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ORAL AND MAXILLOFACIAL
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CYSTS AND TUMORS
David Webb
CHAPTER 44
1. What is the most common odontogenic cyst and tumor?
The most common odontogenic cyst is the periapical cyst (with an inflammatory etiology). The most
common developmental odontogenic cyst is the dentigerous cyst, which is usually diagnosed between
ages 10 and 30 years. The dentigerous cyst represents a pathologic expansion of the dental follicle: a
sac-like structure surrounding the crown of an unerupted tooth.
The most common odontogenic tumor is the odontoma, with prevalence exceeding that of all
other odontogenic tumors combined. The odontoma is a hamartoma and is classified as complex or
compound. The second most common odontogenic tumor is the ameloblastoma (excluding the KCOT),
with much greater morbidity and mortality than the odontoma.
2. What is the differential diagnosis for a mixed density (radiopaque/radiolucent)
lesion in the posterior mandible above the mandibular canal?
The two most prevalent categories are odontogenic and fibro-osseous. Odontogenic etiology includes
odontoma (mixed density if still forming), ameloblastic fibro-odontoma (usually in children), adenomatoid odontogenic tumor (usually in teenagers), osteoblastoma (younger patients), cementoblastoma
(attached to tooth root), calcifying epithelial odontogenic tumor, calcifying odontogenic cyst, and developing tooth. Fibro-osseous etiology includes cement-osseous dysplasia, fibrous dysplasia (disease of
bone = indistinct lesion margins), and ossifying fibroma (disease in bone = distinct lesion margins).
If the radiographic border of the lesion is poorly demarcated, consider osteomyelitis, metastatic
carcinoma, osteosarcoma/osteochondroma.
3. What if the same lesion crosses the mandibular midline?
Cement-osseous dysplasia, osteomyelitis, metastatic carcinoma, osteosarcoma.
4. What is the differential diagnosis for a multilocular radiolucency in the posterior
mandible above the mandibular canal?
Keratocystic odontogenic tumor, ameloblastoma, myxoma (stepladder appearance with perpendicular
trabeculae), idiopathic bone cavity (traumatic bone cyst is an incorrect term as there is no cyst lining),
and cherubism (bilateral).
5. Define the following terms: enucleation, curettage, peripheral ostectomy, linear
margins, and anatomic margins.
• Enucleation: removal of the soft tissue lining and cyst/tumor produced by the lesion from its bony
cavity
• Curettage: using a curette to scrape or scoop the soft tissue and some hard tissue produced by the
lesion from its bony cavity
• Peripheral ostectomy: removal of a layer of hard tissue from a bony cavity (usually with a rotary
handpiece and bur) after removal of all visible soft tissue
• Linear margin: bony radiographic margin that is measured from the extent of the resected lesion
• Anatomic margin: a distinct tissue layer or vital structure sacrificed or preserved during an ablative
procedure
Both linear and anatomic margins are planned based upon the diagnosis of the lesion. For example,
ablative principles for a solid ameloblastoma of the mandible would call for 1 cm linear margins
(determined radiographically) and one uninvolved anatomic barrier (i.e., a supraperiosteal dissection
in the setting of cortical plate perforation).
6. What is the incidence of development of cystic lesions around retained,
asymptomatic, impacted mandibular third molars?
According to various literature reports, it ranges from 0.3% to 37%.
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7. Is it necessary to remove teeth that are in close association with a cyst?
Appropriate imaging techniques should be obtained to ascertain that teeth are indeed involved by
the lesion. Usually teeth with displaced but intact roots can be treated endodontically and preserved.
Teeth showing root resorption should be extracted. The removal of teeth associated with odontogenic
keratocysts is appropriate to prevent recurrence.
8. What is the accepted diameter required to radiographically diagnose a
nasopalatine duct cyst?
