Download Tumors of the Hard Palate and Upper Alveolar Ridge

The University of Texas Medical Branch
Department of Otolaryngology
Grand Rounds Presentation
April 22, 2011
Regina Rodman, MD
Faculty Advisor: Tammara Watts, MD, PhD
Aided by Guy Petruzzelli, MD, PhD, MBA

Incisive Fossa
◦ Slight depression posterior
to central incisor teeth
◦ Nasopalatine nerve
• Greater palatine foramina
 Medial to 3rd Molar
 Greater palatine vessels and
nerve
• Lesser palatine foramina
 Lesser Palatine nerves and
vessels to soft palate

Greater palatine artery

Superior Alveolar Arteries
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
The Greater Palatine artery
is a branch of the third part
of the maxillary artery. The
greater palatine artery
descends with its
accompanying nerve in the
palatine canal.
The superior alveolar
arteries are terminal
branches of the
nasopalatine artery
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The greater palatine
emerges on the hard
palate from the
greater palatine
foramen
runs forward in a
groove on the inferior
surface of the bony
palate almost to the
incisor teeth
supplies the gums
and the mucosa and
glands of the hard
palate.4

The venous
drainage is to the
pterygoid plexus
and subsequently
to the internal
jugular venous
system.

The nasopalatine nerves

Greater Palatine Nerves


The nasopalatine nerves
are branches of the
maxillary division of the
trigeminal nerve.
They enter the palate at
the incisive foramen
supply the anterior part
of the hard palate
behind the incisor
teeth.5


Greater (and Lesser)
Palatine run through the
palatine canal and exit at
the Great and Lesser
Palatine Foramens,
respectively.
Parasympathetic
postganglionic
secretomotor fibres from
the pterygopalatine
ganglion run with the
nerves to supply the
palatine mucous glands.

Tumors spreading
by perineural
extension can be
discovered by
radiographic
enlargement of the
palatine foramina
or widening of the
palatine canals or
the foramen
rotundum.6

The upper alveolar
ridge consists of
mucosa overlying
the alveolar process
of the maxilla and
extends from the
gingivobuccal
sulcus laterally to
the junction of the
hard palate
medially.
Squamous Cell
Adenoid Cystic
Adenocarcinoma
Mucoepidermoid Ca
Other
Anaplastic Ca
Histology
The palate is covered by thick mucosa bound tightly to the underlying
periosteum.
The submucosa in the posterior half of the hard palate contains glands of
the mucous minor salivary type.
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
The mucosa is covered
by keratinizing stratified
squamous epithelium
which shows regional
variations and may be
ortho- or
parakeratinized.
This keratinization may
explain the decreased
incidence of squamous
cell carcinoma in the
hard palate as compared
to other areas of the oral
cavity.
Adj of a specific type of epithelium; its four layers include a keratin component whose cells
are nuclei-free. Most oral mucosa consists of parakeratinized epithelium, which contains
nucleated keratinocytes.

Lifestyle
◦ tobacco
◦ Alcohol
◦ diet lacking in antioxidants

Other factors:
◦ HPV 16 virus,
 has been shown have shown an increased odds ratio of 2.2
for squamous cell CA in individuals who were seropositive
for HPV 166
 the exact role of HPV in oral carcinogenesis is still being
defined.

Tobacco, particularly cigarettes, and alcohol
remain the primary factors in the etiology of
squamous cell oral cancer in the United States.7,8

In parts of India and South-East Asia chewing
betel quid with tobacco and areca nuts is the
primary risk factor for oral cancer.
Placed in the mouth or chewed and remaining in contact with the mucosa, usually
containing one or both of the two basic ingredients, tobacco and/or areca nut, in raw or
any manufactured or processed
There are several types of chewing habits
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betel quid
pan masala
mainpuri
mawa, khaini
gutka
smokeless tobaccos
Survey regarding socioecomics and oral cancer udy done in Sri
Lanka10
◦ half of the betel chewers consisted of farmers or estate laborers in these
areas.
◦ One betel quid is ½- 1/10th the price of smoking.
◦ Both betel quid and beedi are life-threatening habits for low income people.
◦ Late presentation: The access of the people living in rural areas to hospitals
is limited because of a number of reasons; besides the money concern, it
may also be risky for keeping a job, a trouble that reflects upon the entire
family.
The cost of a betel quid is only 5 Rs. for these inhabitants, which makes betel chewing preferable to cigarette
smoking (7.5 to 10 Rs. per cigarette). Beedi (or bidi), which is made by rolling a dried, rectangular piece of the
temburni leaf into a conical shape containing a small amount of finely cut tobacco, is very popular and cheap (50
cents) in India, Sri Lanka and other Southeast Asian countries.
Composition of betel quid: Betel leaves (A) with slaked lime (B), areca nut (C) and tobacco (D).

