Uncategorized

A New Target to Ameliorate the Damage of Periodontal Disease: The Role of Transient Receptor Potential Vanilloid Type-1 in Contrast to That of Specific Cannabinoid Receptors in Rats.

By May 11, 2019 May 13th, 2019 No Comments
2019 May 11. doi: 10.1002/JPER.18-0766.
[Epub ahead of print]

Abstract

BACKGROUND:

Transient receptor potential vanilloid type-1 (TRPV1) is expressed in oral tissues cells and its activity can be regulated by inflammation products and anandamide. The aim of the present study was to evaluate the effects of blocking TRPV1 or specific cannabinoid receptors 1 (CB1r) and 2 (CB2r) on periodontal status of rats subjected to experimental periodontitis (EP).

METHODS:

Male rats were distributed in groups 1) control, 2) lipopolysaccharide induced EP (LPS) and 3) LPS plus capsazepine (Capz, TRPV1 antagonist) application (LPS+Capz). EP was induced by injections of LPS (1 mg/ml) around first molars and treatment was performed with Capz (2 ug/ml) applied locally during six weeks. Additional experiment was performed by applying CB1r and CB2r antagonists (AM251 and AM630) to rats with EP.

RESULTS:

Capz prevented alveolar bone loss (ABL) on the external crests and in the interradicular bone of the first molars (Periodontal space height: LPS, 270.7±33.5μm versus LPS+Capz, 216.4±19.9μm; ρ<0.01). Inflammatory mediators, like tumor necrosis factor alpha (TNFα) and prostaglandin E2 (PGE2 ), increased by LPS-induced EP, were diminished in gingival tissue of rats treated with Capz. In contrast, application of AM251 and AM630 exacerbated ABL and gingival inflammatory mediators, increased by LPS, altering also biomechanical properties.

CONCLUSIONS:

TRPV1 blockade attenuates periodontal impairment in EP rats, since it reduces local inflammation, unlike CB1r and CB2r blockade. This work lays the foundations for developing therapeutics in humans based on the pharmacological manipulation of these receptors to treat periodontal disease. This article is protected by copyright. All rights reserved.

KEYWORDS:

anti-inflammatory agents; cytokines; experimental periodontitis; pathology – oral

PMID: 31077362
DOI: 10.1002/JPER.18-0766

LinkOut – more resources

Full Text Sources

Miscellaneous

Leave a Reply

en English