily, followed by a brachytherapy
boost. Low-energy photons such as 4-MV or 6-MV beams are recommended.
High-volume T3 and T4 cancers are unlikely to be cured with RT alone and are
better treated with surgery and postoperative irradiation. EBRT fields are similar to
those used to treat patients with irradiation alone. A petroleum jelly gauze bolus is
placed over incisions to ensure that the surface dose is adequate. The fields are
extended to the skull base along the course of the third division of the fifth cranial
nerve if perineural invasion is present. The dose depends on the surgical margins:
negative (R0), 60 Gy; microscopically positive (R1), 66 Gy; and gross residual
disease (R2), 70 Gy. Patients are treated once daily at 2 Gy per fraction, 5 days a
week, in a continuous course.
Complications
After RT, there is gradual atrophy of the irradiated tissues. The irradiated lip must be
protected from sun exposure by use of hats and ultraviolet protectants. Because the
anterior teeth and gingiva are protected by lead shields when radiation is given by
EBRT, radiation caries, bone exposure, and osteoradionecrosis are uncommon.
Floor of the mouth
The floor of the mouth is a crescent-shaped region of mucosa overlying the
mylohyoid and hyoglossus muscles, extending from the inner aspect of the lower
alveolar ridge to the underside of the anterior two thirds of the tongue.
Posteriorly, the floor of the mouth is continuous with the base of the anterior
tonsillar pillar, and anteriorly the frenulum of the tongue divides it into two sides.
On either side of the frenulum is the sublingual caruncle, marking the orifices of the
submandibular duct.

Posterolaterally from the orifices is a rounded ridge called the sublingual fold, which
overlies the upper border of the sublingual salivary glands.
The paired mylohyoid muscles constitute a muscular diaphragm and provide the
structural support of the anterior floor of the mouth.
They arise from the mylohyoid lines of the mandible and insert into the hyoid bone.
Their borders unite in the midline as a median raphe that extends from the
symphysis of the mandible to the hyoid bone
The hyoglossus muscle partly supports the extreme posterior floor of the mouth;
it is a flat, quadrilateral muscle extending upward into the tongue from the body and
greater horn of the hyoid, partly above and partly behind the mylohyoid muscle.
An important point of surgical anatomy is that the lingual nerve, submandibular
duct, sublingual gland, and twelfth cranial (hypoglossal) nerve lie lateral to the
hyoglossus muscle, whereas the lingual artery runs deep (medial) to it.
Medially, the space between the mylohyoid muscle and the mucosa of the floor of
the mouth contains the three extrinsic muscles of the tongue: the hyoglossus,
genioglossus, and the styloglossus.
Laterally, this space contains the sublingual gland, the submandibular gland duct,
the lingual nerve, and branches of the lingual artery.
The lingual artery and vein supply the floor of the mouth.
The artery arises from the external carotid and enters the oral cavity deep to the
hyoglossus muscle.
After giving rise to the dorsal lingual artery, which supplies the base of the tongue,
the lingual artery terminates in the sublingual and deep lingual arteries, which
supply the floor of the mouth.
A branch of the mandibular nerve (V3) supplies the mylohyoid muscle.
Branches of the lingual nerve provide sensory innervation to the floor of the mouth.
The lymph vessels of the floor of the mouth spring from an extensive submucosal
plexus that forms two discrete systems: a superficial mucosa and a deep collecting.
The superficial system has crossing afferent lymphatic vessels in the anterior floor of
the mouth, where no definite midline exists. These channels drain into the ipsilateral
and contralateral preglandular lymph nodes.

