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Anisotropy, inhomogeneity, and tension-compression nonlinearity of human glenohumeral cartilage in finite deformation.

The tensile and compressive properties of human glenohumeral cartilage were determined by testing 120 rectangular strips in uniaxial tension and 70 cylindrical plugs in confined compression, obtained from five human glenohumeral joints. Specimens were harvested from five regions across the articular surface of the humeral head and two regions on the glenoid. Tensile strips were obtained along two orientations, parallel and perpendicular to the split-line directions. Two serial slices through the thickness, corresponding to the superficial and middle zones of the cartilage layers, were prepared from each tensile strip and each compressive plug. The equilibrium tensile modulus and compressive aggregate modulus of cartilage were determined from the uniaxial tensile and confined compression tests, respectively. Significant differences in the tensile moduli were found with depth and orientation relative to the local split-line direction. Articular cartilage of the humeral head was significantly stiffer in tension than that of the glenoid. There were significant differences in the aggregate compressive moduli of articular cartilage between superficial and middle zones in the humeral head. Furthermore, tensile and compressive stress-strain responses exhibited nonlinearity under finite strain, while the tensile modulus differed by up to two orders of magnitude from the compressive aggregate modulus at 0% strain, demonstrating a high degree of tension-compression nonlinearity. The complexity of the mechanical properties of human glenohumeral cartilage was exposed in this study, showing anisotropy, inhomogeneity, and tension-compression nonlinearity within the same joint. The observed differences in the tensile properties of human glenohumeral cartilage suggest that the glenoid may be more susceptible to cartilage degeneration than the humeral head.

Aged↗

A transversely isotropic, transversely homogeneous microstructural-statistical model of articular cartilage.

Articular cartilage is a multi-phasic, composite, fibre-reinforced material. Therefore, its mechanical properties are determined by the tissue microstructure. The presence of cells (chondrocytes) and collagen fibres within the proteoglycan matrix influences, at a local and a global level, the material symmetries. The volumetric concentration and shape of chondrocytes, and the volumetric concentration and spatial arrangement of collagen fibres have been observed to change as a function of depth in articular cartilage. In particular, collagen fibres are perpendicular to the bone-cartilage interface in the deep zone, their orientation is almost random in the middle zone, and they are parallel to the surface in the superficial zone. The aim of this work is to develop a model of elastic properties of articular cartilage based on its microstructure. In previous work, we addressed this problem based on Piola's notation for fourth-order tensors. Here, mathematical tools initially developed for transversely isotropic composite materials comprised of a statistical orientation of spheroidal inclusions are extended to articular cartilage, while taking into account the dependence of the elastic properties on cartilage depth. The resulting model is transversely isotropic and transversely homogeneous (TITH), the transverse plane being parallel to the bone-cartilage interface and the articular surface. Our results demonstrate that the axial elastic modulus decreases from the deep zone to the articular surface, a result that is in good agreement with experimental findings. Finite element simulations were carried out, in order to explore the TITH model's behaviour in articular cartilage compression tests. The force response, fluid flow and displacement fields obtained with the TITH model were compared with the classical linear elastic, isotropic, homogeneous (IH) model, showing that the IH model is unable to predict the non-uniform behaviour of the tissue. Based on considerations that the mechanical stability of the tissue depends on its topological and microstructural properties, our long-term goal is to clearly understand the stability conditions in topological terms, and the relationship with the growth and remodelling mechanisms in the healthy and diseased tissue.

Cartilage, Articular↗

Site specific changes in gene expression and cartilage metabolism during early experimental osteoarthritis.

