Objective：This study aimed to examine the effects of kilohertz-frequency alternating current (KFAC) on muscle performance and adverse event in patients with neuromuscular skeletal disorders.Methods：A literature search was conducted in PubMed, PEDro, CINAHL, and Cochrane CENTRAL until September 2017. The reviewer extracted data on subject characteristics, intervention, target muscle, and outcome measures in accordance with the Cochrane Handbook.Results：The literature search yielded 1295 studies, and 3 studies met the inclusion criteria (n＝32；mean age：45.3 years). KFAC stimulation combined with land-based exercise was likely more effective in increasing the quadriceps femoris muscle strength than exercise alone in patients after total knee arthroplasty (TKA). However, KFAC was not superior to low-frequency pulsed current in increasing pedaling work in patients with spinal cord injury. No severe adverse event relevant to KFAC was reported in all 3 studies. The quality of evidence was very low according to the GRADE approach.Conclusion：Additional KFAC may be more effective than exercise alone in improving the quadriceps femoris muscle strength in patients after TKA without any severe adverse event. Further studies to investigate the effects of KFAC are warranted to increase the confidence for the effects of KFAC treatment.

Clinical studies have shown that Aggregatibacter actinomycetemcomitans(A.actinomycetemcomitans)is associated with aggressive periodontitis and can potentially trigger or exacerbate rheumatoid arthritis(RA).However,the mechanism is poorly understood.Here,we show that systemic infection with A.actinomycetemcomitans triggers the progression of arthritis in mice anti-collagen antibody-induced arthritis(CAIA)model following IL-1β secretion and cell infiltration in paws in a manner that is dependent on caspase-11-mediated inflammasome activation in macrophages.The administration of polymyxin B(PMB),chloroquine,and anti-CD11b antibody suppressed inflammasome activation in macrophages and arthritis in mice,suggesting that the recognition of lipopolysaccharide(LPS)in the cytosol after bacterial degradation by lysosomes and invasion via CD11b are needed to trigger arthritis following inflammasome activation in macrophages.These data reveal that the inhibition of caspase-11-mediated inflammasome activation potentiates aggravation of RA induced by infection with A.actinomycetemcomitans.This work highlights how RA can be progressed by inflammasome activation as a result of periodontitis-associated bacterial infection and discusses the mechanism of inflammasome activation in response to infection with A.actinomycetemcomitans.