The deep collecting system drains into the ipsilateral preglandular nodes.
Only the most anterior collecting vessels of the deep system cross the midline.
Lymph channels from the posterior portion of the floor of the mouth drain directly
into the jugulodigastric and jugulocarotid nodes.
Malignant tumors of the floor of the mouth usually occur anteriorly near the midline
and spread to such contiguous structures as the root of the tongue and the
mandible.
Tumors near the orifice of the submandibular duct frequently track along the duct.
Tumors may also extend far along the lingual nerve.
As cancer encroaches on the lingual cortex of the mandible, it extends downward
through the mylohyoid into the submandibular space to involve the submandibular
gland and occasionally the subcutaneous tissues and skin.
The tongue is no barrier to the spread of cancer from the anterior floor of the
mouth.
The tumor frequently invades the anterior musculature of the tongue and tracks
inferiorly as far as the hyoid bone and, in rare instances, into the prelaryngeal space.
Pathology and Patterns of Spread
Most floor of mouth neoplasms are squamous cell carcinomas; most are moderately
differentiated. Adenoid cystic and mucoepidermoid carcinomas arise from the minor
salivary glands and account for 2% to 3% of floor of mouth malignant tumors.
Most floor of mouth carcinomas are located in the anterior midline adjacent to
Wharton’s ducts. Extension toward the gingiva and periosteum occurs early and
frequently.
Small to moderate-size (stage T1 and T2) lesions are associated with metastases to
the ipsilateral regional lymph nodes in 15% to 38% of cases, depending on the size
and depth of invasion of the primary tumor.

Floor of Mouth Carcinomas: Correlation of Primary Tumor Thickness with Neck
FailureThickness (mm) T1N0 T2N0
0.1 to 1.5 1/38 (3%) 0/19
1.6 to 3.5 1/5 (20%) 3/7 (43%)
≥3.6 7/11 (64%) 2/4 (50%)
shows the distribution of clinically positive neck nodes at diagnosis and depicts
the distribution of pathologically positive nodes after elective neck dissection in
patients with carcinoma of the floor of the mouth.64 The incidence of positive
lymph nodes was 19% for those with T1 or T2 lesions and 26% for patients with
T3 or T4 cancers.
Carcinoma of the floor of the mouth.

The distribution of involved neck nodes in the N0 neck
Clinical Manifestations, Patient Evaluation, and Staging
Floor of mouth carcinomas usually present as slightly elevated mucosal lesions
with well-defined borders. A background of leukoplakia may be present. The
lesions are often diagnosed by a dentist or physician during a routine physical
examination.
T1 and T2 tumors may be noted initially when the patient feels a lump in the
floor of the mouth with the tip of the tongue. Advanced lesions tend to produce
pain, bleeding, foul breath, loose teeth, and change in speech as the result of
fixation of the tongue.

Bimanual palpation is necessary to accurately determine the extent of induration
and degree of fixation to the periosteum. Extensive lesions may exhibit invasion
into the soft tissues of the neck or skin.
The AJCC staging system is based on tumor size and invasion of adjacent
structures such as bone or soft tissue of the neck. Radiographic studies may
facilitate staging with reference to (1) the status of the mandible and teeth,
(2) the deep extent of the tumor,
(3) the evaluation of the regional lymph
nodes. CT scans should be obtained in essentially all patients. The mandible may
be evaluated by panoramic x-ray films, dental films, and CT scanning. Magnetic
resonance imaging (MRI) is useful to evaluate marrow space invasion and
perineural involvement.
The role of PET scanning as part of the initial staging workup for oral cavity
cancers has not gained widespread acceptance. It may, however, be useful in
early detection of recurrences and in prediction of which patients may benefit
from elective neck dissection after chemoradiation.
Treatment
Early Lesions (T1 and Superficial T2)
Surgery and radiation therapy produce equal cure rates for T1 and superficial T2
lesions. The risk of irradiation-induced bone and soft tissue necrosis is significant.
Therefore, surgery is usually the treatment of choice. The neck is also treated
with an elective neck dissection,70 although some advocate observation of the
neck in select patients with clinically negative nodes (cN0).

Treatment algorithm for de novo floor of mouth cancer. *Treat neck with neck
dissection or radiotherapy in any patient with a primary lesion that is more than
1.5 mm thick.60 † Concomitant chemotherapy may be used.
Sentinel lymph node biopsy is being investigated for possible use in oral cavity
cancers. However, a recent study showed that this procedure was less sensitive
for floor of mouth cancers (80%) compared with other oral sites (100%).
Some patients present after excisional biopsy of the primary tumor. If the
margins are either close or involved and there is no evidence of visible or
palpable residual tumor, an interstitial implant alone to the primary site is a good
alternative provided that the depth of invasion is less than 1.5 mm. Re-excision
may not be feasible, because the surgeon does not know exactly what to
remove. An additional advantage of RT is the ability to treat a larger area.
Moderately Advanced Lesions (Large T2 and Exophytic T3)
Infiltrative lesions with fixation or tethering to inner tables of the mandible are
best treated by excision with resection of the periosteum with or without a rim of

