Hypohidrotic Ectodermal Dysplasia
Transcription
Hypohidrotic Ectodermal Dysplasia
Earn 1 CE credit This course was written for dentists, dental hygienists, and assistants. 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 Go Green, Go Online to take your course 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. 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 92 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- www.rdhmag.com 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 www.rdhmag.com 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 www.rdhmag.com 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. www.rdhmag.com 95 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 Reader Feedback 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. We encourage your comments on this or any PennWell course. For your convenience, an online feedback form is available at www. ineedce.com. Online Completion Use this page to review the questions and answers. Return to www.ineedce.com and sign in. If you have not previously purchased the program select it from the “Online Courses” listing and complete the online purchase. Once purchased the exam will be added to your Archives page where a Take Exam link will be provided. Click on the “Take Exam” link, complete all the program questions and submit your answers. An immediate grade report will be provided and upon receiving a passing grade your “Verification Form” will be provided immediately for viewing and/or printing. Verification Forms can be viewed and/or printed anytime in the future by returning to the site, sign in and return to your Archives Page. 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 ANSWER SHEET Hypohidrotic Ectodermal Dysplasia Name: Title: Address: E-mail: City: State: Telephone: Home ( ) Office ( Specialty: ZIP: ) Country: Lic. Renewal Date: 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 1 CE credit. 6) Complete the Course Evaluation below. 7) Make check payable to PennWell Corp. For Questions Call 216.398.7822 Educational Objectives If not taking online, mail completed answer sheet to Academy of Dental Therapeutics and Stomatology, 1. List the more common syndromes associated with oligodontia A Division of PennWell Corp. 2. List the various signs and symptoms of ectodermal dysplasia P.O. Box 116, Chesterland, OH 44026 or fax to: (440) 845-3447 3. List and describe the global incidence of female carriers for ectodermal dysplasia Course Evaluation Pleaseevaluatethiscoursebyrespondingtothefollowingstatements,usingascaleofExcellent=5toPoor=0. 1. Were the individual course objectives met? Objective #1: Objective #2: Yes Yes No NoO Yesbejcvti#e3: No For IMMEDIATE results, go to www.ineedce.com to take tests online. Answer sheets can be faxed with credit card payment to (440) 845-3447, (216) 398-7922, or (216) 255-6619. Payment of $29.00 is enclosed. (Checks and credit cards are accepted.) 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