The nasopalatine duct cyst (NPDC) is the most common nonodontogenic cyst in the maxilla. Radiolu-
cencies >6 mm in the area of the incisive foramen are considered pathologic. 28% of NPDCs contain
respiratory epithelium on histologic analysis.
9. How can chronic inflammation affect the prognosis of an untreated odontogenic
cyst?
Malignant transformation is one concern when tissue is exposed to chronic inflammation. Primary
intraosseous squamous cell carcinoma ex-odontogenic cyst is most commonly associated with
radicular cyst, dentigerous cyst, and keratocystic odontogenic tumor. Clinical features of pain,
swelling, perforation of the buccal and lingual cortical plates, and adherence of the cyst lining to the
bony cavity are all suspicious for malignancy. The estimated incidence of malignant change in cysts is
between 0.31% and 3%.
10. Why was the odontogenic keratocyst (OKC) redesignated as the keratocystic
odontogenic tumor (KCOT)?
Redesignation of the OKC as the KCOT by the World Health Organization in 2005 was due to behavior,
histology, and genetics. Abnormal function of the tumor suppressor gene PTCH occurs in both nevoid
basal cell carcinoma syndrome and sporadic KCOTs.
11. How are odontogenic keratocysts treated?
Evidence suggests that these cysts can be managed effectively by a conservative approach. Good
results have been achieved with decompression or marsupialization with or without later cystectomy,
enucleation combined with excision of overlying mucosa and Carnoy solution application to the bony
defect, and enucleation combined with liquid nitrogen application to the osseous cavity. It appears that
although odontogenic keratocysts are notorious for their capricious nature relative to their tendency to
recur, block resection of these lesions is hardly justifiable.
12. What is the difference among a Partsch I, Partsch II, and decompression
procedure?
A Partsch I procedure is synonymous with marsupialization. In this one-step procedure, the cystic
cavity is converted into a pouch by creating a bony window over the cyst and suturing the cut edges
of the cyst lining to the surrounding oral mucosa. A Partsch II procedure is enucleation of the lesion
followed by primary closure. Decompression is distinguished from marsupialization by making a
smaller window into the lesion and securing a tube for daily irrigation. A second surgery is necessary
for definitive enucleation when using the decompression method.
13. What are the three possible reasons for persistence of a keratocystic odontogenic
tumor?
First, incomplete removal: KCOTs are difficult to enucleate as the epithelial lining is thin (five to eight cell
layers) and friable. Multilocular lesions further complicate complete removal. Second, some authors believe
daughter or satellite tumors persist within the bone beyond the perceived margin. This may explain the high
recurrence rate or rather persistence for marsupialization or enucleation alone as definitive treatment. Last,
epithelial remnants from the dental lamina may reside within the attached alveolar mucosa overlying the
primary lesion. These harboring remnants can potentially develop into new lesions. For this reason, some
authors recommended excision of the overlying mucosa in addition to the lesion.
14. Name the five types of ameloblastomas and treatment of each.
See Table 44-1.
15. What are the six histologic patterns of solid/multi-cystic ameloblastoma?
Follicular (most common), plexiform, acanthomatous, granular cell, desmoplastic, and basal cell
(least common). The desmoplastic pattern is unique as it may present as a mixed density lesion
radiographically.
