Comparison of Dehydrated Human Amnion-Chorion and Type 1 Bovine Collagen Membranes in Alveolar Ridge Preservation: A Clinical and Histological Study.

Alveolar ridge preservation maintains ridge dimensions and bone quality for implant placement. The aim of this randomized controlled clinical study is to compare the use of a human amnion-chorion membrane to a collagen membrane in an exposed-barrier ridge preservation technique. Furthermore, this study will determine if intentional membrane exposure compromises ridge dimensions and bone vitality. Forty-three patients requiring extraction and delayed implant placement were randomly assigned into either the experimental or control group. Twenty-one participants received human amnion-chorion membrane (test) during ridge preservation while 22 participants received the collagen membrane (control). In both groups, demineralized freeze-dried bone allografts were used to graft the socket and primary closure was not achieved. The patients underwent implant placement after an average healing period of 19.5 weeks, and 2.7 × 8-mm core bone specimens were obtained for histomorphometric analyses. The clinical ridge dimensions were measured after extraction and at the time of delayed implant placement. No significant difference was observed in the mean vital bone formation between the experimental (51.72 ± 8.46%) and control (49.96 ± 8.31%; P > .05) groups. The bone height and width did not differ, as determined by clinical measurements (P > .05). Using either a human amnion-chorion membrane or type 1 bovine collagen as the open barrier did not change healing, compromise ridge dimensions, or affect bone vitality between the 2 groups.

MicroRNA-223 coordinates cholesterol homeostasis.

MicroRNAs (miRNAs) regulate a wide variety of biological processes and contribute to metabolic homeostasis. Here, we demonstrate that microRNA-223 (miR-223), an miRNA previously associated with inflammation, also controls multiple mechanisms associated with cholesterol metabolism. miR-223 promoter activity and mature levels were found to be linked to cellular cholesterol states in hepatoma cells. Moreover, hypercholesterolemia was associated with increased hepatic miR-223 levels in athero-prone mice. miR-223 was found to regulate high-density lipoprotein-cholesterol (HDL-C) uptake, through direct targeting and repression of scavenger receptor BI, and to inhibit cholesterol biosynthesis through the direct repression of sterol enzymes 3-hydroxy-3-methylglutaryl-CoA synthase 1 and methylsterol monooxygenase 1 in humans. Additionally, miR-223 was found to indirectly promote ATP-binding cassette transporter A1 expression (mRNA and protein) through Sp3, thereby enhancing cellular cholesterol efflux. Finally, genetic ablation of miR-223 in mice resulted in increased HDL-C levels and particle size, as well as increased hepatic and plasma total cholesterol levels. In summary, we identified a critical role for miR-223 in systemic cholesterol regulation by coordinated posttranscriptional control of multiple genes in lipoprotein and cholesterol metabolism.