Autografts vs Synthetics for Cruciate Ligament Reconstruction: A Systematic Review and Meta-Analysis.

To describe the outcomes of autografts and synthetics in anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL) reconstruction with respect to instrumented laxity measurements, patient-reported outcome scores, complications, and graft failure risk. We searched PubMed, Cochrane Library, and EMBASE for published randomized controlled trials (RCT) and case controlled trials (CCTs) to compare the outcomes of the autografts versus synthetics after cruciate ligament reconstruction. Data analyses were performed using Cochrane Collaboration RevMan 5.0. Nine studies were identified from the literature review. Of these studies, three studies compared the results of bone-patellar tendon-bone (BPTB) and ligament augmentation and reconstruction system (LARS), while six studies compared the results of four-strand hamstring tendon graft (4SHG) and LARS. The comparative study showed no difference in Lysholm score and failure risk between autografts and synthetics. The combined results of the meta-analysis indicated that there was a significantly lower rate of side-to-side difference > 3 mm (Odds Ratio [OR] 2.46, 95% confidence intervals [CI] 1.44-4.22, P = 0.001), overall IKDC (OR 0.40, 95% CI 0.19-0.83, P = 0.01), complications (OR 2.54, 95% CI 1.26-5.14, P = 0.009), and Tegner score (OR -0.31, 95% CI -0.52-0.10, P = 0.004) in the synthetics group than in the autografts group. This systematic review comparing long-term outcomes after cruciate ligament reconstruction with either autograft or synthetics suggests no significant differences in failure risk. Autografts were inferior to synthetics with respect to restoring knee joint stability and patient-reported outcome scores, and were also associated with more postoperative complications.

Adenovirus-mediated transduction with Histone Deacetylase 4 ameliorates disease progression in an osteoarthritis rat model.

BACKGROUND: Downregulation of histone deacetylase-4 (HDAC4) contributes to cartilage degeneration in osteoarthritis (OA) because it promotes upregulation of runt-related transcription factor-2 (Runx-2) and osteoarthritis-related genes. The effect of HDAC4 upregulation on cartilage damage in OA remains unknown. METHODS: Rat chondrocytes were infected with Ad-GFP or Ad-HDAC4-GFP for 48 h, stimulated with interleukin-1ß (IL-1ß, 10 ng/mL) for 24 h, and then harvested for RT-qPCR. Male Sprague-Dawley rats in 3 groups were given anterior cruciate ligament transection (ACLT) or sham operation, and knee injections with different adenovirus (Ad) vectors at 48 h after surgery and every 3 weeks thereafter: ACLT+Ad-GFP (n = 17); ACLT+Ad-HDAC4-GFP (n = 20); and sham+Ad-GFP (n = 15). Three ACLT-Ad-HDAC4-GFP rats were sacrificed at different times to examine the expression of HDAC4. Two ACLT-Ad-GFP rats and two ACLT-Ad-HDAC4-GFP rats were euthanized at week-2; articular cartilage was harvested and expression of HDAC4 was determined by RT-qPCR. All other rats were euthanized at week-8. Cartilage damage and OA progression was assessed using radiography, fluorescence molecular tomography (FMT), histology, immunohistochemistry (IHC), ELISA, and RT-qPCR. RESULTS: Overexpression of HDAC4 in chondrocytes stimulated by IL-1ß reduced the levels of Runx-2, MMP-13, and Collagen X, but increased the levels of Collagen II and Aggrecan. Upregulation of HDAC4 reduced osteophyte formation and cartilage damage, and increased articular cartilage anabolism. CONCLUSION: HDAC4 attenuated articular cartilage damage by repression of Runx-2, MMP-13, and collagen X and induction of collagen II and ACAN in this rat model of OA. Upregulation of HDAC4 may provide chondroprotection in OA patients.

Contribution of IL-1ß, 6 and TNF-α to the form of post-traumatic osteoarthritis induced by "idealized" anterior cruciate ligament reconstruction in a porcine model.

BACKGROUND: It has been noted that anterior cruciate ligament (ACL) injury-induced cartilage degeneration is the key risk factor for post-traumatic osteoarthritis (PTOA). However, whether the cartilage degeneration after ACL injury is caused by inflammation, abnormal biomechanics or both remains largely unknown, as there has been no animal model for separating the two factors so far. METHODS: Eighteen-month-old female mini-pigs were divided into an "idealized" anterior cruciate ligament reconstruction (IACLR) group and a control group (n = 16 limbs per group). Real-time PCR, safranine O staining and indian ink staining were performed to verify whether animal models were successfully established or not. Multiple linear regression analysis was used to evaluate the correlation between levels of the inflammatory factors (including interferon [IFN]-γ, interleukin [IL]-1ß, IL-4, IL-6, IL-8, IL-10, IL-12 and tumor necrosis factor [TNF]-α measured by the Luminex method) and changes in cartilage histology (quantified by morphological scoring) after surgery. RESULTS: A significant OA cartilage damage with increased MMP-1, MMP-13 mRNA levels and reduced aggrecan mRNA/protein levels was observed in IACLR groups. As a result, the IACLR gross morphology score was dramatically increased than control. Moreover, IACLR significantly increased the levels of IL-1ß, IL-4, IL-6 and TNF-α in the synovial fluid of the knee. Most importantly, a close relationship was found between IL-1ß, IL-6 and TNF-α concentrations and morphological score of PTOA, respectively. CONCLUSION: These results demonstrated that inflammatory factors are independently responsible for the onset of PTOA.