Efficacy of acupuncture and laser acupuncture in temporomandibular disorders: a systematic review and meta-analysis of randomized controlled trials.

OBJECTIVE: The aim of this study is to perform a qualitative and quantitative analysis of the scientific literature regarding the use of acupuncture and laser acupuncture in the treatment of pain associated with temporomandibular disorders (TMDs). The aim of this article was to assess the clinical evidence for acupuncture and laser acupuncture therapies as treatment for temporomandibular joint disorder (TMD). MATERIALS AND METHODS: This systematic review includes randomized clinical trials (RCTs) of acupuncture and laser acupuncture as a treatment for TMD compared to other treatments. Systematic searches were conducted in 3 electronic databases up to July 2023; PubMed, EMBASE, and SCOPUS databases. All RCTs of acupuncture for TMD were searched without language restrictions. Studies in which no clinical data and complex interventions were excluded. The Cochrane risk of bias tool (RoB 2) tool was employed to analyze randomized controlled trials. A Meta-analysis was performed in order to investigate a quantitative analysis comparing acupuncture and laser acupuncture to placebo. RESULTS: A total of 11 RCTs met our inclusion criteria. The findings show that acupuncture is short-term helpful for reducing the severity of TMD pain with muscle origin. Meta-analysis revealed that the Acupuncture group and Laser Acupuncture group had a higher efficacy rate than the Placebo control group, showing a high efficacy of Acupuncture and Laser Acupuncture group in the treatment of temporomandibular. CONCLUSIONS: In conclusion, our systematic review demonstrate that the evidence for acupuncture as a symptomatic treatment of TMD is limited. Further rigorous studies are, however, required to establish beyond doubt whether acupuncture has therapeutic value for this indication. However high efficacy of Laser Acupuncture in the treatment of temporomandibular disorders was reported.

Polycomb YY1 is a critical interface between epigenetic code and miRNA machinery after exposure to hypoxia in malignancy.

Yin Yang 1 (YY1) is a member of polycomb protein family involved in epigenetic modifications and transcriptional controls. We have shown that YY1 acts as positive regulator of tumor growth and angiogenesis by interfering with the VEGFA network. Yet, the link between polycomb chromatin complex and hypoxia regulation of VEGFA is still poorly understood. Here, we establish that hypoxia impairs YY1 binding to VEGFA mRNA 3'UTR (p<0.001) in bone malignancy. Moreover, RNA immunoprecipitation reveals the formation of triplex nuclear complexes among YY1, VEGFA DNA, mRNA, and unreached about 200 fold primiRNA 200b and 200c via Dicer protein. In this complex, YY1 is necessary to maintain the steady-state level of VEGFA expression while its silencing increases VEGFA mRNA half-life at 4 h and impairs the maturation of miRNA 200b/c. Hypoxia promotes histone modification through ubiquitination both of YY1 and Dicer proteins. Hypoxia-mediated down-regulation of YY1 and Dicer changes post-transcriptional VEGFA regulation by resulting in the accumulation of primiRNA200b/c in comparison to mature miRNAs (p<0.001). Given the regulatory functions of VEGFA on cellular activities to promote neoangiogenesis, we conclude that YY1 acts as novel critical interface between epigenetic code and miRNAs machinery under chronic hypoxia in malignancy.

Deletion of Yin Yang 1 protein in osteosarcoma cells on cell invasion and CXCR4/angiogenesis and metastasis.

We know that the Yin Yang 1 protein (YY1) overexpression is positively and strongly correlated with the degree of malignancy of bone tumors. Therefore, we questioned whether we could influence cell invasiveness by deleting YY1 in human osteosarcoma cells (SaOs-2), as tested in Matrigel-coated filters and metastasis implantation of such osteosarcoma cells in vivo, by serial analysis with nuclear magnetic resonance. Moreover, we focused our work on the chemokine receptor CXCR4 and its inhibition by T22 antibody, as well as on systemic (direct in vivo assay) and computer-assisted imaging of angiogenesis-related metastasis. Results showed that cell invasiveness and metastasis implantation by wild-type SaOs-2 cells, as evaluated by histology and immunohistochemistry, are associated with up-regulation of CXCR4 expression, which in turn was significantly reduced by T22. In addition, deletion of YY1 (siRNAYY1-SaOs-2) induced a significant decrease of cell invasion and metastasis growth. This phenomenon was associated with decreased vascular endothelial growth factor (VEGF)/angiogenesis and a complex rearrangement of the gene expression profile as evaluated by microarray analysis. In conclusion, YY1 and VEGF/CXCR4 seem to intervene in the pathogenesis of the malignant phenotype of osteosarcoma by acting on cell invasiveness and metastasis growth.

Physical training and metabolic supplementation reduce spontaneous atherosclerotic plaque rupture and prolong survival in hypercholesterolemic mice.

Moderate physical exercise (PE) combined with metabolic treatment (MT) (antioxidants and l-arginine) are well known to reduce atherosclerotic lesion formation in hypercholesterolemic mice. However, the long-term beneficial effects on unstable atheroma remain poorly understood. We started early PE training in large groups of 6-week-old hypercholesterolemic mice (by graduated swimming) alone or in combination with nutritional supplementation (1.0% vitamin E added to the chow and 0.05% vitamin C and 6% l-arginine added to the drinking water). Inactive controls did not receive PE. The spontaneous development of atherosclerotic plaque rupture (associated with advanced atherosclerosis) and survival rates were evaluated. Moderate PE elicited an increase in plasma levels of nitric oxide. Early combined treatment with PE and MT in the hypercholesterolemic mice significantly reduced lesions (also detected noninvasively at 10 months) and spontaneous atherosclerotic plaque rupture and prolonged survival more effectively than each intervention alone. Thus, early concerted actions of MT and PE improve the natural history of atherosclerotic lesions and reduce the plaque instability in hypercholesterolemic mice.