<<Disclaimer: Verify this information before applying it to your situation.>> Below are comments I received from list members on this topic. Lynn Rainwater http://www.geocities.com/alamoceliac Just search PubMed/Medline using Dental Enamel Celiac as the search terms, and you'll find 36 citations, most with abstracts, some with reference to adults. I'm one of the adults with enamel problems. I have seen dental enamel defects listed as an association w/ celiac. I do not know if what I read stated specifically that it was for children, adults or both. I was just diagnosed earlier this year and I am 32. I have had underdeveloped enamel my whole life and we never really knew the cause of it, but I am sure it is due to undiagonosed celiac. Sorry I can't give you any more specific info, but hope this helps. No articles. Just sharing that I most certainly have little or no enamel. I was told that it was due to not processing calcium when I was a child, and not on a totally gf diet...My mom tried, but didn't have all of the info that we have now. Sounds plausible. I have not looked up articles on the subject, but I know from personal experience with malabsorption (probably resulting from a lifetime of undiagnosed CD) that my own history of unrelenting tooth decay and then bone loss was significantly reversed after going gf and taking adequate calcium supplements (1500 mgs a day). In response to suggestions I ran across on this list I have my calcium (and other essential nutrients) levels checked regularly to be sure I absorb what I ingest. I only have anectdotal information. My son was diagnosed in Dec last year. However because of dr testing etc. we did not start a gf diet until almost May. In the past year he has "suddenly" had terrible problems with decay and has had urine tests showing very high levels of calcium which one dr says is related to digestive problems. Gluten Intolerance Group (GIG) had a newsletter article about tooth enamel within the last 2 years. I can't give you any sites, but I can tell you that I have had dental enamel problems since being an adult. About five years ago, way before being diagnosed, my dentist was suddenly alarmed by the changes she saw in my mouth. My gums that were previously pink & firm, were suddenly red, puffy & tender. The enamel on the tongue side of my teeth suddenly showed pitting that had not been there just 6 months earlier. She thought that I must be eating hard candies all day, sucking on lemons or vomiting frequently. None was the case. My dentist could tell that I had some kind of systemic inflammatory disease, but my doctor couldn't pinpoint it. It wasn't until I was diagnosed celiac in April of this year that I realized that the problems were celiac related. I attended a Gluten Intolerance Group conference in June of this year. A dentist told us that pitting enamel & gingivitis can be caused from celiac disease in adults. Quoted below is information provided by Don Wiss. Lynn Rainwater http://www.geocities.com/alamoceliac From the CCA's "Celiac News" dated Spring '94. For subscription info see: http://www.celiac.ca/ Excerpts from "Update" Nov. 93, a publication of the College of Dental Surgeons of British Columbia. Reprinted with permission. Children with celiac disease often reveal pathognomonic enamel defects systematically and chronologically in all four quadrants. Dentists can play an important role in screening patients possibly suffering from celiac disease. Patients with symmetrical enamel hypoplasia in permanent teeth should be advised to seek serologic screening using sensitive and/or invasive tests for evidence of small bowel mucous villous atrophy. Celiac Disease as Classified by Enamel Defects are: Grade 0: No defect. Grade I: Defect in colour of enamel only; single or multiple cream, yellow or brown opacities with clearly defined or diffused margins; all or part of the enamel surface is without a natural glaze. Grade II: Minor structural defects; rough enamel surface, horizontal grooves or shallow pits, light opacities and/or discoloration may be found; or part of the enamel surface is without a natural glaze. Grade III: Evident structural defects; all or part of the enamel surface is rough with deep horizontal grooves of varying width; may have large vertical pits; large opacities of strong and varying discoloration. Grade IV: Severe structural defects; the shape of the tooth may be abnormal with cusp tips sharply pointed and/or the incisal edges unevenly thinned and roughened; margins of the lesions are well defined and strongly discoloured. =================================== From: Ron Hoggan <[log in to unmask]> Date: Sun, 26 May 1996 23:41:37 -0700 (MST) Subject: tooth defects, bone minerals, etc Here are some references: 1. Maki, et. al. "Dental enamel defects in first-degree relatives of coeliac disease patients" LANCET, Vol. 337, pages 763-764, March 30, 1991. 