1. Porphyromonas gingivalis is one of the bacteria likely to be related to
pain in
periodontitis. Several
enzymes isolated from P. gingivalis have been reported to have
kininogenase activity. Since
kinin release could be held responsible for inflammatory symptoms and
pain in
periodontitis, we investigated whether the inflammatory and algesic effects of a sonic extract from P. gingivalis (PGSE) could be inhibited by the potent
bradykinin B2 receptor antagonist,
icatibant (
Hoe 140). 2. In anaesthetized rats, the subplantar injection of PGSE (0.1 and 1.0 mg) caused a dose-dependent oedema of the hind paws. The net increase of the paw volume 60 min after the injection was 23 +/- 5% and 77 +/- 12%, respectively. The oedema was rich in
plasma proteins as determined by the
Evans blue method. Pretreatment with
icatibant (300 nmol kg-1, s.c.) significantly reduced the effect of 1.0 mg of PGSE whereas the effects of 0.1 mg of PGSE remained unaffected. 3. The subplantar injection of 1.0 mg of PGSE in unanaesthetized rats caused nociceptive behavioural responses which started about 5 min after the injection and lasted for about 10-15 min. These responses were completely prevented by pretreatment with
icatibant (300 nmol kg-1, s.c.). 4. The present results show that the plasma extravasation induced by non-algesic doses of a sonic extract from P. gingivalis are caused by mechanisms other than B2
kinin receptor activation whereas inflammatory effects of algesic doses are due to the action of
kinins. The
pain elicited by the extract is solely mediated by
kinins and can be prevented by
icatibant. The
bradykinin antagonist could thus have a potential for a clinical use against
pain associated with periodontal
inflammation.