Download Oral Cancer Detection: The Role of Adjunctive Technology

Oral Cancer Detection:
The Role of Adjunctive Technology
C
CouErse
Written by Denis P. Lynch, D.D.S., Ph.D.
Educational Objectives
1. Know the incidence of oral cancer in the United States and understand the risk
factors
2. Understand screening methods available for the detection of oral cancer
3. Understand the role of chromosomal aberrations in the risk of malignant
transformation
Abstract
In the United States in 2007, over 34,000 new cases of oral cavity and oropharyngeal
cancer will be diagnosed. With a five-year relative survival rate estimated at 59.1%
overall during 1996–2003. Early detection based on diagnoses of suspicious lesions
is increased through regular screening of patients. In recent years, screening
technologies have become available that supplement the visual examination. The
ultimate goals are to reduce mortality and morbidity, and to improve patients’ quality
of life.
Introduction/Overview
In the United States in 2007, over 34,000 new cases of oral cavity and oropharyngeal
cancer will be diagnosed. During the same time period, over 7,000 affected individuals
will die of these cancers.1 In the United States, the most common sites for oral cancer
are the tongue and lip.
Risk Factors
The single greatest risk factor for oral cancer in the United States is the use of
tobacco, with combustible and smokeless tobacco being associated with 75% of all
cases of oral cancer. Oral cancer is also six times more likely to develop in alcohol
drinkers than in non-drinkers. The combination of tobacco use and alcohol abuse
is particularly hazardous, posing a fifteen-fold risk of oral cancer compared to nonusers.2 Other factors associated with increased oral cancer risk include ultraviolet
radiation (lip exposure) and HIV seropositivity (Table 1). A strong association has
been found with the presence of HPV in oral tissues, independent of smoking or
drinking habits.3,4,5 One study of 143 patients found HPV-16, present in 16.8% of
head and neck squamous cell carcinomas.6 A reduced risk of oral cancer has been
associated with a high dietary fruit and vegetable intake.7
10
Table 1. Risk factors for oral cancer
Risk factors
Predisposing risk factors
Smoking and/or chewing tobacco
Increasing age
Drinking alcohol
Male gender
Betel quid chewing
Genetics
Areca nut use
Socioeconomic status
HPV
HIV seropositivity
Use (abuse) of narcotics
Negative association
High dietary fruit and
vegetable intake
Cannabis use
Sunlight exposure (lower lip)
Previous oral or other cancer
Morbidity and mortality
Oral cancer is associated with significant morbidity and mortality. The five-year relative
survival rate for oral and pharyngeal cancer is estimated at 59.1% overall for cases
diagnosed during 1996–2003.8 Survival rates vary with the stage of the disease and
site. The best prognosis exists for lip cancer, with a 97% five-year relative survival rate
if the tumor is localized and completely excised. Oral cancers in other anatomic sites
can be clinically occult and asymptomatic. Fifty percent of tongue carcinomas have
metastasized by the time they are diagnosed.9 Early diagnosis significantly improves
the patient’s long-term survival and reduces morbidity. The excision of an oral cancer,
depending on the site and size of the tumor, can severely compromise the patient’s
quality of life and in some cases may not even be possible.
Initial lesions
Preventing disease progression relies on early detection, a diagnosis, and appropriate
treatment. Early detection of oral cancer is complicated by the fact that many lesions in
their earlier stages may be completely asymptomatic.
Clinically, cancerous and pre-cancerous lesions may present as ulcers, leukoplakia,
erythroplakia, erythroleukoplakia, soft tissue masses, or other lesions that will not heal
even after removal of the presumptive etiology (Figures 1–2).