mandible. Postoperative RT is indicated for patients with close (≤5 mm) or
positive margins, perineural invasion, and/or lymphatic space invasion.
One common indication for adjuvant RT is the inability of the surgeon to obtain
adequate margins of resection, because this often leads to local recurrence,
even if immediate re-excision is performed. Jacobs and associates and Laramore
and colleagues reported a large intergroup study where adjuvant postoperative
EBRT (60 Gy) was administered for locally advanced cancers. They found that
the relapse rate was 11% in patients with satisfactory margins and 26% in those
with unsatisfactory margins. Unsatisfactory margins tend to reflect a higher
residual tumor burden; therefore it may be prudent to deliver a higher dose of
postoperative RT. At the University of Florida, patients with involved margins
receive hyperfractionated irradiation to increase the dose given to the primary
site while minimizing the potential late morbidity.
Locally Advanced Lesions (Endophytic T3 and T4)
Patients with locally advanced floor of mouth cancers are treated with surgery
followed by postoperative RT. In some cases, preoperative irradiation can be
used for unresectable tumors. Patients with extensive tongue invasion with
fixation or extension into the soft tissues of the neck, as well as those with
massive neck disease, can be treated with palliative RT (30 Gy in 10 fractions or
20 Gy in 2 fractions with a 1-week interfraction interval).
Concomitant Postoperative Chemoradiation
The issue of whether concomitant chemotherapy is beneficial when administered
with postoperative irradiation for head and neck cancer was recently addressed
by two randomized trials (RTOG 9501 and EORTC 22931). Each of these showed

an improvement in locoregional control and DFS when cisplatin (100 mg/m2) was
given on days 1, 22, and 43 of the EBRT regimen. Severe acute effects are seen
more frequently with chemoradiation compared with postoperative RT alone
Irradiation Techniques
Because of the proximity of the gingival ridge, which is vulnerable to high-dose
irradiation-induced soft tissue injury or osteoradionecrosis, the floor of the mouth
has a lower radiation therapy tolerance than other portions of the oral cavity.
Therefore preirradiation and postirradiation oral care is critical.
T1 and T2 Cancers
Patients with superficial (≤4 mm thick), well-differentiated squamous cell
carcinomas of the floor of the mouth may be treated either with brachytherapy
alone or, when accessible, with intraoral cone irradiation. Brachytherapy is not
feasible if the tumor abuts or extends onto the mandibular alveolar ridge because
of the risk of bone exposure. Brachytherapy may be performed with either rigid
cesium needles mounted in a customized template or with iridium using the
plastic tube technique. The rigid needles are preferable because although the
needles are active, the implant can be accomplished rapidly because the needles
are mounted in a rigid template . An additional advantage of this technique is
that the geometry of the implant is optimal and dosimetry can be obtained
before the implant. The vertical needles are spaced approximately 1 cm apart
with a crosser to ensure an adequate surface dose. The implant is anchored in
place by a suture placed through the submentum into the floor of the mouth.

Custom-made implant device for T1 to T2 cancers of the floor of the mouth. Note the single crossing needle
through the center of the device (arrowheads). The device is now machined from nylon. Cesium needles
have replaced the radium needles.

Intraoral cone irradiation is administered with either orthovoltage x rays or electrons.
Orthovoltage x rays are preferred because there is less beam constriction and the
surface dose is higher. Before each treatment, it is necessary for the radiation
oncologist to verify the position of the tumor relative to the intraoral cone. Because
a small volume of tissue is included in the intraoral cone field, the dose per fraction
may be increased to 2.5 to 3 Gy once daily.
Cancers thicker than 4 mm and those that are poorly differentiated have an
increased risk of subclinical disease in the regional nodes. The first-echelon nodes
for the floor of the mouth are the level I and II nodes. EBRT is delivered with either
4-MV or 6-MV x-rays using parallel opposed fields that encompass the primary tumor
as well as the first-echelon nodes. An intraoral stent is placed in the mouth to
displace the maxilla and upper lip out of the fields
The EBRT fields are treated to 46 Gy in 23 fractions once daily or 38.4 Gy at 1.6
Gy per fraction twice daily. Brachytherapy follows the EBRT if that is the
technique selected to boost the tumor. If intraoral cone radiation therapy is
selected to boost the tumor, it precedes the EBRT so the extent of the tumor can
be optimally defined and because it may be difficult to place the cone after EBRT
because of patient discomfort. The total dose ranges from 65 to 70 Gy.

