Aim. Septic arthritis of the hip is a rare entity among the adult population, but with a potential severe repercussion. The most accepted treatment is the hip debridement, even though a notorious proportion of the cases need further hip replacement owing to the cartilage destruction. The aim of this study is to analyse all our cases of septic arthritis of the hip treated with a 2-stage strategy using an antibiotic-loaded cement spacer. Method. We present a retrospective review of all our cases of septic arthritis of the hip diagnosed between 2004 and 2016 that were treated with an antibiotic-loaded cement spacer. We analysed age, gender, comorbidities, aetiology, duration of symptoms, C-reactive protein values, erythrocyte sedimentation rate, initial treatment, cultures, definitive treatment and evolution. Results. A total of 14 cases were included with a mean age of 47 years: 8 men and 6 women. The aetiology of the arthritis was: haematogenous in 8 cases, after osteosynthesis in 5 cases and after arthroscopy in 1 case. An initial debridement was performed in 6 cases whereas the spacer was directly implanted in 8 cases. The cultures were positive for: Staphylococcus aureus (4 cases), Candida albicans (2 cases), Staphylococcus epidermidis (1 case), Pseudomonas aeruginosa (1 case), Enterococcus faecium (1 case), Serratia marcescens (1 case), Streptococcus dysgalactiae (1 case), Salmonella spp (1 case) and negative in 2 cases. The evolution was: total hip arthroplasty in 10 cases, spacer preserved in 2 cases, pending of hip replacement in 1 case and exitus in 1 case. All cases presented negative cultures at the moment of implantation of the definitive prosthesis. Conclusions. A 2-stage strategy using an antibiotic-loaded cement spacer prior to the definitive hip prosthesis is a good treatment for the septic arthritis of the hip in cases with important cartilage destruction

Aberrant infrapatellar fat metabolism is a notable feature provoking inflammation and fibrosis in the progression of osteoarthritis (OA). Irisin, a secretory subunit of fibronectin type III domain containing 5 (FNDC5) regulate adipose morphogenesis, energy expenditure, skeletal muscle, and bone metabolism. This study aims to characterize the biological roles of Irisin signaling in an infrapatellar fat formation and OA development. Injured articular specimens were harvested from 19 patients with end-stage knee OA and 11 patients with the femoral neck fracture. Knee joints in mice that overexpressed Irisin were subjected to intra-articular injection of collagenase to provoke OA. Expressions of Irisin, adipokines, and MMPs probed with RT-quantitative PCR. Infrapatellar adiposity, articular cartilage damage, and synovial integrity verified with histomorphometry and immunohistochemistry. Infrapatellar adipose and synovial tissues instead of articular cartilage exhibited Irisin immunostaining. Human OA specimens showed 40% decline in Irisin expression than the non-OA group. In vitro, the gain of Irisin function enabled synovial fibroblasts but not chondrocytes to display minor responses to the IL-1β provocation of MMP3 and MMP9 expression. Of note, Irisin signaling reduced adipogenic gene expression and adipocyte formation of mesenchymal progenitor cells. In collagenase-mediated OA knee pathogenesis, forced FNDC5 expression in articular compromised the collagenase-induced infrapatellar adipose hypertrophy, synovial hypercellularity, and membrane hyperplasia. These adipose-regulatory actions warded off the affected knees from cartilage destruction and gait aberrance. Likewise, intra-articular injection of Irisin recombinant protein mitigated the development of infrapatellar adiposity and synovitis slowing down the progression of cartilage erosion and walking profile irregularity. Affected joints and adipocytes responded to the Irisin recombinant protein treatment by reducing the expressions of cartilage-deleterious adipokines IL-6, leptin, and adiponectin through regulating PPAR&gamma, function. Irisin dysfunction is relevant to the existence of end-stage knee OA. Irisin signaling protects from excessive adipogenesis of mesenchymal precursor cells and diminished inflammation and cartilage catabolism actions aggravated by adipocytes and synovial cells. This study sheds emerging new light on the Irisin signaling stabilization of infrapatellar adipose homeostasis and the perspective of the therapeutic potential of Irisin recombinant protein for deescalating knee OA development