OBJECTIVES: To characterize the molecular events underlying cartilage injury in the early phase of mono-iodoacetate-induced osteoarthritis (OA) in rats. METHODS: Experimental osteoarthritis was induced by intra-articular injection of 0.03mg mono-iodoacetate (MIA) in Wistar rats. Animals were killed 2, 5, 10, 15 and 20 days post-injection. Synovial tissue and standardized biopsies from different areas of knee cartilage were examined. Proteoglycan synthesis ((35)S incorporation) and gelatinase activities (zymography), semi-quantitative RT-PCR and immunohistochemistry for IL1beta, iNOS, COX2 and PPARgamma, were performed on these samples. RESULTS: Changes in proteoglycan synthesis and gelatinase activities were time and site-dependent. Proteoglycan synthesis inhibition was maximal by day 2 while the highest gelatinase activities were observed at day 5. Central part of patella and posterior plateaus and condyles, i.e. the weight-bearing cartilage areas, were the most affected. IL1beta and iNOS transcripts were induced early in cartilage at time of maximal proteoglycan synthesis inhibition, especially in weight-bearing areas. COX-2 was slightly up-regulated whereas PPARgamma gene expression remained unchanged. Gene expression profile in synovium paralleled that of cartilage, except for PPARgamma which was up-regulated at day 15 and 20. Immunostaining for IL1beta and iNOS showed that proteins were located in diseased cartilage areas at early stage of the experimental OA (day 2). At later time-points (day 20), IL1beta and iNOS were expressed in perilesional areas whereas immunostaining became below control level for COX-2 and PPARgamma. CONCLUSIONS: Time-dependent degradation of cartilage after injection of low dose of MIA (0.03mg) into rat knee joint can be related to early loss of proteoglycan anabolism, increased gelatinase activities and expression of IL1beta and downstream inflammatory genes. Increased susceptibility to MIA in weight-bearing areas of cartilage further indicate that MIA-induced experimental OA is a relevant model to study not only metabolical but also biomechanical aspects of human OA.

Animals↗

Expression and localization of connective tissue growth factor (CTGF/Hcs24/CCN2) in osteoarthritic cartilage.

OBJECTIVE: The investigation of the expression and localization of connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24/CCN family member 2 (CTGF/Hcs24/CCN2) in normal and osteoarthritic (OA) cartilage, and quantification of CTGF/Hcs24-positive cells. METHODS: Cartilage samples of patients (n=20) with late stage OA were obtained at total joint replacement surgery. Morphologically normal cartilage was harvested for comparison purposes from the femoral heads of 6 other patients with femoral neck fracture. Paraffin-embedded sections were stained by Safranin O. The severity of the OA lesions was divided into four stages (normal, early, moderate, and severe). The localization of protein and mRNA for CTGF/Hcs24 was investigated by immunohistochemistry and in situ hybridization, respectively. The population of CTGF/Hcs24-positive chondrocytes in OA cartilage and chondro-osteophyte was quantified by counting the number of the cells under light microscopy. RESULTS: Signals for CTGF/Hcs24 were detected in a small percentage of chondrocytes throughout the layers of normal cartilage. In early stage OA cartilage, the CTGF/Hcs24-positive chondrocytes were localized mainly in the superficial layer. In moderate to severe OA cartilage, intense staining for CTGF/Hcs24 was observed in proliferating chondrocytes forming cell clusters next to the cartilage surface. In chondro-osteophyte, strong signals were found in the chondrocytes of the proliferative and hypertrophic zones. CONCLUSION: CTGF/Hcs24 expression was detected in both normal and OA chondrocytes of human samples. The results of the current study suggested that expression of CTGF/Hcs24 was concomitant with development of OA lesions and chondrocyte differentiation in chondro-osteophyte.

Adult↗

Histopathological correlation of cartilage swelling detected by magnetic resonance imaging in early experimental osteoarthritis.

OBJECTIVE: We previously reported that an increase of cartilage thickness is the earliest measurable change by magnetic resonance imaging (MRI) in early stages of experimental osteoarthritis (OA). Our present objective was to study the microscopic translation of this finding in order to know whether the cartilage thickness increment represents the earliest structural damage or whether it alternatively constitutes a non-progressive reversible phenomenon. METHODS: OA was induced by partial medial meniscectomy in rabbits. Normal and sham-operated animals were used as controls. Gross and microscopic cartilage changes were sequentially assessed after surgery at 0, 2, 4, 6, 8, 10 and 52 weeks, and compared to MRI findings. RESULTS: The swelling of cartilage detected by MRI correlated with depletion in matrix proteoglycans and cellular loss, which were closely related to the progression of OA at the earliest stages. Abnormalities of the cartilage structure appeared only in advanced OA. CONCLUSION: Cartilage swelling detected by MRI is due to proteoglycan depletion and represents the earliest abnormality in OA. Because it is accompanied by cellular loss, it cannot be merely attributed to surgical trauma and represents true tissue damage. The biological meaning of volume variations detected by MRI should be assessed carefully taking into account the disease stage as an increase in cartilage height also reflects cartilage damage and not a reparative process.

