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Surg Oncol Clin N Am. Author manuscript; available in PMC 2016 September 10.
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Published in final edited form as:

Surg Oncol Clin N Am. 2015 July ; 24(3): 491–508. doi:10.1016/j.soc.2015.03.006.

CANCER OF THE ORAL CAVITY

Pablo H. Montero, MD* and Snehal G. Patel, MD*
*Head and Neck Surgery Service, Department of Surgery, Memorial Sloan-Kettering Cancer
Center

Keywords
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oral cavity cancer; oral cancer; squamous cell carcinoma; head and neck cancer

INTRODUCTION
Cancer of the oral cavity is one of the most common malignancies,1 especially in developing
countries, but also in the developed world2. Squamous cell carcinoma (SCC) is the most
common histology and the main etiological factors are tobacco and alcohol use3. Although
early diagnosis is relatively easy, presentation with advanced disease is not uncommon. The
standard of care is primary surgical resection with or without postoperative adjuvant therapy.
Improvements in surgical techniques combined with the routine use of postoperative
radiation or chemoradiation therapy have resulted in improved survival statistics over the
past decade 4. Successful treatment of patients with oral cancer is predicated on
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multidisciplinary treatment strategies to maximize oncologic control and minimize impact of

therapy on form and function.

ANATOMY OF THE ORAL CAVITY

The oral cavity extends from the vermilion border of the lips to the circumvallate papillae of
the tongue inferiorly and the junction of the hard and soft palate superiorly. The oral cavity
is divided into several anatomical subsites: lip, oral tongue, floor of mouth, buccal mucosa,
upper and lower gum, retromolar trigone and hard palate (Figure 1). Despite their proximity,
these subsites have distinct anatomical characteristics that need to be taken into account in
planning oncologic therapy.
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EPIDEMIOLOGY AND ETIOLOGY

Worldwide, 405,000 new cases of oral cancer are anticipated each year, and the countries
with the highest rates are Sri Lanka, India, Pakistan, Bangladesh, Hungary and France5

Corresponding Author: Dr. Snehal G. Patel, Head and Neck Surgery, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, New
York, NY 10065. Telephone: 212-639-3412, patels1@mskcc.org.
The Authors have nothing to disclose.
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our
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 Montero and Patel Page 2

(Figure 2). In the European Union there are an estimated 66,650 new cases each year. The
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American Cancer Society estimates that there will be 42,440 new cancers of the oral cavity
and pharynx in the U.S. causing 8,390 deaths in 20146. Tobacco smoking and alcohol are the
main etiological factors in SCC of the oral cavity (SCCOC)3, 7. Other habits such as betel
nut and tobacco chewing have been implicated in the Asian population.

Tobacco contains many carcinogenic molecules, especially polycyclic hydrocarbons and

nitrosamines. A directly proportional effect exists between the pack years of tobacco used
and the risk of SCCOC8. This risk can be reduced after tobacco cessation, but it does not
fully abate (30% in the first 9 years and 50% for those over 9 years)910. A decreased
incidence of oral cavity cancer has been reported in the last 15 years, widely attributed to a
reduction in tobacco use11.

Alcohol and tobacco seem to have a synergistic effect in the etiology of oral and
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oropharyngeal SCC3, 12, 13. However, alcohol is linked to an increased risk of cancer even in
non-smokers14. Other factors such as poor oral hygiene 15, wood dust exposure 16, dietary
deficiencies17, red meat and salted meat consumption18, 19 have been reported as etiologic
factors. The herpes simplex virus (HSV) has been suspected but has not been implicated in
the etiology of SCCOC20. Despite the emerging evidence supporting the role of the human
papilloma virus (HPV) in the etiology of oropharyngeal cancer, it has not been conclusively
linked to SCCOC21. Host factors such as immune system alterations in transplant
patients22, 23 and HIV-infected patients with AIDS24, and genetic conditions like xeroderma
pigmentosum, Fanconi anemia and ataxia telangiectasia are associated with an increased
incidence of head and neck cancer25–28.

Oral cancer is more common in men and usually occurs after the 5th decade of life. About
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1.5% will have another synchronous primary in the oral cavity or the aero-digestive tract
(larynx, esophagus or lung)29. Metachronous tumors develop in 10% to 40% in the first
decade after treatment of the index primary30, 31 and therefore regular post-therapy
surveillance and lifestyle alteration are important strategies for secondary prevention.

