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Background A tourniquet is commonly used in total knee arthroplasty (TKA). However, the effectiveness and safety of tourniquets are debated. We performed this study to investigate whether patients benefit from the use of tourniquets in TKA. Methods The literature search was conducted using Pub-Med, Cochrane Library, MEDLINE, Embase, and other medical databases. After a literature search, 26 randomized controlled trials involving 1,450 knees were analyzed. Results Tourniquet use significantly decreased intraoperative blood loss, transfusion rate, and operation time but not postoperative blood loss, measurable total blood loss, calculated total blood loss, transfusion volume, incidence of pulmonary embolism, or duration of hospital stay. It also slowed down joint functional recovery in the short term and increased the incidence of deep vein thrombosis and other minor wound complications. Conclusions Data from this meta-analysis indicate that patients may benefit from the use of a tourniquet in TKA; however, it use is accompanied by disadvantages and complications. Because of the very low-evidence quality and lower grading of recommendations, assessment, development, and evaluation recommendation strength, no guidelines can be developed based on current evidence.

Overproduction of nitric oxide (NO) and matrix metalloproteinases (MMPs) plays an important role in the pathogenesis of osteoarthritis (OA). In present study, we investigated whether vorinostat can inhibit the catabolic effects of IL-1β in vitro, especially the inhibition of MMPs and inducible nitric oxide synthase (iNOS) through the attenuation of nuclear factor kappa-B (NF-κB) and mitogen activated protein kinase (MAPK) pathways in human chondrocytes. Human OA chondrocytes were either left untreated or treated with various concentrations of vorinostat followed by incubation with IL-1β (5ng/mL). Effects of vorinostat on IL-1β-induced gene and protein expression of iNOS, MMP-1, MMP-13 and tissue inhibitors of metalloproteinase-1 (TIMP-1) were verified by quantitative real time-PCR and Western blot analysis. Production of NO, MMP-1, MMP-13 and TIMP-1 released in culture supernatant was estimated using commercially available kits. The roles of NF-κB and MAPK pathways in the regulation of targeted genes and the mechanism involved in vorinostat mediated modulation of these genes were determined by Western blot using specific antibodies. We found that vorinostat down-regulated iNOS, MMP-1 and MMP-13 expression and up-regulated TIMP-1 expression in human OA chondrocytes. In addition, the release of NO, MMP-1 and MMP-13 secreted from IL-1β stimulated chondrocytes was also suppressed by vorinostat. Interestingly, vorinostat selectively inhibited IL-1β-induced p38 and ERK1/2 activation without affecting JNK activation. Furthermore, we observed that vorinostat inhibited NF-κB pathway by suppressing the degradation of I-κBα and attenuating NF-κB p65 translocation to the nucleus. These results suggest that vorinostat may be a promising therapeutic agent for the prevention and treatment of OA.