Improvement of gingival and alveolar bone status in periodontitis‐affected hamsters treated with 15‐methyl prostaglandin E₁

Abstract

Exogenous PGE1 at pharmacological doses suppresses acute and chronic inflammation manifestations. As periodontitis possesses features of both acute and chronic inflammation, attenuation of periodontal destruction in hamsters was attempted by using 15-M-PGE1, a stable PGE1 analog. The agent was tested at 2 different doses (100 and 150 micrograms/kg/d) and its effects were matched against disease-free and periodontitis-affected animals. No effect was found with the 100 micrograms regimen. In contrast, in the 150 micrograms group, in the gingiva around the first right mandibular molar the pocket epithelium and infiltrated connective tissue (ICT) areas, the mean vascular lumen, the number of PMNLs adherent to blood vessels and infiltrating the ICT were significantly reduced. The number of osteoclasts was markedly diminished as well, but their intrinsic activity was enhanced. Bone formation was totally inhibited in this treatment group. These results indicated that 15-M-PGE1 effectively improved gingival inflammation mostly by reducing edema and PMNL recruitment and controlled alveolar bone destruction by reducing the osteoclast recruitment. From a therapeutic point of view the complete inhibition of formation seems to contraindicate its use.

Cyclooxygenase-2-dependent Prostaglandin E2 Down-regulates Intercellular Adhesion Molecule-1 Expression via EP2/EP4 Receptors in Interleukin-1ß-stimulated Human Gingival Fibroblasts

“…it has becin shown that PG analogs ol' the F -scrics hax\c antiinflammatory activities suchI as prevention ol adjU\ Jt1 arthritis, inhibitioni of edema torimation, suppiessioln ol Iloinflammatory cytokine release (ZtII ier and QuaL' ,t 971; 1 959 .,s,, -,Y, ,YQ Perretti, 1994;Strassmann et al, 1994;Widomski et al, 1997). Furthermore, PG analogs of the Eseries have been demonstrated to induce periodontal regeneration in adult dogs and to inhibit gingival inflammation and bone resorption in periodontitis-affected hamsters (Capillon and Saffar, 1994;Marks and Miller, 1994). It has been suggested that ICAM-l expressed in HGF may play an important role in the accumulation and retention of LFA-1-bearing lymphocytes in periodontal lesions (Crawford et al, 1992;Hayashi et al, 1994;Takahashi et al, 1994).…”

The roles of cyclooxygenase‐2 and prostaglandin E2 in periodontal disease

“…Local application of prostaglandin E 1 has been shown to stimulate bone formation adjacent to the site of delivery in the canine mandible (72). The use of a stable prostaglandin E 1 analog in a hamster periodontitis model improved bone status (11). It has also been reported that local delivery of prostaglandin E 1 increases cementum, alveolar bone, and periodontal ligament cell formation in adult dogs (73).…”

Periodontal repair in dogs: histologic observations of guided tissue regeneration with a prostaglandin E1 analog/methacrylate composite

“…Other evidence suggests that the same agents may also stimulate bone formation. The use of a stable PGE1-analog in a hamster periodontitis model controlled alveolar bone resorption (Caillon & Saffar 1994). Miller & Marks (1988, 1933a, b, 1994 have shown that local application of PGE1 in adult dogs stimulates alveolar bone formation in a dose-dependent manner, and formation of cementum and periodontal ligament.…”