Scoliosis is diagnosed as idiopathic in 70 % of structural deformities affecting the spine in children and adolescents, probably reflecting our current misunderstanding of this disease. By definition, a structural scoliosis should be the result of some primary disorder. The goal of this article is to give a comprehensive overview of the currently proposed etiological concepts in idiopathic scoliosis regarding genetics, molecular biology, biomechanics, and neurology, with particular emphasis on adolescent idiopathic scoliosis (AIS). Despite the fact that numerous potential etiologies for idiopathic scoliosis have been formulated, the primary etiology of AIS remains unknown. Beyond etiology, identification of prognostic factors of AIS progression would probably be more relevant in our daily practice, with the hope of reducing repetitive exposure to radiation, unnecessary brace treatments, psychological implications, and costs-of-care related to follow-up in lowrisk patients.

The course of the spondylodiscitis' infantile form is characterized by a mild-to-moderate clinical and biologic inflammatory response. Unfortunately, blood and disk/vertebral aspiration cultures show a high percentage of negative results. However, detecting Kingella kingae DNA in the oropharynx provided reasonable suspicion, to our opinion, that this microorganism is responsible for the spondylodiscitis.

Kingella kingae is a Gram-negative bacterium that is today recognized as the major cause of joint and bone infections in young children. This microorganism is a member of the normal flora of the oropharynx, and the carriage rate among children under 4 years of age is approximately 10%. K. kingae is transmitted from child to child through close personal contact. Key virulence factors of K. kingae include expression of type IV pili, Knh-mediated adhesive activity and production of a potent RTX toxin. The clinical presentation of K. kingae invasive infection is often subtle and may be associated to mild-to-moderate biologic inflammatory responses, highlighting the importance a high index of suspicion. Molecular diagnosis of K. kingae infections by nucleic acid amplification techniques enables identification of this fastidious microorganism. Invasive infections typically respond favorably to medical treatment, with the exception of cases of endocarditis, which may require urgent valve replacement

The use of organism-specific real-time PCR assays markedly improves the detection rate of the pathogen responsible for PEASAO, and K. kingae is the most commonly detected pathogen. The literature highlights a biphasic age distribution of PEASAO in children. The infantile form affects children from one to less than four years of age, accounting for approximately 75% of all PEASAO cases. The second form, in older children, is more likely to be associated with fever and systemic symptoms. The femur and the tibia are the most commonly affected long bones. Laboratory data are usually noncontributory for diagnosing PEASAO, and blood cultures are often sterile. Although K. kingae is the most commonly detected microorganism in children less than four years of age, S. aureus is responsible for most PEASAO in older children. Antibiotic treatment is usually sufficient to eradicate the pathogen.

During a two-stage revision for prosthetic joint infections (PJI), joint aspirations, open tissue sampling and serum inflammatory markers are performed before re-implantation to exclude ongoing silent infection. We investigated the performance of these diagnostic procedures on the risk of recurrence of PJI among asymptomatic patients undergoing a two-stage revision. A total of 62 PJI were found in 58 patients. All patients had intraoperative surgical exploration during re-implantation, and 48 of them had intra-operative microbiological swabs. Additionally, 18 joint aspirations and one open biopsy were performed before second-stage reimplantation. Recurrence or persistence of PJI occurred in 12 cases with a mean delay of 218 days after re-implantation, but only four pre-or intraoperative invasive joint samples had grown a pathogen in cultures. In at least seven recurrent PJIs (58%), patients had a normal C-reactive protein (CRP, <10 mg/l) level before re-implantation. The sensitivity, specificity, positive predictive and negative predictive values of pre-operative invasive joint aspiration and CRP for the prediction of PJI recurrence was 0. 58, 0.88, 0.5, 0.84 and 0.17, 0.81, 0.13, 0.86, respectively. As a conclusion, pre-operative joint aspiration, intraoperative bacterial sampling, surgical exploration and serum inflammatory markers are poor predictors of PJI recurrence. The onset of reinfection usually occurs far later than reimplantation.

Our data suggest that for native septic arthritis, in the absence of clinical sepsis immediate joint drainage does not appear to reduce the risk of sequelae compared with delayed drainage.

Background: 1st and 2nd generation cephalosporins used for perioperative prophylaxis in orthopaedic surgery do not cover non-fermenting Gram-negative rods (NFR).Methods: Epidemiological cohort study of adult patients operated for orthopedic infections between 2004 and 2014 with perioperative cefuroxim or vancomycin prophylaxis. Exclusion of polyneuropathic ischemic foot infections and septic bursitis cases.Results: Of the total 1840 surgical procedures in the study, 430 grew Gram-negative pathogens (23%), of which 194 (11%) were due to NFR and 143 (8%) to Pseudomonas aeruginosa. Overall, 634 episodes (35%) involved orthopaedic implants (321 arthroplasties, 135 plates, 53 nails, and others). In multivariate analysis and group comparisons, especially preoperative antibiotic use (124/194 vs. 531/1456; p<0.01) was significantly associated with NFR.Conclusions: Overall proportion of NFR oscillated between 9% and 13% among our orthopaedic infections. Variables associated with NFR were antibiotic use prior to hospitalization. The low infection rate of NFR following elective surgery and the community-based epidemiology, has led us to keep our standard perioperative prophylaxis unchanged.

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