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PubMed2005

[Efficient isolation of chondrocytes from rabbit articular cartilage with three-step enzymatic digestion and observation of their biological characteristics during cultivation in vitro].

OBJECTIVE: To observe the effect of isolating the chondrocytes from articular cartilage with the method of three-step enzymatic digestion, and the biological characteristics of the isolated chondrocytes during cultivation in vitro in order to evaluate their biological activity. METHODS: The method of three-step enzymatic digestion was designed that the articular cartilage was digested one by one with the 1 g/L trypsin and 1 g/L EDTA, 1 g/L hyaluronidase and 2 g/L collagenase I in the culture medium to isolate chondrocytes. The harvesting and viability rate of the primary chondrocytes were detected. During the passage cultivation in vitro, the changes of the chondrocytes shape and growth were observed, the changes of the collagen type I and II and aggrecan in the extracellular matrix were investigated and detected. RESULTS: (1) The extracellular matrix of articular cartilage was completely dissolved by the three-step enzymatic digestion, and the chondrocytes were completely isolated from the solid matrix. The number of the harvested chondrocytes from every gram of wet cartilage was 50.3 x 10(6) on average, and their viability rate was 98.8% on average. (2) The primary and first passage chondrocytes had triangle or multi-angle shape, and became elliptic shape at the growing confluence with the positive immunohistochemical stain of collagen type II and the strong heterochromia to toluidine blue. The content of sulfate glycosaminoglycans (GAG) in the extracellular matrix of the primary passage cells was (92 +/- 10) microg/cm(2). The chondrocytes after the third passaging gradually became spindle shape with the negative stain of collagen type II and the weak heterochromia to toluidine blue. The content of sulfate GAG of the fourth passage cells was (48 +/- 12) microg/cm(2). CONCLUSION: (1) The method of three-step enzymatic digestion can make the extracellular matrix of articular cartilage completely degraded, and has advantages in the high efficiency of harvesting primary chondrocytes, high cellular viability rate and simple manipulation. (2) The primary and first passage chondrocytes have fine biological activity, and the chondrocytes after the third passaging have lost their special biological activity.

Animals↗
PubMed2005

Ultrasonic measurement of depth-dependent transient behaviors of articular cartilage under compression.

We previously reported an ultrasound method for measuring the depth-dependent equilibrium mechanical properties of articular cartilage using quasi-static compression. The objective of this paper was to introduce our recent development for nondestructively measuring the transient depth-dependent strains of full-thickness articular cartilage specimens prepared from bovine patellae. A 50 MHz focused ultrasound transducer was used to collect ultrasound echoes from articular cartilage specimens (n=8) and sponge phantoms with open pores (n=10) during tests of compression and subsequent stress-relaxation. The transient displacements of the tissues at different depths along the compression direction were calculated from the ultrasound echoes using a cross-correlation tracking technique. An LVDT sensor and a load cell were used to measure the overall deformation of the tissue and the applied force, respectively. Results showed that the tissues inside the cartilage layer continued to move during the stress-relaxation phase after the compression was completed. In the equilibrium state, the displacements of the cartilage tissues at the depths of 1/4, 1/2, and 3/4 of the full-thickness reduced by 51%+/-22%, 54%+/-17%, and 50+/-17%, respectively, in comparison with its peak value. However, no similar phenomenon was observed in the sponge phantoms. Our preliminary results demonstrated that this ultrasound method may provide a potential tool for the nondestructive measurement of the transient depth-dependent processes involved in biological and bioengineered soft tissues as well as soft biomaterials under dynamic loading.

Animals↗
PubMed2003

Topographic and zonal distribution of tenascin in human articular cartilage from femoral heads: normal versus mild and severe osteoarthritis.

