Crohn’s Disease: Is it related to Periodontal Disease?

Crohn’s Disease: Is it related to Periodontal Disease?

By William D Nordquist DMD MS

Inflammatory bowel diseases have become a significant public health problem because of the increase in the incidence of inflammatory bowel diseases, particularly Crohn’s disease, in the U.S. population[1]. Ulcerative colitis and Crohn’s disease are chronic intestinal disorders of unknown cause. Crohn’s disease is characterized by tissue wall penetration and infiltration by inflammation of immune cells; i.e., lymphocytes, macrophages, and plasma cells. In 70% of the cases, granulomas (a roughly spherical mass of immune cells that forms when the immune system attempts to wall off substances; especially infectious microbes) are found. Despite the intense interest in transmissible agents, abnormal changes in cell lines, and the role of cell-wall deficient pseudomonads (L forms of amoebas) investigated at the time Van dyke[2] (1986) reported his findings there was still no evidence for an infective etiology for Inflammatory bowel diseases.

Van dyke when on to report in his study a total of 20 patients with inflammatory bowel disease (Crohn’s disease, ulcerative colitis) were evaluated with regard to the role of infectious agents and host response. Patients were selected based upon oral manifestations of their disease, 10 with periodontal disease and 10 without. Microbiologic studies of the periodontal flora of inflammatory bowel disease-affected patients revealed a unique microflora composed predominantly of small, motile, gram-negative rods, which were most consistent with the genus Wolinella. Further studies of the host response of these patients revealed a serum-mediated defect in neutrophil chemotaxis (movement of immune cells toward infectious bacteria) in all 10 patients with periodontal disease. Neutrophil phagocytosis (ability of immune cells to “eat” invading bacteria) was normal. Test tube studies of neutrophil immune cell function in response to Wolinella extracts and culture concentrates revealed inhibition of neutrophil chemotaxis in a dose-response fashion. The organism was “eaten” by neutrophils but not attached to them close enough to be “eaten”. In other words, the immune system was suppressed by the bacteria. The data suggest that unusual microorganisms colonizing the oral cavity of Crohn’s disease patients potentially play a role in the pathogenesis of the disease as infectious agents or modifiers of the host response or both.

Areas affected far away from the intestinal tract include manifestations of mouth ulcers, severe periodontal disease, and involvement of heart and lungs, skin, joints, liver, and urine tracts[3] [4] [5] [6] [7] [8]. More recent studies have shown the Vitamin D dysfunction and elevated 1,25-D levels in Crohn’s disease patients indicates cell-wall deficient bacteria within macrophages may play a role in the immune suppression aspect of the disease process[9]. If this is the case, then Crohn’s disease has a bacterial cause and could very well be instigated by bacteria that come from the mouth. Nordquist and Krutchkoff further discuss the Vitamin D dysfunction and its cause related to bacteria that get into the body through bleeding diseased “gums” resulting from periodontal disease[10]. If you have Crohn’s disease, it wouldn’t hurt to get your “gums” checked for periodontal disease.


[1] Sleisenger, M. H. 1981. Pathophysiology of the gastrointestinal tract, p. 1506-1689. In L. H. Smith and S. 0. Thie (ed.), Pathophysiology: the biologic principles of disease. The W. B. Saunders Co., Philadelphia.

[2] Van Dyde T, Dowell V, Offendbacker S, Snyder W and Hersh T. Potential Role of Microorganisms Isolated from Periodontal Lesions in the Pathogenesis of Inflammatory Bowel Disease. Infection and immunity. Sept 1986: 671-677.

[3] Bartlett, J. G., and S. M. Finegold. 1972. Anaerobic pleuropulmonary infections. Medicine (Baltimore) 51:413-450.

[4] Bartlett, J. G., S. L. Gorbach, F. P. Tally, and S. M. Finegold. 1974. Bacteriology and treatment of primary lung abscess. Am. Rev. Respir. Dis. 109:510-518.

[5] Frederick, J., and A. I. Braude. 1974. Anaerobic infection of the paranasal sinuses. N. Engi. J. Med. 209:135-137.

[6] Hodgson, H. J. E., B. J. Potter, and D. P. Jewell. 1977. Immune complexes in ulcerative colitis and Crohn’s disease. Clin. Exp. Immunol. 29:187-196.

[7] Nastro, L. J., and S. M. Finegold. 1973. Endocarditis due to anaerobic gram-negative bacilli. Am. J. Med. 54:482-496.

[8] Nielsen, H., V. Binder, H. Daughtarty, and S. E. Svehag. 1978. Circulating immune complexes in ulcerative colitis. I. Correlation to disease activity. Clin. Exp. Immunol. 31:72-80.

[9] Waterhouse JC Marshall TG Fender B et al. High levels of active 1,25-Dihydroxyvitamin D despite low levels of 25-Hydroxyvitamin D Precursor-Implications of dysregulated vitamin D for diagnosis and treatment of chronic disease. In: Vitamin D New Research, Stolt, 2006 Nova Science Publications, Inc.

[10] Nordquist W & Krutchkoff D. The Silent Saboteur. 2010. Bio-Med Publishing Group.

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