Animals↗

A review of the effects of insulin-like growth factor and platelet derived growth factor on in vivo cartilage healing and repair.

Growth factors may enhance current cartilage repair techniques via multiple mechanisms including recruitment of chondrogenic cells (chemotaxis), stimulation of chondrogenic cell proliferation (mitogenesis) and enhancement of cartilage matrix synthesis. Two growth factors that have been studied in cartilage repair are insulin-like growth factor (IGF) and platelet derived growth factor (PDGF). IGF plays a key role in cartilage homeostasis, balancing proteoglycan synthesis and breakdown. Incorporating IGF into a fibrin clot placed in an equine cartilage defect improved the quality and quantity of repair tissue and reduced synovial inflammation. PDGF is a potent mitogenic and chemotactic factor for all cells of mesenchymal origin, including chondrocytes and mesenchymal stem cells. Resting zone chondrocytes cultured with PDGF demonstrated increased cell proliferation and proteoglycan production, while maturation of these cells along the endochondral pathway was inhibited. Pretreating chondrocytes with PDGF promotes heterotopic cartilage formation in the absence of any mechanical stimulus. PDGF has also been shown to be a potent stimulator of meniscal cell proliferation and migration. These studies and others suggest a potential role for these potent biological regulators of chondrocytes in cartilage repair. More work needs to be performed to define their appropriate dosing and the optimum delivery method. Combining tissue growth factors with a biological matrix can provide a physical scaffold for cell adhesion and growth as well as a means to control the release of these potent molecules. This could result in biological devices that enhance the predictability and quality of current cartilage repair techniques.

Animals↗

Articular cartilage MR imaging and thickness mapping of a loaded knee joint before and after meniscectomy.

OBJECTIVE: We describe a technique to axially compress a sheep knee joint in an MRI scanner and measure articular cartilage deformation. As an initial application, tibial articular cartilage deformation patterns after 2 h of static loading before and after medial meniscectomy are compared. METHODS: Precision was established for repeated scans and repeated segmentations. Accuracy was established by comparing to micro-CT measurements. Four sheep knees were then imaged unloaded, and while statically loaded for 2 h at 1.5 times body weight before and after medial meniscectomy. Images were obtained using a 3D gradient echo sequence in a 4.7 T MRI. Corresponding 3D cartilage thickness models were created. Nominal strain patterns for the intact and meniscectomized conditions were compared. RESULTS: Coefficients of variation were all 2% or less. Root mean squared errors of MR cartilage thickness measurements averaged less than 0.09 mm. Meniscectomy resulted in a 60% decrease in the contact area (P=0.001) and a 13% increase in maximum cartilage deformation (P=0.01). Following meniscectomy, there were greater areas of articular cartilage experiencing abnormally high and low nominal strains. Areas of moderate nominal strain were reduced. CONCLUSIONS: Medial meniscectomy resulted in increased medial tibial cartilage nominal strains centrally and decreased strains peripherally. Areas of abnormally high nominal strain following meniscectomy correlated with areas that are known to develop fibrillation and softening 16 weeks after medial meniscectomy. Areas of abnormally low nominal strain correlated with areas of osteophyte formation. Studies of articular cartilage deformation may prove useful in elucidating the mechanical etiology of osteoarthritis.

Animals↗

T(2) relaxation time mapping reveals age- and species-related diversity of collagen network architecture in articular cartilage.