11
Figure 1. Erythroplakia
Figure 2. Erythroleukoplakia
Leukoplakia, erythroplakia, and erythroleukoplakia (speckled leukoplakia) are clinical
terms for white, red, or mixed red/white lesions, respectively, that cannot be wiped
off, do not have an obvious clinical diagnosis, and have an unclear etiology.10 An
estimated 85% of oral premalignant and malignant lesions present clinically as
leukoplakias11 and the rate of malignant transformation of leukoplakia is estimated to
be 7%, occurring on average seven years following initial diagnosis.12
Non-homogenous leukoplakia has been found to have a seven times greater risk of
malignant degeneration than homogenous leukoplakia. Lesions greater than 2 cm in
size had a 5.4 times greater risk of developing malignancy than smaller lesions.13 In
the case of erythroplakias, 70%14 to 90%15 have been found to be severely dysplastic
or frankly malignant at the time of initial biopsy. The definitive diagnosis of oral cancer
can only be determined by histopathologic examination of a biopsy specimen and
ranges from normal, through varying degrees of dysplasia, to carcinoma-in-situ to
invasive malignancy.
The detection of suspicious lesions is increased through routine, regular screening of
patients.16 Early detection will result in earlier diagnosis, less aggressive treatment, and
decreased need for complicated post-treatment management.
Early detection and technology
Historically, unaided visual examination, palpation, and radiographs were available
for oral cancer screening. Supplemental screening technologies now available that
help the clinician identify suspicious lesions include the use of special wavelength
lights and chemiluminescence, as well as dyes that selectively stain lesions. Standalone screening devices include the Microlux/DL (AdDent), VELScope (LED Dental, Inc.),
and ViziLite and ViziLite Plus (Zila Pharmaceuticals, Inc.).
Microlux/DL
Microlux/DL is a hand-held device that uses light-emitting diodes (LEDs) as the
illumination source. The patient rinses for 30–60 seconds with 1% acetic acid, and
upon illumination the abnormal tissue will appear white (“aceto-white”).
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VELScope
VELScope is a hand-held device that emits a blue light to fluoresce the mucosa. No
pre-rinse is required. When exposed to the blue light, normal mucosa emits a pale
green autofluorescence, while abnormal tissue appears dark green to black (Figures
3a, b). Highly inflamed mucosa results in a loss of fluorescence which may result in
a false positive.17 The VELScope has been found to help delineate the extent of visible
lesions, as well as to identify lesions that were difficult to appreciate with unaided
visual examination.18 In one study, 12 of 19 VELScope-positive lesions were biopsied
and found to exhibit loss of heterozygocity.19
Figure 3a. Lesion
prior to use of VELScope
Figure 3b. Appearance
following autofluorescence
ViziLite and ViziLite-Plus
ViziLite is a hand-held device that emits chemiluminescent light. The patient rinses for
30–60 seconds with 1% acetic acid and the ViziLite device is used to illuminate the oral
cavity. Abnormal areas will appear white (“aceto-white”). The light increases both the
brightness and the sharpness of lesions.20
Chemiluminescence has been found to significantly assist the clinician in identifying
white and erythroleukoplakic lesions. In one study of 134 patients, use of ViziLite
identified two lesions that were not found by unaided visual examination, one of
which was a squamous cell carcinoma of the tongue.21 Kerr et al. studied 501 patients
and ninety-eight lesions found in when ViziLite was used with 77 of these considered
suspicious, including six that had been missed with unaided visual examination.22 The
adjunctive use of T-Blue630 is a feature specific to the ViziLite-Plus system. This is the only
FDA-cleared device and in-vivo staining system for the marking and identification of oral
lesions. After using the ViziLite to identify abnormal “aceto-white” areas, T-Blue630 can be
used to mark suspicious areas for further evaluation (Figures 4a, b).23
Figure 4a. Lesion prior to use of T-Blue
Figure 4b. Lesion after use of T-Blue
13
T-Blue630 is the brand name for pharmaceutical-grade tolonium chloride, a toluidine blue
dye. Generic toluidine blue is not FDA-cleared for human use.