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Table 44-1. Types of Ameloblastomas and Treatment
AMELOBLASTOMA
TYPE DESCRIPTION TREATMENT
Peripheral
ameloblastoma
Unicystic
ameloblastoma
Solid (multi-cystic)
ameloblastoma
Malignant
ameloblastoma
Ameloblastoma
carcinoma
Firm, exophytic, non-ulcerative, painless
gingival mass
Well-circumscribed radiolucency (90%
unilocular, 10% multilocular) usually posterior mandible, associated
with impacted tooth in 20 yo. Three
histologic patterns: intraluminal,
luminal, and mural
Multilocular radiolucency, posterior
mandible, painless expansion in 20
to 60 yo. Desmoplastic variant can
appear radiographically as mixed
density lesion
A benign ameloblastoma with meta-
static potential whose metastatic
foci will also be benign
A malignant ameloblastoma with meta-
static potential whose metastatic foci
will also be malignant
Excision with 2 to 3 mm margins
(include one uninvolved layer)
Intraluminal, luminal are enucle-
ated (+/− curettage). Mural
must be resected. Be wary of
enucleate/curettage after incisional biopsy yields intraluminal
or luminal as mural ameloblastoma may exist elsewhere in
the cyst lining
Resect all six histologic patterns
with 1 to 1.5 cm linear margins
and one uninvolved anatomic
layer
Resection/excision of primary and
metastatic tumors (see solid)
Radical resection, +/− chemo-
therapy, +/− XRT
16. Are all unilocular radiolucent ameloblastomas unicystic?
No. While ∼90% of unilocular radiolucent ameloblastomas are unicystic, ∼10% are multi-cystic.
Conversely, ∼10% of multilocular radiolucent ameloblastomas are unicystic.
17. What is the doubling time of ameloblastoma vs. oral cavity squamous cell carcinoma (OCSCC), and when does each most often recur?
Doubling time of ameloblastoma is 2 to 5 years versus OCSCC ∼1 month. Average recurrence of
ameloblastoma is ∼5 years vs. OCSSC within first year.
18. What is the recommended length of follow-up for recurrent odontogenic tumors
such as ameloblastoma, myxoma, calcifying epithelial odontogenic tumor, and
keratocystic odontogenic tumor?
These lesions can recur after decades with no prior evidence of disease. Accordingly, indefinite follow-
up with imaging annually for the first 5 years and biannually thereafter is prudent.
19. Why is the adenomatoid odontogenic tumor (AOT) referred to as the lesion of
two-thirds?
The AOT occurs during the second decade of life in two-thirds of cases, maxilla:mandible is 2:1, and
F:M is 2:1. This tumor is commonly associated with an unerupted maxillary canine and can often be
distinguished from a dentigerous cyst by radiolucency surrounding the apex, not just crown, of the
involved tooth. The circumscribed unilocular radiolucency occasionally contains snowflake radiopacities, further differentiating the AOT from a dentigerous cyst. The thick capsule facilitates easy
enucleation with almost no recurrence.
20. What histologic features are present in the calcifying epithelial odontogenic tumor
(CEOT)?
The CEOT is a slow-growing tumor of odontogenic origin. Most common between ages of 30 to 50,
usually a painless, slow expansion of the posterior mandible paired with radiographic findings of
a uni- or multilocular radiolucency. Radiopaque calcifications may be present. The histopathologic
features are unique and may include sheets of polyhedral cells, amyloid deposits, and multiple
CHAPTER 44 ORAL AND MAXILLOFACIAL CYSTS AND TUMORS 425
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calcifications (Leisegang rings). After staining with Congo red, the amyloid exhibits apple-green
birefringence under polarized light. Treatment involves resection with 1.0 to 1.5 cm margins.
21. What common anatomic structures share histologic features with the odontogenic myxoma?
The developing dental papilla and hyper-plastic tooth follicle are strikingly similar to the myxoma
microscopically. If located in the maxillary sinus, nasal polyps can also resemble myxoma. It is important to distinguish these structures using clinical and radiographic correlation. Treatment of myxoma
includes surgical resection with 1.0 to 1.5 cm bony margins and one uninvolved anatomic barrier.
22. What histologic features are present in the calcifying odontogenic cyst (COC)?
Like the ameloblastoma, the COC is an uncommon lesion that can have cystic, solid, and peripheral
variants, with the solid variant being the most aggressive. The lesion is considered by many to be
a neoplasm rather than a cyst. Intraosseous lesions can be cystic or solid (neoplastic) with a very
small number of solid types known to be malignant (odontogenic ghost cell carcinoma). Diagnostic
histologic findings include ghost cells. 10% to 20% of COCs are involved with an odontoma.