Buccal mucosa
The buccal mucosa includes the entire membrane lining of the interior surface of
the cheek and lips, from the opposing lip’s line of contact to the
pterygomandibular raphe posteriorly and to the line of attachment of the alveolar
ridge mucosa above and below.
The buccal mucosa forms the lateral wall of the oral vestibule.
The buccinator muscle is the lateral muscular wall of the oral cavity and, along
with the orbicular mouth muscle, helps to determine oral competence.
It extends from the superior constrictor of the pharynx and blends with orbicular
muscle fibers in the upper and lower lips.
Tumors of the buccal mucosa may extend laterally through the buccinator muscle
to involve the buccal fat pad posteriorly or subcutaneous tissues and skin of the
cheek.
The buccal branch of CN VII is the motor supply to the buccinator muscle.
It runs in the same direction as the buccal branch of CN V (V3), which provides
sensory innervation to the cheek.
The infraorbital (V2) and mental (V3) nerves provide additional sensory
innervation to the anterior buccal mucosa.
Lymphatics of the buccal mucosa arise from a submucosal capillary network and
drain to lymph nodes located in the submental and submandibular triangles.
Upper and lower alveolar ridges
The alveolar ridges include the alveolar processes of the mandible and maxilla
and their mucosal covering that, in the case of the lower alveolar ridge, extends
from the line of attachment of mucosa in the buccal gutter to the line of free
mucosa in the floor of the mouth.
Posteriorly, the lower alveolar ridge’s mucosa extends to the ascending ramus of
the mandible.

The upper alveolar ridge’s mucosa extends from the line of attachment of
mucosa in the upper buccal gutter to the junction of the hard palate.
Its posterior margin is the upper end of the pterygopalatine arch. Malignancies of
the upper gingiva readily invade underlying bone and may extend upward into
the floor of the nasal cavity or into the maxillary antrum.
Lateral spread will result in involvement of the upper buccal sulcus and buccal
mucosa. Medial extension will involve the hard palate.
The maxillary nerve (V2) provides innervation to the teeth of the upper jaw
through the posterosuperior and anterosuperior alveolar nerves.
Different sensory branches of the maxillary nerve innervate the lingual and labial
gingiva of the upper alveolus.
The greater palatine nerve supplies the lingual side of the alveolus behind the
premaxilla.
The nasopalatine nerve supplies the lingual gingiva of the premaxilla; two
different branches of the maxillary nerve innervate the labial surface of the upper
alveolar gingiva.
The posterosuperior alveolar nerve, which descends on the infratemporal surface
of the maxilla, supplies the gingiva posterior to the premaxilla.
Branches of the infraorbital nerve supply the labial gingiva.
The mandibular nerve (V3) innervates the teeth and gingiva of the lower jaw.
The teeth are also innervated by the inferior alveolar nerve, which enters the
mandibular foramen and runs the length of the mandible in the mandibular canal
to exit the mental foramen.
Malignancies arising on the alveolus may infiltrate bone and reach the
mandibular canal, where the tumor may follow the mandible along the nerve
toward the skull base or through the mental foramen and into the skin of the
lower lip and chin.

