Our previous investigation showed that in P. gingivalis several genes associated with oxidative stress and sodium translocation were part of the RprY regulon, suggesting a possible role in Na + metabolism and the response to redox changes [9]. The goals of the present study were to determine the activation signal(s) for rprY and clarify its role in the oxidative stress response. We found that the regulator was essential for growth of P. gingivalis under sodiumlimited growth conditions. While the parent strain adapted and was able to grow, albeit slowly, under these conditions, an rprY mutant strain could not, indicating that RprY was essential for the response to this stress and hence viability. By transcription profiling and metabolite analyses we determined that sodium limitation induced an oxidative stress response in both parent and rprY mutants strains. However, the response was highly amplified in the mutant and was accompanied by dysregulation of genes encoding protein chaperones. We found that RprY interacted directly with the promoters of several chaperone genes, and collectively our **data** indicate that the regulator acts as a repressor of their expression. We hypothesize that in the absence of RprY, P. gingivalis is unable control oxidative stress and protein chaperone responses compromising growth of the mutant under stress conditions.