OBJECTIVE: The extracellular matrix glycoprotein tenascin (TN) is upregulated in articular cartilage with severe osteoarthritis (OA). This study gives a detailed description of TN expression in areas of articular cartilage from femoral heads with mild OA showing structural lesions and in structurally normal areas of the same femoral heads compared with normal cartilage and cartilage with severe OA. METHODS: Immunohistochemical evaluation was performed on cryosections stained with antibodies against TN. Sections were selected as follows: from each macroscopically normal femoral head (n=6) a normal central and peripheral biopsy; from each femoral head with macroscopically mild OA (n=8) a central biopsy that showed structural lesions and a peripheral normal biopsy; from each femoral head with severe OA (n=9) a central and a peripheral biopsy with structural lesions. Central biopsies represent load bearing areas, whereas peripheral biopsies are non-load bearing. RESULTS: Central cartilage with mild OA contains significantly higher levels of TN in the superficial zone than structurally normal, peripheral cartilage from the same femoral heads. Normal cartilage and cartilage with severe OA do not display this topographic variation. Central cartilage with mild OA shows significantly higher levels of TN than normal, central cartilage. Peripheral, normal cartilage with mild OA shows significantly less TN than peripheral cartilage with severe OA. CONCLUSIONS: In femoral heads with mild OA, TN is accumulated in areas displaying structural damage. This proposes mild OA to be a localized disorder. Extreme caution is necessary for sampling of articular cartilage, especially from joints with mild OA.

Cartilage, Articular↗
PubMed2003

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↗
PubMed2003

Articular cartilage bioreactors and bioprocesses.

This review summarizes the major approaches for developing articular cartilage, using bioreactors and mechanical stimuli. Cartilage cells live in an environment heavily influenced by mechanical forces. The development of cartilaginous tissue is dependent on the environment that surrounds it, both in vivo and in vitro. Chondrocytes must be cultured in a way that gives them the proper concentration of nutrients and oxygen while removing wastes. A mechanical force must also be applied during the culturing process to produce a phenotypically correct tissue. Four main types of forces are currently used in cartilage-culturing processes: hydrostatic pressure, direct compression, "high"-shear fluid environments, and "low"-shear fluid environments. All these forces have been integrated into culturing devices that serve as bioreactors for articular cartilage. The strengths and weaknesses of each device and stimulus are explored, as is the future of cartilage bioreactors.

Animals↗
PubMed2000

Ultrastructural study of upper surface layer in rat articular cartilage by "in vivo cryotechnique" combined with various treatments.

The ultrastructures of the upper surface layer of rat articular cartilage were studied with our "in vivo cryotechnique" followed by freeze-substitution method for scanning electron microscopy (SEM) or transmission electron microscopy (TEM). Rat hip or knee articular cartilage was quickly frozen by the in vivo cryotechnique with liquid isopentane-propane cryogen (-193 degrees C), and surface areas of some frozen specimens were freeze-fractured with a scalpel in liquid nitrogen. They were freeze-substituted and freeze-dried, ion-sputtered, and then observed in SEM. Other frozen specimens were routinely freeze-substituted and embedded in epoxy resin for TEM. Many globular structures were detected in the thick upper surface layer that had not been revealed by the conventional fixation methods. Their sizes were reduced by Triton X-100 treatment, and their localization was also detected in synovial fluid, as revealed by SEM. Such globular lipid-like structures in the upper surface layer of hip or knee articular cartilage might contribute to joint lubrication.

Animals↗
PubMed1994

Transforming growth factor-beta and insulin-like growth factor-1 restore proteoglycan metabolism of bovine articular cartilage after depletion by retinoic acid.

