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Hypohidrotic Ectodermal Dysplasia A Peer-Reviewed Publication Written by Sherri Lukes RDH, MS and Jennifer S. Sherry RDH, MSEd

This course has been made possible through an unrestricted educational grant. The cost of this CE course is $29.00 for 1 CE credit. Cancellation/Refund Policy: Any participant who is not 100% satisfied with this course can request a full refund by contacting PennWell in writing.

Publication date: November 2010Expiry date: October 2013

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Educational ObjectivesThe overall goal of this article is to provide the reader with in-formation on the signs and symptoms of ectodermal dysplasia and carrier status among patients. Upon completion of this course, the reader will be able to do the following:1. List the more common syndromes associated with

oligodontia2. List the various signs and symptoms of ectodermal

dysplasia3. List and describe the global incidence of female carriers for

ectodermal dysplasia

AbstractMore than 120 syndromes are associated with oligodontia, including ectodermal dysplasia. The signs and symptoms of ec-todermal dysplasia include sparse hair; dry skin; few, malformed teeth; deficient sweat glands and dystrophic fingernails. Ecto-dermal dysplasia is most commonly the hypohidrotic X-linked version, affecting 80% of sufferers and the syndrome is carried by females. Knowing the signs and symptoms of ectodermal dysplasia may assist dentists and dental hygienists in identifying patients with the disease and possibly potential carriers.

IntroductionDental professionals commonly observe congenitally miss-ing teeth during the process of care. They should, however, be cognizant of various conditions and/or syndromes in which missing teeth and other dental abnormalities are manifestations. Hypodontia, which technically is defined as the absence of six teeth or less,1 is a common developmental anomaly in dentistry. Among the commonly missing teeth are third molars, maxillary lateral incisors and mandibular second premolars. Oligodontia, on the other hand, is defined as the absence of more than six teeth, excluding third molars, and is a less common finding.1,2 It is typically just one of a variety of signs manifested in several syndromes and can be one of the first signs that a person is af-fected by the syndrome.

There are over 120 syndromes in which oligodontia is one of the associated findings.2 The majority are hereditary. Those most commonly associated with missing teeth are ectodermal dysplasia (ED) and Down syndrome,3 and many of the remain-ing syndromes are very rare. When diagnosing oligodontia, the dental professional must look for additional manifestations of a syndrome, as there is an array of findings among the numerous syndromes. Some of the many syndromes in which oligodontia can be a finding include Seckel syndrome, Rieger syndrome, Wolf-Hirschhorn syndrome and Klippel-Feil syndrome.4,5,6,7

The ectodermal dysplasias represent a group of genetic disorders characterized by 150-170 clinical conditions.8,9 It can be the result of autosomal dominant, autosomal recessive or X-linked genetic expression and occurs in populations world-wide with an estimated incidence of one per 100,000 births.8-12 The most common form is the X-linked, hypohidrotic form, constituting 80% of those affected by the condition. The tissues

affected in their development are those derived from ectoderm and include skin, hair, nails, teeth and glands.8-19 Among the various sign and symptoms of hypohidrotic ectodermal dys-plasia (HED) are dry, hypoplastic skin; sparse scalp and body hair (alopecia or hypotrichosis); dystrophic fingernails; deficient sweat glands (hypohidrosis); oligodontia; and other dental de-fects. The few teeth that are present in HED patients tend to be malformed and smaller in size. Alveolar edentulous areas are often exemplified as hypoplastic, sharp and narrow ridges.15,20 These dental abnormalities are especially important in the early diagnosis of HED so appropriate treatment can be planned for the patient from childhood to adulthood.16,18

As with most diseases, there is great variability of signs and symptoms in those affected by HED. Since the syndrome is inherited as an X-linked recessive gene, it is only fully ex-pressed in males, which means all signs and symptoms are more numerous and severe in males than in females.13,16,21,22 The combined signs of HED result in a quite characteristic dento-craniofacial appearance for affected males (fig. 1), dis-tinguished by thin, fine hair; sunken eyes and nasal bridge (also called “saddle nose”); prominent forehead; and everted lips.20 Dental abnormalities include oligodontia or anodontia, coni-cally shaped anterior teeth, bud-shaped crowns, taurodontism, decreased mesio-distal diameter of molars and hypoplastic alveolar ridge.9,15,16,22

