The aim of this 1-year study was to evaluate and compare crestal bone loss and clinical outcomes of immediate and delayed loaded implants supporting mandibular overdentures with Locator attachments. In a randomised controlled clinical trial, 36 completely edentulous patients (mean age 59.6 years) who desired to improve the stability of their mandibular dentures were randomly assigned into two groups. Each patient received two implants in the canine area of the mandible after a minimal flap reflection. Implants were loaded by mandibular overdentures either 3 months (delayed loading group, G1) or the same day (immediate loading group, G2) after implant placement. Locator attachments were used to retain all overdentures to the implants. Peri-implant vertical (VBL) and horizontal (HBLO) bone losses and clinical parameters [plaque scores (PI), gingival scores (GI), probing depths (PD) and implant stability (ISQ)] were assessed at time of overdenture insertion (T0), 6 months (T6) and 12 months (T12) after overdenture insertion. After 12 months of overdenture insertion, two implants (5.5%) failed in G2. Vertical bone loss was significantly higher in G2 compared with G1, while HBLO demonstrated insignificant differences between groups. All clinical parameters (PI, GI, PD and ISQ) did not differ significantly between groups. Vertical bone loss was significantly correlated with PD and HBLO. Immediately loaded two implants supporting a Locator-retained mandibular overdenture are associated with more vertical bone resorption when compared to delayed loaded implants after 1 year. Clinical outcomes do not differ significantly between loading protocols.

Resilient telescopic attachments are associated with increased chewing efficiency and MBF compared bar attachments when used to retain overdentures to the implants in patients with atrophied mandibles.

This review is concerned with cardiac malfunction as a result of an imbalance in protein proteostasis, the homeostatic balance between protein removal and regeneration in a long remodeling process involving the endoplasmic reticulum (ER) and the unfolded protein response (UPR). The importance of this is of special significance with regard to cardiac function as a high energy requiring muscular organ that has a high oxygen requirement and is highly dependent on mitochondria. The importance of mitochondria is not only concerned with high energy dependence on mitochondrial electron transport, but it also has a role in the signaling between the mitochondria and the ER under stress. Proteins made in the ER are folded as a result of sulfhydryl groups (-SH) and attractive and repulsive reactions in the tertiary structure. We discuss how this matters with respect to an imbalance between muscle breakdown and repair in a stressful environment, especially as a result of oxidative and nitrosative byproducts of mitochondrial activity. The normal repair is a remodeling, but under this circumstance, the cell undergoes or even lysosomal "self eating" autophagy, or even necrosis instead of apoptosis. We shall discuss the relationship of the UPR pathway to chronic congestive heart failure (CHF).

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BACKGROUND: The cannabinoid receptor 2 (CB2) plays a pleiotropic role in the innate immunity and is considered a crucial mediator of liver disease. Cannabinoid CB2 receptor activation has been reported to attenuate liver fibrosis in CCl4 exposed mice and also plays a potential role in liver regeneration in a mouse model of I/R and protection against alcohol-induced liver injury. AIM: In this study, we investigated the impact of CB2 receptors on the antifibrotic and regenerative process associated with cholestatic liver injury. METHODS: Twenty-six rats had bile duct ligation co-treated with silymarin and AM1241 for 3 consecutive weeks. Serum hepatotoxicity markers were determined, and histopathological evaluation was performed. RESULTS: Following bile duct ligation (BDL) for 3 weeks, there was increased aminotransferase levels, marked inflammatory infiltration and hepatocyte apoptosis with induced oxidative stress, as reflected by increased lipid peroxidation. Conversely, following treatment with the CB2 agonist, AM-1241, BDL rats displayed a reduction in liver injury and attenuation of fibrosis as reflected by expression of hydroxyproline and α-smooth muscle actin. AM1241 treatment also significantly attenuated lipid peroxidation end-products, p53-dependent apoptosis and also attenuated inflammatory process by stimulating IL-10 production. Moreover, AM1241 treated rats were associated with significant expression of hepatic progenitor/oval cell markers. CONCLUSION: In conclusion, this study points out that CB2 receptors reduce liver injury and promote liver regeneration via distinct mechanisms including IL-10 dependent inhibition of inflammation, reduction of p53-reliant apoptosis and through stimulation of oval/progenitor cells. These results suggest that CB2 agonists display potent hepatoregenrative properties, in addition to their antifibrogenic effects.