Abstract
Inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), can be associated with several extra-intestinal manifestations requiring a multidisciplinary management both in terms of work-up and therapy. Oral lesions are common in patients with IBD, with a prevalence ranging from 5% to 50%. These can represent an oral location of IBD as well as a side-effect of drugs used to treat the intestinal disease. Oral manifestations, occurring in patients with IBD, can be divided in nonmalignant, specific, and non-specific ones, and malignant lesions. While there is undoubtedly a need to search for an IBD in patients with oral lesions associated with intestinal symptoms, the work-up of those with an exclusive oral lesion should be personalized. Fecal calprotectin is a non-invasive marker of intestinal inflammation and may be used to select which patients need to undergo endoscopic examination, thereby avoiding unnecessary investigations. The pharmacological armamentarium to treat oral lesions associated with IBD includes topical or systemic corticosteroids, immunosuppressive agents, and biologic drugs.
Highlights
Inflammatory bowel disease (IBD) comprises chronic heterogeneous disorders of unknown etiology, resulting from multifactorial environmental precipitants in genetically susceptible individuals [1]
Granulomas are found in only 24–61% of patients with Crohn’s disease (CD), whereas in those with orofacial granulomatosis, granuloma formation in the oral lesions occurs in 70–100% of cases, irrespective of coexisting CD
The specific oral lesions include indurated tag-like lesions, cobblestoning, mucogingivitis, lip swelling with vertical fissures, and deep linear ulcerations (Table 1)
Summary
Inflammatory bowel disease (IBD) comprises chronic heterogeneous disorders of unknown etiology, resulting from multifactorial environmental precipitants in genetically susceptible individuals [1]. Common genetic background (IBD1 gene [8], MHC allele HLADRB1*0103 [9], ABCB1 gene [10]) between the two conditions may be the predisposing cause, but the detailed mechanisms remain unknown, especially because the environmental triggers responsible for disease onset have not been elucidated. Bacteria belong to four phyla (Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria) the majority are from either Firmicutes or Bacteroidetes [12] It remains to be clarified, in IBD patients, if there is a decrease in microbial diversity as a consequence of intestinal changes, or if this could play a role in the pathogenesis of these diseases. Because of the potential wide spectrum of involvement and of the genetic commonalities, it has been hypothesized that IBD represents a systemic disease with a predominantly intestinal manifestation [13]
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