OBJECTIVE: The magnetic resonance imaging (MRI) parameter T(2) relaxation time has been shown to be sensitive to the collagen network architecture of articular cartilage. The aim of the study was to investigate the agreement of T(2) relaxation time mapping and polarized light microscopy (PLM) for the determination of histological properties (i.e., zone and fibril organization) of articular cartilage. METHODS: T(2) relaxation time was determined at 9.4 T field strength in healthy adult human, juvenile bovine and juvenile porcine patellar cartilage, and related to collagen anisotropy and fibril angle as measured by quantitative PLM. RESULTS: Both T(2) and PLM revealed a mutually consistent but varying number of collagen-associated laminae (3, 3-5 or 3-7 laminae in human, porcine and bovine cartilage, respectively). Up to 44% of the depth-wise variation in T(2) was accounted for by the changing anisotropy of collagen fibrils, confirming that T(2) contrast of articular cartilage is strongly affected by the collagen fibril anisotropy. A good correspondence was observed between the thickness of T(2)-laminae and collagenous zones as determined from PLM anisotropy measurements (r=0.91, r=0.95 and r=0.91 for human, bovine and porcine specimens, respectively). CONCLUSIONS: According to the present results, T(2) mapping is capable of detecting histological differences in cartilage collagen architecture among species, likely to be strongly related to the differences in maturation of the tissue. This diversity in the MRI appearance of healthy articular cartilage should also be recognized when using juvenile animal tissue as a model for mature human cartilage in experimental studies.

Adult↗

Matrix metalloproteinase-9 expression, tartrate-resistant acid phosphatase activity, and DNA fragmentation in vascular and cellular invasion into cartilage preceding primary endochondral ossification in long bones.

Vascular and cellular invasion into cartilage are essential for endochondral ossification. Recently it has been shown that matrix metalloproteinase-9 (MMP-9)/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. To study vascular and cellular invasion into cartilage preceding primary endochondral ossification in long bones, precursor femurs from 13- to 16-day-old murine embryos were sectioned. Tartrate-resistant acid phosphatase (TRAP) activity, in situ hybridization for matrix metalloproteinase-9 (MMP-9), immunostaining for CD31, and in situ detection of apoptosis (TUNEL) were studied. TRAP activity, MMP-9 mRNA, and CD31 expression were initially detected in the intertrabecular spaces of the perichondral collar, and then in cells migrating into the cartilage. The first cells involved in the primary invasion into cartilage were CD31-positive vascular endothelial cells and MMP-9-positive cells, followed by TRAP-positive cells. At the cartilage-marrow interface, CD31-positive vascular endothelial cells and MMP-9-positive cells were predominant. These results suggest that MMP-9-positive cells cooperate with vascular endothelial cells in cartilage angiogenesis. TUNEL-positive staining was detected on chondrocytes attached to the inner surface of the perichondral collar, and also detected in the area where cartilage was removed. These results suggest that chondrocytes separated from the cartilage matrix may undergo apoptosis.

Acid Phosphatase↗

Hyaline cartilage degenerates after autologous osteochondral transplantation.

OBJECTIVES: Autologous osteochondral grafting is a well-established clinical procedure to treat focal cartilage defects in patients, although basic research on this topic remains sparse. The aim of the current study was to evaluate (1) histological changes of transplanted hyaline cartilage of osteochondral grafts and (2) the tissue that connects the transplanted cartilage with the adjacent cartilage in a sheep model. METHOD: Both knee joints of four sheep were opened surgically and osteochondral grafts were harvested and simultaneously transplanted to the contralateral femoral condyle. The animals were sacrificed after three months and the received knee joints were evaluated histologically. RESULTS: Histological evaluation showed a complete ingrowth of the osseous part of the osteochondral grafts. A healing or ingrowth at the level of the cartilage could not be observed. Histological evaluation of the transplanted grafts according to Mankin revealed significantly more and more severe signs of degeneration than the adjacent cartilage, such as cloning of chondrocytes and irregularities of the articular surface. CONCLUSION: We found no connecting tissue between the transplanted and the adjacent cartilage and histological signs of degeneration of the transplanted hyaline cartilage. In the light of these findings, long-term results of autologous osteochondral grafts in human beings have to be followed critically.

Animals↗

Heterogeneous three-dimensional strain fields during unconfined cyclic compression in bovine articular cartilage explants.