Figure 1. Affected male

With permission from NFED

Females are gene carriers for the disorder, which means the spectrum for signs and symptoms in females can range from unobservable to full expression of HED.10,15,20,21 Global studies report oligodontia, however, as one of the most common signs of carrier females, noting that 75% or more female carriers had abnormalities associated with their permanent teeth.14,15,22 Some researchers also note that carriers may go undiagnosed for HED if hypodontia is minor and no other signs and symptoms are noticed.2,15 Early prosthetic therapy is recommended for patients who present with the various forms of hypodontia.20

During the assessment phase of the dental hygiene process of care, it is possible that dental hygienists can aid in the diag-

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nosis of female carrier states of HED through identification of dental abnormalities. The following case study is suspect for a carrier state of HED, undiagnosed as of yet by medical and dental professionals.

Case Study

Medical HistoryPatient “X” is a 35-year-old Caucasian female who sched-uled a routine dental examination and prophylaxis ap-pointment in the clinic within a dental hygiene program at a Midwestern university. Her medical history was unremarkable, revealing no current diseases or pathologic conditions. She did have a history of taking the medications Advil and Zantac as well as a birth control pill. The patient used tobacco products for 15 years and continues to smoke about 10 cigarettes per day. She tried the smoking cessa-tion medication Chantix in the past but was unsuccessful at quitting. There is a family history of hypertension as well as diabetes.

Blood pressure was recorded as 130/90 (other vitals within normal limits)Weight: 230 pounds (reported by the patient)Height: 5’2” (reported by the patient)

Dental HistoryPatient “X” could not recall the date of her last dental ex-amination, prophylaxis or radiographs. She had a history of fever blisters on her lips but did not elaborate on specific information regarding this condition. The patient noted a history of clenching and grinding her teeth. When asked about one or both of her parents losing teeth in the past, she mentioned that her father (deceased) was congenitally missing several of his permanent teeth. She reported previ-ous orthodontic treatment. The patient stated she was not satisfied with the appearance of her teeth and would not be disturbed if she had to wear false teeth/dentures. Patient “X” worked in retail and did not have dental insurance.

Oral AssessmentIntra- and Extraoral ExaminationThe intra- and extraoral examination elicited a number of find-ings. The intra- and extraoral findings were as follows: Temporomandibular joint popping Small lesion on lower lip Slight hairy tongue Unable to classify occlusion due to missing teeth;

open bite was visible on the panoramic radiograph Multiple missing teeth (excluding third molars): #2, 4, 5, 6, 7, 10, 12, 15, 20, 21, 22, 23, 28, 29 and 31 Retained deciduous teeth “A,” “L,” and “T” with no successor Amalgam restorations: #3-O, #14-O, #18-O, #30-O and “T”-O

Gingival/periodontal status: localized areas of gingivitis, moderate supra- and subgingival calculus noted on the entire dentition

4 mm. pockets on #3-ML, #13-DL and #30-MB “T”: recession of 4 mm on the buccal surface “A”: recession of 3 mm on the buccal surface Periodontal diagnosis: localized chronic periodontitis

with slight (< 2 mm) clinical attachment loss (CAL) Oral hygiene: plaque-free score 86.6%

Figure 2. Panoramic radiograph

Radiographic assessmentThe radiographic findings were as follows:Panoramic radiograph (fig. 2): • Mandibularrightmidlinedeviation(fig.3)• Apicalrootresorption:#8,9severeresorption“A,”“T,”

and “L”(no mobility noted)• 45degreerotation:#13• Abnormalmorphology:#18–macrodontia• Boneloss:localizedareasofhorizontalandverticalbone

loss • Hypoplasticcrestofmandibularbone,rightposterior

alveolar ridge• Prematurewearonsuperioraspectofrightcondyle Periapical radiographs (figs. 4-6): • Conicalrootstructure:#3,“A”• Severerootresorption/bonelosson“T”–appearstohave

little to no supporting bone, Patient “X” later stated “T” is sensitive to pressure

• Abnormalmorphology:#18–increasedmesial/distalwidth of crown with abnormally wide pulp chamber

