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increasing resistance to antibiotics and the potential for recurrent infection suggests more targeted and longer-lasting approaches are needed to reduce the levels of P. gingivalis in the oral cavity.To achieve this goal, a thorough knowledge of the biology of P. gingivalis is needed.Periodontal diseases are triggered by microorganisms and manifest themselves in inflammation, bleeding, and destruction of soft and tooth tissues.P. gingivalis is found in healthy sites such as the buccal mucosa, tongue, tonsils, palate and supragingival dental plaque on the tooth enamel surface (86), but its numbers are significantly elevated in the subgingival environment and especially in diseased areas (92), suggesting the bacterium is well adapted and benefits from the hostile inflammatory state of the host.To survive in the diseased periodontal pocket the pathogen must be able to escape host defenses and acquire sufficient nutrients that will sustain its growth.One such nutrient required for growth of P. gingivalis is iron, and its presence has a profound effect on the bacterium's virulence.Using a mouse abscess model, the Ebersole group demonstrated that bacteria grown under heminlimitation were less virulent than their counterparts grown in hemin-excess (64,83,87).In this review, we discuss the mechanisms of iron acquisition by P. gingivalis.We also describe regulatory mechanisms, because excess iron reacts with peroxide to generate hydroxyl radicals that are detrimental to the bacterial cell.P. gingivalis is distantly related to bacteria in which iron acquisition and homeostasis mechanisms are well known, so this review provides novel supportive information with regard to iron acquisition mechanisms in bacteria.
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Janina P. Lewis (2009) studied this question.
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