The Effects of Subcrestal Implant Placement on Crestal Bone Levels and Bone-to-Abutment Contact: A Microcomputed Tomographic and Histologic Study in Dogs.

Purpose: Implant design and the implant-abutment interface have been regarded as key influences on crestal bone maintenance over time. The aim of the present study was to determine crestal bone changes around implants placed at different depths in a dog model.

Materials And Methods: Thirty-six two-piece dental implants with a medialized implant-abutment interface and Morse taper connection (Ankylos, Dentsply) were placed in edentulous areas bilaterally in six mongrel dogs.

Endothelial cell-derived interleukin-6 regulates tumor growth.

Background: Endothelial cells play a complex role in the pathobiology of cancer. This role is not limited to the making of blood vessels to allow for influx of oxygen and nutrients required for the high metabolic demands of tumor cells. Indeed, it has been recently shown that tumor-associated endothelial cells secrete molecules that enhance tumor cell survival and cancer stem cell self-renewal.

Propolis decreases lipopolysaccharide-induced inflammatory mediators in pulp cells and osteoclasts.

Background: Intracanal medicaments are used to disinfect the root canal system, reduce interappointment pain and inflammation, and prevent resorption. Bacterial components such as lipopolysaccharide (LPS) are implicated in the development of pulpal and periapical inflammation and inducing osteoclastogenesis. Propolis is a natural, non-toxic substance collected from bee's wax that has been used for many years in folk medicine.

Type 1 diabetes-associated TLR responsiveness of oral epithelial cells.

In type 1 diabetes (T1D), a Toll-like receptor (TLR)-hyper-inflammatory monocytic phenotype has been implicated as a mechanism of exacerbated tissue destruction. Other cells of the periodontium, including oral epithelial cells (OECs), express innate immune receptors, including TLRs. To delineate the TLR responses of OECs derived from T1D participants and to determine effects of the anti-inflammatory agent triclosan on the TLR-hyper-inflammatory phenotype, primary human OECs from individuals with T1D and diabetes-free individuals were stimulated with TLR ligands in the presence and/or absence of triclosan.