2. Ballinger, et. al. "Dental enamel defects in coeliac disease" LANCET vol. 343, pages 230-231, Jan. 22, 1994 3. Mazure, et. al. "Bone Mineral Affection in Asymptomatic Adult Patients with Celiac Disease" THE AMERICAN JOURNAL OF GASTROENTEROLOGY, vol. 89, no. 12, page 2130-2134, 1994 4. Marsh, Michael N. "Bone Disease and Gluten Sensitivity: Time to Act, to Treat, and To Prevent" THE AMERICAN JOURNAL OF GASTROENTEROLOGY vol. 89, no. 12, pages 2105-2107, 1994. There are, of course, many other references in the literature, that indicate that such symptoms are the result of not absorbing minerals, and the vitamins also necessary for metabolizing these minerals, as a result of the poorer absorption that is part of gluten intolerance. As my mother was first diagnosed with fibromyalgia, and then her blood demonstrated antigliadin antibodies at 40% above the normal range, I am inclined to think that her arthritic pain is also the result of gluten intolerance. Because this intolerance is a genetic ailment, and because I have gluten intolerance, my mother's medical profile is becoming rapidly clearer. I sincerely hope it is not too late to reverse some of the damage that gluten has done. I should point out that my 24 year old daughter has had muscle pain since puberty. She was diagnosed with gluten intolerance last year, and she says that mineral and vitamin supplementation of much the same sort as outlined my Ms. Williamson is necessary for her continued comfort, in addition to the gluten-free diet. I hope these references are helpful. If you need more, I can have a bunch for you by end of business tomorrow Mountain Daylight Time. Best Wishes, Ron Hoggan ============== "Research Report on Dermatitis Herpetiformis" by Elaine I. Hartsook, Ph.D.,R.D. (Gluten Intolerance Group of North America,1993) : Dental enamel defects similar to those previously seen in both children and adults with celiac sprue (Aine, 1989; Aine,1990) have been shown to be present in adults and children with DH (Aine, 1991; Aine,1992). These enamel defects occur while the crowns of the teeth are forming, that is, usually before the age of 7 years. Celiac-type enamel defects are found on'matched' teeth on both sides of the mouth (that is, they are symmetrical) and they appear in the same location on the tooth surface, showing that they occurred at same time (that is, they are chronologically matched). Enamel damage has been classified by Aine and her coworkers as : Grade 1 = enamel lesions include defects in the color of the enamel; Grade 2 slight structural defects with a rough enamel surface and horizontal grooves or shallow pits; Grade 3 evident structural defects with part of all of the surface of the enamel rough and filled with deep horizontal grooves varying in width or with large vertical pits; and Grade 4 severe structural defects in which the shape of the tooth has also changed. Celiac-type dental defects were shown to be, overall, less severe in those with DH than those with celiac sprue. Eighty-three percent of 40 adult subjects with celiac sprue were shown to have enamel defects in Aine's 1990 study. Children with celiac sprue had the most severe defects, with 11% showing Grade 4 enamel defects (Aine, 1986). In Aine's 1992 study, 53% of the 30 adult study subjects with DH had celiac-type dental defects, while only 2% of the 66 control subjects showed these types of defects. The defects in those with DH were mild, Grade 1 and Grade 2. Severity of enamel defects did not relate to the degree of damage to the lining of the small intestine in these DH subjects. When the total number of affected teeth were counted, 51% of the 793 teeth in DH subjects showed dental enamel defects as opposed to only 18% of the 1,780 teeth from the normal