Increase in cartilage degeneration in all knee compartments after failed ACL reconstruction at 4 years of follow-up.

PURPOSE: Degeneration of the cartilage after anterior cruciate ligament reconstruction (ACL-R) is known, and further deterioration can be expected in patients with tunnel malplacement or partial meniscal resection. It was hypothesized that there is a significant increase in cartilage degeneration after failed ACL-R. MATERIAL AND METHODS: Isolated ACL revision surgery was performed in 154 patients at an interval of 46 ± 33 months (5-175 months) between primary and revision surgery. Cartilage status at the medial, lateral femorotibial, and patellofemoral compartments were assessed arthroscopically during primary and revision ACL-R in accordance with the Outerbridge classification. Tunnel placement, roof angle, and tibial slope was measured using anteroposterior and lateral radiographic views. RESULTS: Cartilage degeneration increased significantly in the medial femorotibial compartment, followed by the lateral and patellofemoral compartments. There was a correlation between both cartilage degeneration in the patellofemoral compartment (PFC) (rs = 0.28, p = 0.0012) and medial tibial plateau (Rs = 0.24, p = 0.003) in relation to the position of tibial tunnel in the frontal plane. Worsening of the cartilage status in the medial femorotibial compartment, either femoral or tibial, was correlated with the tibial aperture site in the lateral view (Rs = 0.28, p < 0.001). Cartilage degeneration in the lateral compartment of the knee, on both femoral or tibial side, was inversely correlated with the femoral roof angle (Rs = -0.1985, p = 0.02). Meniscal tears, either at the medial or lateral site or at both, were found in 93 patients (60%) during primary ACL-R and increased to 132 patients (86%) during revision ACL-R. DISCUSSION: Accelerated cartilage degeneration and high prevalence of meniscal lesions are seen in failed ACL-R. Tunnel placement showed significant impact on cartilage degeneration and may partially explain the increased risk of an inferior outcome when revision surgery is required after failed primary ACL-R. LEVEL OF EVIDENCE: Level IV-retrospective cohort study.

Joint effusion, anteroposterior stability, muscle strength and degree of patellofemoral osteoarthritis significantly impact outcome following revision ACL reconstruction.

PURPOSE: Effusion, impaired muscle function and knee instability are considered as some of the most important factors effecting outcome following anterior cruciate ligament reconstruction (ACL-R) but the impact on revision ACL-R remains unclear. It was hypothesized that these factors will significantly worsen clinical outcome following revision ACL-R. METHODS: Seventy knees (13 female and 57 male) were followed retrospectively after revision ACL-R at a mean follow-up of 47.8 ± 20.7 months. Clinical examination was based on the International Knee Documentation Evaluation Form-2000 (IKDC), Tegner activity scale. Instrumented measurement of anterior tibial translation was performed using the Rolimeter® (DJO Global, Freiburg, Germany). Bilateral circumference of the thigh was measured 10 and 20 cm proximal to the medial joint space. Cartilage was assessed according to Outerbridge classification during both primary and revision ACL-R. RESULTS: Tegner activity scale decreased significantly from 7.8 ± 1.4 points at primary ACL-R to 7 ± 1.8 points at revision ACL-R, and 5.8 ± 1.7 points at the time of follow up (p < 0.001). Joint effusion (r = - 0.47, p < 0.01) and side to side differences in single leg hop test (r = - 0.48, p < 0.1) significantly correlated with inferior outcome. Cartilage lesions were found in 67% of the patients at the time of revision ACL-R compared to 38% at the time of primary ACL-R. According to the IKDC classification A was graded in three patients (4.3%), B in 35 (50%), C in 29 (41.4%) and D in three (4.3%). Joint effusion was measured in 35% of patients at the time of follow-up. Degeneration at the patellofemoral compartment of > grad 2 was responsible for IKDC grade C and D (p = 0.035). Instrumented anteroposterior site-to-site difference of ≥3 mm showed significant impact on clinical outcome (p < 0.019). CONCLUSION: The study has shown that chronic effusion, quadriceps dysfunction, cartilage lesions especially at the patellofemoral compartment and side to side difference in anteroposterior stability significantly influences patient outcome after revision ACL-R. These factors require special attention when predicting patient's outcome. LEVEL OF EVIDENCE: Level-IV, case-controlled study.

