Cannabidiol decreases bone resorption by inhibiting RANK/RANKL expression and pro-inflammatory cytokines during experimental periodontitis in rats

Cannabidiol (CBD) is a cannabinoid component from Cannabis sativa that does not induce psychotomimetic effects and possess anti-inflammatory properties. In the present study we tested the effects of CBD in a periodontitis experimental model in rats. We also investigated possible mechanisms underlyin...

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Veröffentlicht in:International immunopharmacology 2009-02, Vol.9 (2), p.216-222
Hauptverfasser: Napimoga, Marcelo H., Benatti, Bruno B., Lima, Flavia O., Alves, Polyanna M., Campos, Alline C., Pena-dos-Santos, Diego R., Severino, Fernando P., Cunha, Fernando Q., Guimarães, Francisco S.
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Sprache:eng
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Zusammenfassung:Cannabidiol (CBD) is a cannabinoid component from Cannabis sativa that does not induce psychotomimetic effects and possess anti-inflammatory properties. In the present study we tested the effects of CBD in a periodontitis experimental model in rats. We also investigated possible mechanisms underlying these effects. Periodontal disease was induced by a ligature placed around the mandible first molars of each animal. Male Wistar rats were divided into 3 groups: control animals; ligature-induced animals treated with vehicle and ligature-induced animals treated with CBD (5 mg/kg, daily). Thirty days after the induction of periodontal disease the animals were sacrificed and mandibles and gingival tissues removed for further analysis. Morphometrical analysis of alveolar bone loss demonstrated that CBD-treated animals presented a decreased alveolar bone loss and a lower expression of the activator of nuclear factor-κB ligand RANKL/RANK. Moreover, gingival tissues from the CBD-treated group showed decreased neutrophil migration (MPO assay) associated with lower interleukin (IL)-1β and tumor necrosis factor (TNF)-α production. These results indicate that CBD may be useful to control bone resorption during progression of experimental periodontitis in rats.
ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2008.11.010