23. What are the two variants of ameloblastic fibroma?
Literature suggests the ameloblastic fibroma can be categorized into neoplastic and hamartomatous
variants based on clinical and radiographic features. Lesions in patients over the age of 22 are considered true neoplasms, while those in younger patients may be either true neoplasms or odontomas in
early stages of development. Histologic analysis of the two are indistinguishable. Asymptomatic small
unilocular lesions with no or minimal bone expansion are likely developing odontomas, while large
expansile lesions with extensive bone destruction are neoplasms.
24. Which jaw lesions include histology containing multinucleated giant cells?
Central giant cell lesion, giant cell tumor, brown tumor of hyperparathyroidism, cherubism, and aneu-
rysmal bone cyst
25. Compare and contrast the aneurysmal bone cyst (ABC) with the idiopathic bone
cavity (IBC).
Both the ABC and SBC share a peak incidence in the second decade of life. Both lesions lack an
epithelial lining and are not true cysts. Both have an unknown etiology, though the ABC is believed
to be reactive, resulting either as a primary entity stemming from trauma or secondary to a dilated
vascular bed in a preexisting bony lesion. Clinical features of both include swelling, mild painful
symptoms, and vital teeth with or without tooth displacement. The IBC is located almost exclusively
in the mandible, with a tendency for the body of the mandible. The ABC has predominance in the
posterior mandible with more uniform distribution in the maxilla. Surgical exploration into the
IBC reveals either an empty cavity or cavity filled with serosanguineous fluid. Surgically the ABC
appears as a blood-soaked sponge, usually without marked hemorrhage, and is known to have a
high recurrence rate.
26. Which genetic diseases are central giant cell lesions associated with?
The brown tumor of hyperparathyroidism associated with neurofibromatosis-1 (NFM-1), cherubism,
and Noonan syndrome all are characterized by central giant cell lesions, often multifocally. For this
reason, parathormone levels may be indicated with a histologic diagnosis of central giant cell lesion,
as well as genetic testing to rule in/out Noonan syndrome. Noonan syndrome is an uncommon
disorder characterized by short stature, short neck with webbing, deformity of the sternum, cardiac
anomalies, and cryptorchidism. Craniofacial features include dysmorphism, hypertelorism, downward
eye slant, ptosis, and low-set posteriorly rotated ears. Cherubism is an autosomal dominant disease
process that ceases after puberty. In the absence of severe functional disturbance, treatment is usually deferred until disease stabilization and/or regression.
27. How does one treat giant cell lesions?
Central giant cell lesions can be aggressive or nonaggressive but share the same benign histology.
Aggressive lesions tend to recur, are large, can erode teeth, and can be associated with pain. As
such, nonaggressive lesions can be definitively treated with enucleation while aggressive lesions may
require en bloc resection. Generally speaking, surgery and chemotherapy are indicated if patients
are ≤10 years old. For patients >10 years old, only surgery is required. Adjunctive chemotherapy
options include intranasal or subcutaneous calcitonin, intralesional glucocorticoids, and antiangiogenic
therapy with interferon alpha.
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28. What types of chemotherapy regimens are used to treat giant cell lesions?
• Interferon alpha : 3 million units/m2 SQ daily. Side effects can include fatigue, fever, headache, and
hair loss. Favorable response has been reported, especially in patients <10 years old.
• Systemic calcitonin : 50 IU SQ QD until tolerated, then advance to 50 IU SQ BID until tolerated, then
advance to 100 IU SQ QD for 6 to 9 months (until lesion resolves radiographically). The downside to
calcitonin is decreased serum Ca2+ levels and peptic ulcer disease.
• Intralesional steroids : Weekly injections of 30 mg triamcinolone (often combined with local anes-
thetic) for 6 weeks. GCLs are very vascular lesions so one drawback for intralesional steroid use
includes systemic absorption potentially resulting in a cushingoid response.