PATHOLOGY
Squamous cell carcinomas (SCC) constitute more than 90% of all oral cancer. Other
malignant tumors can arise from the epithelium, connective tissue, minor salivary glands,
lymphoid tissue, and melanocytes or metastasis from a distant tumor.

A variety of premalignant lesions have been associated with development of SCC32. The
more common premalignant lesions including leukoplakia, erythroplakia, oral lichen planus,
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and oral submucous fibrosis have varying potential for malignant transformation33. The
WHO (2005) classifies premalignant lesions according to degree of dysplasia into mild,
moderate, severe, and carcinoma in situ.

Leukoplakia is a clinical term defined as a “white patch or plaque that cannot be

characterized clinically or pathologically as any other disease”34. This lesion is usually
associated with smoking and alcohol use. The prevalence of leukoplakia worldwide is about
2%. Dysplastic changes are seen in only 2–5% of patients. The annual rate of malignant

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transformation for leukoplakia is 1%. Risk factors for malignant transformation include
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presence of dysplasia, female gender, long duration of leukoplakia, location on the tongue or
floor of mouth, leukoplakia in non-smokers, size greater than 2cm, and non-homogeneous
type. In addition to lifestyle alteration to avoid tobacco and alcohol use, excision constitutes
the only definitive modality for accurate diagnosis and treatment.

Erythroplakia is a “bright red velvety patch that cannot be characterized clinically or

pathologically as being caused by any other condition”34. Surgical excision is recommended
as these lesions have higher malignant potential than leukoplakia and are commonly
associated with dysplasia and carcinoma in situ.

Non-squamous cell carcinomas of the oral cavity are uncommon. Minor salivary gland
carcinomas represent less than 5% of the oral cavity cancers. They frequently arise on the
hard palate (60%), lips (25%) and buccal mucosa (15%)35. Mucoepidermoid carcinoma is
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the most common type (54%), followed by low-grade adenocarcinoma (17%), and adenoid
cystic carcinoma (15%)49,50.

Mucosal melanomas are rare but usually present as locally aggressive tumors, mainly of the
hard palate and gingiva. Bony tumors including osteosarcoma of the mandible or maxilla
and odontogenic tumors such as ameloblastoma can present within the oral cavity and may
be mistaken for a mucosal lesion if there is surface ulceration.

CLINICAL PRESENTATION AND EVALUATION

Despite easy self-examination and physical examination, patients often present with
advanced stage disease. A comprehensive head and neck exam is mandatory in patients with
suspected oral cavity cancer. Visual inspection and palpation allow an accurate impression of
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the extent of the disease, the third dimension of tumor, the presence of bone invasion, or skin
breakdown. Appropriate documentation with drawings and photographic records of the
tumor are useful in staging, decision-making and further follow up.

The clinical TNM stage should be recorded at first encounter and modified as evaluation
progresses. The initial workup consists of diagnosis by biopsy. Accessible lesions may be
adequately biopsied in the clinic using punch forceps, core needle or fine-needle aspiration.
Some patients will require examination under general anesthesia (EUA) in order to access
posteriorly located lesions, or to complete a physical exam limited by pain and trismus.
Radiographic imaging is crucial for evaluation of the relation of the tumor to adjacent bone
and for assessing regional lymph nodes. CT scan is the study of choice for evaluation of
bone and neck nodes, especially early cortical involvement and extracapsular nodal spread.
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MRI provides complementary information about soft tissue extent and perineural invasion
and is also helpful for evaluating the extent of medullary bone involvement because adult
marrow is normally replaced by fat. Most patients with oral cancer are not at risk for distant
metastases and therefore the role of PET scan in initial assessment is debatable. However, a
preoperative PET scan may be useful as a baseline if adjuvant treatment is anticipated and a
PET scan will be used for radiation therapy planning (though this is undertaken differently
from a “diagnostic” PET scan). Patients with locally advanced tumors require appropriate

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multidisciplinary consultations with the reconstructive surgeon, medical specialists for

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presurgical optimization, dental professionals, speech and swallowing pathologists, and

behavioral therapists for smoking cessation and other lifestyle alterations.

