The Effect of Celiac Disease on the Oral Cavity: A Review

Celiac disease is one of the most common chronic systemic autoimmune disorders. It is triggered by the ingestion of gluten, which is a protein found in wheat, rye, and barley [1]. Only a part of the gluten complex plays a significant role in the pathogenesis of Celiac disease; this includes gliadin in wheat, secalin in rye, hordein in barley, and avenin in oats [2]. Celiac disease generally presents after the sixth month of life, when gluten is normally introduced in the human diet [3,4]. In humans, gluten is not completely digested; it is only broken down into peptides, which are transferred across the intestinal wall and modified by tissue transglutaminase (TTG). TTG is generally present in an inactivated form, and the cause of its activation in Celiac disease remains unknown. TTG activation leads to the production of negatively charged peptide molecules, which complement the positively charged structures of HLA DQ2 and HLA DQ8 antigens. Subsequently, escalation of the immune response results in the production of specific autoantibodies, which are the bases of disease diagnostics. This process results in an inflammatory state in the intestinal wall and consequent damage to the intestinal villi, which affects the absorption process and leads to progressing malnutrition and related consequences [5]. Celiac disease can be typical or atypical. The typical (classic) type develops when gluten is introduced in the diet, usually between 6 and 24 months of age. Typical features include insufficient height and weight and gastrointestinal symptoms such as abdominal bloating and pain, vomiting, constipation, and diarrhea. The atypical type, on the other hand, affects older children and adults. Celiac disease is diagnosed on the basis of clinical symptoms; serological tests for the detection of serum immunoglobulin (Ig) A (IgA), TTG antibody, and IgA-endomysial antibody; and histopathological examination of biopsy specimens from the intestinal mucosa [6,7]. Recently, genetic studies identifying HLA DQ2/DQ8 antigens have been utilized more frequently [8], because the spontaneous disappearance of antibodies over time has been observed in a proportion of children with Celiac disease [9]. Approximately 83% patients remain undiagnosed or are misdiagnosed, which can result in irreversible medical and dental complications [10]. Celiac disease is a multifactorial disorder, with both genetic and environmental factors playing a role in the etiology [11]. Genetically close relatives of a patient with celiac disease are at significant risk of developing the disorder (5%–15%) [12]. In addition, patients with autoimmune disorders such as type 1 diabetes mellitus, Williams syndrome, IgA deficiency, autoimmune thyroiditis, and Down syndrome, carry a higher risk of Celiac disease development [13]. Among environmental factors, the most important one is early introduction of gluten in a child’s diet. In fact, the disease can be prevented by early introduction of gluten in a child’s diet to build the immune tolerance [14]. The current dietetic recommendations advise that gluten should be gradually introduced in the diet between 4 and 6 months of age, with careful observation for undesired reactions. Late introduction of gluten may result in atypical Celiac disease, with delayed diagnosis or undiagnosed disease for several years [11]. Alterations in the oral cavity are frequently observed in patients with Celiac disease and may allow for early diagnosis and treatment. Specifically, dental enamel defects, recurrent aphthous stomatitis (RAS), delayed eruption of teeth, and malocclusion have been found to be more common in this patient population. Awareness of Celiac disease among health professionals remains poor, and delays in diagnosis are common. Therefore, as clinicians, it is very important to be aware of the potential presentations, particularly in the oral cavity, in order to facilitate early diagnosis and prevent consequences that can affect the overall health status of the patient.