29. How should fibrous dysplasia be treated?
Re-contouring is usually performed in cases in which aesthetic and functional improvement is
required, but it is more effective when the dysplastic site has undergone maturation. Although complete resection of fibrous dysplasia has been decried in the past, current refined instrumentation and
craniofacial surgical techniques allow a more aggressive, non-disabling approach, particularly when
vital anatomic structures are affected by the lesion.
30. What surgery is indicated for osteosarcoma of the mandible?
Wide surgical resection (2.0 to 3.0 cm margins). Adjuvant therapy has been shown to be beneficial in
cases when surgical margins are positive or uncertain.
31. What are the workup and treatment for a diagnosis of solitary plasmacytoma of
bone?
A solitary plasmacytoma is a unifocal, monoclonal, neoplastic proliferation of plasma cells occurring
most often within bone but may be found within soft tissue. The disease mostly affects men over the
age of 50. It is rarely found in the jaws, with mandible more common than maxilla. Plasmacytosis
must be ruled out with a complete radiographic survey and a bone marrow biopsy. Urine and serum
electrophoresis demonstrate a monoclonal immunoglobulin M spike in up to 25% of cases. 70% of
patients with solitary lesions develop multiple myeloma. Treatment of solitary plasmacytoma includes
radiation therapy.
CANCER OF THE ORAL CAVITY
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David L. Hirsch, Lauren G. Bourell, Ray Cheng
1. What is the typical presentation of oral cancer?
Oral cancer may present as an irregular color change or thickening in the mucosa. It may be a mass
that is exophytic or endophytic, ulcerated or non-ulcerated. When larger, it is typically indurated. It
may be friable and bleed and is usually, although not always, painful.
2. What is the prevalence of oral cancer?
Worldwide, oral cancer is the twelfth most common cancer; all head and neck cancers combined rank
fifth overall. In the US, there are about 45,000 new head and neck cancer cases per year, of which
about 12,000 are oral cavity cancers. Oral cancer is more common in males by a ratio of 2:1 and
most common in the fifth to sixth decades of life.
3. What is the most common location in the oral cavity for cancer to present?
The most common sub-site is tongue, followed by floor of mouth. Buccal mucosa and retromolar
trigone areas are next in frequency.
4. What does TNM stand for, and what is the TNM system in reference to oral
cancer?
Tumor Node Metastases (TNM) is a staging system for cancer of the oral cavity. TNM staging can be
different in different head and neck sub-sites. (See Table 45-1.)
5. How is oral cancer staged? What is the average 5-year survival for each stage?
See Table 45-2.
6. What is the difference between clinical staging and pathologic staging?
Clinical staging depends on clinical examination of tumor size, palpable lymph nodes, and radiologic
evidence of cervical lymph nodes and distant metastasis. Pathologic staging is determined by the size
of tumor and evidence of cervical lymph nodes based on final pathology.
7. What are the common risk factors for oral cancer?
Tobacco and alcohol use (which has a synergistic effect when combined with tobacco) are two of the
most common risk factors for oral cancer. In parts of the world were paan or betel quid (arica nut)
products are used, this is also a risk factor. Diets low in fresh fruits and vegetables are associated
with an increased cancer risk as well.
8. What is the role of HPV (human papillomavirus) in oral cancer?
Particular strains of the HPV, especially HPV-16, are independent risk factors for oropharyngeal
squamous cell carcinoma. For oral squamous cell carcinoma, the rate of HPV+ in oral cavity cancer is
significantly lower, and its association with oral cavity cancer is controversial.
9. Which oral lesions are considered premalignant?
Potentially malignant lesions of the oral cavity include leukoplakia, erythroplakia, lichen planus,
lichenoid reaction, submucous fibrosis, discoid lupus erythematosus, actinic keratosis, and epithelial
dysplasia.
