LPS Dental specializes in enabling dentists of all specialties to monetize a portion of their practice value for cash today at today’s low tax rates with silent partners known as IDSOs (Invisible Dental Support Organizations). The doctors continue as owners leading their practices under their brand, team and strategy for years or decades while diversifying their largest investment. The process also enables clinicians to accelerate their growth and gain access to the capital needed to expand or acquire new offices and territories.
Endotoxin, or lipopolysaccharide LPS Dental (LPS), is a virulence factor released by Gram-negative bacteria that triggers inflammation and a host response leading to bacterial colonization, invasion, infection and/or inflammatory pulpitis [1]. It acts through activation of Toll-like receptor 2 (TLR2) or 4 (TLR4) receptors which in turn activate NF-kB and MAPK pathways resulting in expression of adhesion molecules (ICAM-1, VCAM-1), chemotactic factors (IL-6, IL-8), metalloproteases and odontoblastic differentiation proteins.
In addition to the aforementioned molecular effects, LPS induces alterations in DNA methylation pattern and promotes production of proinflammatory mediators (IL-1b, IL-6). It downregulates mRNA and protein level of DNA methyltransferases 3B (DNMT3B) and 1 (DNMT1) and upregulates miR-21-5p which decreases NF-kB p65 phosphorylation and expression of IL-6 and IL-8. It also attenuates COX-2 expression, inhibits cellular protein production and increases cell death (pyroptosis).
The results of the present study show that EGCG significantly reduces LPS-induced inflammatory mediators. Moreover, the expression of DNMT3B and DNMT1 was downregulated in cells exposed to LPS while EGCG increased Wnt5a expression. In addition, EGCG reduced the expression of cytolysin, which inhibits dentinogenesis.
The results indicate that ECGE may be a useful adjunct to traditional dental treatment for patients with periodontal disease because it enhances tooth pulp healing in patients undergoing root canal therapy or deep caries. In this way, ECGE could increase the chances of successful endodontic treatment while protecting against inflammatory responses induced by LPS. In addition, the results of this investigation suggest that DNMT1 demethylation may be responsible for the protection against inflammatory mediators produced by hDPSCs under the influence of LPS. However, further research is required to evaluate this hypothesis.