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ABSTRACT
Background: Probiotic bacteria with anti-inflammatory properties have the potential to be of therapeutic benefit in gingivitis.
Objective: To evaluate the effects of potential probiotic strains on inflammatory mediators involved in early gingivitis using an ex vivo inflammation model.
Methods: Strains were screened in viable and attenuated forms for effects on bacterial lipopolysaccharide (LPS)-stimulated release of interleukins (IL)-Iß, -6 and -8, tumor necrosis factor-a, prostaglandin E2and 8-isoprostane from human primary monocytes, and then, if anti-inflammatory effects were shown, on IL-1 ß-stimulated release of inflammatory mediators from primary gingival fibroblasts. Lead strains were evaluated for optimal dosing, batch-to-batch variation and functional consistency in toothpaste.
Results: Twenty-one of 73 strains showed anti-inflammatory effects in monocytes; of which, seven showed effects in both viable and attenuated forms. Seven of 14 strains showed effects in fibroblasts. Strains Lactobacillus paracasei LPc-G110(SYBIO-15) and Lactobacillus plantarum GOS42(SYBIO-41) induced statistically significant dose-dependent reductions in the release of multiple inflammatory mediators from monocytes, which were consistent across batches. Viable L. paracasei LPc-G110 tooth paste significantly reduced IL-6, IL-8 and prostaglandin E2 release from monocytes versus placebo.
Conclusion: Strains L. paracasei LPc-G110 and L. plantarum GOS42 have potential for use as probiotics in oral care products to reduce gingival inflammation.
ARTICLE HISTORY
Received 11 April 2018
Revised 28 June 2018
Accepted 6 July 2018
KEYWORDS
Gingivitis; inflammation; bacteria; oral hygiene; dental plaque; biofilms; probiotics
Introduction
Inflammation of the gingivae (gingivitis) occurs in response to the accumulation of dental plaque on tooth surfaces near the gingival margin. In particular, bacterial lipopolysaccharide (LPS) from Gram-negative bacteria, which increase in number and proportion in plaque as it matures, provokes a non-specific inflammatory immune response [1,2]. This response is mediated by proinflammatory cytokines (e.g. tumor necrosis factor-a [TNF-a] and interleukin [IL]-1ß), chemokines (e.g. IL-8) and prostaglandins (e.g. prostaglandin E2 [PGE2]) secreted by gingival epithelial cells, fibroblasts and resident leukocytes [2-4]. These inflammatory mediators influence various cellular processes, including recruitment and chemotaxis of neutrophils, and promote increased vascular dilation and blood flow in the gingiva [5]. Persistent gingival inflammation can progressively exert selective pressure for the development of a dysbiotic and inflammophilic plaque microbiota [6]. In susceptible individuals, these changes can lead to chronic periodontitis, which is characterized by chronic inflammation and irreversible destruction of the supporting tissues of...