10. What is the risk of progression to oral cancer for these premalignant lesions?
For leukoplakias without dysplasia and for lichen planus and lichenoid reactions, the risk of malignant
transformation is <1%. Erythroplakia has a much higher rate of malignant transformation of 23.4%,
while leukoplakias with dysplasia have the highest rate of transformation at 36.4%.
11. What is the management of these premalignant lesions?
Smoking and alcohol cessation should be encouraged for all patients with leukoplakia. Various forms of
surgical treatment, including scalpel excision, NdYAG laser or CO2 laser-assisted excision, or photodynamic therapy, have been advocated as treatment for leukoplakia with or without evidence of dysplasia.
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CHAPTER 45
Table 45-1. Oral Cavity Squamous Cell Carcinoma TNM Description
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PRIMARY
TUMOR (T)
T
X
T
0
T
is
T
1
T
2
Primary tumor cannot be
assessed
No evidence of primary tumor N
Carcinoma in situ N
Tumor size 2 cm or less N
Tumor size between 2 and 4 cm N
REGIONAL LYMPH
NODES (N)
N
X
0
1
2
2a
Regional lymph nodes cannot be
assessed
No regional lymph node
metastasis
Met in single ipsilateral lymph
node less than 3 cm
Met in single ipsilateral lymph
node greater than 3 cm less
than 6 cm
T
3
T
4a
Tumor size greater than 4 cm N
Tumor invades adjacent struc-
tures only (cortical bone, deep
2b
N
2c
Multiple ipsilateral lymph nodes,
none greater than 6 cm
Bilateral or contralateral lymph
nodes, all less than 6 cm
extrinsic muscle of tongue,
maxillary sinus, skin of face)
T
4b
Tumor invades masticator space,
pterygoid plates, or skull base
N
3
Mets in lymph node greater than
6 cm in size
and/or encases internal carotid
artery
From Edge SB, Byrd DR, Compton CC, et al., editors: AJCC cancer staging manual, ed 7, New York, 2010, Springer.
DISTANT
METASTASIS (M)
M
0
M
1
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No distant metastasis
Distant metastasis
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Table 45-2. Oral Cavity Squamous Cell Carcinoma TNM Staging
Stage T N M 5-Year Survival
0 T
I T
II T
III T
IVA T
is
1
2
1
T
2
T
3
4a
T
4a
T
1
T
2
T
3
T
4a
IVB Any T N
T
4b
IVC Any T Any N M
From Edge SB, Byrd DR, Compton CC, et al., editors: AJCC cancer staging manual, ed 7, New York, 2010,
Springer.
N
0
N
0
N
0
N
1
N
1
N
1
N
0
N
1
N
2
N
2
N
2
N
2
3
Any N M
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
0
1
91%
77%
61%
32%
25%
4%
Erythroplakia and lesions demonstrating dysplasia should be treated more seriously as they
carry a higher risk of malignancy. Patients with lichen planus require an initial biopsy and periodic
follow-up.
12. What is PVL (proliferative verrucous leukoplakia), and what is its premalignant
potential?
PVL is a corrugated-appearing, papillomatous lesion of the oral cavity, more common in elderly women
who had leukoplakia for many years, with no etiologic factors proven to date. There is an approximately
74% rate of malignant transformation to squamous cell carcinoma or verrucous carcinoma, recurrences
after treatment in 86.7% of cases, new lesions during follow-up in 83.3%, and oral cancer eventually in
63.3% with high incidence on the gingival.
13. How does depth of invasion of cancer of the oral tongue affect prognosis?
Tumors with greater thickness and greater depth of invasion into underlying structures represent
later stage disease. Tumors with depth of invasion <4 mm have increased locoregional control and
better disease-specific and overall survival compared to tumors with depth of invasion ≥4 mm,
which have worse locoregional control and decreased survival. There is also an increased risk of
neck metastasis with >4 mm depth of invasion. According to Shah et al. there is also an increased
risk of neck recurrence in patients with low-risk T1-2 tongue cancer with >4 mm thickness who
underwent partial glossectomy and ipsilateral elective neck dissection without postoperative
radiation.
