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 Table of Contents  
Year : 2015  |  Volume : 27  |  Issue : 3  |  Page : 412-415

Oral health presentations and considerations in gastrointestinal diseases

Department of Oral Medicine and Radiology, Chettinad Dental College and Research Institute, Kanchipuram, Tamil Nadu, India

Date of Submission03-Dec-2014
Date of Acceptance11-Nov-2015
Date of Web Publication25-Nov-2015

Correspondence Address:
Christeffi Mabel Rolands
No.1, AF-3, AL-Syed Builders, II Main Road, Dhandeeswaram Nagar, Velachery, Chennai - 600 042, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-1363.170475

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Lesions of the gastrointestinal tract (GIT) run the gamut from the merely annoying heartburn that has affected many a partakers of a large and spicy meal to the highly lethal cancers. Distressing to the physician is that all disorders of the esophagus tend to produce similar symptoms, namely heartburn, dysphagia, pain, and/or hematemesis. The GIT plays a prominent part in the immune system. The pH (ranging from 1 to 4) of the stomach is acidic which proves fatal for a number of microbes which pass through it. Also, mucus in the stomach (containing IgA antibodies) and enzymes present in the saliva and bile neutralize many of these microorganisms. Lesions of the GIT also present with oral symptoms, which is of significance for an oral physician to recognize and treat them.

Keywords: Crohn′s disease, oral manifestations, ulcerative colitis

How to cite this article:
Rolands CM. Oral health presentations and considerations in gastrointestinal diseases. J Indian Acad Oral Med Radiol 2015;27:412-5

How to cite this URL:
Rolands CM. Oral health presentations and considerations in gastrointestinal diseases. J Indian Acad Oral Med Radiol [serial online] 2015 [cited 2020 Feb 29];27:412-5. Available from: http://www.jiaomr.in/text.asp?2015/27/3/412/170475

   Introduction Top

Dentists, in general, and oral physicians, in particular, are expected to identify, diagnose, and treat oral conditions associated with gastrointestinal (GI) diseases. To provide safe and appropriate dental care, dentists are typically concerned with the proper diagnosis of oral manifestations of GI disorders, homeostasis, risk of infection, drug actions and interactions and, many a times, this could be a warning alarm for diagnosing the systemic disorder of the patient. The present article offers a detailed review of the oral manifestations of various GI diseases or conditions.

   Diseases of the Upper Digestive Tract Top

Gastroesophageal reflux disease

It is one of the most common diseases affecting the upper gastrointestinal tract (GIT). Gastroesophageal reflux disease (GERD) is generally perceived to be less common in Asia in comparison with the western world. However, several population-based studies have shown a prevalence of more than 10%. In gastroesophageal reflux, the gastric contents (chyme) move passively up from the stomach into the esophagus. Heart burn is the cardinal sign of GERD. Chest pain is another important symptom. Dysphagia is also a common presenting complaint. [1] The "burp" mechanism is due to the relaxation of the lower esophageal sphincter so that the pressure in the stomach is relieved. When this lower esophageal sphincter fails, gastric contents may make their way into the esophagus and cause reflux, and the severity of the symptoms depends on the amount of acid refluxate. [2] In populations with a high prevalence of Helicobacter pylori infection, a significant proportion of patients with GERD have concomitant peptic ulcer disease. Empirical treatment based on "typical" GERD symptoms alone may not be appropriate. [3]

Oral health presentation in GERD

Loss of taste or altered taste sensation and dental erosion are the two major manifestations. Severe erosion gives a smooth shiny surface to the teeth and may lead to pulpitis with acute pain. This occurs most commonly in the maxillary anterior teeth, particularly the palatal surface. Palatal mucosa may also disclose microscopic alteration. Erythema and mucosal atrophy due to the acidic refluxate are also common. [4] Enamel loss in patients with GERD may act as an indicator of the duration, frequency, and severity of the disease. This might be of help to the gastroenterologist in treating the patient. Moreover, many a times, these patients report to the dentist with a complaint of hypersensitivity of teeth and only when the dentist explains the underlying cause, they understand their medical state and seek treatment for GERD.

Oral health considerations in patients with GERD

Patients under H2 antagonists experience toxic reaction to lidocaine. H2 receptor antagonists (cimetidine) also inhibit the absorption and, therefore, affect the blood concentration of azole antifungal agents. Esophageal stricture and fibrosis can affect the insertion of intubation tube during oral surgical procedures.