Articular cartilage provides critical load-bearing and tribological properties to the normal function of diarthrodial joints. The unique properties of cartilage, as well as heterogeneous deformations during mechanical compression, are due to the nonuniform microstructural organization of tissue components such as collagens and proteoglycans. A new cartilage deformation by tag registration (CDTR) technique has been developed by the authors to determine heterogeneous deformations in articular cartilage explants. The technique uses a combination of specialized MRI methods, a custom cyclic loading apparatus, and image processing software. The objective of this study was to use the CDTR technique to document strain patterns throughout the volume of normal bovine articular cartilage explants during cyclic unconfined compression at two physiologically-relevant applied normal stress levels (1.29 and 2.57 MPa). Despite simple uniaxial cyclic compressive loading with a flat, nonporous indenter, strain patterns were heterogeneous. Strains in the thickness direction (E(yy)) were compressive, varied nonlinearly with depth from the articular surface from a maximum magnitude of 11% at the articular surface, and were comparable despite a 2-fold increase in applied normal stress. Strains perpendicular to the thickness direction (E(xx) and E(zz)) were tensile, decreased linearly with depth from the articular surface from a maximum of 7%, and increased in magnitude 2.5-fold with a 2-fold increase in applied normal stress. Shear strains in the transverse plane (E(xz)) were approximately zero while shear strains in the other two planes were much larger and increased in magnitude with depth from the articular surface, reaching maximum magnitudes of 2% at the articular cartilage-subchondral bone interface. In general, strain patterns indicated that cartilage osteochondral explants exhibited depth-dependent nonisotropic behavior during uniaxial cyclic loading. These results are useful in verifying constitutive formulations of articular cartilage during cyclic unconfined compression and in characterizing the micromechanical environment likely experienced by individual chondrocytes throughout the tissue volume.

Animals↗

Vascular endothelial growth factor isoforms and their receptors are expressed in human osteoarthritic cartilage.

To assess the possible involvement of vascular endothelial growth factor (VEGF) in the pathology of osteoarthritic (OA) cartilage, we examined the expression of VEGF isoforms and their receptors in the articular cartilage, and the effects of VEGF on the production of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in OA chondrocytes. Reverse transcriptase-polymerase chain reaction analyses demonstrated that mRNAs for three VEGF isoforms (VEGF(121), VEGF(165), and VEGF(189)) are detectable in all of the OA and normal (NOR) cartilage samples. However, the mRNA expression of their receptors (VEGFR-1 = Flt-1, VEGFR-2 = KDR and neuropilin-1) was recognized only in the OA samples. The protein expression of VEGFR-1 and VEGFR-2 in OA chondrocytes was also demonstrated by immunohistochemistry of the OA cartilage tissue and cultured OA chondrocytes. In situ hybridization and immunohistochemistry indicated that VEGF is expressed in the chondrocytes in the superficial and transitional zones of OA cartilage. A linear correlation was obtained between VEGF immunoreactivity and Mankin scores in the cartilage (r = 0.906, P < 0.001). The production levels of VEGF determined by enzyme-linked immunosorbent assay were significantly 3.3-fold higher in OA than in NOR samples (P < 0.001). Among MMP-1, -2, -3, -7, -8, -9, and -13, TIMP-1 and -2 measured by their sandwich enzyme immunoassay systems, the production of MMP-1 and MMP-3 but not TIMP-1 or TIMP-2 was significantly enhanced by the treatment of cultured OA chondrocytes with VEGF (P < 0.05), whereas no such effect was obtained with cultured NOR chondrocytes. These results demonstrate that VEGF and its receptors are expressed in OA cartilage, and suggest the possibility that VEGF is implicated for the destruction of OA articular cartilage through the increased production of MMPs.

Aged↗

Effects of warm ischemia and cryopreservation on cartilage viability of tracheal allografts.

BACKGROUND: For clinical use of a cryopreserved tracheal allograft, it is important to evaluate cartilage viability. We assessed cell viability of the cartilage in a cryopreserved tracheal allograft by measurement of Na2 35SO4 incorporation. We also investigated the effects of warm ischemic time on tracheal cartilage viability. METHODS: The tracheas from Lewis rats were harvested and preserved at different warm ischemic times from cardiac death to preservation (0, 1, 2, 4, 6, 9, and 12 hours, each group n = 8). The cartilage was labeled with 4 muCi/mL of Na2 35SO4. The specimen was hydrolyzed in 0.5 mol/L NaOH, and a solution of the extracts was then counted by liquid scintillation counter. Tracheas were transplanted into Brown Norway rats. RESULTS: 35Sulfur incorporation in the cartilage decreased as warm ischemic time increased. In addition, 35Sulfur incorporation decreased from 76% to 67% after cryopreservation. Histologic examinations of the normal tracheal cartilage before preservation and after thawing were done in all the groups. After transplantation, the cartilage had severe fibrous changes, and its layer was almost nonobservable in the 9- and 12-hour groups. CONCLUSIONS: The viability of the tracheal cartilage decreased with warm ischemic time and from 76% to 67% after cryopreservation. In the rat tracheal transplantation model, a cryopreserved tracheal allotransplant could be done safely with a graft that was cryopreserved within 6 hours of warm ischemic time.

