Hypohidrotic Ectodermal Dysplasia

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Hypohidrotic
Ectodermal Dysplasia
A Peer-Reviewed Publication
Written by Sherri Lukes RDH, MS and Jennifer S. Sherry RDH, MSEd
Publication date: November 2010
Expiry date: October 2013
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Educational Objectives
The overall goal of this article is to provide the reader with information 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
oligodontia
2. List the various signs and symptoms of ectodermal
dysplasia
3. List and describe the global incidence of female carriers for
ectodermal dysplasia
Abstract
More than 120 syndromes are associated with oligodontia,
including ectodermal dysplasia. The signs and symptoms of ectodermal dysplasia include sparse hair; dry skin; few, malformed
teeth; deficient sweat glands and dystrophic fingernails. Ectodermal 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.
Introduction
Dental professionals commonly observe congenitally missing 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 affected 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 remaining 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 worldwide 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
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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 dysplasia (HED) are dry, hypoplastic skin; sparse scalp and body
hair (alopecia or hypotrichosis); dystrophic fingernails; deficient
sweat glands (hypohidrosis); oligodontia; and other dental defects. 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 expressed 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), distinguished 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, conically 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
Someresearchersalsonotethatcarriersmaygoundiagnosedfor
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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January 2011
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 History
Patient “X” is a 35-year-old Caucasian female who scheduled a routine dental examination and prophylaxis appointment 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 cessation 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 History
Patient “X” could not recall the date of her last dental examination, 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 previous 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 Assessment
Intra- and Extraoral Examination
The intra- and extraoral examination elicited a number of findings. 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
January 2011
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 assessment
The radiographic findings were as follows:
Panoramic radiograph (fig. 2):
• Mandibular right midline deviation (fig. 3)
• Apical root resorption: #8, 9 severe resorption “A,”“T,”
and “L”(no mobility noted)
• 45 degree rotation: #13
• Abnormal morphology: #18 – macrodontia
• Bone loss: localized areas of horizontal and vertical bone
loss
• Hypoplastic crest of mandibular bone, right posterior
alveolar ridge
• Premature wear on superior aspect of right condyle
Periapical radiographs (figs. 4-6):
• Conical root structure: #3, “A”
• Severe root resorption/bone loss on “T” – appears to have
little to no supporting bone, Patient “X” later stated “T” is
sensitive to pressure
• Abnormal morphology: #18 – increased mesial/distal
width of crown with abnormally wide pulp chamber
• Little to no bone support on distal, “L”
• Overall trabecular pattern was within normal limits
Figure 3. Midline deviation
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93
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 shifting 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 fabrication of partial dentures to fill spaces caused by the congenitally
missing teeth. She reported wearing the appliances for the appropriate 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 became 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 commonly 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.
Figure 4. Periapical radiograph
Figure 5. Periapical radiograph
Discussion
Figure 6. Periapical radiograph
Additional Assessment Results
After the oral and radiographic assessment, supervising faculty 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 family 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
94
Several 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 having 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 oligodontia. 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 significant 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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January 2011
The combination of her missing teeth and abnormal
tooth morphology is also significant because these two specific characteristics occurring together have been utilized in
studies investigating the expressed traits of females in families 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 Professionals
Dental professionals owe it to their patients to assist in identifying 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 experience. Since dental anomalies can be the primary manifestation 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 assessment. 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 planning 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 affect 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. Interestingly, 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.”
January 2011
Conclusions
Recent 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 protocols for the treatment of hypohidrotic ectodermal dysplasia in
the future, significantly changing the lives of those with the genetic 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 possible for patients. Additional information about the ectodermal
dysplasias can be accessed at www.nfed.org.
References
1. Cobourne MT. Familial human hypodontia – is it all in the genes? 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 Oral
Maxillofac Surg. 2007;36:473-480.
3. Ulm MR, Kratochwil A, Ulm B, Solar P, Aro G, Bernaschek G. Threedimensional 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,
delayed eruption, and dentin dysmineralization: a new variant? J Oral
Pathol Med. 2006;35:639-641.
5. Wang Y, Zhao H, Zhang X, Feng H. Novel identification of a four-basepair 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. Paradowska A, Szelag J, Slawecki K. Klippel-Feil Syndrome – Review of
the 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;62:989996.
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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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.