Hiatal hernia

The esophagus passes through the hiatus into the stomach. In some patients, the hiatus may be weak or enlarged, so a portion of the stomach herniates into the chest cavity. Infants usually regurgitate blood-stained food and have difficulty in breathing and swallowing. In adults, hiatal hernias may present with symptoms of esophageal reflux and, conversely, esophageal reflux disease often is associated with hiatal hernia. Hiatal hernias mostly are asymptomatic. There are two types of hiatal hernia. The most common by far (90%) is a sliding hiatal hernia where, as the name implies, a portion of the proximal stomach herniates or slides into the chest. As a consequence, the cardioesophageal junction is displaced into the chest as well. [5]

Oral health presentations

Dry mouth (xerostomia), class V caries, and root caries are the oral health symptoms. If reflux enters into the oral cavity, then symptoms similar to GERD have been reported. [6]

   Diseases of the Lower Digestive Tract Top

Peptic ulcer

Peptic ulcer is yet another common disease encountered by the dentist while reviewing patients' medical history. Peptic ulcer is a disease of the GIT characterized by mucosal damage secondary to pepsin and gastric acid secretion. It usually occurs in the stomach (gastric ulcer) and proximal duodenum (duodenal ulcer); other sites include lower esophagus, distal duodenum, or jejunum. [7] H. pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAIDs) are the predominant causes of peptic ulcer disease. In 1997, the Center for Disease Control and Prevention (CDC) propagandized the link between H. pylori and ulcers and also insisted that peptic ulcers are curable infections with appropriate antibiotics.

Oral health presentations

Erosion in the palatal aspect of maxillary anterior teeth, malodor, aphthous ulcers, oral candidiasis, [8] vascular malformations of the lip, and low salivary secretion may contribute to decreased efficacy of H. pylori eradication. H. pylori has been isolated from dental plaque, implicating the oral cavity as the major source of this organism.

Oral health considerations

Lengthy dental procedures should be avoided to reduce stress. NSAID (acetoaminophen is preferred) and steroid administration should be avoided as GI bleeding and ulceration may occur with their use. Caution and care needs to be taken in patients with perforation as it would lead to anemia. Long-term use of cimetidine and rantidine can cause thrombocytopenia. [9]

Ulcerative colitis

Ulcerative colitis is caused due to chronic inflammation of the colonic mucosa and the extent and severity of colon involvement are variable. There are two common presentations. In its most limited form, it may be restricted to the distal rectum and in the second presentation, the most extended form, the entire colon is involved. [10] If the disease is mild, there may be granular appearance of the mucosa and if fulminant, stripping of the mucosa, with areas of sloughing, ulceration, and bleeding can occur. Psychological or autoimmune reaction has been proposed as a cause for this condition and the hallmark of this condition is rectal bleeding and diarrhea, abdominal cramps, erythema nodosum of the thighs and legs, episcleritis, uveitis, corneal ulcers, retinitis, anemia of microcytic and hypochromic type, leukocytosis, electrolyte imbalance, hypoalbuminemia, and low serum magnesium and potassium levels.

Oral health presentations

Aphthous stomatitis (major or minor), pyoderma gangrenosum (deep ulcers which may ulcerate through the tonsillar pillar), and pyostomatitis vegetans (pustules which could be aggregated or linear, seen commonly on the buccal mucosa and may involve other non-keratinized mucosa) are the oral health presentations. These pustules eventually rupture to form snail-track ulcers which are pathognomonic to this disease. These ulcers are usually epithelialized and their severity is, many a times, directly proportional to the severity of the GI disease. The oral lesions may be the first sign of the disease, but they usually co-exist. Long-standing oral lesions may become granular, polypoid, or fissured. 10% of patients develop inflammatory bowel disease-associated arthritis of the temporomandibular joints.

Oral health considerations

Delayed healing, increased risk of infection due to anemia, and long-term steroid therapy increase the risk of vertebral compression fractures. So, careful positioning of these patients in the dental chair is advised. Chronic use of glucocorticosteroid can cause adrenal suppression, and side effects of long-term corticosteroid use like hypertension and hyperglycemia should also be addressed. In patients with history of bowel surgery, malabsorption of Vit. K can occur.

Crohn's disease

Crohn's disease (CD) is a chronic idiopathic condition characterized by relapsing inflammation of the bowel. This was reported by Crohn et al. in 1932 as regional ileitis. This could affect any segment of the GIT from the mouth to the anus, with the ileum, colon, and perineum most widely involved. Extraintestinal manifestations (EIMs) may occur in the skin, joints, liver/biliary tree, and eyes. Mutations at gene loci coding for immune molecules and pathways, identified via Genome-Wide Association Studies (GWAS), have implicated a range of immunological "culprits" involved in the pathogenesis of CD. [11] It is common in women of age range 20-39 years. Tiny erosions of the overlying normal mucosal lymphoid tissue eventually coalesce to form small aphthous ulcers or more diffuse ulceration. As the disease progresses, there is marked hyperplasia of the lymphoid tissue extending through the wall, resulting in fibrosis and muscular hypertrophy leading to constrictures and inflammatory tracts. Granulomas are present in about 50% of patients, and CD is diagnosed by colonoscopy and with endoscopic biopsies.

