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Year : 2017  |  Volume : 2  |  Issue : 1  |  Page : 22-25

Periodontitis in late childhood: Associated with immune-mediated enteropathy

1 Department of Pediatric and Preventive Dentistry, Surendra Dental College and Research Institute, Sri Ganganagar, Rajasthan, India
2 Department of Periodontology and Implantology, Surendra Dental College and Research Institute, Sri Ganganagar, Rajasthan, India

Date of Submission05-Mar-2018
Date of Acceptance16-Mar-2018
Date of Web Publication27-Apr-2018

Correspondence Address:
Dr. Kanika Gupta Verma
52-Satnam Nagar, P. O. Model Town, Jalandhar City - 144 003, Punjab
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijas.ijas_3_18

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Celiac disease is a chronic intestinal disease with immunological responsiveness to ingested gluten and is associated with poor absorption and digestion, affecting both developing dentition and oral mucosa. The article presents a clinical case showing the impact on the general and oral health of a 10-year-old patient. The case presented as a special situation in clinical pediatric practice that must be taken into account more often.

Keywords: Autoimmune, enteropathy, gluten, periodontitis

How to cite this article:
Verma KG, Juneja S, Salaria SK, Sukhija M. Periodontitis in late childhood: Associated with immune-mediated enteropathy. Imam J Appl Sci 2017;2:22-5

How to cite this URL:
Verma KG, Juneja S, Salaria SK, Sukhija M. Periodontitis in late childhood: Associated with immune-mediated enteropathy. Imam J Appl Sci [serial online] 2017 [cited 2021 May 12];2:22-5. Available from:

  Introduction Top

Celiac disease (CD) is a lifelong immune-mediated enteropathy found in genetically susceptible participants, characterized by permanent intolerance mediated by T-lymphocytes to the polypeptide fragments of gluten, a protein contained in some cereals, such as wheat, rye, and barley.[1] It is associated with severe atrophy of mucosa of the upper small intestine, resulting in poor absorption of majority of nutrients and vitamins. The characteristic clinical features are chronic diarrhea, tiredness, abdominal distension and bloating, vomiting, weight loss, muscle weakness, and loose stools.[2] When undiagnosed, it can cause developmental problems in childhood, severe gastrointestinal (GI) symptoms, depression, and reduced bone mineral density. It is a rare malabsorptive disorder of infancy and childhood; however, it is now considered to be a common, chronic, multisystem disorder that can present at any age when gluten is present in the diet.[1],[2]

CD presents various oral manifestations, which are dental enamel defects, recurrent aphthous stomatitis (RAS), and caries experience. Diagnostic criteria include serological tests (e.g., endomysial antibodies – EmA-IgA), characteristic small intestinal histology (lymphocytes infiltration and villous atrophy), and genetic testing, for example, determining human histocompatibility antigens, i.e. human leukocyte antigen DQ2/DQ.[3]

The treatment is lifelong adherence to a gluten-free diet (GFD), which usually results in remission, but delay in diagnosis can lead to a variety of complications, including nutritional deficiencies, such as anemia and osteoporosis, reproductive disorders, increased risk of developing other autoimmune disorders, and intestinal lymphoma.[3],[4]

Here, we present a case of 10-year-old boy who came to the department for multiple mobile teeth, and on investigation, it was diagnosed to be a case of CD.

  Case Report Top

A 10-year-old boy reported to the department of pediatric and preventive dentistry with a chief complaint of mobile teeth in the right upper, right, and left lower region for 4–5 months. History of present illness dated back to 1–1.5 years when the patient first noticed mobility in a tooth in the right upper region. However, for 4–5 months, mobility of various teeth increased with time. Medical history revealed that patient suffered from diarrhea, nausea, cramps, flatulence, abdominal distension, colic, difficulty with falling asleep, and lack of appetite since childhood. Parents got him examined, and the patient was diagnosed with CD and allergic to wheat. There was no relevant prenatal, natal, and family history. General physical examination revealed that the patient was of athletic built, well oriented, and cooperative. Extraoral examination revealed no abnormality. Intraoral examination revealed retained 63, congenitally missing 14 and chronic localized periodontitis with respect to 15, 16, 34, 36, and 46 [Figure 1]. Grade III mobility was noticed with respect to 16, 36, and 34. Extraoral radiological investigations were done by taking orthopantomograph, hand and wrist radiographs, and feet radiographs [Figure 2]. Intraoral radiographic investigations were done with intraoral periapical radiographs. The radiographic investigations revealed severe bone loss with respect to 16, 34, 35, 36, 45, and 46 [Figure 3]a,[Figure 3]b,[Figure 3]c,[Figure 3]d. Complete blood examination revealed raised level of lymphocytes (41%) and raised erythrocyte sedimentation rate (40 mm/h). Treatment planned was diet management with GFD. Extraction of 36 and 34 was done as there was gross mobility and the patient was unable to chew properly. Mesial root resorption was noticed with respect to 36 [Figure 3]e. Granulomatous tissue was observed in relation with 34 [Figure 3]g and sent for histopathological investigation that revealed densely infiltrated acute and chronic inflammatory cells [Figure 3]f and [Figure 3]h.
Figure 1: Intraoral photographs (a) Front occlusal view; (b) Localized periodontitis with respect to 15 and 16; (c) Maxillary occlusal view left side; (d) Localized periodontitis with respect to 46; (e) Localized periodontitis with respect to 34 and 36

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Figure 2: Extraoral radiographs (a and b); hand and wrist radiographs; (c and d) feet radiographs; (e) Orthopantomograph

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Figure 3: (a-d) Intraoral radiographs; (e) extracted 36; (f) histopathology with respect to 36; (g) extracted 34; (h) histopathology of granulomatous tissue with respect to 34