14. What is the current staging system for oral cancer?
The TNM staging system is shown in Tables 45-3 to 45-5.
Some inherent inadequacies of this system have prompted the proposal of certain modifications
and revisions in an effort to enhance its prognostic significance.
15. Which levels are commonly associated with regional metastasis from oral cavity
SCC?
Levels I-III are the most commonly involved sites in neck metastasis. Level IV only represents a very
small subgroup of patients. Level IV lymph node may be at a higher risk when the presence of metastasis in levels I-III is found. Level V is an uncommon finding in oral cavity SCC but significant in other
head and neck cancer sites.
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Table 45-3. Tumor Classification of Cancer of the Oral Cavity
CLASS TUMOR SIZE
T
1
T
2
T
3
T
4
From Edge SB, Byrd DR, Compton CC, et al., editors: AJCC cancer staging manual, ed 7, New York, 2010, Springer.
Table 45-4. Node Classification of Cancer of the Oral Cavity
CLASS DESCRIPTION
N
X
N
0
N
1
N
2
Regional lymph nodes cannot be assessed
No regional lymph node metastasis
Metastasis in a single ipsilateral lymph node, ≤3 cm at greatest dimension
Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than 6 cm at
greatest dimension
or
Multiple ipsilateral lymph nodes, none more than 6 cm at greatest dimension
or
Bilateral or contralateral lymph nodes, none more than 6 cm at greatest dimension
N
2a
N
2b
N
2c
N
3
From Edge SB, Byrd DR, Compton CC, et al., editors: AJCC cancer staging manual, ed 7, New York, 2010, Springer.
Metastasis in a single ipsilateral lymph node, >3 cm but ≤6 cm at greatest dimension
Metastasis in multiple ipsilateral lymph nodes, none >6 cm at greatest dimension
Metastasis in bilateral or contralateral lymph nodes, none >6 cm at greatest dimension
Metastasis >6 cm at greatest dimension in a lymph node
≤2 cm at greatest dimension
>2 cm but ≤4 cm at greatest dimension
>4 cm at greatest dimension
Tumor invades adjacent structures
Table 45-5. Metastasis Classification of Cancer of the Oral Cavity
CLASS DESCRIPTION
M
X
M
0
M
1
From Edge SB, Byrd DR, Compton CC, et al., editors: AJCC cancer staging manual, ed 7, New York, 2010, Springer.
16. What is meant by the term neck dissection in reference to surgical treatment of
oral cancer?
A neck dissection is a lymphadenectomy, or removal of lymph nodes, from the cervical region of the
neck extending below the mandible to just above the clavicle and posteriorly to the trapezius muscle.
Depending on the type of neck dissection, the sternocleidomastoid muscle, internal jugular vein, and/
or spinal accessory nerve may also be included in the neck dissection specimen. Neck dissection is a
therapeutic, diagnostic, and staging procedure for the oral cancer patient.
17. What are the types of neck dissections?
There are various systems for classifying neck dissections. The most aggressive approach is called
a radical neck dissection. This refers to removal of all lymph nodes in the neck from levels I-V
along with the SCM (sternocleidomastoid), the internal jugular, and the spinal accessory nerve. The
modified radical neck dissection is a version of the radical neck that removes all lymph nodes from
levels I-V but spares one (or more) of the named structures. A type I modified radical neck dissection
spares the spinal accessory, type II spares the spinal accessory and the internal jugular, and type III
Distant metastasis cannot be assessed
No distant metastasis
Distant metastasis
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spares all three: spinal accessory, internal jugular, and SCM. There is also a selective neck dissection that includes removal of selected lymph nodes only, from levels of the neck most likely to be
involved with a particular tumor (as an example, a selective neck dissection for an oral cavity cancer
would usually include levels I-III—sometimes also referred to as a supraomohyoid neck dissection).