Oral health presentations

Recurrent aphthous ulcers are the most common manifestations. Pyostomatitis vegetans and granulomatous lesions are observed in the salivary glands, where they may cause rupture of the ducts and localized mucocele formation, diffuse swellings of the lips and face, polypoid tag-like lesions of buccal mucosa and retromolar pad, and persistent deep linear ulceration with hyperplastic margins. Anti-inflammatory and sulfa-containing drugs, which are commonly used for inflammatory bowel disease (IBD), cause oral lichenoid drug reactions. Superinfection with Candida is often seen in the oral lesions of these patients. The GI lesions are preceded by the oral manifestations in 60% of the cases. The oral lesions are multifocal, linear, nodular, polypoid, or diffuse mucosal thickenings, with a predilection for occurrence in the labial and buccal mucosa, and the mucobuccal folds give cobblestone appearance. They are characteristically firm, pink, and painless to palpation, unless there are ulcerations that may cause pain on touch or when eating acidic, spicy, or hot foods. Fatahzadeh et al. (2009) described three types of mucocutaneous findings in CD depending on the origin:

  1. Granulomatous oral and perianal changes caused by direct extension of intestinal disease as well as granulomatous skin findings non-contiguous with the GIT;
  2. Reactive conditions in association with CD, such as pyoderma gangrenosum, erythema nodosum, Sweet's syndrome, erythema multiforme, and cutaneous vasculitis; and
  3. Changes related to therapy directed against CD or disease-induced nutritional deficiencies such as acrodermatitis enteropathica and marasmic striae.

   Conclusion Top

Oral health care providers must have a comprehensive understanding of the GI system and how normal and abnormal function may affect the oral health care of patients, and also be efficient enough to provide good care for those patients. Vice versa, GI diseases could be diagnosed with respect to their oral presentations, which would help the patients in being relieved of their symptoms of GI diseases.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Goh KL. Gastroesophageal reflux disease in Asia: A historical perspective and present challenges. J Gastroenterol Hepatol 2011;26(Suppl 1):2-10.  Back to cited text no. 1
Guimarães EV, Marguet C, Camargos PA. Treatment of gartroesophageal reflux disease. J Pediatr (Rio J) 2006;82(Suppl): S133-45.  Back to cited text no. 2
World Gastroenterology Organisation. WGO Global Guidelines. Coping with common GI symptoms in the community (Long Version). Milwaukee, WI: The Organisation; 2013. p. 35.  Back to cited text no. 3
Greenberg MS, Glick M, Ship JA. Burket′s Oral Medicine. 11 th ed. Hamilton, Ontario: McGraw Hill Education; 2008. p. 345-62.  Back to cited text no. 4
Stein HJ, Barlow AP, DeMeester TR, Hinder RA. Complications of gastroesophageal reflux disease. Role of the lower esophageal sphincter, esophageal acid and acid/alkaline exposure and duodenogastric reflux. Ann Surg 1992;216:35-43.  Back to cited text no. 5
Daley TD, Armstrong JE. Oral manifestations of gastrointestinal diseases. Can J Gastroenterol 2007;21:241-44.  Back to cited text no. 6
Ramakrishnan K, Scheid DC. Treatment options for insomnia. Am Fam Physician 2007;76:517-26.  Back to cited text no. 7
Idan HM, Abdul-Razaq FD. Oral manifestations, microbial study and enzyme analysis in patients with peptic ulcers. J Bagh Coll Dentistry 2011;23:56-60.  Back to cited text no. 8
Edwards CR, Boucher IA. Davidson′s Principles and Practice of Medicine. 17 th ed. London: Churchill Livingston; 1996. p. 405-82.  Back to cited text no. 9
Ardizzone S. Ulcerative colitis. Orphanet Encyclopedia. 2003. Available from: http://www.orpha.net/data/patho/GB/uk-UC.pdf. [Last accessed on 2014 Nov 03].  Back to cited text no. 10
Hendy P, Hart A. A review of Crohn′s disease. EMJ Gastroenterol 2013;1:116-23.  Back to cited text no. 11


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