Those who use tobacco and alcohol
simultaneously are thought to have a
significantly increased risk of oral cancer
relative to using either one alone, likely
because the combined use of nicotine and
ethanol (known cytotoxins) significantly
increases the penetration of NNitrosonornicotine (NNN), a known
carcinogen found in tobacco, across the oral
mucosa.11

Squamous cell
tumors may arise
anywhere in the oral
cavity but the favored
locations are
◦ Floor of mouth
◦ Ventral surface of
tongue
◦ Soft Palate
◦ Base of Tongue
◦ Gingiva
◦ Lower lip
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

The likely reason for the increased incidence of
cancer in these areas is due to the histology of
the region.
The majority of the oral cavity mucosa (including
the hard palate) consists of a thick layer of
squamous cells with well-developed rete pegs
and a prominent superficial keratin layer.
Floor of the mouth and the ventral surface of the
tongue are lined by thin, atrophic mucosa with
shallow rete pegs and little surface keratin.
thick layer of squamous cells
well-developed rete pegs
prominent superficial keratin layer
thin, atrophic mucosa
shallow rete pegs
little surface keratin

This phenomenon, together with the fact that
this area is constantly bathed by a pool of
saliva containing potential carcinogens, is a
possible reason for the high incidence of oral
carcinoma in these areas.
Still most common cancer of the hard palate


A large portion of palatal tumors are minor
salivary gland tumors, and the etiology of
these tumors is less clear.
One study found that there showed that
smoking, alcohol consumption did not
independently or jointly increase the risk of
salivary gland cancer.14


Another study demonstrates that there is a
possible increased risk for salivary gland tumors
in patients who received radiation treatment to
the head and neck, ultraviolet light treatment or
full mouth dental x-rays before 1955, when the
exposure dose was substantially higher.15
Still, this does not account for all patients with
minor salivary gland tumors, and more research
needs to be done regarding the etiology of such
neoplasms.
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Malignant Histiocytoma
Malignant Melanoma
Malignant Mixed Tumor
Osteosarcoma
Ameloblastoma
Verrucous Carcinoma
Extramedullary Plasmacytoma

Melanoma of the
oral mucosa is a
rare tumor, but
when it does occur
the most common
locations are the
palate and
maxillary gingiva.
Black pigmentation, pinpoint satellite lesions, and
peripheral erythema characteristic pf malignant
melanoma

Amelanotic Malignant Melanoma
The etiology of these
tumors is unclear, but
possible etiologic
mechanisms include
solar irradiation,
mechanical trauma,
ill-fitting dentures,
oral habits, self
medication and
exposure to
formaldehyde.
Vegetative, amelanotic malignant melanoma; palate and alveolar
ridge
Patient with T/NK cells angiocentric lymphoma, which shows
destructive ulcerative lesion in hard palate and extensive zones
of necrosis

One clear etiology
for hard palate
tumors is seen in
areas of India
where the practice
of chutta, or
reverse smoking, is
practiced.

This practice of
holding the lit end
of the cigarette in
the mouth causes
smoke to hit the
hard palate directly.

