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Kava‐241 reduced periodontal destruction in a collagen antibody primed Porphyromonas gingivalis model of periodontitis
Author(s) -
Alshammari Abdulsalam,
Patel Jayesh,
AlHashemi Jacob,
Cai Bin,
Panek James,
Huck Olivier,
Amar Salomon
Publication year - 2017
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.12784
Subject(s) - porphyromonas gingivalis , periodontitis , dental alveolus , medicine , inflammation , antibody , pharmacology , immunology , dentistry
Aim The aim of this study was to evaluate the effect of Kava‐241, an optimized Piper methysticum Kava compound, on periodontal destruction in a collagen antibody primed oral gavage model of periodontitis. Methods Experimental periodontitis was induced by oral gavage of Porphyromonas gingivalis ( P. gingivalis) + type II collagen antibody ( AB ) in mice during 15 days. Mice were treated with Kava‐241 concomitantly or prior to P. gingivalis gavage and compared to untreated mice. Comprehensive histomorphometric analyses were performed. Results Oral gavage with P. gingivalis induced mild epithelial down‐growth and alveolar bone loss, while oral gavage with additional AB priming had greater tissular destruction in comparison with gavage alone ( p < .05). Kava‐241 treatment significantly ( p < .05) reduced epithelial down‐growth (72%) and alveolar bone loss (36%) in P. gingivalis + AB group. This Kava‐241 effect was associated to a reduction in inflammatory cell counts within soft tissues and an increase in fibroblasts ( p < .05). Conclusion Priming with type II collagen antibody with oral gavage is a fast and reproducible model of periodontal destruction adequate for the evaluation of novel therapeutics. The effect of Kava‐241 shows promise in the prevention and treatment of inflammation and alveolar bone loss associated with periodontitis. Further experiments are required to determine molecular pathways targeted by this therapeutic agent.