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Abstracts / Bone 48 (2011) S261–S265
outgrowth regulation. Since osteophytic growth is characteristic for the degenerative joint disease, we hypotheses that synovial membrane is the site of the molecular factors production which are proved to be stimulative for osteophytic growth. Material and methods: The study was performed on series of 14 synovial tissue samples collected during knee joint surgery of the individuals undergoing total joint replacement. As a control samples we used synovial tissue from the autopsy cases, without any degenerative or inflamatory changes in knee joint tissue. The tissue samples were embedded in parafin, cut on 5 micrometers thin slices and immunostained with specific antibodies against defined BMPs and BMPs antagonists. Results: BMP −2 and −4 were not detected by immunohistochemistry in OA synovial tissue. This finding was additionally proved by postive (positively stained subependimal cells in mouse brain) and negative control (negatively stained synovial cells in immunoprotocol without primary antibodies). BMP −7 was strongly expressed in the lining layer cells (intracytoplasmatic brown staining). Noggin and chordin were expressed in both layers of the synovial epithelium and also in the stromal fibroblasts and extracellular matrix. Noggin expression was found in higher percentage of the cells when compared to chordin. Gremlin was expressed in the lining layer of the synovial epithelium and also inside the blood vessels. Imunostaining for gremlin was detected as a membranous staining. Distribution of the follistatin was not equally expressed in all the samples. But it was regularly positive in the wall of the blood vessels. Conclusion: The BMPs were differentially expressed in synovial tissue from normal and OA knee joint. In OA synovial membrane BMP −2 and −4 were negative in contrast to BMP −7 which is strongly expressed in the lining layer cells. BMP antagonists were also differentially expressed in OA synovial tissue: gremlin and noggin were predominantly expressed in the lining layer in contrast to follistatin and chordin which were predominantly expressed in perivascular synovial tissue fibroblasts. This article is part of a Special Issue entitled ECTS 2011. Disclosure of interest: None declared.
doi:10.1016/j.bone.2011.03.648
PP518-M (Recipient of a 2011 ECTS/IBMS Travel Award) Contribution of statistical shape model and predefined geometry parameters in prediction of hip osteoarthritis M.C. Castano Betancourt a,⁎, J. Van Meurs a, S. Bierma Zeinstra b, F. Rivadeneira a, A. Hofman c, H. Weinans d, A. Uitterlinden a, E. Waarsing d a Internal Medicine, Erasmus MC, Rotterdam, Netherlands b General Practice, Erasmus MC, Rotterdam, Netherlands c Epidemiology, Erasmus MC, Rotterdam, Netherlands d Orthopaedics, Erasmus MC, Rotterdam, Netherlands Abstract: Hip morphology variation has been associated with hip osteoarthritis (HOA). Specific aspects of hip geometry are commonly quantified through predefined geometry measures (PGM), typically lengths, widths and angles. Alternatively, Active Shape Modeling (ASM) quantifies patterns of total variation in hip shape (modes). Our aim is to determine how much these hip morphology parameters add to prediction of HOA in addition to known clinical OA risk factors (age, gender, BMI and joint damage at baseline Kellgren–Lawrence (KL)). Methods: The population is part from the prospective population-based cohort: Rotterdam study. Baseline and follow up radiographs were scored for HOA using KL. Only hips without osteoarthritis (KL ≤ 1) at baseline were selected. Incident OA was defined as KL ≥ 2 or THR at two visits (mean 5.5 and 11 years). ASM generated 24 modes. Additionally, 12 geometry measures were determined (n = 1283 hips). The association between hip morphology and incident HOA was analyzed using Generalized Estimating Equations adjusting for age, gender, BMI and KL-grade where applicable. Prediction of HOA was quantified using areas under the receiver operator characteristics (AUC–ROC). Results: At first follow up (5.5. years) 132 hips had incident OA. In total 3 PGM (Neck Width (NW), triangular index (TI), pelvic width (PW)) and 2 statistical shape modes (modes 5 and 9) were significant predictors of OA (p = 3.61*10−7, 1.27*10−8, 0.003 and 6.08*10−7, 0.002 respectively). Hip morphology (shape and geometry) alone demonstrated moderate discriminative value for incident HOA (AUC: 0.64). Prediction of HOA was high for known clinical risk factors including KL (AUC: 0.80). PGM and ASM added 2% and 4% respectively to the prediction of HOA (AUC: 0.82, 0.84). During a longer follow up time (11 years), 197 incident HOA cases were present. TI, NW, Spherical sector and mode 12 were significant predictors of OA (p = 3.38*10−7, 1.48*10−5, 0.002 and mode 12 p = 0.001). Also here, PGM and ASM added little discriminative value to the known OA clinical risk factors (AUC: 0.73, 0.74 versus 0.72 clinical factors alone). Conclusions: Variation in hip morphology measured by ASM and PGM contributed little in prediction of HOA to known clinical risk factors. The predictive power of hip geometry and known clinical risk factors decreased with a longer follow up. Wider femoral neck, increased acetabular roof and deformation of the femoral head might appear as early signs of HOA. This article is part of a Special Issue entitled ECTS 2011. Disclosure of interest: None declared.