It has been
demonstrated that
there is a close
correlation between
reverse smoking,
nicotine stomatitis
and carcinoma or
the hard palate.21

Other possible etiologic mechanisms include
◦ poor oral hygiene
◦ mechanical irritation from ill fitting dentures
◦ syphilis

Perforation of the hard palate
due to gummatous destruction
Infammatory reaction from
ill fitting dentures

Pain and discomfort most common
presenting symptom
Ulceration, foul odor and bleeding (if not
submucosal)
Fit of dentures changes

Minor Salivary Gland:


◦ Asymptomatic
◦ Smooth
◦ Mucosa covered
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
Study from Pittsburg showed that there was a
delay in diagnosis of months to years in many
patients. 22
Extension superiorly into the maxillary
antrum and nasal cavity
present with nasal obstruction
Posterior extension into the structures of the
oropharynx, into pterygoid muscles
present with trismus, malocclusion
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
History and thorough head and neck exam
Lymph nodes in neck
Middle ear effusion
◦ Extension into nasopharynx
◦ Invasion of the tensor veli palatini m. or eustachian tube

Absent trigeminal blink reflex or palatal
hypesthesia
 Involvement of maxillary division of trigeminal nerve in the
sphenopalatine fossa

Masseter or temporalis wasting
◦ Involvement of the mandibular division of the trigeminal
nerve

CT scan
◦ Axial: define the anterior-posterior dimension,
assess bone destruction, especially of erosion of
pterygoid plastes and skull base
◦ Coronal: superior extension and paranasal sinus
involvement

MRI
◦ May be useful in evaluating cranial base and CNS

Ulcerated, exposed lesions
◦ Transoral punch or cup foreceps

Mucosa covered
◦ Incisional biopsy

Small, well circumscribed covered with intact
mucosa


Complete excision, defect will granulate
If nodes are present
◦ FNA


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Small Lesions transorally
Large, requiring partial maxillectomy lateral
rhinotomy incision or midface degloving
If cancer extends through the palatetotal
maxillectomy


The palate is a midline structure, therefore
treatment to neck should be bilateral.
The areas at risk for metastatic disease include
the retropharyngeal lymphatics and the jugular
(zone II) lymphatics bilaterally.22
◦ Patients who present with cervical mets from palatal
cancer is poor.

The question of whether or not to perform an
elective neck dissection in an N0 neck is
answered differently depending on the type of
tumor.

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
Elective neck dissection should be offered to
patients with squamous cell cancer of the hard
palate and the maxillary alveolus due to the
significant rates of occult cervical metastasis,
both locally and regionally.23
Elective selective neck dissection should also be
performed in tumors occurring on the lateral and
buccal surfaces of the alveolar ridge.
In the majority of tumors not fitting the above
qualifications, elective neck dissection is not
routinely advocated.

Must recognize that if the tumor is in the
anterior upper gum and significantly involves
the lip and the nasal vestibule
lymphatic drainage may be along the
facial artery.
cancer can spread to buccinator chain of
nodes
 ultimately to submental triangle, possibly
pre-auricular nodes



An area where much has been published is the area of
adjuvant therapy, and the prognosis/survival compared
across treatment modalities including surgery vs. radiation
treatment vs. combination therapy.
A few papers have been written that specifically focus
adjuvant therapy for tumors of the hard palate and upper
alveolar ridge.
Radiation is effective for both squamous cell tumors and
salivary gland tumors, and that while surgery has a role in
management of hard palate tumors,22 so does radiation
therapy.23


Most patients will benefit from combination
therapy.
It is believed that some patients may receive
more benefit from radiotherapy alone20
◦ Very early lesions
◦ Unfit for surgery

Retrospective studies, and the treatment
modality chosen was based on factors that affect
prognosis
◦ Radiation group: poor surgical candidates
◦ unressectable disease
◦ neoplasms so small they can be treated without surgery

Small sample size due to the relative rarity of
tumors in this location.

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Discrepancy between that which is clinically significant and
what proves to be statistically significant.
To date, no studies which have created a forward
facing matched pair analysis.
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Are radioresponsive, with dose response
relationship
Combination therapy showed better local control,
 however did not improve overall survival due
to the better salvage rate in the surgery only
group25
However, in the case of adenoid cystic carcinoma,
combination therapy has been shown to increase
overall survival , likely because radiation controls
for the adenoid cystic tumors propensity for
perineural invasion. 26, 27
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Until a substantial conclusion can be reached
regarding the role of radiotherapy as a stand
alone treatment, it is recommended that
radiation therapy be used as adjuvant therapy
only.
Adjuvant therapy should be used in patients
with
◦
◦
◦
◦
demonstrated cervical metastasis
Positive margins
adenoid cystic carcinoma
high grade tumors
 particularly high grade mucoepidermoid carcinomas.

