Psychological stress is known to increase the circulating levels of the catecholamine hormones noradrenaline and adrenaline, which have been shown to influence the growth of a large number of bacterial species by acting in a siderophore-like manner or by inducing the production of novel autoinducers of growth. As we have previously demonstrated that periodontal organisms display differing growth responses to noradrenaline and adrenaline, the aim of this study was to determine whether these growth effects were based upon either siderophore-like or autoinducer mechanisms. Initial inocula of 43 microbial organisms normally found within the subgingival biofilm were established under anaerobic conditions (35 degrees C). Each strain was re-inoculated into a serum-based minimal medium and growth was assessed by optical density (OD(600 nm)) with test and control cultures performed in triplicate. Test cultures were supplemented with either 50 mum ferric nitrate or a previously described Escherichia coli autoinducer of growth. Significant growth effects for supplementation with ferric nitrate (13 species responding positively) and E. coli autoinducer (24 species responding positively) were observed, with differences in growth response within bacterial species and within microbial complexes. When data for all organisms were compared with published responses to catecholamines there were only weak correlations with Fe (r = 0.28) and E. coli autoinducer (r = 0.34) responses. However, large positive responses (> 25% increase) to free Fe and/or E. coli autoinducer were significantly more prevalent in the group of organisms (n = 12) known to exhibit similar responses to catecholamine hormones (P < 0.01; chi2 = 4.56). The results support the view that catecholamines may exert their effects on subgingival organisms by initiating autoinducer production, or simply by acting in a siderophore-like manner, scavenging bound iron from the local environment. It is possible that autoinducer mechanisms may play an important role in the response of oral microorganisms to stress hormones, thereby contributing to the clinical course of stress-associated periodontal diseases.