Screening protocol
Early detection of oral cancer and related premalignancy requires an appropriate
screening and diagnosis protocol (Figure 5). All oral structures must be thoroughly
examined, and any abnormalities should be recorded on a mouth map. If suspicious
lesions are found, the lesion must be biopsied or the patient referred to a specialist
for further evaluation. It has been recommended that all adult patients 18 and over be
screened annually,24 even if medical and dental histories elicit no risk factors. Known-risk
patients should be screened every six months.
Figure 5. Screening and biopsy protocol
Medical and Dental History
Extra-oral Examination:
Visual and Palpation
Intra-oral Examination:
Unaided Visual
Radiographs
Palpation
Autofluorescence
Chemiluminescence
T-Blue
Clinically Suspicious Lesion
No Staining By T-Blue
Clinically Suspicious Lesion
Staining By T-Blue
Known Risk:
Semi-Annual or
More Frequent
Screening
Biopsy
Malignant
Treat
No Clinically
Suspicious Lesion
Clinically
Suspicious Lesion
Biopsy
No Known Risk:
Routine Annual
Screening
Malignant
Non-Malignant
Treat
Frequent Follow-Up
Risk Prediction
Non-Malignant
Frequent Follow-Up
Risk Prediction
Biopsy protocol
The two basic biopsy techniques for definitive diagnosis of oral mucosal lesions are
incisional biopsy and excisional biopsy. The brush biopsy (CDx) is a less-invasive,
preliminary diagnostic tool and may also be useful as an intermittent preliminary
diagnostic technique in patients under observation,25 but is insufficient to provide
a definitive diagnosis. Incisional or excisional biopsy is the standard-of-care for
definitive diagnosis.
14
The ability to predict risk of a benign lesion undergoing malignant transformation
could help determine the frequency of follow-up and/or earlier intervention.
Risk differentiation and prediction
Dysplasia and risk prediction
The conventional wisdom is that the more severe a lesion’s dysplasia, the more likely
it is that it will undergo malignant transformation. A number of recent studies do not
support this presumption.26,27
While dysplasia can be predictive, that is not always the case.28 Rosin et al. found that
forty-seven percent of leukoplakias classified as having either no dysplasia or mild
dysplasia developed into a secondary oral malignancy. Primary tumor stage, grade,
and location were not significantly associated with the outcome.29
Chromosomal abnormalities and risk prediction
Recent microscopic studies have investigated loss of heterozygocity (LOH) in tumor
cells and its potential role as a risk predictor for malignant transformation. LOH has
been found to indicate high risk of transformation or conversion to malignancy. In
particular, aberrations in the 3p, 9p, and 17p chromosomal arm sites have been
implicated as high-risk predictors.30,31,32,33,34 LOH in multiple chromosome arms, and
in particular in 3p and 9p sites, has also been found to be predictive of a secondary
malignancy.35
Summary
The importance of routine screening to improve early diagnosis of oral malignancies
cannot be overemphasized. It is incumbent upon the clinician to screen all adult
patients for oral cancer. Available screening technologies include the use of LED lights,
autofluorescence, chemiluminescence, and the combined use of chemiluminescence
and T-Blue630. Recent advances have shown that the risk of malignant transformation is
associated with chromosomal aberrations. The ability to identify lesions and to predict
which lesions will undergo malignant transformation would facilitate early diagnosis
and subsequent disease management.
References
1 American Cancer Society. Available at: http://www.cancer.org/docroot/CRI/content/CRI_2_4_1X_.
Accessed June 15, 2007.
2 Oral Cancer Facts. Available at: http://www.oralcancerfoundation.org/facts/index.htm.
Accessed July 19 2007.
3 Gillison ML, Shah KV. Human papillomavirus-associated head and neck squamous cell
carcinoma: mounting evidence for an etiologic role for human papillomavirus in a subset of
head and neck cancers. Curr Opin Oncol. 2001;13:183–188.
