Gingival crevicular fluid prostaglandins and gingival phospholipids in experimentally-induced periodontitis in the dog

Activation of Blood Coagulation Factor X by Arginine-specific Cysteine Proteinases (Gingipain-Rs) from Porphyromonas gingivalis

“…Thus, it may be natural for 95-kDa gingipain R adhesin domains to bind to phospholipids. However, phospholipids augmented neither Boc-Ile-Glu-Gly-Arg-MCA hydrolysis, prekallikrein activation, nor fibrinogen degradation by the complexed form, 4 hence the phospholipids effect appears to be specific for factor X activation. The augmentation of 95-kDa gingipain R factor X activation by phospholipids, together with the lower K m and much higher k cat values of 95-kDa gingipain R than those of the 50-kDa form (Table III), indicates a further function for the adhesin domains in increasing the affinity to factor X as well as facilitating substrate cleavage.…”

“…Thus, in blood there is likely to be the simultaneous production of each by gingipain Rs, and for this reason it is believed that both may also be involved in the production of gingival crevicular fluid (24) and of prostaglandins and interleukin-1 (13)(14)(15), respectively, during infectious episodes. Hence, the elevated levels of prostaglandins and interleukin-1 in gingival crevicular fluid of adult periodontitis patients (3,4,6) may be connected to the thrombin produced by P. gingivalis proteinases. In addition, thrombin and fibrinopeptide B, released from fibrinogen by thrombin are each neutrophil chemotactic factors (44,45) and may contribute to infiltration of these phagocytic cells at periodontitis sites (46).…”

“…Recent studies indicate that the initial activation of coagulation in sepsis is primarily dependent on activation of the extrinsic pathway, initiated by tissue factor expressed on monocytes (50). Since endotoxin, itself, or endo- 4 T. Imamura, unpublished data. toxin-induced tumor necrosis factor-␣ can stimulate monocytes to express tissue factor (51,52), the tendency has been to recognize such factors as the primary bacterial agents involved in the induction of DIC coagulation in sepsis.…”

“…It is the most common cause of tooth loss in adults, primarily because of the declining incidence of dental caries in the general population (1,2). Although the pathogenesis of periodontitis is not completely understood, prostaglandins (3,4) and interleukin-1 (5,6), which increase in gingival crevicular fluid in periodontal pockets, are considered to be predominant factors in the tissue destruction process associated with this disease. However, the mechanism of the production of these inflammatory mediators is still unclear.…”

A modified method for inducing periodontitis in dogs using a silk-wire twisted ligature

“…Several studies have induced experimental periodontitis using a more invasive method in which a full-thickness gingival flap is made and the alveolar bone is destroyed prior to ligation [3,18]. These methods take several months to promote advanced periodontitis, and thread-type ligatures might be lost due to loosening or wearing during this period.…”