control group. Enamel defects are thought to be caused by nutritional or immunological factors. BIBLIOGRAPHY: *Aine, L.: Dental enamel defects and dental maturity in children and adolescents with coeliac disease. Proceedings of the Finnish Dental Society, 82 (Suppl 3), pges 1-71, 1986 *Aine, l., Maki,M., Collin,P., and Keyrilainen, O.: Dental enamel defects in celiac disease. Journal of Oral Pathology and Medicine. Vol. 19, pges 241-245, 1990 *Aine, L., Reunala, T., and Maki, M.,: Dental enamel defects in children with dermatitis herpetiformis. Journal of Pediatrics. Vol. 118, pges 572-574, 1991. *Aine, L., Maki, M., and Reunala, T.: Coeliac-type dental enamel defects in patients with dermatitis herpetiformis. Acta Derm Venereol (Stockh). Vol. 72, pges25-27, 1992. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997 Dec;84(6):646-650 Dental enamel defects in celiac patients. Aguirre JM, Rodriguez R, Oribe D, Vitoria JC Departamento de Estomatologia, Universidad del Pais Vasco/E.H.U., Bilbao, Vizcaya, Spain. OBJECTIVE: The incidence and distribution of enamel defects among patients with celiac disease were examined. STUDY DESIGN: The oral cavity was explored in 137 patients with celiac disease (mean age 16.2 years; age range 5 to 68 years) and in 52 control patients (mean age 19.8 years; age range 5 to 64 years). Permanent dentition enamel defects were recorded, along with their number and locations. The decayed, missing, and filled teeth index rates were also established, and an investigation was made of the human leukocyte antigens among the patients with celiac disease. The results obtained were analyzed with the chi-squared test, statistical significance being regarded for p < or = 0.05. RESULTS: Enamel defects were observed in 72 (52.5%) of the patients with celiac disease (52 patients had systematic defects) and in 22 (42.3%) of the control patients (9 patients had systematic defects). Systematic defects were significantly more common in the celiac disease group. In the patients with celiac disease, 72.2% were symmetrical, compared with 40.9% of the defects in the control patients. The incisors were the most frequently affected teeth, the extent of involvement being significantly greater in the celiac disease group. In patients with celiac disease, DR7, DR3, and DQ2 were the most commonly observed human leukocyte antigens. The mean decayed, missing, and filled teeth index rates were 4.8 and 6.2 in the celiac disease group and the control group, respectively. CONCLUSIONS: Enamel defects are common among patients with celiac disease. They tend to be bilateral and symmetrical, and they are chronologically distributed. The lesions affect mainly the incisors and the molars. Patients with such characteristics should be evaluated for possible celiac disease. PMID: 9431534, UI: 98093599 Pediatr Dent 1996 Nov;18(7):461-464 The oral manifestations of intestinal lymphangiectasia: case report. Ralph PM, Troutman KC Bronx Lebanon Hospital, New York, USA. Intestinal lymphangiectasia is a rare autosomal dominant disorder or acquired condition that leads to lymph obstruction, poor chyle transport, and concomitant problems of hypoproteinemia, lymphocytopenia, hypogammaglobulinemia, and peripheral edema. Patients develop diarrhea, steatorrhea, and hypocalcemia secondary to fat-soluble vitamin malabsorption. Treatment is a restrictive diet of low fat, medium chain triglycerides. Oral manifestations are gingivitis due to poor PMN function and enamel defects due to poor calcium absorption. A case of a 14-year-old boy with both gingival and enamel problems secondary to intestinal lymphangiectasia is reported. PMID: 8970209, UI: 97125105 Acta Paediatr Suppl 1996 May;412:47-48 Dental enamel defects and screening for coeliac disease. Martelossi S, Zanatta E, Del Santo E, Clarich P, Radovich P, Ventura A Istituto di Clinica Pediatrica, Istituto per l'Infanzia IRCCS Trieste, Italy. Specific dental enamel defects (DEDs) in permanent teeth are frequently observed in coeliac patients. We examined the permanent teeth in 6949 secondary school children living in Trieste (78% of 8724 children born between 1978 and 1982). Children with DEDs were tested for serum antigliadin antibodies (AGAs) and antiendomysium antibodies (AEAs), and those positive for serum AGAs and/or AEAs underwent