Previous studies showed that retinoic acid is a powerful resorbing agent for articular cartilage at physiological doses (10(-8) to 10(-10) M); the possible role of individual cytokines in the reversal of this effect is now explored in bovine articular cartilage organ cultures. Seven days of treatment with the retinoid under serum-free conditions, at 1 x 10(-8) M, led to a suppression of proteoglycan synthesis of 90 +/- 5% (n = 6; n = cultures from different animals; mean +/- SD) and to a net loss of 64 +/- 14% (n = 6). Removal of the retinoid from the feeding medium did not significantly increase proteoglycan synthesis nor diminish the further loss of proteoglycans. Thus, transforming growth factor-beta (TGF-beta) and insulin-like growth factor-1 (IGF-1), cytokines which independently maintain proteoglycan homeostasis (Morales and Roberts, 1988, J. Biol. Chem. 263, 828; and Luyten et al., 1988, Arch. Biochem. Biophys. 267, 416), were tested. TGF-beta (10 ng/ml) or IGF-1 (10 ng/ml) added for 7 days to serum-free medium following retinoic acid treatment led to recoveries of proteoglycan synthesis of 74 +/- 24% (n = 12) and 69 +/- 18% (n = 12), respectively, as compared to controls switched from serum-free conditions to corresponding cytokine treatments. TGF-beta + IGF-1 restored activity to 95 +/- 17% (n = 12) of controls. TGF-beta s 1-3 exhibited identical responses in control and experimental cultures. IGF-2 replaced IGF-1, but a fourfold higher concentration was required; insulin also had IGF-1-like effects, but even at 500 ng/ml it was 25% less effective than IGF-1. In contrast to the cultures switched from retinoic acid treatment to serum-free conditions, the cultures switched to IGF-1, TGF-beta, or IGF-1 + TGF-beta were stabilized from further proteoglycan loss by the treatment; after 1 week, tissue levels were 97 +/- 19, 96 +/- 22, and 114 +/- 15% (n = 6), respectively, compared to the content before switching. Measurements of catabolism were in agreement with these observations. It is proposed that retinoic acid, TGF-beta, and IGF-1 are parts of an endogenous system involved in the reversible modulation of proteoglycan homeostasis in articular cartilage.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2004

Autologous bone marrow stromal cell transplantation for repair of full-thickness articular cartilage defects in human patellae: two case reports.

This study assessed the effectiveness of autologous bone marrow stromal cell transplantation for the repair of full-thickness articular cartilage defects in the patellae of a 26-year-old female and a 44-year-old male. These two patients presented in our clinic because their knee pain prevented them from walking normally. After thorough examination, we concluded that the knee pain was due to the injured articular cartilage and decided to repair the defect with bone marrow stromal cell transplantation. Three weeks before transplantation, bone marrow was aspirated from the iliac crest of each patient. After erythrocytes had been removed by use of dextran, the remaining nucleated cells were placed in culture. When the attached cells reached subconfluence, they were passaged to expand in culture. Adherent cells were subsequently collected, embedded in a collagen gel, transplanted into the articular cartilage defect in the patellae, and covered with autologous periosteum. Six months after transplantation, clinical symptoms (pain and walking ability) had improved significantly and the improvement has remained in effect (5 years and 9 months posttransplantation in one case, and 4 years in the other), and both patients have been satisfied with the outcome. As early as 2 months after transplantation, the defects were covered with tissue that showed slight metachromatic staining. Two years after the first and 1 year after the second transplantation, arthroscopy was performed and the defects were repaired with fibrocartilage. Results indicate autologous bone marrow stromal cell transplantation is an effective approach in promoting the repair of articular cartilage defects.

Adult↗
PubMed1998

Magnetic resonance imaging of articular cartilage: an overview.

MR imaging is the best noninvasive method for the evaluation of articular cartilage. Recent studies have clarified the MR appearance of normal articular cartilage and proven that MR imaging can detect chondral lesions with high accuracy. Quantitative imaging holds promise for the accurate determination of cartilage volumes and thickness measurements, as well as the ability to detect early chondral degeneration and biochemical changes before gross morphologic changes occur.

Cartilage, Articular↗
PubMed1995

The potential of magnetic resonance imaging (MRI) for quantifying articular cartilage thickness -- a methodological study.