• Littletonobonesupportondistal,“L”• Overalltrabecularpatternwaswithinnormallimits

Figure 3. Midline deviation

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Figure 4. Periapical radiograph

Figure 5. Periapical radiograph

Figure 6. Periapical radiograph

Additional Assessment ResultsAfter the oral and radiographic assessment, supervising fac-ulty at the dental hygiene clinic suspected a syndrome such as hypohidrotic ectodermal dysplasia as an explanation for the patient’s missing teeth. This required additional questioning, which revealed more details about her medical, dental and fam-ily history that was significant for the differential diagnosis. Patient “X” reported having no missing deciduous teeth that she could recall, and none of her permanent teeth were ever

extracted. She did report, however, that two retained primary teeth were extracted at the approximate age of 30, due to decay. Of the three currently retained primary teeth, she reported “T” as sensitive to pressure during mastication, resulting in shift-ing food to the opposite side of the mouth while eating. When questioned further about her orthodontic treatment, she stated that the objective of orthodontics had been to enable fabrica-tion of partial dentures to fill spaces caused by the congenitally missing teeth. She reported wearing the appliances for the ap-propriate time, after which she received a partial denture, first for the mandibular arch. No removable retainer was delivered, however, and she was told to leave the partial out at night. This resulted in mobilization of the mandibular teeth, and she be-came unable to wear it due to poor fit. For financial reasons, Patient “X” did not seek care for additional partial dentures.

When questioned about other ectodermal structures com-monly affected by hypohidrotic ectodermal dysplasia, Patient “X” reported a history of dry and sensitive skin. She also reported heat intolerance, recalling a fainting incident due to heat exposure on one occasion while at the beach. Fingernails and hair appeared normal, but she stated her mother told her she had little to no hair until the age of four. Patient “X” was also asked additional questions about the dental and medical history of her father, who had been deceased several years. She could recall only that he indeed had several teeth not present and that upon entrance into the military his remaining teeth were extracted and he received a set of dentures. She had no knowledge of other affected ectodermal structures.

DiscussionSeveral assessment findings from her father’s dental history as well as her medical history tend to suggest that Patient “X” could be an undiagnosed case of HED. The multiple missing teeth experienced by her father indicate he could possibly have been mildly affected by HED and undiagnosed. The patient also reported having dry skin, being heat intolerant and hav-ing delayed childhood development of scalp hair, all of which could be indicators of the syndrome.21 More significant than the self-reported dental/medical history for Patient “X” are the dental abnormalities noted for her during the subsequent oral and radiographic examinations, several of which could indicate a carrier state of HED. The most significant finding is the multiple missing teeth, or oligodontia. It is unlikely that her missing teeth constitute a nonsyndromic form of oligodon-tia. While it is more common than HED, in nonsyndromic hereditary oligodontia, tooth agenesis is usually the only trait expressed.1,23 Patient “X” exhibited oligodontia, as well as the additional dental abnormalities of pyramidal/cuneiform roots on tooth #3 and abnormal size/morphology of #18 (figs. 2, 4, 5). The areas of the mouth involved in tooth agenesis are sig-nificant as well. The pattern for nonsyndromic tooth agenesis is restricted to the front or the back of the mouth, but rarely both. In contrast, HED patients have generalized tooth agenesis, which is the pattern expressed in Patient “X.”24

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The combination of her missing teeth and abnormal tooth morphology is also significant because these two spe-cific characteristics occurring together have been utilized in studies investigating the expressed traits of females in fami-lies affected by HED.22 In addition, two of the teeth Patient “X” is missing are the maxillary lateral incisors. This is yet another characteristic that is consistent with the literature, as the maxillary lateral incisors are the most frequently missing teeth in heterozygous females.11,25 One last observation from the radiographs exposed for Patient “X” is the hypoplastic crest of mandibular bone, on the right posterior alveolar ridge. Again, this is a finding consistent with the literature for patients affected by HED.15,19,20 The thin, narrow ridge can be problematic for replacement of missing teeth with dental implants or other types of restorations.

