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Improvement of gingival and alveolar bone status in periodontitis‐affected hamsters treated with 15‐methyl prostaglandin E 1
Author(s) -
Caillon P.,
Saffar J. L.
Publication year - 1994
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1994.tb01102.x
Subject(s) - periodontitis , dental alveolus , inflammation , bone resorption , connective tissue , medicine , edema , osteoclast , prostaglandin e2 , resorption , pathology , endocrinology , dentistry , receptor
Exogenous PGE 1 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‐PGE 1 , a stable PGE 1 analog. The agent was tested at 2 different doses (100 and 150 μg/kg/d) and its effects were matched against disease‐free and periodontitis‐affected animals. No effect was found with the 100 μg regimen. In contrast, in the 150 μg 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‐PGE 1 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.