The TNM system is the most widely accepted prognostic system due to its relatively simple
design and user-friendliness. The clinical staging of the oral cavity tumors consists of
primary tumor characteristics, the neck, and assessment for distant metastases (Table 1).
This information allows TNM stage grouping for the tumor (Table 2)36. The basic elements
in staging of the primary site are the tumor size and invasion of deep structures. Advanced
disease is defined by invasion of structures such as medullary bone, deep muscle of the
tongue, maxillary sinus, and skin for T4a disease, or masticator space, pterygoid plates, or
skull base and/or encasement of the internal carotid artery for T4b disease. Lymphatic
spread into the neck generally occurs in a step-wise, orderly and predictable fashion. The
lymph node echelons of the neck are described using the terminology standardized by the
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American Head and Neck Society Guidelines37 (Figure 3).

Knowledge of the patterns of nodal metastasis has practical implications in the design of
neck dissection for patients with oral cancer. The patient with a clinically negative neck is at
highest risk of metastasis to levels I–III38. Skip metastases to level IV do occur, especially in
cancer of the anterior tongue. Metastases to level V are extremely rare (1%) even in patients
with clinically positive neck. Oral tongue tumors have the greatest propensity of all oral
cancers for metastasis to the neck, and tumor thickness (Figure 4) is a major predictor of risk
of nodal metastasis39.

TREATMENT
Surgical resection is the treatment of choice for SCCOC. Surgical resection allows accurate
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pathologic staging, with information about the status of margins, tumor spread and
histopathologic characteristics which can then be used to inform subsequent management
based upon assessment of risk versus benefit. Adjuvant radiotherapy ± chemotherapy is used
for specific indications in locoregionally advanced tumors. A multidisciplinary team is
absolutely essential to ensure a favorable outcome. Multiple factors are taken into account in
selecting treatment for an individual patient. The risk of treatment-related complications
should be assessed based on physiological age, comorbid conditions (e.g. cardiopulmonary
status), lifestyle (smoking or alcohol), surgical resectability, and patient expectations.

Surgical Management
A detailed description of surgical technique for management of oral cavity cancers is beyond
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the scope of this publication and the reader is referred to specialized texts for this
information40. Broad principles of surgical management will be discussed and these include
access to the oral cavity, management of the mandible, management of neck nodes, and
reconstruction of oral cavity surgical defects.

Surgical access—The transoral approach is usually used for premalignant lesions and
small, superficial tumors of the anterior floor of mouth, alveolus and tongue. A more
invasive approach becomes necessary for posteriorly located tumors or if there are

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limitations due to trismus or inadequate surgical exposure (Figure 5). The lip-splitting
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paramedian mandibulotomy approach is used for larger posteriorly located tumors of the
tongue. The upper cheek flap and midfacial degloving approaches are useful for gaining
access to the maxilla.

Management of the mandible—Mandibular invasion can occur early in tumors of the

floor of the mouth, the ventral surface of the tongue and the gingivobuccal sulcus. The
mechanism of invasion of these tumors into the mandible has been well studied41–43.
Tumors invade the mandible through the dental sockets in the dentate mandible, and through
the dental pores of the alveolar process in the edentulous mandible.

Early cortical invasion of the mandible is difficult to assess with plain radiography, or
orthopantomograms but CT scans are more sensitive. On a practical basis, tumors that are in
close juxtaposition to the mandibular cortex will require consideration for marginal
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mandibulectomy in order to achieve an adequate margin of resection irrespective of

radiographically demonstrable early cortical invasion. The role of marginal resection might
be limited in patients with reduced vertical height of the body of the mandible due to the
higher risk of early involvement of the body of mandible and the risk of pathologic fracture
if a marginal resection is performed. Adequate tumor clearance in edentulous patients may
therefore necessitate a segmental mandibulectomy. The indications for segmental resection
are listed in Table 3.

Management of the neck—Sixty percent of patients with early stage oral cancer will
present with a clinically negative neck (cN0). Approximately 20–30% will have
microscopically evident nodal metastasis on histologic examination after elective neck
dissection (END). The risk of nodal metastasis is related to several factors (Table 4)44, 45.
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Cervical lymph node metastasis is the single most important prognostic factor in oral cancer:
survival chances are reduced by 50% when compared to those with similar primary tumors
without neck metastases46, 47. SCC of the oral tongue and the floor of the mouth are more
likely to metastasize to the neck, and these patients should be offered END, even for early
stage tumors, if they are thicker than about 4mm48. The hard palate and the upper gum have
a relatively lower rate of occult nodal metastasis and END may not be indicated49.

Sentinel node biopsy is an alternative to END for staging the cN0 neck in early stage (T1–2)
SCCOC. The technique was first reported in 2001 by Shoaib et al50 and has been analyzed
in several single institutional studies as well as two prospective multicenter trials, one in
Europe51, 52 and the other in the US53. The procedure is technically challenging and
successful identification of sentinel nodes and detecting occult metastasis depends on
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expertise and experience. Therefore, it should be undertaken only in centers with the
necessary proficiency and the appropriate volume of cases54.

