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Editor,—The association between coeliac disease and dental enamel defects (DED) is already known.1 These defects range from discolouring to pitting, grooving, and total loss of enamel, and are considered to be coeliac disease specific when distributed symmetrically and chronologically in all four sections of dentition. The Italian Society of Pediatric Gastroenterology and Hepatology (SIGEP) promoted a multicentre study for evaluating the prevalence of DED in a large group of Italian patients with coeliac disease.
A total of 603 children with coeliac disease were studied (327 girls, 276 boys, mean age 17.8 years) in 13 Italian centres for paediatric gastroenterology. All subjects had permanent or mixed (permanent plus primary) dentition. The diagnosis of coeliac disease had been made in all cases using the criteria of the European Society of Paediatric Gastroenterology and Nutrition.2 The dental enamel inspection was performed in each centre by a paediatric gastroenterologist experienced in identifying enamel defects, with a dentist present. A group of 6949 schoolchildren (mean age 12.4 years) served as healthy controls. When a subject from the control group presented with DED, an antiendomysium antibody assay was performed (indirect immunofluorescence, Endomisium Eurospital, Trieste, Italy), leading to small bowel biopsy in subjects testing positive. Student’st test was used for statistical analysis.
Altogether, 195 of our 603 patients with coeliac disease (32 4%) had systematic enamel defects with a fair degree of variation between centres (table 1). Mean age at diagnosis of coeliac disease was significantly higher in the group with DED (8.1 v 4.1 years, p<0.01). In the group of 6949 healthy controls, specific DED were found in 52 subjects (0.59%) (p<0.00001 in respect of the coeliac disease patients). Ten of them tested positive for antiendomysium antibodies, nine underwent intestinal biopsy (one refusal), and four had a flat mucosa.
DED are therefore present in one third of Italian patients with coeliac disease, with a prevalence lower than that found in the Finnish studies1 but higher than that found in UK.3This study also suggests that DED may be connected to late diagnosis of coeliac disease. The mechanism of development of DED in coeliacs is not clear, but it seems more likely that they are the consequence of immune mediated enamel damage rather than related to malnutrition. In fact, similar lesions that appear to be associated with HLA DR3 aplotype,4 are common in autoimmune disease (such as polyendocrinopathy), but are rare in nutrition disorders such as rickets. Our study also confirms that coeliac disease can be symptomless or can present with an atypical clinical picture. We recommend that subjects with symmetrical DED in permanent teeth undergo serological testing for antiendomysium antibodies and intestinal biopsy when testing positive.
Participants to the Italian Society of Paediatric Gastroenterology and Hepatology DED study group: R Lazzari, C Corvaglia (Bologna), S De Virgilis (Cagliari), A Miano, M Marani (Cesena), F Bascietto (Chieti), M Sanfilippo (Fiesole), G Magazzu’ (Messina), A M Giunta, I Prampolini (Milano, ‘De Marchi’), C Bianchi, G. Barera (Milano ‘S Raffaele’), F Balli, P Bertolani (Modena), F Cataldo (Palermo), G Maggiore (Pisa), M Bonamico (Roma), M S Scotta (Varese).
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