01926nas a2200169   4500000000100000008004100001100001800042700002100060700001800081700001400099245010200113856005800215300001100273490000900284520144900293022001401742       2015                            d1 aCortela D C B1 aSouza Junior A L1 aVirmond M C L1 aIgnotti E00aInflammatory mediators of leprosy reactional episodes and dental infections: A systematic review.  uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539113/   a5485400 v20153 a<p>Reactional episodes in leprosy are a result of complex interactions between the immune system, Mycobacterium leprae, and predisposing factors, including dental infections. To determine the main inflammatory mediators in the immunopathological process of dental infections and leprosy reactions, <em>we conducted a systematic review of primary literature published between 1996 and 2013</em>. A three-stage literature search was performed (Stage I, "leprosy reactions" and "inflammatory mediators"; Stage II, "dental infections" and "inflammatory mediators"; and Stage III, "leprosy reactions," "dental infections," and "inflammatory mediators"). Of the 911 eligible publications, 10 were selected in Stage I, 68 in Stage II, and 1 in Stage III. Of the 27 studied inflammatory mediators, the main proinflammatory mediators were IL-6, IFN-γ, TNF-α, IL-1β, and IL-17; the main anti-inflammatory mediators were IL-10 and IL-4. Serum IL-6 and TNF-α concentrations were significant during periodontal and reactional lesion evolution; IFN-γ and IL-1β were associated with types 1 and 2 reactions and chronic periodontal disease. The proinflammatory mediators in dental infections and leprosy reactions, especially IL-6 and TNF-α, were similar across studies, regardless of the laboratory technique and sample type. IFN-γ and IL-1β were significant for leprosy reactions and periodontal diseases. This pattern was maintained in serum.</p>
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