In patients with clinically or radiographically involved neck nodes, a therapeutic

comprehensive neck dissection is indicated (Table 5). It involves dissection of levels I to V.
The need to sacrifice other structures such as the spinal accessory nerve,
sternocleidomastoid muscle, or internal jugular vein depends on the location of the
metastasis and its characteristics. The most common type of comprehensive neck dissection

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is the modified radical neck dissection, MRND Type 1. Radical neck dissection is rarely
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performed unless there is direct infiltration of the relevant structures by gross extranodal
extension of disease (Table 5).

In a patient with a clinically negative neck, the risk of occult metastasis is mainly to levels I
through III. Potential compromise of levels IV and V is very rare. For these reasons, a
supraomohyoid neck dissection (SOHND)(Table 5) is usually adequate to stage the cN0
neck. In patients with primary oral tongue SCCOC dissection of level IV may be indicated
due to the possibility of skip metastasis. For patient with positive nodes on END, neck
recurrence is observed in 10–24%55. Appropriately selected patients benefit from
postoperative radiation therapy56, 57. For cN0 patients who are proven pathologically N0,
failure rates of less than 10% have been reported58.

Reconstructive surgery—Restoration of form and function after ablative cancer surgery

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is the ultimate goal of treatment and is achieved by choosing the appropriate reconstructive
procedure. Surgical defects after resection of early stage tumors can usually be reconstructed
with primary closure or the use of skin graft or skin substitutes. Reconstruction of larger and
more complex defects that result from resection of advanced tumors requires participation
from an expert reconstructive surgeon. Microvascular free tissue transfer is the technique of
choice59, 60. For example, in patients with soft tissue defects of the oral tongue, floor of
mouth and retromolar trigone, the free radial forearm flap results in excellent functional
results (Figure 6). In addition to soft tissue cover, free flaps are also a reliable source for
bone reconstruction. The fibula free flap is currently the workhorse in reconstruction of
defects following segmental mandibulectomy (Figure 6). Other composite microvascular
flaps include the radial forearm osteocutaneous flap, iliac crest and scapula free flaps.
Several studies have demonstrated the reliability and low morbidity of microvascular free
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flap reconstruction techniques61. The ability reliably to reconstruct large surgical defects has
contributed to improved oncologic outcomes in patients with locally advanced cancers by
enabling more complete resections62. Pedicled myocutaneous flaps such as the pectoralis
major, latissimus dorsi or trapezius flaps are reliable alternatives if surgical expertise is not
available or if the patient is not a good candidate for microvascular reconstruction.

Adjuvant treatment
Adjuvant postoperative treatment is indicated in patients with high risk of locoregional
recurrence. This includes patients with large primary tumors (pT3 or pT4), bulky nodal
disease (pN2 or pN3), metastases to nodal levels IV or V, positive surgical margins,
lymphovascular invasion, perineural invasion, and extracapsular spread. External beam
radiation therapy has been the traditional modality for postoperative adjuvant treatment and
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doses of 66–70 Gy result in good locoregional control63, 64. Two clinical trials have shown
that administration of cisplatin chemotherapy concurrently with postoperative radiotherapy
improves locoregional control and survival (versus radiotherapy alone) in head and neck
cancer patients with extracapsular spread and /or positive surgical margins65, 66. However,
concurrent chemoradiation can result in significant morbidity and is best used at centers
where appropriate expertise and infrastructure is available.

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OUTCOMES OF TREATMENT
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The results of treatment of SCCOC in recently published major series are shown in Table 6.
The overall 5-year survival in a recently analyzed cohort of patients at Memorial Sloan-
Kettering Cancer Center is 63%. This represents a significant improvement compared to
historical cohorts (Figure 7) and may be related to wider use of microvascular free flaps with
enhanced ability to resect large tumors and reconstruct large and complex defects, more
aggressive regional therapy including increasing use of elective selective neck dissections,
and the use of postoperative adjuvant therapy.