Implications for Dental ProfessionalsDental professionals owe it to their patients to assist in iden-tifying and diagnosing conditions that have perhaps been unrecognized as of yet by primary care physicians or dental professionals. In children, cases such as that of Patient “X” can be referred for appropriate care in a timely manner to restore aesthetics and function for a normal childhood experi-ence. Since dental anomalies can be the primary manifesta-tion of HED in some patients and especially in carriers, a case can be made for exposing dental radiographs in the very young patient beyond just those for routine caries assess-ment. A panoramic view of the dentition after two years of age can be extremely helpful in the diagnosis of HED and other genetic disorders. The extent of hypodontia as well as morphologic defects can be assessed so that treatment plan-ning can begin for prosthetic restoration. Placing prostheses early in HED patients is important not only for aesthetics but also to maintain the alveolar ridge for implant placement later in the child’s life.19 Had Patient “X” been referred as a child, she could have had oral reconstruction at an early age, less dissatisfaction with her physical appearance and a more fully functional dentition as an adult.

From this case study, an argument can also be made for more extensive history taking in dental patients, the objective being recognition of possible genetic disorders that may af-fect the dentition. Knowledge about the various syndromes manifesting hypodontia would be beneficial for all dental professionals to enhance the history-taking process.

Patient “X” received routine preventive care at the dental hygiene clinic and was referred to the National Foundation for Ectodermal Dysplasia (NFED) for genetic testing. Interest-ingly, NFED is located approximately 150 miles from where Patient “X” resides. Among the many resources within the foundation is an international patient registry and assistance in obtaining genetic testing for definitive diagnosis of HED. The foundation also has relationships with two area dental schools and sometimes assists patients in obtaining care. This could be a possibility for Patient “X.”

ConclusionsRecent advances in research make the future much brighter for families affected by HED. Positive results from canine research are showing promise for replication in humans.24,26 Studies in progress could provide the necessary data to implement proto-cols for the treatment of hypohidrotic ectodermal dysplasia in the future, significantly changing the lives of those with the ge-netic defect responsible for the disorder. It is prudent for dental professionals to stay abreast of upcoming developments in the diagnosis and treatment of HED to provide the best care pos-sible for patients. Additional information about the ectodermal dysplasias can be accessed at www.nfed.org.

References1. CobourneMT.Familialhumanhypodontia– is itall in thegenes?Br

Dent J. 2007;203(4):203-208.2. Worsaae N, Jensen BN, Holm B, Holsko J. Treatment of severe

hypodontia-oligodontia – an interdisciplinary concept. Int J OralMaxillofac Surg. 2007;36:473-480.

3. Ulm MR, Kratochwil A, Ulm B, Solar P, Aro G, Bernaschek G. Three-dimensional ultrasound evaluation of fetal tooth germs. Ultrasound Obstet Gynecol. 1998;12:240-243.

4. De Coster PJ, Verbeeck MH, Holthaus V, Marten LC, Vral A. Seckel syndrome associated with oligodontia, microdontia, enamel hypoplasia, delayederuption,anddentindysmineralization:anewvariant?JOralPathol Med. 2006;35:639-641.

5. Wang Y, Zhao H, Zhang X, Feng H. Novel identification of a four-base-pair deletion mutation in PITX2 in a Rieger Syndrome Family. J Dent Res. 2003;82(12):1008-1012.

6. Nieminen P, Kotilainen J, Aalto Y, Knuutila S, Pirinen S, Thesleff I. MSX1 gene is deleted in Wolf-Hirschhorn Syndrome patients with oligodontia. J Dent Res. 2003;82(12):1013-1017.

7. ParadowskaA,SzelagJ,SlaweckiK.Klippel-FeilSyndrome–Reviewofthe literature. Dent Med Probl. 2007;44(4):491-494.

8. Talo T, Acun Kaya F. The effects of ectodermal dysplasia on periodontal tissues. J Int Dent Med Res. 2009;2(2):53-57.

9. Bani M, Tezkirecioglu AM, Akal N, Tuzuner T. Ectodermal dysplasia with anodontia: a report of two cases. Eur J Dent. 2010;4:215-222.

10. Huang C, Yang Z, Ke T, Wang H, Wang X, Shen J, Tu X, Tian J, Yu Liu J, Wang QK, Liu M. A novel de novo frame-shift mutation of the EDA gene in a Chinese Han family with hypohidrotic ectodermal dysplasia. J Hum Genet. 2006;51:1133-1137.