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, MSEd
Jennifer S. Sherry RDH, MSEd, is an assistant professor in the Dental Hygiene
Program at Southern Illinois University,
Carbondale, IL. She teaches radiology and
is a clinic supervisor for the third-year dental hygiene students. Her research interests
include children’s health issues, school nutrition programs,
school-based health clinics and pediatric dentistry.
Author Profiles
Disclaimer
Sherri Lukes RDH, MS
Sherri 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 Community Oral Health, Multicultural Applied Experience
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Questions
1. There are more than ________ in which
oligodontia is one of the associated findings and the majority are ________.
a.
b.
c.
d.
60 syndromes; acquired
90 syndromes; hereditary
120 syndromes; hereditary
120 syndromes acquired
2. The syndromes most commonly associated with missing teeth are ________ and
________.
a.
b.
c.
d.
ectodermal dysplasia; Seikel’s syndrome
Seikel’s syndrome; Down syndrome
Down syndrome; ectodermal dysplasia
Regan’s syndrome; ectodermal dysplasia
3. ________ is associated with oligodontia.
a.
b.
c.
d.
Rieger syndrome
Seckel syndrome
Klippel-Feil syndrome
all of the above
4. Ectodermal dysplasia can be the result of
________genetic expression.
a.
b.
c.
d.
autosomal dominant
autosomal recessive
X-linked
all of the above
5. Hypohidrotic ectodermal dysplasia is
associated with ________.
a.
b.
c.
d.
96
dry, hypoplastic skin
sparse scalp and body hair
dystrophic fingernails
all of the above
6. ________ is/are associated with ectodermal dysplasia.
a.
b.
c.
d.
Over-expressed sweat glands
Over-expressed tuftelin
Deficient sweat glands
none of the above
7. The most common form of ectodermal
dysplasia is the ________.
a.
b.
c.
d.
X-linked, hypohidrotic form
Y-linked, hypohidrotic form
X-linked, hyperhidrotic form
Y-linked, hyperhidrotic form
8. ________ are important in the early
diagnosis of ectodermal dysplasia.
a. Small, malformed teeth
b. Alveolar edentulous areas with hypoplastic, sharp
and narrow ridges
c. A reduced number of teeth
d. all of the above
9. ________ is a characteristic sign of
ectodermal dysplasia in an affected male.
a.
b.
c.
d.
Sunken eyes
Everted lips
Thin, fine hair
all of the above
10. More than ________ of female carriers
present with abnormalities associated with
their permanent teeth.
a.
b.
c.
d.
25%
50%
75%
90%
11. Decreased mesio-distal diameter of
molars is seen in ________.
a.
b.
c.
d.
12. Ectodermal dysplasia carriers may go
undiagnosed if ________.
a. hyperdontia is minor and other signs and
symptoms are present
b. hypodontia is major and other signs and symptoms
are present
c. hypodontia is minor and no other signs and
symptoms are present
d. all of the above
13. Female carriers of ectodermal dysplasia
may mention that their________.
a. dog had several missing teeth
b. father had several missing teeth due to early
extraction caused by infection
c. father had several congenitally missing teeth
d. none of the above
14. A female suspected of being a carrier for
ectodermal dysplasia may complain of
________.
a.
b.
c.
d.
intolerance to heat
intolerance to cold
intolerance to humidity
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.
b.
c.
d.
www.rdhmag.com
Male carriers for ectodermal dysplasia
Males with ectodermal dysplasia
Males with ectodermal hyperplasia
Females with ectodermal hyperplasia
bitewing
occlusal
panoramic
all of the above
January 2011
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Hypohidrotic Ectodermal Dysplasia
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1. List the more common syndromes associated with oligodontia
A Division of PennWell Corp.
2. List the various signs and symptoms of ectodermal dysplasia
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3. List and describe the global incidence of female carriers for ectodermal dysplasia
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The author(s) of this course has/have no commercial ties with the sponsors or the providers of
the unrestricted educational grant for this course.
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 PennWell or the administration of this course to
Machele Galloway, 1421 S. Sheridan Rd., Tulsa, OK 74112 or macheleg@pennwell.com.
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: macheleg@pennwell.com.
www.ineedce.com
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 verification
form. Verification forms 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 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/COST
All 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.
Customer Service 216.398.7822
RECORD KEEPING
PennWell 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 PennWell in writing.
© 2010 by the Academy of Dental Therapeutics and Stomatology, a division
of PennWell