4 D’Souza G, Kreimer AR, Viscidi R, Pawlita M, Fakhry C, Koch WM, Westra WH, Gillison ML.
Case-control study of human papillomavirus and oropharyngeal cancer. N Engl J Med.
2007;356(19):1944–1956.
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5 Rosenquist K. Risk factors in oral and oropharyngeal squamous cell carcinoma: a populationbased case-control study in southern Sweden. Swed Dent J Suppl. 2005;(179):1–66.
6 Braakhuis BJM, Snijders PJF, Keune W-JH, Meijer CJLM, Ruijter-Schippers HJ, et al. Genetic
patterns in head and neck cancers that contain or lack transcriptionally active human
papillomavirus. JNCI J Nat Cancer Inst. 2004;96(13):998–1006.
7 Pavia M, Pileggi C, Nobile CG, Angelillo IF. Association between fruit and vegetable consumption
and oral cancer: a meta-analysis of observational studies. Am J Clin Nutr. 2006;83(5):1126–1134.
8 National Cancer Institute. SEER Cancer Statistics Review 1975–2004. Available at: seer.cancer.
gov/csr/1975_2004/results_merged/sect_20_oral_cavity. Accessed June 19, 2007.
9 Landis S, Murray T, Bolden S, et al. Cancer Statistics, 1998. CA Cancer J for Clin. 1998;48(1):6–29.
10 Axell T, et al. Oral white lesions with special reference to precancerous and tobacco-related
lesions: conclusions of an international symposium held in Uppsala, Sweden, May 18–21 1994.
International Collaborative Group on Oral White Lesions. J Oral Pathol Med. 1996;25(2):49–54.
11 Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and Maxillofacial Pathology. 2nd ed.
Philadelphia: WB Saunders; 2002.
12 Silverman S. Oral Cancer. 5th ed.
13 Holmstrup P, Vedtofte P, Reibel J, Stoltze K. Long-term treatment outcome of oral premalignant
lesions. Oral Oncol. 2006;42(5):461–474.
14 Oral Cavity and Oropharyngeal Cancer. American Cancer Society. Available at: http://
documents.cancer.org/5043.00/5043.00.pdf. Accessed June 27, 2007.
15 Neville B, Damm D, Allen C, Bouquot J. Oral and Maxillofacial Pathology. 2nd ed. Philadelphia:
WB Saunders; 2002.
16 Carvalho AL, Nishimoto IN, Cali-fano JA, Kowalski LP. Trends in incidence and prognosis for
head and neck cancer in the United States: a site-specific analysis of the SEER database. Int. J.
Cancer 2005;114: 806–816.
17 Kois JC, Truelove E. Detecting oral cancer: a new technique and case reports. Dent Today.
2006;25(10):94, 96–97.
18 Poh CF, Ng SP, Williams PM, Zhang L, Laronde DM, Lane P, Macaulay C, Rosin MP. Direct
fluorescence visualization of clinically occult high-risk oral premalignant disease using a simple
hand-held device. Head Neck. 2007;29(1):71–76.
19 Poh CF, Zhang L, Anderson DW, Durham JS, Williams PM, Priddy RW, Berean KW, Ng S, Tseng
OL, MacAulay C, Rosin MP. Fluorescence visualization detection of field alterations in tumor
margins of oral cancer patients. Clin Cancer Res. 2006;12(22):6716–6722.
20 Huber MA, Bsoul SA, Terezhalmy GT. Acetic acid wash and chemiluminescent illumination as
an adjunct to conventional oral soft tissue examination for the detection of dysplasia: a pilot
study. Quintessence Int. 2004;35(5):378–384.
21 Epstein JB, Gorsky M, Lonky S, Silverman S Jr, Epstein JD, Bride M. The efficacy of oral
lumenoscopy (ViziLite) in visualizing oral mucosal lesions. Spec Care Dentist. 2006;26(4):171–174.