11. Lexner MO, Bardow A, Hertz JM, Nielsen LA, Kreiborg S. Anomalies of tooth formation in hypohydrotic ectodermal dysplasia. Int J Ped Dent. 2007;17:10-18.

12. Gruber J, Kreitzberg, G. Ectodermal dysplasia: a seven-year case report. NYSDJ. 2006;28-31.

13. Guckes AD, Roberts MW, McCarthy GR. Pattern of permanent teeth present in individuals with ectodermal dysplasia and severe hypodontia suggests treatment with dental implants. Ped Dent. 1998;20(4):278-280.

14. Clarke A, Phillips DIM, Brown R, Harper PS. Clinical aspects of X-linked hypohidrotic ectodermal dysplasia. Arch Dis Childhood. 1987;62:989-996.

15. Glavina D, Majstorovic M, Lulic-Dukic O, Juric H. Hypohidrotic ectodermal dysplasia: dental features and carriers detection. Coll Anthropol. 2001;25(1):303-310.

16. Clauss F, Maniere MC, Obry F, Waltmann E, Hadj-Rabia S, Bodemer C, Alembik Y, Lesot H, Schmittbuhl M. Dento-craniofacial phenotypes and underlying molecular mechanisms in hypohidrotic ectodermal dysplasia (HED): a review. J Dent Res. 2008;87(12):1089-1099.

17. Lin TK, Huang CY, Lin MH, Chao SC. A novel 7-bp deletion mutation in a Taiwanese family with X-linked hypohidrotic ectodermal dysplasia. Clin Exper Derm. 2004;29:536-538.

18. Sarikaya I, Guler AU. Prosthodontic treatment of a patient with ectodermal dysplasia: a case report. Internet J Dent Sci. 2009;7(2).

19. Freiman A, Borsuk D, Barankin B, Sperber GH, Krafchik B. Dental manifestations of dermatologic conditions. J Am Acad Dermatol. 2009;60:289-298.

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96 www.rdhmag.com January 2011

20. Tarjan I, Gabris K, Roxsa N. Early prosthetic treatment of patients with ectodermal dysplasia: a clinical report. J Prosthetic Dent. 2005;93:419-424.

21. Kerr CB, Wells RS, Cooper KE. Gene effect in carriers of anhidrotic ectodermal dysplasia. J Med Genet. 1966;3:169-176.

22. Crawford PJM, Aldred MJ, Clarke A. Clinical and radiographic dental findings in X-linked hypohidrotic ectodermal dysplasia. J Med Genet. 1991;28:181-185.

23. Song S, An D, Qu H, Gong Y, Wu H, Zhang X, Zhong N, Feng H. EDA gene mutations underlie non-syndromic oligodontia. J Dent Res. 2009;88(2):126-131.

24. National Foundation for Ectodermal Dysplasias. Connecting Lives. Winter 2010, p.12.

25. Airenne P. X-linked hypohidrotic ectodermal dysplasia in Finland. A clinical, radiographic and genetic stud. Proc Finn Dent Soc. 1981;77(suppl. I):1-107.

26. Casal ML, Lewis JR, Mauldin EA, Tardivel A, Ingold K, Favre M, Paradies F, Demotz S, Gaide O, Schneider P. Significant correction of disease after postnatal administration of recombinant ectodysplasin A in canine X-linked ectodermal dysplasia. Amer J Hum Gen. 2007;81:1050-1056.

Author ProfilesSherri Lukes RDH, MSSherri Lukes RDH, MS, is an associate professor in the dental hygiene program at Southern Illinois University Carbondale, where she has taught oral pathology for the past 20 years. Other teaching responsibilities include Com-munity Oral Health, Multicultural Applied Experience

in Dental Hygiene and Advanced Periodontics clinic. Her research has been focused on oral pathology, migrant and seasonal farmworker oral health and issues affecting a range of other underserved groups.

Jennifer S. Sherry RDH, MSEdJennifer S. Sherry RDH, MSEd, is an as-sistant professor in the Dental Hygiene Program at Southern Illinois University, Carbondale, IL. She teaches radiology and is a clinic supervisor for the third-year den-tal hygiene students. Her research interests include children’s health issues, school nutrition programs, school-based health clinics and pediatric dentistry.