Animals↗

Quantitative spatially resolved measurements of mass transfer through laryngeal cartilage.

The scanning electrochemical microscope (SECM) is a scanned probe microscope that uses the response of a mobile ultramicroelectrode (UME) tip to determine the reactivity, topography, and mass transport characteristics of interfaces with high spatial resolution. SECM strategies for measuring the rates of solute diffusion and convection through samples of cartilage, using amperometric UMEs, are outlined. The methods are used to determine the diffusion coefficients of oxygen and ruthenium(III) hexamine [Ru(NH3)6(3+)] in laryngeal cartilage. The diffusion coefficient of oxygen in cartilage is found to be approximately 50% of that in aqueous electrolyte solution, assuming a partition coefficient of unity for oxygen between cartilage and aqueous solution. In contrast, diffusion of Ru(NH3)6(3+) within the cartilage sample cannot be detected on the SECM timescale, suggesting a diffusion coefficient at least two orders of magnitude lower than that in solution, given a measured partition coefficient for Ru(NH3)6(3+) between cartilage and aqueous solution, Kp = [Ru(NH3)6(3+)]cartilage/[RU(NH3)6(3+)]solution = 3.4 +/- 0.1. Rates of Ru(NH3)6(3+) osmotically driven convective transport across cartilage samples are imaged at high spatial resolution by monitoring the current response of a scanning UME, with an osmotic pressure of approximately 0.75 atm across the slice. A model is outlined that enables the current response to be related to the local flux. By determining the topography of the sample from the current response with no applied osmotic pressure, local transport rates can be correlated with topographical features of the sample surface, at much higher spatial resolution than has previously been achieved.

Animals↗

Contribution of meniscal extrusion and cartilage loss to joint space narrowing in osteoarthritis.

OBJECTIVE: This study was undertaken to determine the contribution of meniscal extrusion and cartilage loss to joint space narrowing on conventional radiographs by correlation with magnetic resonance imaging (MRI). SUBJECTS AND METHODS: Sixty-two consecutive patients, 32 patients with osteoarthritis and 30 without osteoarthritis, over the age of 60 years that were referred for both radiographic and MRI of the knee were included in the study. In each case, relative joint space narrowing on conventional AP radiographs was assessed utilizing the Kellgren-Lawrence scoring system. Subsequently, the degree of meniscal extrusion and the integrity of articular cartilage were evaluated from MR in the same patients. RESULTS: Each of 30 patients with normal joint space (Kellgren Grade 0) were noted to have normal articular cartilage, grade 1 meniscal extrusion was identified in only three of these patients. In comparison, meniscal extrusion was identified in all 32 patients with joint space narrowing (Kellgren Grades 1-4). Definite thinning or loss of articular cartilage was identified in only 15 of the 32 cases. In 17 patients with radiographic joint space narrowing (Kellgren Grades 1-3) and meniscal extrusion, no loss of articular cartilage was observed. A statistically significant correlation (P<0.001) was observed between Kellgren Grade and degree of meniscal extrusion and cartilage thinning on MRI. CONCLUSION: Conventional radiographs are an unreliable method of evaluating for articular cartilage loss in patients with early osteoarthritis. Initial joint space narrowing on conventional radiographs is secondary to meniscal extrusion rather than thinning of articular cartilage in most cases.

Aged↗

Comparison of the equilibrium response of articular cartilage in unconfined compression, confined compression and indentation.

