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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”). 12 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. 15 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 Name: Title: Mailing Address: E-mail Address: City: State: Telephone: Home ( ) Specialty: ZIP: Office ( ) Requirements for successful completion of the course and to obtain dental continuing education credits: 1) Read the entire course.2) Complete all information above. 3) Complete answer sheets in either pen or pencil. 4) Mark only one answer for each question. 5) A score of 70% on this test will earn you 2 CE credits. 6) Complete the Course Evaluation below. 7) Make check payable to The Academy of Dental Therapeutics and Stomatology OR PennWell Corp. Mail completed answer sheet to 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 For IMMEDIATE results, go to www.ineedce.com and click on the button “Take Tests Online.” Answer sheets can be faxed with credit card payment to (440) 845-3447, (216) 398-7922, or (216) 255-6619. Course Evaluation ■ Please evaluate this course by responding to the following statements, using a scale of Excellent = 5 to Poor = 0. 1. Were the individual course objectives met? Objective #1: Yes No Objective #3: Yes No Payment of $24.00 is enclosed. (Checks and credit cards are accepted.) If paying by credit card, please complete the following: ■ MC ■ Visa ■ AmEx ■ Discover Objective #2: Yes No 2. To what extent were the course objectives accomplished overall? 5 4 3 2 1 0 3. Please rate your personal mastery of the course objectives. 5 4 3 2 1 0 4. How would you rate the objectives and educational methods? 5 4 3 2 1 0 5. How do you rate the author’s grasp of the topic? 5 4 3 2 1 0 Acct. Number: _______________________________ Exp. Date: _____________________ 6. Please rate the instructor’s effectiveness. 5 4 3 2 1 0 7. Was the overall administration of the course effective? 5 4 3 2 1 0 8. Do you feel that the references were adequate? Yes No 9. Would you participate in a similar program on a different topic? Yes No Charges on your statement will show up as Pennwell 10. If any of the continuing education questions were unclear or ambiguous, please list them. ___________________________________________________________________ 11. Was there any subject matter you found confusing? Please describe. ___________________________________________________________________ ___________________________________________________________________ 12. What additional continuing dental education topics would you like to see? AGD Code 734, 739 ___________________________________________________________________ ___________________________________________________________________ PLEASE PHOTOCOPY ANSWER SHEET FOR ADDITIONAL PARTICIPANTS. AUTHOR DISCLAIMER Dr. Lynch lectures on oral cancer for Zila Pharmaceuticals, Inc. SPONSOR/PROVIDER This course was made possible through an unrestricted educational grant. No manufacturer or third party has had any input into the development of course content. All content has been derived from references listed, and or the opinions of clinicians. Please direct all questions pertaining to the ADTS or the administration of this course to Machele Galloway, 1421 S. Sheridan Rd., Tulsa, OK 74112 or [email protected]. COURSE EVALUATION and PARTICIPANT FEEDBACK We encourage participant feedback pertaining to all courses. Please be sure to complete the survey included with the course. Please e-mail all questions to: [email protected]. INSTRUCTIONS All questions should have only one answer. Grading of this examination is done manually. Participants will receive confirmation of passing by receipt of a certificate. Certificates will be mailed within two weeks after taking an examination. EDUCATIONAL DISCLAIMER The opinions of efficacy or perceived value of any products or companies mentioned in this course and expressed herein are those of the author(s) of the course and do not necessarily reflect those of the ADTS. Completing a single continuing education course does not provide enough information to give the participant the feeling that s/he is an expert in the field related to the course topic. It is a combination of many educational courses and clinical experience that allows the participant to develop skills and expertise. COURSE CREDITS/COST All participants scoring at least 70% (answering 14 or more questions correctly) on the examination will receive a certificate verifying 2 CE credits. The formal continuing education program of this sponsor is accepted by the AGD for Fellowship/Mastership credit. Please contact ADTS for current term of acceptance. Participants are urged to contact their state dental boards for continuing education requirements. The cost for courses ranges from $24.00 to $110.00. Many ADTS self-study courses have been approved by the Dental Assisting National Board, Inc. (DANB) and can be used by dental assistants who are DANB Certified to meet DANB’s annual continuing education requirements. To find out if this course or any other ADTS course has been approved by DANB, please contact DANB’s Recertification Department at 1-800-FOR-DANB, ext. 445. RECORD KEEPING The ADTS maintains records of your successful completion of any exam. Please contact our offices for a copy of your continuing education credits report. This report, which will list all credits earned to date, will be generated and mailed to you within five business days of receipt. CANCELLATION/REFUND POLICY Any participant who is not 100% satisfied with this course can request a full refund by contacting the Academy of Dental Therapeutics and Stomatology in writing. © 2007 by the Academy of Dental Therapeutics and Stomatology 19