In edentulous persons the alveolar bone is absorbed, and the mandibular canal
may be only a few millimeters from the mandible’s upper margin, providing for
early access of the tumor into the mandible’s medullary portion.
Branches of the lingual nerve supply the entire lingual gingiva of the lower
alveolus.
The buccal nerve (V3) supplies the labial surface behind the canine tooth; the
mental nerve supplies the surface in front of the canines.
The posterosuperior alveolar artery and vein provide the blood supply to the
upper alveolus. The greater palatine artery and vein also contribute to the lingual
aspect. The inferior alveolar artery and vein primarily supply the lower alveolus.
Lymphatics of the buccal aspect of the upper and lower alveolar ridges drain to
submental and submandibular lymph nodes.
Lymphatics from the lingual aspect of the upper and lower gingiva pass chiefly to
upper deep jugular and lateral retropharyngeal lymph nodes.
Some channels may drain to lymph nodes adjacent to the tail of the parotid
gland (subparotid). Lymphatics from the lingual surface of the lower alveolus also
may end in submandibular nodes.
Retromolar trigone
The retromolar trigone is the attached gingiva overlying the ascending ramus of
the mandible.
The distal surface of the last lower molar forms the base of this triangular area,
and its apex terminates at the maxillary tuberosity.
The upward extension of the oblique line of the mandible to the coronoid process
forms the triangle’s lateral side, and a line connecting the distal lingual cusp of
the last molar and the coronoid process forms the medial side.
The triangle’s base is continuous laterally with the gingivobuccal sulcus and
medially with the gingivolingual sulcus.
The triangle’s lateral side is continuous with the buccal mucosa, and the medial
side blends into the anterior tonsillar pillars.

The mucosa adheres closely to the underlying bone in the region of the
retromolar trigone, and malignant tumors arising in this area may readily
infiltrate the mandible.
The inferior alveolar nerve enters the mandibular foramen at a point just
posterior to the midpoint of the trigone’s medial side and may be affected by
neoplasm early in the course of disease.
Nerve twigs from the ninth cranial (glossopharyngeal) nerve and branches of the
lesser palatine nerve (V2) provide sensory innervation to the retromolar triangle.
The contribution of CN IX accounts for the referred ear pain that may be
observed in patients with cancer arising in this region
Hard palate
The hard palate is a semilunar area consisting of mucous membranes covering
the horizontal laminae of the palatine bones.
The upper alveolar ridge partly surrounds the hard palate, which extends from
the inner surface of the superior alveolar ridge to the posterior edge of the
palatine bone.
Each palatine bone is somewhat L-shaped.
The palate’s horizontal lamina meets the other side’s lamina in the midline,
forming the secondary palate, and the perpendicular lamina runs upward,
forming the posterolateral wall of the nasal passage.
The fusion of the palatine processes of the two maxillae, known as the primary
palate, forms the bony palate in front of the palatine bone’s horizontal laminae.
The primary palate is part of the premaxilla, or the bone that bears the incisor
teeth. Its union with the posterior portion of the hard palate is marked in the
midline by the incisive fossa.
Two or more foramina are located posterolaterally on either side near the
junction of the hard and soft palate.

The larger is the greater palatine foramen, and behind this are one or two lesser
palatine foramina.
These foramina represent the lower end of the pterygopalatine canal, through
which nerves and vessels are conducted from the pterygopalatine fossa to supply
the hard and soft palate.
The foramina provide access for tumor spread into the pterygopalatine fossa and
regions of the skull base.
Likewise, the incisive fossa and canal provide a pathway for tumor extension into
the nasal cavity.
The hard palate receives its vascular supply from the greater palatine artery and
vein, which are terminal branches of the sphenopalatine vessels.
They gain access to the palate through the greater palatine foramen.
The greater palatine nerve supplies the secondary palate and exits the foramen.
The nasopalatine nerve, a branch of the maxillary nerve (V2) that descends
through the incisive canal from the nasal passage, innervates the primary palate.
Lymphatics of the hard palate are sparse compared with other sites in the oral
cavity.
Drainage is similar to that of the lingual surface of the upper alveolus. Most of
the lymphatics drain into upper deep jugular (subdigastric) or lateral
retropharyngeal nodes.
Lymph channels draining the primary palate may terminate in the prevascular
and retrovascular group of submandibular nodes.
Anterior two thirds of the tongue
The anterior two thirds of the tongue, known as the oral tongue, are considered
part of the oral cavity.
The oral tongue is the freely mobile portion of the tongue that extends anteriorly
from the line of the circumvallate papillae to the root.