The thickness of patellar articular cartilage was assessed in a cadaveric human knee joint by magnetic resonance imaging. Imaging was conducted at 1.0 T, using three-dimensional gradient-echo sequences. From each of the sequences the total cartilage volume, the size of the articular surface, the mean cartilage thickness and the regional distribution of cartilage thickness were determined by image analysis. These values were then compared with those obtained from anatomical sections. The fat-suppressed FLASH sequence was found to allow the most accurate evaluation of the total volume and the regional distribution of the articular cartilage. Slight underestimation of the cartilage thickness by about 5% may be due to the fact that the calcified layer is not made visible by magnetic resonance imaging. There is, however, a very high degree of similarity between the distribution patterns obtained from the MR images and the anatomical sections. The contrast-to-noise ratios and reproducibility were also highest with the fat-suppressedFLASH sequence. This pulse sequence can therefore be recommended for experimental and clinical use.

Journal Article↗
PubMed1998

Chondrocyte apoptosis increases with age in the articular cartilage of adult animals.

BACKGROUND: Apoptosis in vivo has been identified in developing cartilage from embryonic chick sterna and avian and murine growth plates. To date, no evidence exists that chondrocytes in articular cartilage undergo apoptosis. METHODS: We examined the distribution of cells demonstrating fragmented DNA in the articular knee cartilage of C57BL/6 mice (aged 11, 18, 24, and 30 months) and Wistar rats (aged 6, 12, and 24 months) using a DNA end-labeling technique. RESULTS: Control experiments utilizing retinoic acid-induced apoptosis in a chondrocyte cell line, established that DNA end-labeling correlated with DNA ladder formation. In vivo, apoptotic cells were detected in articular cartilage tissue in both species examined. The percentage of apoptotic cells increased significantly (P < 0.05 with age) for all joint surfaces in both species. No significant difference was found between the medial and lateral or femoral and tibial joint surfaces of the knee. Apoptotic cells were observed in both the calcified and uncalcified regions of the articular cartilage of C57 mice. In the rat, only the calcified region of articular cartilage contained apoptotic cells. CONCLUSIONS: These results suggest that apoptosis plays a role in some aspect of maintenance, remodeling, or turnover of mature articular cartilage. In addition, the increase in apoptosis associated with aging could contribute to the greater risk for cartilage degeneration.

Aging↗
PubMed1979

Deformation of the articular cartilage and joint space of the human knee joint under static load.

In order to define the deformation of articular cartilage and the joint space under statically loaded knee joints, we studied serial sections in the frontal plane of knee joints which were frozen under the application of a load. Normal articular cartilage surfaces did not make contact even under loads of 100kg or more, leaving always a space between. The compressive deformation of articular cartilage mainly occurred at the central area near to the intercondylar notch or prominence, but the deformation of cartilage in the area covered by menisci was negligible.

Adult↗
PubMed2002

Ultrastructural localization of type VI collagen in normal adult and osteoarthritic human articular cartilage.

OBJECTIVE: Type VI collagen is a major component of the pericellular matrix compartment in articular cartilage and shows severe alterations in osteoarthritic cartilage degeneration. In this study, we analysed the exact localization of type VI collagen in its relationship to the chondrocyte and the (inter)territorial cartilage matrix. Additionally, we were interested in its ultrastructural appearance in normal and osteoarthritic cartilage. DESIGN: Distribution and molecular appearance was investigated by conventional immunostaining, by multilabeling confocal scanning microscopy, conventional transmission, and immunoelectron microscopy. RESULTS: Our analysis confirmed the pericellular concentration of type VI collagen in normal and degenerated cartilage. Type VI collagen formed an interface in between the cell surface and the type II collagen network. The type VI collagen and the type II collagen networks appeared to have a slight physical overlap in both normal and diseased cartilage. Additionally, some epitope staining was observed in the cell-associated interterritorial cartilage matrix, which did not appear to have an immediate relation to the type II collagen fibrillar network as evaluated by immunoelectron microscopy. In osteoarthritic cartilage, significant differences were found compared with normal articular cartilage: the overall dimension of the lacunar volume increased, and a significantly increased type VI collagen epitope staining was observed in the interterritorial cartilage matrix. Also, the banded isoform of type VI collagen was found around many chondrocytes. CONCLUSIONS: Our study confirms the close association of type VI collagen with both, the chondrocyte cell surface and the territorial cartilage matrix. They show severe alterations in type VI collagen distribution and appearance in osteoarthritic cartilage. Our immunohistochemical and ultrastructural data are compatible with two ways of degradation of type VI collagen in osteoarthritic cartilage: (1) the pathologically increased physiological molecular degradation leading to the complete loss of type VI collagen filaments from the pericellular chondrocyte matrix and (2) the transformation of the fine filaments to the band-like form of type VI collagen. Both might implicate a significant loss of function of the pericellular microenvironment in osteoarthritic cartilage.