Approximately a third of patients treated for SCCOC relapse, and locoregional recurrence is
the most common pattern of failure. The clinical stage at presentation is an important
predictor of survival (Figure 8) but the most powerful predictor of outcome is the presence
of metastatic lymph nodes (Figure 9). Other clinical signs of locally advanced disease and
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poor prognosis include trismus, which indicates invasion of the pterygoid, temporalis or
masseter muscle; reduced tongue mobility, which indicates invasion of the extrinsic
musculature of the tongue or the hypoglossal nerve; and skin invasion with dermal
lymphatic infiltration. Significant histopathologic predictors of outcome include depth of
invasion of the primary tumor, positive margins of surgical resection, perineural invasion and
major extracapsular nodal extension.

Follow up
Oral cancer patients have a high risk of locoregional recurrence and developing subsequent
new primary cancers, but the risk of distant recurrence is low67. The possibility of a second
head and neck primary is about 4–7% a year and comprehensive clinical examination and a
high suspicion are the cornerstones of early diagnosis68. Control of lifestyle-related risk
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factors, such as tobacco and alcohol consumption, is a priority in these patients because of
the higher risk of treatment failure and second primaries69. Unfortunately, there is no
effective chemoprevention and close follow up remains the most important tool in secondary
prevention70. Baseline imaging studies are often obtained about 3–6 months following
completion of treatment and then as needed based on clinical suspicion. Chest imaging is not
routinely needed but may be beneficial in patients with a significant smoking history. Other
ancillary measures include speech and swallowing rehabilitation as indicated, monitoring of
thyroid stimulating hormone levels if the neck been treated with radiation therapy, and
regular dental evaluation.

CONCLUSION
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Treatment results for patients with oral cancer have improved considerably over the last
several decades due to improvements in reconstruction and adjuvant treatment. Further
improvements in survival have been hampered by attrition from second and subsequent
primary tumors in long-term survivors. Primary and secondary prevention of oral cancer
requires better education about lifestyle related risk factors, and improved awareness and
tools for early diagnosis.

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Key Points
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• Cancer of the oral cavity is a common malignancy in the United States

and around the world.

• The standard of care is primary surgical resection with or without

postoperative adjuvant therapy.

• Multidisciplinary treatment is crucial to improve the oncologic and

functional results in oral cancer patients

• Primary and secondary prevention of oral cancer requires education

about lifestyle-related risk factors, and improved awareness and tools
for early diagnosis.
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Figure 1.
Anatomic sites of the oral cavity
From Shah JP, Patel SG, Singh B, et al. Jatin Shah's head and neck surgery and oncology.
4th ed. Philadelphia, PA: Elsevier/Mosby; 2012, 232–244 with permisison.
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Figure 2.
Incidence of oral cavity cancer among both sexes expressed by level of Age-standardized
rate (ASR) in countries of the world (From GLOBOCAN 2012 International Agency for
Research on Cancer (http://globocan.iarc.fr/Pages/Map.aspx.))
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Figure 3.
Cervical lymph node level classification
From Shah JP, Patel SG, Singh B, et al. Jatin Shah's head and neck surgery and oncology.
4th ed. Philadelphia, PA: Elsevier/Mosby; 2012, 232–244, with permisison.
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Figure 4.
Incidence of lymph node metastasis and survival stratified by the thickness of the primary
tumor. (From Shah JP, Patel SG, Singh B, et al. Jatin Shah's head and neck surgery and
oncology. 4th ed. Philadelphia, PA: Elsevier/Mosby; 2012, 232–244, with permisison.)
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Figure 5.
Various surgical approaches. A, Peroral. B, Mandibulotomy. C, Lower cheek flap. D, Visor
flap. E, Upper cheek flap. (From Shah JP, Patel SG, Singh B, et al. Jatin Shah's head and
neck surgery and oncology. 4th ed. Philadelphia, PA: Elsevier/Mosby; 2012, 232–244, with
permisison.)
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Figure 6.
Fibular (left) and radial forearm (right) free flaps are two of the most common flaps used in
oral cavity reconstruction after major resections.
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Figure 7.
Outcomes of treatment of SCCOC in three cohorts treated during different time periods at
Memorial Sloan-Kettering Cancer Center (1960–2005). Courtesy of Memorial Sloan-
Kettering database, New York, NY.
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Figure 8.
Clinical stage at presentation is an important predictor of outcome. Courtesy of Memorial
Sloan-Kettering database, New York, NY.
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Figure 9.
Impact of clinically palpable lymph node metastasis on disease-specific survival in SCCOC.
Courtesy of Memorial Sloan-Kettering database, New York, NY.
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Table 1