22 Kerr AR, Sirois DA, Epstein JB. Clinical evaluation of chemiluminescent lighting: an adjunct for
oral mucosal examinations. J Clin Dent. 2006;17(3):59–63.
23 Epstein JB, Scully C, Spinelli J. Toluidine blue and Lugol’s iodine application in the assessment of
oral malignant disease and lesions at risk of malignancy. J Oral Pathol Med. 1992;21(4):160–163.
24 Joseph BK. Oral cancer: prevention and detection. Med Princ Pract. 2002;11(1S):32–35.
25 Kosicki DM, Riva C, Pajarola GF, Burkhardt A, Gratz KW. OralCDx brush biopsy — a tool for early
diagnosis of oral squamous cell carcinoma. Schweiz Monatsschr Zahnmed. 2007;117(3):222–227.
26 Holmstrup P, Vedtofte P, Reibel J, Stoltze K. Long-term treatment outcome of oral premalignant
lesions. Oral Oncol. 2006 May;42(5):461–474.
27 Holmstrup P, Vedtofte P, Reibel J, Stoltze K. Oral premalignant lesions: is a biopsy reliable? J
Oral Pathol Med. 2007;36(5):262–266.
16
28 Scully C, Sudbø J, Speight PM. Progress in determining the malignant potential of oral lesions. J
Oral Pathol Med. 2003;32(5):251–256.
29 Rosin MP, Lam WL, Poh C, Le ND, Li RJ, et al. 3p14 and 9p21 loss is a simple tool for predicting
second oral malignancy at previously treated oral cancer sites. Cancer Res. 2002;62:6447–6450.
30 Tabor MP, Brakenhoff RH, van Houten VMM, Kummer JA, Snel MHJ, et al. Persistence of
genetically altered fields in head and neck cancer patients: Biological and clinical implications.
Clin Cancer Res. 2001;7:1523–1532.
31 Partridge M, Pateromichelakis S, Phillips E, Emilion GG, Ahern RP, Langdon JD. A casecontrol study confirms that microsatellite assay can identify patients at risk of developing oral
squamous cell carcinoma within a field of cancerization. Cancer Res. 2000; 60:3893–3898.
32 Mao L, Lee JS, Fan YH, Ro JY, Batsakis JG, Lippman S. et al. Frequent microsatellite alterations
at chromosomes 9p21 and 3p14 in oral premalignant lesions and their value in cancer risk
assessment. Nat. Med. 1996;2:682–685.
33 Guo Z, Yamaguchi K, Sanchez-Cespedes M, Westra WH, Koch WM, Sidransky D. Allelic losses
in OraTest-directed biopsies of patients with prior upper aerodigestive tract malignancy. Clin
Cancer Res. 2001;7(7):1963–1968.
34 Nawroz H, van der Riet P, Hruban RH, Koch W, Ruppert JM, Sidransky D. Allelotype of head and
neck squamous cell carcinoma. Cancer Res. 1994;54:1152–1155.
35 Rosin MP, Lam WL, Poh C, Le ND, Li RJ, et al. 3p14 and 9p21 loss is a simple tool for predicting
second oral malignancy at previously treated oral cancer sites. Cancer Res. 2002;62:6447–6450.
Author Profile
Denis P. Lynch, D.D.S., Ph.D.
Dr. Lynch received his Doctor of Dental Surgery degree from the
University of California at San Francisco in 1976. He subsequently
completed a residency in oral and maxillofacial pathology at
the University of Alabama at Birmingham, as well as a Ph.D. in
Experimental Pathology. Dr. Lynch is currently Professor of Oral
and Maxillofacial Pathology and Associate Dean for Academic
Affairs at Marquette University School of Dentistry in Milwaukee,
as well as Professor of Dermatology at the Medical College of
Wisconsin. He is the author of numerous scientific articles and book chapters, as well
as the coauthor of The Mouth: Diagnosis and Treatment.
Disclaimer
Dr. Lynch lectures on oral cancer for Zila Pharmaceuticals, Inc.
