Oral Manifestations of Gastrointestinal Diseases
Inflammatory bowel diseases (IBDs), most notably
Crohn disease and ulcerative colitis, are primary intestinal diseases. Both
main forms demonstrate a spectrum of oral lesions. These manifestations may be
the initial presentation of the disease, and the course of the lesions may be
dependent on or independent of bowel disease activity. The incidence of oral
lesions in IBD is estimated to be 20% to 50%; lesions are most commonly seen in
children with Crohn disease. Oral lesions specific to Crohn disease are
histopathologically granulomatous and typically visualized on the buccal
mucosa, gingiva, lips, and vestibular and retromolar areas. Four oral lesions
specific to Crohn disease have been described:
(1) White reticular tags, seen most frequently in the labial, buccal, and retromolar regions, form non-caseating granulomas, referred to as indurated taglike lesions. (2) Cobblestoning of the buccal mucosa, most often in the posterior region, is created by hyperplasia and fissuring of the mucosa, primarily in the posterior buccal region and palate; the fissuring results from the formation of mucosa-colored papules that degenerate into firm painful plaques. (3) Mucogingivitis is an edematous, granular, hyperplastic gingiva without ulcerations. (4) Lip swelling occurs, with vertical fissures, deep linear ulcerations in the buccal sulci, and midline labial fissuring. None of these oral lesions vary with disease activity. All can be treated with immunosuppressive medications; topical drugs are most often used, but systemic drugs can be used if disease is severe.
(1) White reticular tags, seen most frequently in the labial, buccal, and retromolar regions, form non-caseating granulomas, referred to as indurated taglike lesions. (2) Cobblestoning of the buccal mucosa, most often in the posterior region, is created by hyperplasia and fissuring of the mucosa, primarily in the posterior buccal region and palate; the fissuring results from the formation of mucosa-colored papules that degenerate into firm painful plaques. (3) Mucogingivitis is an edematous, granular, hyperplastic gingiva without ulcerations. (4) Lip swelling occurs, with vertical fissures, deep linear ulcerations in the buccal sulci, and midline labial fissuring. None of these oral lesions vary with disease activity. All can be treated with immunosuppressive medications; topical drugs are most often used, but systemic drugs can be used if disease is severe.
Nonspecific oral lesions can be seen
in IBD patients, as well as in the general population. Aphthous stomatitis is
seen in IBD patients, with greater frequency in rheumatologic patients and
lesser frequency in the general population. The lesions are round, shallow
ulcerations with fibrinous exudate and an erythematous border.
Pyostomatitis vegetans, a chronic mucocutaneous ulcerative condition,
presents with multiple miliary white or yellow pustules surrounded by an
erythematous, edematous mucosal base; it is most often visible in the labial,
gingival, and buccal mucosa. The pustules rupture and coalesce to form a
linear, or snail track, ulceration. This type of ulceration has also been
described in secondary syphilis. These lesions are non-specific to IBD, but
when they are associated with IBD, the type of disease is most frequently
ulcerative colitis. Gastroesophageal reflux disease (GERD) results from
movement of the gastric contents cephalad, traversing the lower esophageal
sphincter, esophagus, and upper esophageal sphincter and moving into the oral
cavity. Dental erosions, specifically those occurring on the lingual and
palatal surfaces of the teeth, are complications of this condition. Acid is the
likely corrosive agent in this process. The critical pH for demineralization is
5.5, but it varies inversely with the concentration of calcium and phosphate in
saliva. Several studies have indicated that halitosis could be
considered an extraesophageal manifestation of GERD. The etiology of this
relationship is less clear but is likely explained physiologically by the
degradation of anaerobic bacteria of sulfur-containing amino acids.
Peutz-Jeghers syndrome is an autosomal dominant disease characterized by
multiple gastrointestinal tract hamartomatous polyps and mucocutaneous
pigmentation. The pigmentation is due to macrophage-filled melanin-pigmented,
flat blue-gray or brown spots of 1 to 5 mm located in the dermis of the lips
and buccal region. The diagnosis can be made by histologic examination of one of
the luminal polyps in an index case or by gross identification of the polyps or
noting the presence of mucocutaneous pigmented lesions in an individual who has
a first-degree relative in whom the disease was previously diagnosed.
Gardner syndrome is an autosomal dominant disorder characterized by
colorectal polyps and extracolonic tumors. Similar to familial adenomatous
polyposis (FAP), the genetic mutation responsible for the disease is the
adenomatous polyposis gene. The risk of malignant transformation of the
colorectal polyps is significant. Unlike FAP, Gardner syndrome is characterized
by the presence of multiple osteomas, epidermoid cysts, desmoid tumors, and
cutaneous fibromas. The osteomas most often develop in the maxilla and
mandible. Dental abnormalities can be seen in about 30% of patients even in the
absence of osteomas. The abnormalities seen include supernumerary teeth,
compound odontomas, hypodontia, abnormal tooth morphology, and multiple
impacted teeth.