When there is significant bony involvement
◦ greater risk of radiation induced complications
 Thin palatal mucoperiosteum offers little protection
◦ More resistant to radiation therapy
 Oxygen poor environment

Rarely develops in this region when there is no
exposed bone
28,29
◦ Radiation oncologist agree that when there is bony
involvement, treat with surgery and post op radiation

If it does, it is not as disabling as when it occurs
in the maxilla.
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Tissue Reconstruction vs. Obturator
Compared to mandible, the residual maxilla
does not move, making a prosthesis a good
option for functional recovery
Obturator was the “gold standard” for years.
However, advancements in reconstructive
surgery have lead to multiple publications in
recent years advocating tissue reconstruction.
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Dental oncologist
Endodontist
Maxillofacial prosthedontist
Head and Neck Surgeon
Reconstructive Surgeon
Patient
Patient’s Family/Caregivers

Genden et al 2004: (12/12)

Morena et al 2010 (73/40)

Small Case Series describing successful FTT
◦ Equal in diet, mastication, articulation
◦ Equal satisfaction with appearance, chewing, and taste
◦ RFFF reported higher satisfaction scores in speech, comfort,
convenience, and social interaction
◦ Moderate defects (<50%) Speech intelligibility and postoperative
diet were
◦ Large defects (>50%) free flap reconstruction was superior in both
◦
◦
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Bare serratus anterior muscle fascia and scapular bone
Radial Forearm osseocutaneous
Temporalis muscle
Iliac Crest

Disease Biology

Oral Anatomy and Physiology

Patient Factors

Defect Analysis
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Need cavity surveillance32
Ameleoblastoma
Myxoma
Mucosal Melanoma
Study by Moreno et al
showed there was no
significant difference in
local recurrence detection
between groups.33

Trismus

Teeth?
◦ Free flap is better as it will not require daily removal and
maintenance that obturator does.
◦ + May plan osteotomy planes
through the existing tooth sockets
preserve the support of adjacent
teeth (abutments), may be strategic
for retention of a prosthesis.
◦ - Edentulous or partially edentulous patients have difficulty
with retention of obturator and, in some cases, difficulty
with support as well.
 In these cases, osseointegrated implants can anchor and
support the obturator prosthesis. Usually with bone graft s/p
radiation.

Need to be able to remove prosthesis BID

Therefore, the following are NOT good candidates for
obturator
◦ cleaning prosthesis
◦ irrgation of the defect with baking soda and salt
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◦
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Trismus
Decreased manual dexterity
Decreased vision
Altered mental status
Patient preference
◦ Unwilling to live with defect
Tongue comes out through nose
Unable to answer the phone in the
night


Many papers arguing success and failure of
obturators and free tissue transfer
Paper by Okay et al, in 2001 gives summary of
how to assess the defect and plan for
reconstruction.
Based on 4 Pillars
of stability
1) Molars
2) Canines
+/- 3) Prior RT

Okay, Genden, Buchbiner, Urken at
Mt Sinai
Class I
Class 1a defects involve any portion of hard palate
but not tooth-bearing maxillary alveolus
Class Ib
involve premaxilla or any portion of maxillary
alveolus and dentition posterior to canines.
<50%
Class II
Class II defects involve any portion of hard palate and tooth-bearing
maxillary alveolus and only one canine. Anterior margin of defect lies
within premaxilla. This class includes transverse palatectomy defects
that involve less than 50% of hard palate.
>50%
Class III
Class III defects involve any portion of hard palate and tooth-bearing
maxillary alveolus, including both canines. This class includes total and
transverse palatectomy defects that involve more than 50% of hard palate.

Class I

Class II

Class III
Soft Tissue Recon
or
Prosthesis
Local Flap
Free Flap
Vascularized Bone Free Flap
or
Prosthesis
Vascularized Bone Free Flap
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1. Think outside the squam when you see a tumor of
the hard palate
2. Etiology is less clear in these tumors. The patient
may not be our typical “head and neck patient”
3. Work up: imaging, biopsy
4. Surgical excision (except very small and too large
tumors)
5. Neck Dissection in N+, all squamous cell, and
lateral tumors
6. Adjuvant therapy for N+ neck, Adenoid cystic,
High grade mucoepidermoid
7. Reconstruction depends on Okay criteria and
resources available to you and the patient.
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