Local anatomical abnormalities vary in congenital hip disease patients. Authors often present early to mid-term total hip arthroplasty clinical outcomes using different techniques and implants randomly on patients with different types of the disease, making same conclusions difficult. We report long term outcomes (13 to 23 years) of the treatment of low and high dislocation cases (separately) with total hip arthroplasty using TM technology acetabular cups (Implex initially and then Zimmer) and short fluted conical (Zimmer) femoral stems. From 2000 to 2010, 418 congenital hip disease hip joints were treated in our department with total hip arthroplasty. According to Hartofilakidis et al's classification, 230 hips had dysplasia, 101 low dislocation, (group A) and 87 high dislocation (group B). Pre-operative and post-operative values, at regular intervals, of HHS, SF-12, WOMAC, OHS and HOOS were available for all patients. Patient, surgeon and implant related failures and complications were recorded for all patients. In all cases an attempt was made to restore hip center of rotation. In group A the average lengthening was 2.8 cm (range: 1 to 4.2) and in group B 5.7 cm (range: 4.2 to 11). In both groups, no hips were revised due to aseptic loosening of either the acetabular cup or the femoral stem. In group A, a cumulative success rate of 95.6% (95% confidence interval, 92.7% – 97.4%) and in group B a cumulative success rate of 94.8% (95% confidence interval, 92.6%–96.9%) was recorded, at 20 years, with revision for any reason as an end point. No s.s. differences were found between groups when mean values of HHS, SF-12, WOMAC and OKS were compared. Satisfactory long-term clinical outcomes can be achieved in treating different types of congenital hip disease when appropriate surgical techniques combined with “game changing” implants are used.
Septic arthritis induced by Staphylococcus aureus causes a rapid destruction of joint cartilage and periarticular bone. The mechanisms behind this phenomenon are not fully understood. Toll-like receptors (TLRs) are essential in host defense against pathogens by virtue of their capacity to detect microbes and initiate the immune response. TLR2 is seen as the most important receptor for gram-positive bacteria. TLR2 signaling can lead to the activation of NF-kB through myeloid differentiation factor 88 (MyD88) dependent pathway. The purpose of this study was to examine the catabolic role of TLR2 mediated by the NF-kB pathway in human septic arthritic chondrocytes. Septic arthritic (SA) chondrocytes (n=7) and fibroblast-like synoviocytes (n=7) infected by gram-positive bacteria, mainly Staphylococcus aureus, as well as chondrocytes from healthy individuals (n=5) were used for this study. The expression of TLR2 in septic articular cartilage and normal cartilage was analyzed by real time reverse transcription polymerase chain reaction as well western blot analysis. Production of matrix metalloproteinase MMP- 13 and IL-1b was evaluated by enzyme-linked immunosorbent assay. MyD88 protein expression levels and NF-kB activation were evalutated by western blot analysis. Downregulation of TLR2 expression was achieved after transfection with specific siRNA against TLR2 using liposomes. We observed that TLR2 mRNA and protein expression was significantly up-regulated in septic arthritic cartilage. Also MMP-13 and IL-1b production were significantly increased in septic arthritic chondrocytes compared to normal. Blocking TLR2 in septic chondrocytes resulted in significant reduction of MyD88 and NF-kB protein levels as well as reduction in MMP-13 and IL-1b expression. It could be suggested that stimulation of TLRs by microbial components may represent the initial signal promoting a pro-inflammatory environment that will enhance degeneration of articular cartilage and the surrounding synovial cells. Targeting NF-kB signalling pathway through TLR2 gene silencing may be of potential therapeutic value in treatment of joint diseases.
