Platelet-rich plasma may prevent titanium-mesh exposure in alveolar ridge augmentation with anorganic bovine bone

Objective: Bone augmentation with the titanium-mesh (Ti-mesh) technique is susceptible to a large rate of complications such as morbidity of bone graft donor site, and mesh exposure to the oral cavity. The purpose of this study was to evaluate the effectiveness of anorganic bovine bone (ABB) in alveolar bone augmentation with the Ti-mesh technique. In addition, we investigated the effect of platelet-rich plasma (PRP) in preventing mesh exposure by using it to cover the Ti-mesh. Patients and methods: Patients included in the clinical trial were randomly allocated by a blinded assistant into two groups. The 30 patients recruited for this study underwent 43 alveolar bone augmentation with the Ti-mesh technique using ABB as graft material in all of them. In 15 patients, the Ti-meshes were covered with PRP (PRP group) whereas in the other 15 the Ti-meshes were not (control group). After 6 months, patients were called for clinical, radiographic and histological evaluation, and implant placement surgery. A total of 97 implants were placed in the augmented bone and their evolution was followed up for a period of 24 months. Results: Significant differences were found between the two study groups in terms of complications and bone formation. In the control group, 28,5% of the cases suffered from mesh exposure, while in the PRP group, no exposures were registered. Radiographic analysis revealed that bone augmentation was higher in the PRP group than in the control group. Overall, 97,3% of implants placed in the control group and 100% of those placed in the PRP group were successful during the monitoring period. We suggest that the positive effect of PRP on the Ti-mesh technique is due to its capacity to improve soft tissue healing, thereby protecting the mesh and graft material secured beneath the gingival tissues. Conclusions: Alveolar bone augmentation using ABB alone in the Ti-Mesh technique is sufficient for implant rehabilitation. Besides, covering the Ti-meshes with PRP was a determining factor in avoiding mesh exposure. Ti-Mesh exposure provoked significant bone loss, but in most cases it did not affect the subsequent placement implants

Manifesting heterozygotes in McArdle disease:a myth or a realityrole of statins

McArdle disease is an autosomal recessive condition caused by deficiency of the PYGM gene-encoded muscle isoform of glycogen phosphorylase. Some cases of “manifesting” heterozygotes or carriers (i.e., patients who show some McArdle-like symptoms or signs despite being carriers of only one mutated PYGM allele) have been reported in the literature but there is controversy, with misdiagnosis being a possibility. The purpose of our study was to determine if there are actually “manifesting” heterozygotes of McArdle disease and, if existing, whether statin treatment can trigger such condition. Eighty-one relatives of McArdle patients (among a total of 16 different families) were studied. We determined whether they were carriers of PYGM mutations and also collected information on exercise tests (second wind and modified Wingate anaerobic test) and statin intake. We found 50 carriers and 31 non-carriers of PYGM mutations. Although we found existence of heterozygotes manifesting some exercise-related muscle problems such as exacerbated myalgia or weakness, they only accounted for 14% of the carriers and muscle symptoms were milder than those commonly reported in patients. Further, no carrier (whether reporting symptoms or not) showed the second wind phenomenon or a flat blood lactate response to maximal-intensity exercise, both of which are hallmarks of McArdle disease. On the other hand, statin myotoxicity was not associated with muscle symptom onset

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field