Clinical outcome of immediately loaded dental implants bioactivated with plasma rich in growth factors: a 5-year retrospective study

BACKGROUND: The aims of this study were to describe a procedure for the immediate loading of dental implants, evaluate the long-term survival rates of 1,139 immediately loaded dental implants, and analyze the influence of different factors on implant survival. METHODS: A retrospective cohort study design was used. A total of 241 patients received 1,139 immediately loaded implants between 2001 and 2005 in Vitoria, Spain. All implants were placed by one experienced surgeon, and rehabilitations were done by four prosthodontists. Each implant failure was analyzed carefully. The potential influence of demographic, clinical, and surgery-dependent factors and prosthetic variables on implant survival was studied. Implant survival was analyzed using a life-table analysis. RESULTS: The overall survival rates were 99.3%, 96.8%, and 96.9% for the implant-, surgery-, and patient-based analyses, respectively. The mean follow-up period was 28 +/- 15 months. Five of 1,139 implants were lost during the observation period. No variable studied was statistically associated with implant failure. CONCLUSION: Based on these results, the procedure described for the immediate loading of implants can be considered safe and predictable if used under strict clinical protocols.     

Mitochondrial cholesterol contributes to chemotherapy resistance in hepatocellular carcinoma

Cholesterol metabolism is deregulated in carcinogenesis, and cancer cells exhibit enhanced mitochondrial cholesterol content whose role in cell death susceptibility and cancer therapy has not been investigated. Here, we describe that mitochondria from rat or human hepatocellular carcinoma (HC) cells (HCC) or primary tumors from patients with HC exhibit increased mitochondrial cholesterol levels. HCC sensitivity to chemotherapy acting via mitochondria is enhanced upon cholesterol depletion by inhibition of hydroxymethylglutaryl-CoA reductase or squalene synthase (SS), which catalyzes the first committed step in cholesterol biosynthesis. HCC transfection with siRNA targeting the steroidogenic acute regulatory protein StAR, a mitochondrial cholesterol-transporting polypeptide which is overexpressed in HCC compared with rat and human liver, sensitized HCC to chemotherapy. Isolated mitochondria from HCC with increased cholesterol levels were resistant to mitochondrial membrane permeabilization and release of cytochrome c or Smac/DIABLO in response to various stimuli including active Bax. Similar behavior was observed in cholesterol-enriched mitochondria or liposomes and reversed by restoring mitochondrial membrane order or cholesterol extraction. Moreover, atorvastatin or the SS inhibitor YM-53601 potentiated doxorubicin-mediated HCC growth arrest and cell death in vivo. Thus, mitochondrial cholesterol contributes to chemotherapy resistance by increasing membrane order, emerging as a novel therapeutic niche in cancer therapy.