TNM classification of carcinomas of the oral cavity

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T — Primary tumor
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
T4a (lip) Tumor invades through cortical bone, inferior alveolar nerve, floor of mouth, or skin (chin or nose)
T4a (oral cavity) Tumor invades through cortical bone, into deep/extrinsic muscle of tongue (genioglossus, hyoglossus, palatoglossus,
and styloglossus), maxillary sinus, or skin of face
T4b (lip and oral cavity) Tumor invades masticator space, pterygoid plates, or skull base; or encases internal carotid artery
Note: Superficial erosion alone of bone/tooth socket by gingival primary is not sufficient to classify a as T4.
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N - Regional Lymph Nodes

NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimension
N2 Metastasis as specified in N2a, 2b, 2c below
N2a Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than 6 cm in greatest dimension
N2b Metastasis in multiple ipsilateral lymph nodes, none more than 6 cm in greatest dimension
N2c Metastasis in bilateral or contralateral lymph nodes, none more than 6 cm in greatest dimension
N3 Metastasis in a lymph node more than 6 cm in greatest dimension
Note: Midline nodes are considered ipsilateral nodes.
M – Distant metastasis
MX Distant metastasis cannot be assessed
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M0 No distant metastasis
M1 Distant metastasis

From, Edge SB, Byrd DR, Compton CC, eds. AJCC Cancer Staging Manual. 7th ed. New York, NY.: Springer, 2010; 33, with permission.
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Table 2

Oral cancer staging

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Stage T N M
0 Tis N0 M0

I T1 N0 M0

II T2 N0 M0

III T3 N0 M0

T1 N1 M0

T2 N1 M0

T3 N1 M0

IVA T4a N0 M0

T4a N1 M0

T1 N2 M0
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T2 N2 M0

T3 N2 M0

T4a N2 M0

IVB Any T N3 M0

T4b Any N M0

IVC Any T Any N M1

From, Edge SB, Byrd DR, Compton CC, eds. AJCC Cancer Staging Manual. 7th ed. New York, NY.: Springer, 2010; 33, with permission.
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Table 3

Indications for Segmental mandibulectomy

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• Gross invasion of the of the mandible

• Tumor fixation to the majority of the vertical height of the occlusal surface of the mandible in hypoplastic edentulous
mandible with significant loss of vertical height precluding safe performance of rim resection
• Tumor fixed to the mandible following prior radiotherapy to the mandible
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Table 4

Risk factors of nodal metastasis in oral cancer

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• Tumor Size
• Histologic Grade
• Depth of Invasion
• Perineural Invasion
• Vascular Invasion
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Table 5

Types of Neck Dissections

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Lymph Nodes Excised Other Structures Excised Structures Preserved

Radical Neck Dissection Levels I–V Sternocleidomast oid Muscle, Internal
(RND) Jugular Vein, Spinal Accessory Nerve,
Submandibular Gland
Modified Radical Neck Levels I–V Sternocleidomast oid Muscle, Internal Spinal Accessory Nerve
Dissection (MRND) Type I Jugular Vein, Submandibular Gland
Modified Radical Neck Levels I–V Internal Jugular Vein, Submandibular Sternocleidomoid Muscle, Spinal
Dissection (MRND) Type II Gland Accessory Nerve
Modified Radical Neck Levels I–V Submandibular Gland Sternocleidomast oid Muscle,
Dissection (MRND) Type III Internal Jugular Vein, Spinal
Accessory Nerve
Supraomohyoid Neck Levels I–III Submandibular Gland Sternocleidomast oid Muscle,
Dissection (SOHND) Internal Jugular Vein, Spinal
Accessory Nerve
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Table 6

Outcomes in patients treated for squamous carcinoma of the oral cavity in major series around the world.

Series Country Year Total no. of Patients 5-years OS all patients 5-years DSS all patients Stage I Stage II Stage III Stage IV
Loree et al72 USA 1997 398 57.0% - - - - -
Taiwan 1999 7032 36.1% - 72.0% 38.9% 26.7% 11.8%
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Chen et al73
Funk et al74 USA 2000 30,803 43.5% - - - - -

Carvalho et al75 Brazil 2002 3642 43.0% - 74.0% 33.0%

Yeole et al76 India 2000 15051 45.9% - 68.9% 26.6% 9.5%

Rogers et al77 UK 2008 541 56.0% 74.0% - - - -

Listl et al78 Germany 2012 15792 54.6% - - - - -

MSKCC USA 2014 1816 62.5% - 78.5% 68.4% 64.5% 34.5%

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