Histological and cell biological characterization of dissected cartilage fragments in human osteochondritis dissecans of the femoral condyle.

INTRODUCTION: Osteochondritis dissecans (OCD) within the weight-bearing femoral condyle carries a high risk of osteoarthritis. The definitive pathogenetic cause is unclear. Therefore biochemical and cellular features of OCD were analyzed and compared to macroscopically normal cartilage of the same joint surface. MATERIALS AND METHODS: Dissected fragments from 14 patients and biopsies of normal cartilage from the intercondylar notch as controls were harvested at arthroscopy. Staining with safranin O to monitor proteoglycan content, alkaline phosphatase activity, and immunohistochemistry with mouse monoclonal antibodies to collagen types I, II, and X. Chondrocytes were isolated for RT-PCR to detect GAPDH, collagen types I, II, X, aggrecan, TGF-beta, BMP-7, bFGF, VEGF and IL-1. RESULTS: The dissected cartilage displayed significant variability. Apart from normal cartilage matrix components also atypical molecules such as collagen type X and alkaline phosphatase were detected at the tidemark but also across the entire dissecate, suggesting chondrocyte hypertrophy. Extended fibrous degeneration associated with collagen type I deposition was observed at the surface and may indicate chondrocyte dedifferentiation. Viable cells could be extracted from OCD and notch. Both expressed similar mRNA levels for matrix molecules, growth factors, and interleukin-1 (IL-1), however significantly more Col X mRNA was detected in dissecates. CONCLUSION: Histology suggests focal alteration of cartilage matrix originating from the basis of the joint cartilage, potentially the mineralized layer or subchondral bone. The molecular analysis indicates a disorganization of cartilage homeostasis across the joint accompanied by embryogenetic processes. The surprisingly high viability and quality of the extracted cells suggests a still preserved intrinsic repair capacity of those vital dissecates.

Synovial fibroblasts and synovial macrophages from patients with rheumatoid arthritis and other inflammatory joint diseases show chromosomal aberrations.

Chromosomal aberrations were investigated in nuclei extracted from synovial tissue and first-passage synovial fibroblasts (P-1 SFB, 98% enrichment) or macrophages (P-1 Mphi) from patients with rheumatoid arthritis (n=10). The findings were compared with those in other rheumatic diseases (osteoarthritis, n=14; reactive arthritis, n=1), as well as with those in chronic obstructive pulmonary disease (n=8). Controls were paired peripheral blood lymphocytes from arthritic patients, synovial tissue or SFB/Mphi from joint trauma/normals (n=9), and peripheral blood monocytes from normal donors (n=10). GTG banding of metaphase chromosomes and interphase fluorescence in situ hybridization with centromere-specific probes were used. Comparable chromosomal aberrations were observed in synovial tissue and P-1 SFB of patients with rheumatoid arthritis, osteoarthritis, and reactive arthritis (polysomy 7 and aneusomies of chromosomes 4, 8, 9, 12, and 18). Notably, aneusomies of chromosomes 4, 6, 7, 8, 9, 11, 12, and/or X were also detected in P-1 synovial Mphi from rheumatoid arthritis (90% of the cases), osteoarthritis (93%), and reactive arthritis (1/1), as well as bronchial Mphi from chronic obstructive pulmonary disease (25%). No aberrations were detected in paired peripheral blood lymphocytes (except for one osteoarthritis case with a karyotype 45,X[10]/46,XX[17]), or in peripheral blood monocytes and synovial tissue of normals/joint trauma. Because Mphi aberrations were common to chronic joint and pulmonary disease, chronic inflammatory stress may induce chromosomal aberrations with potential functional relevance in local mesenchymal cells and infiltrating leukocytes in an organ-independent fashion.