Risk factors involved in IBDIBD is thought to result from inappropriate and ongoing activation of the mucosal immune system facilitated by defects in both the intestinal epithelium and mucosal immune system. 5 There are both genetic and environmental factors implicated in the aetiology of IBD. 6 Although traditionally associated with the developed world, recent epidemiological studies suggest an increasing incidence in rapidly developing countries, especially in South-East Asia. 7 In addition, the increased risk of IBD in the immigrant populations in the West suggests environment has a role in the development of IBD. 8 Genetic Detailed genetic mapping has identified specific genetic changes on chromosome 16 carried in families which appear linked to CD, however no significant changes have been mapped as of yet to UC. 9,10 Specifically, variants of the NOD2 gene provide the strongest association with susceptibility to CD. NOD2 plays a key role in regulating the gut mucosal barrier involving, specifically, the microbiota, as well as the related response by the innate and adaptive immune system. The IBDchip European Project showed NOD2 has been implicated in ileal location colitis with stenosing and penetrating disease behaviour. 11 A genome wide association study has also identified a strong link between the IL23R gene and CD. 12 The gene in particular codes for interleukin 23 that plays a role in regulating innate immunity within the intestine. 13 Cigarette smoking Unusually, cigarette smoking is associated with decreased rates of incidence of UC and has been associated with protective features to prevent further flare-ups of the condition 14-19 such as relapses, 20 ©SEBASTIAN KAULITZKI/Science Photo Library/Getty J. S. Chandan 1 and T. Thomas 1 summarise the treatments for inflammatory bowel disease (IBD) and how anti-inflammatory medications can have side effects that affect the oral cavity.