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“Background Periodontitis is a complex process affecting tooth-supporting tissues [1]. The pathogenesis of periodontal diseases is largely attributed to localized inflammation, which results from interaction between host and microbial factors [2]. SP600125 The most

common etiological agent of chronic periodontitis is Porphyromonas gingivalis, a Gram-negative anaerobic black-pigmented bacterium [3]. On tooth surfaces, P. gingivalis is a constituent of the complex multispecies biofilm known as dental plaque, which has Ribonucleotide reductase properties of other biofilms found in the human body and in the environment. P. gingivalis can also colonize the tissues and cells of the gingival epithelium [4]. The bacterium can not only invade, but also accumulate inside gingival epithelial cells [5, 6]. Recent evidence demonstrates that the effect of periodontitis might have systemic consequences since the bacterium can spread systemically and locate to other tissues [7–10]. Bacteria living in a biofilm have a physiology different from that of planktonic cells and they generally live under nutrient limitation, including that of iron and heme. The uptake of heme as iron and protoporphyrin IX is an important GSK126 in vivo mechanism by which P. gingivalis and other pathogenic bacteria obtain these compounds for their survival and their ability to establish an infection [11, 12]. Gram-negative bacteria utilize outer-membrane receptors to acquire heme from host hemoproteins directly or through a hemophore or lipoprotein and then transport the captured heme into the cell.