Application of Platelet-Rich Fibrin Derivatives for Mandibular Third Molar Extraction Related Post-Operative Sequelae: A Systematic Review and Network Meta-Analysis.

PURPOSE: Leukocyte- and platelet-rich fibrin (L-PRF) and advanced-platelet-rich fibrin (A-PRF) that are derivatives of PRF (platelet-rich fibrin) accelerate wound healing and reduce postoperative sequelae after tooth extraction. This network meta-analysis aimed to investigate the effectiveness of L-PRF and A-PRF in mandibular third molar extraction and provide suggestions for alleviating postoperative symptoms and signs. METHODS: A comprehensive search of the literature was conducted in PubMed, Embase, Web of Science, and SinoMed databases up to Oct 9, 2020. Three types of randomized controlled trials were included to investigate the effects of PRF derivatives after extracting mandibular third molars: A-PRF and L-PRF groups; A-PRF and control groups; L-PRF and control groups. Their relative effectiveness and ranking were assessed using network meta-analysis and the surface under the cumulative ranking curve (SUCRA) with STATA 16.0 and Revman 5.3, respectively. RESULTS: Ten randomized controlled trials were included, with 307 mandibular third molar extraction patients involved. The results showed that A-PRF had the best effect among the 3 groups in improving postoperative pain on the third (SUCRA = 98.2%) and seventh (SUCRA = 88.4%) days; L-PRF promoted soft tissue healing (MD = -0.90, 95% CI [-1.40, -0.40], P = .0004) on the seventh day compared with the control. However, other comparisons showed no significant differences (P > .05). CONCLUSION: The limited results confirmed that PRF derivatives only reduced some postoperative symptoms and did not prevent them all. Application of A-PRF after third molar extraction reduced postoperative pain, and L-PRF improved the degree of soft tissue healing.

The mechanism by which noncoding RNAs regulate muscle wasting in cancer cachexia.

Cancer cachexia (CC) is a complex metabolic syndrome that accelerates muscle wasting and affects up to 80% of patients with cancer; however, timely diagnostic methods and effective cures are lacking. Although a considerable number of studies have focused on the mechanism of CC-induced muscle atrophy, few novel therapies have been applied in the last decade. In recent years, noncoding RNAs (ncRNAs) have attracted great attention as many differentially expressed ncRNAs in cancer cachectic muscles have been reported to participate in the inhibition of myogenesis and activation of proteolysis. In addition, extracellular vesicles (EVs), which function as ncRNA carriers in intercellular communication, are closely involved in changing ncRNA expression profiles in muscle and promoting the development of muscle wasting; thus, EV-related ncRNAs may represent potential therapeutic targets. This review comprehensively describes the process of ncRNA transmission through EVs and summarizes the pathways and targets of ncRNAs that lead to CC-induced muscle atrophy.

Non-coding RNAs in exosomes and adipocytes cause fat loss during cancer cachexia.

Cancer Cachexia (CC) is a disease that changes various metabolisms in human body. Fat metabolism is significantly affected in CC, leading to fat loss. Non-coding RNAs (ncRNAs) in adipocytes and exosomes secreted by tumor play an important role in fat loss. However, there is no related reviews summarizing how ncRNAs contribute to fat loss during CC. This review screens recent articles to summarize how ncRNAs are packaged, transported in exosomes, and play the role in fat loss. Not only does this review summarize the mechanisms, we also point out the research orientations in the future.