Inflammatory bowel disease: clinics and pathology. Do inflammatory bowel disease and periodontal disease have similar immunopathogeneses?

Inflammatory bowel disease (IBD) comprises two chronic, tissue-destructive, clinical entities Crohn disease (CD) and ulcerative colitis (UC) both apparently caused by immunological overreaction (hypersensitivity) to commensal gut bacteria. Under normal conditions the intestinal immune system shows a down-regulating tone ('oral tolerance') against dietary antigens and the indigenous microbiota. This local homeostasis is disturbed in IBD, leading to hyperactivation of T helper 1 (Th1) cells with abundant secretion of interferon-gamma and tumor necrosis factor (TNF) and production of IgG antibodies against commensal bacteria. In addition, UC includes genetically determined autoimmunity, particularly IgG1-mediated cytotoxic epithelial attack. Breaching of the epithelium is the best-defined event underlying abrogation of oral tolerance, but immune deviation caused by cytokines fiom irritated epithelial cells or subepithelial elements (for example, mast cells, natural killer cells, macrophages) may also be involved. Endogenous infection with local hypersensitivity likewise causes periodontal disease, reflecting 'frustrated' immune elimination mechanisms entertained by antigens from dental plaque. Altogether, perturbation of a tightly controlled cytokine network, with abnormal crosstalk between several cell types, apparently explains the progressive immunopathology of chronic inflammatory mucosal diseases in general. This adverse development will be influenced by numerous immunity genes, the dosage and potential pathogeniciy of commensal bacteria, general health, nutritional status, and psychological factors. Several targets for new therapy have tentatively been identified to block immunopathological mechanisms in IBD, and inhibition of TNF has a striking beneficial effect in CD, supporting a central role of this cytokine.     

Behçet's disease: recent findings. Review of the literature

In this work the author reviews the clinical literature and the pathogenetic hypotheses, with particular attention to the correlations of the HLA, for Beh?et disease. Beh?et's syndrome is a multisystem disorder presenting with recurrent oral and/or genital ulcerations, chronic relapsing uveitis that may cause blindness, and neurologic impairments. Although it has a worldwide distribution, the Beh?et's disease is rare in the Americas and Europe and is more prevalent in Turkey and the Middle and Far East. It affects mainly young adults, with men having more severe disease than women. Beh?et syndrome is often diagnosed in late age for the lack of a correct diagnostic protocol and for the different symptoms that can be present. The need to follow the criteria made by the International Group of study on the disease of Beh?et is underlined.     

Behçet's disease

Beh?et's disease is a multisystem inflammatory disorder, characterized by recurrent oral and genital ulceration and uveitis. Additionally, skin lesions, vasculitis, and arthritis may occur. The disease is chronic, with exacerbations and remissions. Treatment of Behcet's disease is symptomatic depending on the symptoms and their severity. Oral ulcers are seen in 98% of patients with Beh?et's disease. Some aspects of oral health, such as the amount of plaque and the presence of periodontal disease, and possibly also caries, are more prevalent in patients with the disease when compared to healthy persons. All oral health aspects will probably benefit from good oral health care. Medications which can be employed for treatment of the various symptoms of the disease are colchicine, corticosteroids, immunosuppressives, cyclosporine, pentoxyfylline, anticoagulants, and thalidomide.     

Clinical characteristics of Mikulicz’s disease as an IgG4-related disease

Objectives

Mikulicz’s disease (MD) was considered to be a subtype of Sjögren’s syndrome (SS), based on histopathological similarities. However, recent studies have indicated that patients with MD show high serum IgG4 concentration, and suggested that MD is one of “IgG4-related disease” and distinguishable from SS. Therefore, we clinically and histopathologically examined the disease states of MD and SS in detail.

Materials and methods

Twenty patients with Mikulicz’s disease and 18 with SS were comparatively studied to determine clinical characteristics in MD patients.

Results

Sialography in MD patients did not show the “apple-tree sign” typically seen in SS. Serologically, high serum IgG4 levels but not anti-SS-A or anti-SS-B antibodies were observed in MD. SS showed lymphocytic infiltration of various subsets with atrophy or severe destruction of the acini, while MD showed selective infiltration of IgG4+ plasma cells with hyperplastic germinal centers and mild acini destruction. Corticosteroid treatment of MD reduced IgG and IgG4 levels and improved salivary function. A negative correlation between disease duration and increasing rate of salivary flow was observed in MD.

Conclusions

These results suggested that the pathogenesis of MD might be different from those of SS. Clinical Relevance: early diagnosis and treatment of MD is important for the improvement of salivary function.     

Is periodontal disease a risk factor for coronary artery disease (CAD)?

Coronary artery disease (CAD) remains the principal cause of death in most developed countries, despite significant preventive and therapeutic advances. Current epidemiological data imply that recent reductions in the prevalence of this disease are unlikely to be sustained until those at high risk are more precisely targeted. Although dental (especially periodontal) infections have been recently identified as independent risk factors for CAD, current evidence is insufficient to justify treatment of such infections to arrest or reverse CAD or other systemic conditions (e.g., diabetes mellitus, stroke or adverse outcomes of pregnancies).