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  Discussion Top

CD is an immunological disorder emanating from sensitivity of the intestinal mucosa to gluten or prolamine and thus affects primarily the intestinal tissue in genetically predisposed people. Patients affected by CD have a broad range of clinical manifestations due to autoantibody response which is triggered by exposing the intestinal tissue to gluten.[5] Beside the systemic symptoms, extraintestinal signs of the disease involve the oral cavity at both the hard- and soft-tissue levels. Recent epidemiologic data have shown a prevalence of CD approaching 1% in the general population. CD is an autoimmune disease resulting from an inappropriate T-cell-mediated immune response against ingested gluten.[4],[5],[6] Although the proximal part of the intestinal mucosa represents the main site of the gut involved in CD, it has been demonstrated that gluten-driven T-cell activation is not restricted to the small intestine but is present in the whole GI tract. The mouth, the first part of the GI system, represents a site very easy to detect and an oral examination could give a useful diagnostic contribution as lesions of the hard and soft tissues have been reported in CD.[6] As abnormalities of the oral cavity have been reported in CD, noninvasive clinical examination of the oral cavity can contribute to identify patients with atypical or silent CD. Indeed, a wide range of frequencies of enamel defects in CD patients has been reported in other studies. It has been reported that RAS is at least among the fifth most common presentations of CD.[7]

Oral examination in our case revealed generalized gingival recession and missing tooth in relation to 13. The tongue appeared bald and the teeth exhibited black linear discoloration and roughened enamel surface. Individuals suspected to have aggressive periodontitis are at a risk of premature tooth loss. Three primary conditions for a successful diagnosis of aggressive type of periodontitis (systemic health, familiar aggregation, and rapid attachment loss) relay on the patient's recognition.

In this case, the patient had a chief complaint of mobile teeth and she had pale skin and generalized weakness. The main oral signs associated with CD are angular cheilitis, glossitis, and depapillated tongue. The redness and pain in the tongue with papillary atrophy are related to the Vitamin B12, folic acid, and iron deficiencies, whose absorptions in the small intestine may be affected by CD. It is still not clear whether the oral lesions represent a direct manifestation of CD or whether they occur as a result of the indirect effects of poor absorption on the cells of the basal layer of the mucosa, which is in the process of division and already predisposed to irritation by a preexistent disease.[6],[7],[8] In some cases, CD may contribute to the development of protein-calorie malnutrition, and depending on the age at which this is established, it contributes to the appearance of oral alterations, such as delayed tooth eruption, diminished size of the teeth, problems in enamel formation, and salivary gland dysfunction.[9],[10],[11] The cornerstone of treatment for CD is lifelong adherence to a strict GFD. For the majority of patients, a GFD leads to clinical and histological remission, normalization of standardized mortality rates, a reduction in long-term health complications (i.e., osteoporosis), and in some studies, an improvement in psychological well-being and quality of life.

  Conclusion Top

CD is the only treatable autoimmune disease, given that a correct diagnosis is reached and a strict, lifelong GFD is executed. Most patients present with atypical signs and symptoms of disease. Dentist may be the first person to diagnose a case of CD because oral manifestations are present in large number of cases. Appropriate referral and a timely diagnosis can help prevent serious complications of this disorder.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Herwis K, Elturki H, Ali A. Prevalence of dental findings of children with celiac disease in Libya: A comparative study. Case Rep Clin Pathol 2015;2:61-6.  Back to cited text no. 1
Rashid M, Zarkadas M, Anca A, Limeback H. Oral manifestations of celiac disease: A clinical guide for dentists. J Can Dent Assoc 2011;77:b39.  Back to cited text no. 2
Barker JM, Liu E. Celiac disease: Pathophysiology, clinical manifestations, and associated autoimmune conditions. Adv Pediatr 2008;55:349-65.  Back to cited text no. 3
Samasca G, Bruchental M, Butnariu A, Pirvan A, Andreica M, Cristea V, et al. Difficulties in celiac disease diagnosis in children – A case report. Maedica (Buchar) 2011;6:32-5.  Back to cited text no. 4
Murch S, Jenkins H, Auth M, Bremner R, Butt A, France S, et al. Joint BSPGHAN and coeliac UK guidelines for the diagnosis and management of coeliac disease in children. Arch Dis Child 2013;98:806-11.  Back to cited text no. 5
da Silva PC, de Almeida Pdel V, Machado MA, de Lima AA, Grégio AM, Trevilatto PC, et al. Oral manifestations of celiac disease. A case report and review of the literature. Med Oral Patol Oral Cir Bucal 2008;13:E559-62.  Back to cited text no. 6
Acar S, Yetkıner AA, Ersın N, Oncag O, Aydogdu S, Arıkan C, et al. Oral findings and salivary parameters in children with celiac disease: A preliminary study. Med Princ Pract 2012;21:129-33.  Back to cited text no. 7
Ertekin V, Sümbüllü MA, Tosun MS, Selimoǧlu MA, Kara M, Kiliç N. Oral findings in children with celiac disease. Turk J Med Sci 2012;42:613-7.  Back to cited text no. 8
Datta Gupta S. Pathology of celiac disease: A brief review. Trop Gastroenterol 2013;34:207-26.  Back to cited text no. 9
Piscaglia AC. Intestinal stem cells and celiac disease. World J Stem Cells 2014;6:213-29.  Back to cited text no. 10
Fasano A, Catassi C. Clinical practice. Celiac disease. N Engl J Med 2012;367:2419-26.  Back to cited text no. 11


  [Figure 1], [Figure 2], [Figure 3]


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