Acknowledgement
Thanks to Dr. Joel Epstein for providing clinical images for use in this article.
Reader Feedback
We encourage your comments on this or any ADTS course. For your convenience, an
online feedback form is available at www.ineedce.com.
17
Questions
1. In the United States, more than
_____ new cases of oropharyngeal
cancer will be diagnosed in 2007.
a. 17,000
b. 26,000
c. 34,000
d. 42,000
2. The most common site for oral
cancer in patients in the United
States is_____.
a. the tongue
b. the cheek
c. the lip
d. a and c
3. The single greatest risk factor for
oral cancer in the United States is
_____.
a. drinking
b. use of tobacco
c. use of narcotics
d. a and c
4. A reduced risk of oral cancer has
been associated with a high dietary
fruit and vegetable intake.
a. True
b. False
8. The definitive diagnosis of oral
cancer can be determined by _____.
a. brush biopsy
b. incisional or excisional biopsy
c. visual and clinical examination
d. all of the above
9. The detection of suspicious lesions is
increased through regular screening.
a. True
b. False
10. Stand-alone oral cancer screening
devices currently available include
_____.
a. ViziLite Plus
c. Ultrascope
d. a and b
11. _____ is cleared by the FDA as a
stain for the marking of oral lesions.
b. Methylene blue
d. all of the above
12. Studies have shown that use of
ViziLite aids identification of lesions
examination.
a. True
b. False
13. Adjunctive use of T-Blue630
7. Non-homogenous leukoplakia
has a greater risk of malignant
degeneration than homogenous
leukoplakia.
a. True
b. False
18
16. A screening protocol should include
_____.
a. a medical and dental history
b. visual examination
c. palpation
d. all of the above
17. Rosin et al. found that _______ of
leukoplakias in previously treated
sites with either no dysplasia or
mild dysplasia developed into a
secondary oral malignancy.
a. 25%
b. 38%
c. 47%
d. 53%
c. T-Blue630
not found with unaided visual
6. Leukoplakia is estimated to _____.
a. be found in approximately 15% of adults
b. be the clinical presentation in 85% of oral
premalignant and malignant lesions
c. have a 7% rate of malignant transformation
d. b and c
15. Known-risk patients should be
screened more often than patients
with no known risk.
a. True
b. False
b. VELScope
a. Toluidine blue
5. The overall five-year relative survival
rate for oral and oropharyngeal
cancer diagnosed between 1996
and 2003 is estimated to be _____.
a. 51.1%
b. 59.1%
c. 62.3%
d. none of the above
14. If a lesion does not stain with
toluidine blue and remains clinically
suspicious after two weeks, _____.
a. it should still be biopsied
b. it does not need to be biopsied
c. it should be biopsied if it is still present in
six months
d. none of the above
can____.
a. help identify abnormal lesions
b. stain tissue pink
c. provide a definitive diagnosis
d. none of the above
18. Aberrations on certain
chromosomal arms have been
found to be high-risk predictors of
malignant transformation.
a. True
b. False
19. The clinician should screen all
adult patients for oral cancer.
a. True
b. False
20. The ability to predict lesions at high
risk of malignant transformation
would _____.
a. facilitate disease management
b. be relatively unimportant
c. facilitate early diagnosis
d. a and c*
ANSWER SHEET
Oral Cancer Detection: The Role of Adjunctive Technology
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Educational Objectives
Academy of Dental Therapeutics and Stomatology
P.O. Box 116, Chesterland, OH 44026
or fax to: (440) 845-3447
1. Know the incidence of oral cancer in the United States and understand the risk factors
2. Understand screening methods available for the detection of oral cancer
3. Understand the role of chromosomal aberrations in the risk of malignant transformation
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AUTHOR DISCLAIMER
Dr. Lynch lectures on oral cancer for Zila Pharmaceuticals, Inc.
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All content has been derived from references listed, and or the opinions of clinicians.
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