DisclaimerThe author(s) of this course has/have no commercial ties with the sponsors or the providers of the unrestricted educational grant for this course.

Reader FeedbackWe encourage your comments on this or any PennWell course. For your convenience, an online feedback form is available at www.ineedce.com.

Questions

1. There are more than ________ in which oligodontia is one of the associated find-ings and the majority are ________. a. 60 syndromes; acquiredb. 90 syndromes; hereditaryc. 120 syndromes; hereditaryd. 120 syndromes acquired

2. The syndromes most commonly associ-ated with missing teeth are ________ and ________.a. ectodermal dysplasia; Seikel’s syndromeb. Seikel’s syndrome; Down syndromec. Down syndrome; ectodermal dysplasiad. Regan’s syndrome; ectodermal dysplasia

3. ________ is associated with oligodontia.a. Rieger syndromeb. Seckel syndromec. Klippel-Feil syndromed. all of the above

4. Ectodermal dysplasia can be the result of ________genetic expression.a. autosomal dominantb. autosomal recessivec. X-linkedd. all of the above

5. Hypohidrotic ectodermal dysplasia is associated with ________.a. dry, hypoplastic skinb. sparse scalp and body hairc. dystrophic fingernailsd. all of the above

6. ________ is/are associated with ectoder-mal dysplasia.a. Over-expressed sweat glandsb. Over-expressed tuftelinc. Deficient sweat glandsd. none of the above

7. The most common form of ectodermal dysplasia is the ________.a. X-linked, hypohidrotic formb. Y-linked, hypohidrotic formc. X-linked, hyperhidrotic formd. Y-linked, hyperhidrotic form

8. ________ are important in the early diagnosis of ectodermal dysplasia.a. Small, malformed teethb. Alveolar edentulous areas with hypoplastic, sharp

and narrow ridgesc. A reduced number of teethd. all of the above

9. ________ is a characteristic sign of ectodermal dysplasia in an affected male.a. Sunken eyesb. Everted lipsc. Thin, fine haird. all of the above

10. More than ________ of female carriers present with abnormalities associated with their permanent teeth.a. 25%b. 50%c. 75%d. 90%

11. Decreased mesio-distal diameter of molars is seen in ________.a. Male carriers for ectodermal dysplasiab. Males with ectodermal dysplasiac. Males with ectodermal hyperplasiad. Females with ectodermal hyperplasia

12. Ectodermal dysplasia carriers may go undiagnosed if ________.a. hyperdontia is minor and other signs and

symptoms are presentb. hypodontia is major and other signs and symptoms

are presentc. hypodontia is minor and no other signs and

symptoms are presentd. all of the above

13. Female carriers of ectodermal dysplasia may mention that their________.a. dog had several missing teethb. father had several missing teeth due to early

extraction caused by infectionc. father had several congenitally missing teethd. none of the above

14. A female suspected of being a carrier for ectodermal dysplasia may complain of ________.a. intolerance to heatb. intolerance to coldc. intolerance to humidityd. all of the above

15. A ________ view of the dentition after two years of age can be extremely helpful in the diagnosis of HED and other genetic disorders.a. bitewingb. occlusalc. panoramicd. all of the above

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Educational Objectives1. List the more common syndromes associated with oligodontia

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Hypohidrotic Ectodermal Dysplasia

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EDUCATIONAL DISCLAIMERThe 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 PennWell.

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/COSTAll participants scoring at least 70% on the examination will receive a verification form verifying 1 CE credit. The formal continuing education program of this sponsor is accepted by the AGD for Fellowship/Mastership credit. Please contact PennWell for current term of acceptance. Participants are urged to contact their state dental boards for continuing education requirements. PennWell is a California Provider. The California Provider number is 4527. The cost for courses ranges from $29.00 to $110.00.

Many PennWell 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 PennWell course has been approved by DANB, please contact DANB’s Recertification Department at 1-800-FOR-DANB, ext. 445.

RECORD KEEPINGPennWell 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 POLICYAny participant who is not 100% satisfied with this course can request a full refund by contacting PennWell in writing.

© 2010 by the Academy of Dental Therapeutics and Stomatology, a division of PennWell

www.ineedce.com Customer Service 216.398.7822


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