At mechanical equilibrium, articular cartilage is usually characterized as an isotropic elastic material with no interstitial fluid flow. In this study, the equilibrium properties (Young's modulus, aggregate modulus and Poisson's ratio) of bovine humeral, patellar and femoral cartilage specimens (n=26) were investigated using unconfined compression, confined compression, and indentation tests. Optical measurements of the Poisson's ratio of cartilage were also carried out. Mean values of the Young's modulus (assessed from the unconfined compression test) were 0.80+/-0.33, 0.57+/-0.17 and 0.31+/-0.18MPa and of the Poisson's ratio (assessed from the optical test) 0.15+/-0.06, 0.16+/-0.05 and 0.21+/-0.05 for humeral, patellar, and femoral cartilages, respectively. The indentation tests showed 30-79% (p<0.01) higher Young's modulus values than the unconfined compression tests. In indentation, values of the Young's modulus were independent of the indenter diameter only in the humeral cartilage. The mean values of the Poisson's ratio, obtained indirectly using the mathematical relation between the Young's modulus and the aggregate modulus in isotropic material, were 0.16+/-0.06, 0.21+/-0.05, and 0.26+/-0.08 for humeral, patellar, and femoral cartilages, respectively. We conclude that the values of the elastic parameters of the cartilage are dependent on the measurement technique in use. Based on the similar values of Poisson's ratios, as determined directly or indirectly, the equilibrium response of articular cartilage under unconfined and confined compression is satisfactorily described by the isotropic elastic model. However, values of the isotropic Young's modulus obtained from the in situ indentation tests are higher than those obtained from the in vitro unconfined or confined compression tests and may depend on the indenter size in use.

Animals↗

Optical determination of anisotropic material properties of bovine articular cartilage in compression.

The precise nature of the material symmetry of articular cartilage in compression remains to be elucidated. The primary objective of this study was to determine the equilibrium compressive Young's moduli and Poisson's ratios of bovine cartilage along multiple directions (parallel and perpendicular to the split line direction, and normal to the articular surface) by loading small cubic specimens (0.9 x 0.9 x 0.8 mm, n =15) in unconfined compression, with the expectation that the material symmetry of cartilage could be determined more accurately with the help of a more complete set of material properties. The second objective was to investigate how the tension-compression nonlinearity of cartilage might alter the interpretation of material symmetry. Optimized digital image correlation was used to accurately determine the resultant strain fields within the specimens under loading. Experimental results demonstrated that neither the Young's moduli nor the Poisson's ratios exhibit the same values when measured along the three loading directions. The main findings of this study are that the framework of linear orthotropic elasticity (as well as higher symmetries of linear elasticity) is not suitable to describe the equilibrium response of articular cartilage nor characterize its material symmetry; a framework which accounts for the distinctly different responses of cartilage in tension and compression is more suitable for describing the equilibrium response of cartilage; within this framework, cartilage exhibits no lower than orthotropic symmetry.

Animals↗

Fibril reinforced poroelastic model predicts specifically mechanical behavior of normal, proteoglycan depleted and collagen degraded articular cartilage.

Degradation of collagen network and proteoglycan (PG) macromolecules are signs of articular cartilage degeneration. These changes impair cartilage mechanical function. Effects of collagen degradation and PG depletion on the time-dependent mechanical behavior of cartilage are different. In this study, numerical analyses, which take the compression-tension nonlinearity of the tissue into account, were carried out using a fibril reinforced poroelastic finite element model. The study aimed at improving our understanding of the stress-relaxation behavior of normal and degenerated cartilage in unconfined compression. PG and collagen degradations were simulated by decreasing the Young's modulus of the drained porous (nonfibrillar) matrix and the fibril network, respectively. Numerical analyses were compared to results from experimental tests with chondroitinase ABC (PG depletion) or collagenase (collagen degradation) digested samples. Fibril reinforced poroelastic model predicted the experimental behavior of cartilage after chondroitinase ABC digestion by a major decrease of the drained porous matrix modulus (-64+/-28%) and a minor decrease of the fibril network modulus (-11+/-9%). After collagenase digestion, in contrast, the numerical analyses predicted the experimental behavior of cartilage by a major decrease of the fibril network modulus (-69+/-5%) and a decrease of the drained porous matrix modulus (-44+/-18%). The reduction of the drained porous matrix modulus after collagenase digestion was consistent with the microscopically observed secondary PG loss from the tissue. The present results indicate that the fibril reinforced poroelastic model is able to predict specifically characteristic alterations in the stress-relaxation behavior of cartilage after enzymatic modifications of the tissue. We conclude that the compression-tension nonlinearity of the tissue is needed to capture realistically the mechanical behavior of normal and degenerated articular cartilage.

Animals↗