doi:10.1016/j.bone.2011.03.649
PP519-T Monocyte chemoattractant protein-1 is strongly expressed during the process of wearing of metal on metal hip prosthesis M. Montesi a,⁎, A. Beraudi a, S. Stea a, S. Falcioni a, S. Squarzoni b, F. Traina c, A. Toni c a Laboratorio Tecnologia Medica, Istituto Ortopedico Rizzoli, Bologna, Italy b Istituto di Genetica Molecolare, CNR, Bologna, Italy c Ortopedia-Traumatologia e Chirurgia Protesica e Dei Reimpianti D'anca e di Ginocchio, Istituto Ortopedico Rizzoli, Bologna, Italy Abstract: Monocyte chemoattractant protein-1 (MCP-1) is a potent chemoattractant for monocytes and lymphocytes and can be secreted by osteoblasts exposed to particulate wear debris increasing osteoclastogenesis, together with the action of other cytokines. The aim of this study was to investigate whether there are differences in the synovial fluid MCP-1 expression among metal-on-metal, ceramic-on-ceramic hip prosthesis and osteoarthritis patients used as control. We studied 19 patients with painful metal on metal CoCrMo hip prosthesis (Group 1), 14 with noising ceramic on ceramic Alumina (Biolox forte) (Group 2), and 7 osteoarthritis patients receiving primary total hip arthroplasty as control (Group 3). The presence of perisprosthetic osteolysis was evaluated on conventional X-rays. Wear particles were quantified in synovial fluid at SEM and EDX analyses. We excluded patients with any major acute or chronic medical disease, with rheumatoid arthritis or fractures and those who were receiving any therapy that may affect bone or calcium metabolism. Synovial fluid was aspirated with a syringe and stored at −20 °C. The samples were centrifuged to exclude cell components and stored at − 20 °C until analysis. Before analysis, the viscosity of synovial fluid was reduced by treatment with bovine testis hyaluronidase. The levels of MCP-1 in the synovial fluid were measured by the use of high sensitivity enzyme-linked immunosorbent assay kit (DIACLONE, France). The analysis of MCP-1 expression in synovial fluid showed a mean value of about 4100 pg/ml in Group 1, 1800 pg/ml in Group 2 and 500 pg/ml in Group 3. All these differences were statistically significant (Kruskal–Wallis p = 0.003). However, there were no correlations between MCP-1 expression and perisprosthetic osteolysis grade and with wear particles presence. These results confirm the presence of a mild inflammatory reaction typical of ceramic wear process and of a strong inflammatory response characteristic of metal on metal wearing. This article is part of a Special Issue entitled ECTS 2011. Disclosure of interest: None declared.
doi:10.1016/j.bone.2011.03.650
PP520-S Effect of articular cartilage on the strain characteristics of subchondral bone P. Kumar ⁎ Bay of Plenty DHB, Tauranga, New Zealand Abstract: Background: Biomechanically, articular cartilage and subchondral bone are two very distinct entities. In the juxta-articular region, they are biomechanically coupled. Mechanical stress and strain that pass through this biomechanical coupling will exhibit distinctive behavior. Mechanical strain has been shown to be the primary stimulus for bone remodeling and growth. The purpose of this study was to investigate the effect of biomechanically adhered articular cartilage on the mechanical strain engendered by subchondral bone and its effects on the structural and mechanical adaptation of subchondral bone. Methods: We used three finite element analysis models, (A) a 3-dimensional human Hip model, (B) a 3-dimensional human knee model and (C) an ideal model, to investigate the effect of the biomechanical coupling of articular cartilage and subchondral bone on the mechanical strain engendered by subchondral bone. Results: The presence of biomechanically coupled articular cartilage at the joint surface amplified the strain intensity engendered by the subchondral bone. The amplification factor was approximately 42. In the presence of articular cartilage, compressive joint stress engenders preferentially tangential principal strain at the subchondral bone. Conclusions: Biomechanically adhered articular cartilage amplifies and transforms the strain characteristics of subchondral bone. This change in strain characteristics, in accordance with bone remodeling, can explain the unique anatomical and material properties of subchondral bone. Further extrapolation provides an explanation for primary stiffening of subchondral bone related to primary osteoarthritis. Clinical relevance: This study provides an explanation for the distinctive architecture of subchondral bone. In addition, this study is a step toward understanding the etiopathogenesis of primary osteoarthritis. This article is part of a Special Issue entitled ECTS 2011. Disclosure of interest: None declared.
doi:10.1016/j.bone.2011.03.651