Could leprosy reaction episodes be exacerbated by oral infections?

Abstract

Introduction: This study evaluated whether leprosy reactions could be associated with oral infection. Methods: Leprosy patients (n = 38) with (group I) and without (group II) oral infections were selected. Reactions were identified from the clinical and histopathological features associated with serum C-reactive protein (CRP) and10kDa interferon-gamma-induced protein (IP-10) levels, determined before and after elimination of the foci of infection. Results: group I presented more reactions than group II did, and improvement of the reactions after dental treatment. Serum CRP and IP-10 did not differ before and after the dental treatment, but differed between the groups. Conclusions: Oral infection could be an exacerbating factor in leprosy reactions.

The role of human T cell lymphotrophic virus type 1, hepatitis B virus and hepatitis C virus coinfections in leprosy

“…Risk factors for development of LR include borderline form of disease, initiation of multidrug therapy, high bacillary load, stress and coinfections (Shegal & Sharma 1998, Balagon et al 2010, Motta et al 2011.…”

Identification of clinical, epidemiological and laboratory risk factors for leprosy reactions during and after multidrug therapy

“…Oral infections have also been suggested as risk factors for the occurrence of leprosy reactions, as indicated by an observed reduction in the rates of reactions after the establishment of dental treatment ( Motta et al 2011 ). After treatment, an elevated titre of circulating anti-phenolic glycolipid-1 (anti-PGL-1) IgM antibodies has been identified as a relevant marker for a reaction; seropositivity at MDT discharge corresponded to a 10-fold higher probability for the development of a reaction compared with that in patients with negative results ( Brito et al 2011 ).…”

Oral coinfection can stress peripheral lymphocyte to inflammatory activity in leprosy

“…It has been observed that PBMCs present different levels of proliferation index of cytokines when they are stimulated in vitro with Mycobacterium leprae extracts [21][22][23] . On the other hand, we observed that the leprosy reactional episodes are frequent in patients presenting oral infections 14,15 and other coinfections 24 . Therefore, this study attempted to clarify whether chronic oral infections could influence the intracellular production of cytokines in leprosy patients, and to verify the relationship with the development of reactional episodes.…”

“…The coexistence of oral chronic infections with leprosy can modulate the inflammatory reaction by elevation of the intracellular inflammatory markers expression, probably stimulating a spill-over of these inflammatory products into the peripheral circulation where they can act as inducers of an inflammatory reaction, exacerbating the insidious chronic evolution of leprosy and, consequently, acting like an inducer, stimulatory or maintaining factor in leprosy reactions 14,15,24 . In addition, the presence of these chronic infections can influence the production of intracellular cytokines, and can reflect the fact that most of the leprosy patients with coinfection (Group I) presented reactional episodes, corroborating the hypothesis of a synergistic action of the two kinds of inflammatory reaction on the course of leprosy.…”

“…In a previous study evaluating the expression of proinflammatory serum biomarkers we observed that leprosy patients with oral infections presented more leprosy reactions associated with higher C-reactive protein (CRP), chemokine IP-10, interleukin-1 (IL-1) and interleukin-6 (IL-6) levels than leprosy patients without oral infections, suggesting that oral infections can act as a maintenance factor of the proinflammatory state 14,15 . However, these results do not show the real participation of peripheral blood cells and the amount of cytokines produced by each cell population, compromising the understanding of the inflammatory response.…”