The root of the tongue is the undersurface at its junction with the floor of the
mouth.
The oral tongue consists of four anatomic regions: the tip, the lateral borders,
the dorsum, and the undersurface (nonvillous surface).
The base of the tongue is that portion posterior to the circumvallate papillae and
is considered a structure of the oropharynx.
Three extrinsic and three intrinsic muscles on each side compose the tongue.
The extrinsic muscles are the genioglossus, hyoglossus, and styloglossus; these
move the tongue body and alter its shape.
The intrinsic muscles are the inferior lingual, vertical, and transverse; these alter
the shape of the tongue during deglutition and speech.
The tongue has a relatively avascular midline marked by a median fibrous
septum that is attached to the hyoid bone and does not reach the dorsum.
The lingual artery alone provides the arterial supply to the tongue.
It arises from the external carotid artery at the level of the greater horn of the
hyoid and runs forward immediately adjacent to the middle pharyngeal
constrictor, which separates it from the mucosa of the pharynx.
The lingual artery runs deep to the hyoglossus muscle, giving arise to two dorsal
lingual arteries and a single sublingual artery, and continues as the deep artery
to supply the anterior two thirds of the tongue.
Its only anastomosis is with its fellow artery at the tip of the tongue.
Small companion veins accompany the lingual artery. The chief vein of the
tongue, however, is the deep vein, which follows the hyoglossus and is then
joined by the companion veins to form the lingual vein, which ends in the internal
jugular vein.
CN XII runs forward between the submandibular gland and the hyoglossus
muscle well below the lingual nerve.

As it crosses the hyoglossus, the nerve innervates the three extrinsic muscles of
the tongue; at the anterior border of this muscle it plunges into the tongue to
supply the intrinsic muscles.
The sensory nerve supply of the oral tongue is the lingual branch of the
mandibular nerve (V3).
The chorda tympani, a branch of CN VII, travels with the lingual nerve and
provides the sensation of taste.
The posterior third of the tongue (tongue base) has a different origin than the
oral tongue and is supplied by CN IX and the superior laryngeal nerve. Both of
these nerves provide sensation and taste to the tongue base.
Lymphatics of the tongue arise from an extensive submucosal plexus, and all
vessels drain ultimately into the deep jugular lymph nodes between the levels of
the digastric and omohyoid muscles.
The nearer the tip of the tongue the lymphatics arise, the lower is the first-
echelon node; and the farther posterior, the higher the node.
Lymphatic collecting channels of the tongue are the anterior (apex), lateral
(marginal), central, and posterior groups.
Vessels from the apex pierce the mylohyoid muscle and partly drain to first-
echelon submental nodes.
The lateral or marginal trunks partly pierce the mylohyoid to end in
submandibular nodes.
The remaining trunks drain on either side of the hyoglossus muscle to deep
jugular nodes.
The central trunks descend in or near the septum of the tongue and follow the
lingual artery to the deep jugular nodes. Lymph channels from the tongue base
pass through the pharyngeal wall laterally below the tonsil to reach principally
the jugulodigastric nodes.
Cancer of the tongue frequently metastasizes bilaterally, primarily because of the
rich lymphatics in the submucosal plexus, which freely communicate across the
midline.

In addition, collecting lymphatic trunks from the apex, central, and posterior
groups have many collecting channels that cross over to terminate in
contralateral lymph nodes.
Malignancies of the tongue frequently grow to considerable size before producing
symptoms.
The relatively loose connective tissues separating the intrinsic musculature
provide little barrier to the advance of cancer.
Symptoms do not occur until the tumor has grown to a size that interferes with
movement, producing dysfunction of speech and deglutition, or when the tumor
has involved the lingual nerve, producing pain.
Cancer of the tongue or the floor of the mouth involving the lingual nerve causes
pain that is typically referred to the ipsilateral ear.
The lingual nerve is a branch of the mandibular nerve (V3) that also provides
sensation to the external auditory meatus, tympanic membrane, and
temporomandibular joint through the auriculotemporal nerve.
Likewise, cancer of the tongue base may also produce referred ear pain because
CN IX provides sensory innervation to the middle ear.

Malignant neoplasms of the oral cavity

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