RESUMEN
OBJECTIVES: The objective of this study was to evaluate the in vivo effects of a 2.6% edathamil gel (Livionex® Dental Gel) on surface microhardness and microstructure in 180 pre-eroded enamel chips. METHODS: This was a double-blind, randomized study. Two enamel chips each were cut from 90 healthy sterilized extracted teeth. One chip from each pair underwent microhardness testing and scanning electron microscopy (SEM) to establish baselines. The remaining 90 samples were demineralized, and then mounted onto intra-oral retainers worn by nine subjects, with five chips mounted on each retainer for each of the two study arms. In one two-week study arm subjects brushed with the control toothpaste; in the other they used the test gel. Study arms were separated by a two-week washout. Sequence of toothpaste use was randomized. At the end of each study arm, samples underwent microhardness measurements (Knoop) and SEM visualization. RESULTS: After intraoral wear, enamel chips recovered fully from demineralization, with no significant difference in microhardness between the two treatments (p > 0.05). In SEM images, enamel surfaces at study's end also appeared comparable in the two groups. CONCLUSIONS: Pre-eroded enamel chips remineralized intra-orally to a similar level after using a control or a test toothpaste containing 2.6% edathamil.
Asunto(s)
Cariostáticos , Esmalte Dental , Desmineralización Dental , Remineralización Dental , Cariostáticos/uso terapéutico , Esmalte Dental/efectos de los fármacos , Método Doble Ciego , Geles , Dureza , Humanos , Distribución AleatoriaRESUMEN
OBJECTIVES: Lipopolysaccharides (LPSs) and lipoteichoic acids (LTAs), or bacterial endotoxins, bind with Toll-like receptors (TLRs) that are expressed on host cells of the periodontium, thereby contributing to the periodontal pathogenicity of oral bacteria. Stannous fluoride (SnF2), an antibacterial fluoride that treats and controls gingivitis, has been shown to react with lipophilic domains/anionic charges in LPS and LTA. The effects of bacterial species and dental plaque on toll receptors can be studied using genetically engineered cell lines containing linked toll receptors on their surfaces. This randomized, examiner-blinded study examined the clinical effects of stabilized SnF2 dentifrice intervention on gingivitis and dental plaque virulence in populations exhibiting high and low levels of clinical gingivitis. METHODS: Recruited populations were evaluated for gingival inflammation (MGI) and gingival bleeding (GBI) at baseline and assigned into two cohorts of 20 each, those with high (GBI > 20 sites) and low (GBI < 3 sites) levels of observed bleeding/gingivitis. Participants were sampled at baseline for both supra- and subgingival dental plaque at both healthy (no bleeding, PD = 2 mm), as well as clinically diseased sites (bleeding, PD = 3-4 mm), and then provided with an intervention hygiene product including a stabilized SnF2 dentifrice and a new soft bristle manual toothbrush. Following two and four weeks of assigned dentifrice use, participants returned for a re-evaluation of gingival inflammation and bleeding and repeat samplings of dental plaque. Plaque samples were analyzed by anaerobic culturing of gram negative anaerobes (GNA), as well as by incubation of subgingival sampled plaques with TLR4 transfected HEK293 cells, where gene expression was assessed by measurement of a SEAP alkaline phosphatase reporter as a marker of toll receptor activation. RESULTS: Clinical assessments showed statistically significant reductions in MGI (24-26%) and GBI (42-53%) gingivitis in both diseased and healthy cohorts following four weeks of dentifrice intervention. For all clinical examinations, MGI and bleeding sites were statistically significantly different (lower) in the low bleeding versus the higher bleeding cohort. Supragingival and subgingival GNAs were significantly reduced (p < 0.05) in both high and low disease cohorts at bleeding and healthy sites following four weeks of stabilized SnF2 dentifrice use. TLR activation from subgingival sampled plaque was reduced following four weeks of stabilized SnF2 dentifrice use in both high and low disease cohorts and in both healthy, as well as diseased sites. CONCLUSIONS: Collectively, these results support the potential for stabilized SnF2 dentifrice to provide clinical gingivitis benefits via mechanisms beyond control of plaque mass, potentially directly decreasing the pathogenicity of plaque biofilms by blocking reactivity of LPS and LTA ligands with tissue receptors associated with inflammation. Importantly, benefits could be seen in both diseased sites, as well as sites not yet exhibiting symptoms of inflammation, supporting the activity of SnF2 not just in treating diseased sites, but in preventing disease development. These learnings may influence treatment planning for patients susceptible to gingivitis.