18. Which patients are indicated for a neck dissection?
Patients with clinical evidence of cervical lymph node metastasis, either a neck mass on physi-
cal exam or a positive lymph node on diagnostic imaging (>15 mm in size, central lucency, ring
enhancement), are indicated for neck dissection. Patients with T2 and larger tumors usually receive an
ipsilateral neck dissection, with consideration for a contralateral neck dissection if the tumor crosses
the midline or if they have contralateral neck disease.
19. What is an SLNB (sentinel lymph node biopsy) in reference to oral cancer?
The sentinel lymph node is the first lymph node in a chain or group of lymph nodes to receive the
lymphatic drainage from a tumor. This sentinel node can be identified and examined for the presence
of metastatic cancer cells—the presence or absence of cancer cells in the sentinel node is taken as
evidence of the likelihood that cancer has spread to the remainder of the lymph node chain. The benefit of identifying and removing the sentinel node (a sentinel node biopsy) is that for negative sentinel
nodes, the patient can be spared a more invasive neck dissection procedure.
20. Which patients benefit from this technique (SLNB)?
SLNB does not replace traditional neck dissection and is not indicated for patients in whom a neck
dissection is indicated. SLNB is best for patients with small lesions (T1, some T2) and N0 necks.
Patients should be informed that, in the case of a positive SLNB, they will require a formal neck
dissection.
The sensitivity of SLNB was 87.5% and 77.8% for permanent and frozen sections, respectively.
The specificity was 100% for permanent and frozen sections, respectively.
21. What are the types of imaging that may be used in the work-up of an oral cancer
patient?
Panoramic or plain radiography, CT (computed tomography), and MRI (magnetic resonance imaging) may
all be used in the work-up of a patient with known or suspected oral cancer. Imaging of the chest with
plain film or CT scan should also be done initially to rule out metastatic or second primary disease.
Panoramic radiography has good specificity for bony invasion but poor sensitivity and is useful for
imaging the dentition and for periapical/periodontal infections that may be missed by traditional CT.
CT scan has 100% specificity for bony invasion. Intravenous contrast is needed to assess nodal
metastasis in the neck. Dental restoration can adversely affect the quality of imaging.
MRI also has 100% specificity for bony invasion and is slightly more sensitive than traditional CT
scan. MRI may be degraded by motion artifact, and MRI may overestimate bony involvement if edema
is present. MRI is suitable for soft tissue imaging of the primary tumor and cervical lymph nodes (with
contrast).
22. What are the primary treatment modalities of oral cancer?
The preferred treatment for oral cancer is surgical resection, followed by radiation or radiation plus
chemotherapy as needed for high-risk patients. Radiation as a primary treatment for oral cancer has
a small role, although cancers of the oropharynx, larynx, and hypopharynx are more often treated with
radiation as the primary modality.
Randomized controlled trials comparing surgery to radiation for treatment of oral cancer (T2+
lesions) were terminated early due to markedly poorer outcomes in the radiation treatment arm; in
general, the overall survival and disease-free survival of patients receiving primary radiation therapy
for oral cancer is roughly half that of those receiving surgery as their primary modality of treatment.
23. What is the accepted margin of normal (uninvolved) tissue surrounding a tumor
that a surgeon proposes to take during surgical resection of an oral cancer?
A margin of 1 to 1.5 cm circumferentially around a tumor is the goal during resection of oral cancer.
In reality, this margin may not be achievable due to proximity of vital structures. Furthermore, there
is a considerable specimen shrinkage after resection and fixation of tissue that can vary in surgical
site. Mistry et al. found mean shrinkage of tumor margins for tongue and buccal specimen were
23.5% and 21%, respectively. Less shrinkage is appreciated in higher stage T3/T4 than for lower
stage T1/T2 tumors.
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