Plasminogen activator (PA) converts plasminogen to plasmin, and plasmin activates the kinin cascade and latent methalloproteases. It is known that the alteration of the PA-plasmin system affects the progression of periodontal disease. We have reported previously that LPS from Campylobacter rectus, which is associated with adult periodontitis, increased PA production in human gingival fibroblasts (hGF). The effects of in vitro- and in vivo-cellular ageing on PA production from human and rat gingival fibroblasts (rGF) were studied. In vitro cellular aged hGF were prepared by subcultivations of hGF, and in vivo aged rGF was cultured primarily from the gingival tissue of aged rats. The cells were challenged with LPS and PA released into the cultured medium was measured as PA activity. Both in vitro and in vivo cellular aged GFs produced a significantly higher PA activity by LPS compared with young GFs cell. In RT-PCR experiments, tissue type PA (tPA) mRNA levels in both aged hGF and rGF were higher than in young cells, whereas plasminogen activator inhibitor 1 (PAI-1) mRNA remained unchanged and urotype PA (uPA) mRNA was not detected. Since LPS-stimulated PA activity from gingival fibroblasts was stimulated in aged cells using both in vitro- and in vivo-experimental models, the ageing of gingival fibroblasts may have an effect on the severity of inflammation and degradation of the extracellular matrix of gingival tissues by producing a large amount of PA in response to LPS.