intestinal biopsy. Specific DEDs were observed in 52 children (0.59% of the total population examined). Serum AGAs and/or AEAs were positive in 10 cases. Nine patients underwent intestinal biopsy (one refused) and in four cases a flat mucosa was documented (one with short stature, three completely asymptomatic). The known incidence of CD in the study area was 1:1000 before the study programme and 1:670 (an increase of 44%) after it. Dental enamel inspection may be utilized for detecting undiagnosed coeliac disease in symptom-free schoolchildren. This clinical test is probably less sensitive than serum AGA screening test, but deserves some consideration because it is cheap, easy to perform and well accepted by the population. PMID: 8783757, UI: 96377982 Ann Med 1996 Feb;28(1):9-12 Coeliac-type permanent-tooth enamel defects. Aine L Department of Oral and Maxillofacial Surgery, Tampere University Hospital, Finland. Systematic and chronologically distributed permanent-tooth so-called coeliac-type enamel defects are highly prevalent both in children and adults with coeliac disease (gluten-sensitive enteropathy) and dermatitis herpetiformis. Coeliac-type enamel defects were also found in healthy first-degree family members of coeliac disease patients. Our family study showed that these persons with the typical defected enamel were genetically similar to coeliac disease patients (A1;B8;DR3). As coeliac disease patients are often clinically silent with no gastrointestinal symptoms, or they complain only of minimal abdominal discomfort, both dentists and physicians could select patients with coeliac-type enamel defects for gastroenterological and dermatological consultations, including serological screening tests and later jejunal mucosal biopsy. PMID: 8932499, UI: 97086305 Acta Paediatr 1994 Dec;83(12):1272-1275 Coeliac disease, enamel defects and HLA typing. Mariani P, Mazzilli MC, Margutti G, Lionetti P, Triglione P, Petronzelli F, Ferrante E, Bonamico M I Clinica Pediatrica, Universita La Sapienza, Roma, Italia. The presence of dental enamel defects in coeliac disease and their relation to hypocalcaemia or a particular HLA class in 82 Italian children with coeliac disease was studied. Demarcated opacities or hypoplasia were detected in 23 subjects (group 1) while minimal or no dental lesions were found in the remaining 59 patients (group 2); in 189 normal controls, enamel lesions were significantly less frequent than in patients with coeliac disease (14.8% versus 28.0%; p < 0.005). No statistically significant differences were found for age at diagnosis and calcium concentrations between groups 1 and 2. Regression analysis showed a correlation between age at diagnosis and number of teeth with enamel defects. In our patients, the presence of HLA DR3 antigen significantly increased the risk of dental lesions, while genotype DR5,7 seemed to protect against enamel defects. A logistic regression analysis of the variables age, serum calcium concentrations, number of affected teeth, type of enamel defect and DR antigens showed that only DR antigens discriminated coeliac disease patients with from those without enamel defects. PMID: 7734869, UI: 95252719 J Oral Pathol Med 1990 Jul;19(6):241-245 Dental enamel defects in celiac disease. Aine L, Maki M, Collin P, Keyrilainen O Department of Oral and Maxillofacial Surgery, University Hospital of Tampere, Finland. The teeth of 40 adults aged 19 to 67 yr with celiac disease (CD) were examined for dental enamel defects (ED). A total of 33 of the 40 adults with CD (83%) had systematic ED in contrast to only 5 of the 112 clinical controls (4%). Unspecific enamel lesions were found in both groups, but they were more common in the control group (80% vs. 18%). Altogether 69% of the permanent teeth in adults with CD were found to be defected, in clinical controls only 19%. In adults with CD the ED were in contrast to those in controls symmetrically and chronologically distributed in all four sections of dentition. The present study clearly shows that symmetrically and chronologically distributed enamel defects are strongly associated with CD. Therefore in the absence of symptoms and signs of malabsorption dentists could easily select the right patients possibly suffering from CD for gastroenterologic consultations. PMID: 2401959, UI: 90383769