Adult↗
PubMed1996

Evidence for insufficient chondrocytic differentiation during repair of full-thickness defects of articular cartilage.

The main objective of this study was to characterize the cellular phenotypes in the repair tissue of full-thickness defects of articular cartilage by histologic and molecular biologic techniques. Healing of the defects in the articular cartilage of the knee joints of 12 rabbits was analyzed at days 3, 7, 14, 28 and 50 using histology and Northern analysis of mRNA levels for type I, II and III collagens and osteonectin. The cellular source of each mRNA was determined by in situ hybridization. Two novel cDNA clones for rabbit type II and III collagen mRNAs were constructed to obtain species-specific hybridization probes. The repair tissue of full-thickness defects consisted of two types of tissue. At the bottom of the defect, bone-derived cells with high levels of type I collagen and osteonectin mRNA were actively producing new osteoid, while superficially a slow transition from a fibrin clot into undifferentiated mesenchyme with cells containing type III collagen mRNA was observed. This tissue subsequently became fibrocartilaginous, with small groups of cells turning on the transcription of the type II collagen gene and acquiring a phenotype typical for hyaline cartilage. The data suggest that small clusters of cells in the repair tissue of full-thickness articular cartilage defects are capable of turning on an apparently correct chondrocytic phenotype. The low transcription level of the type II collagen gene suggests, however, that insufficient amounts of fundamentally important regulatory factors or progenitor cells are present in the repair tissue. In the future, such factors should be administrable into the joint by novel therapeutic means.

Amino Acid Sequence↗
PubMed2000

Normal and pathological adaptations of articular cartilage to joint loading.

Joints are functional units that transmit mechanical loads between contacting bones during normal daily or specialized activities, e.g., sports. All components of the joint, i.e. articular cartilage, bone, muscles, ligaments/tendons and nerves, participate in load transmission. Failure in any of these components can cause joint malfunction, which, in turn, may lead to accumulation of damage in other joint components. Mechanical forces have great influence on the synthesis and rate of turnover of articular cartilage molecules, such as proteoglycans (PGs). Regular cyclic loading of the joint enhances PG synthesis and makes cartilage stiff. On the other hand, loading appears to have less evident effects on the articular cartilage collagen fibril network. Continuous compression of the cartilage diminishes PG synthesis and causes damage of the tissue through necrosis. The prevailing view is that osteoarthrosis (OA) starts from the cartilage surface through PG depletion and fibrillation of the superficial collagen network. It has also been suggested that the initial structural changes take place in the subchondral bone, especially when the joint is exposed to an impact type of loading. This in turn would create an altered stress pattern on joint surfaces, which leads to structural damage and mechanical failure of articular cartilage. The importance of the neuromuscular system to the initiation and progression of OA is still poorly understood. Many surgical extra- and intra-articular procedures have been used for the treatment of OA. Although some of the new methods, such as autologous chondrocyte transplantation and mosaicplasty, have given good clinical results, it is reasonable to emphasize that the methods still are experimental and more controlled studies are needed.

Animals↗
PubMed1986

Softening of canine articular cartilage after immobilization of the knee joint.

Using the indentation method, effects of immobilization with a splint for 11 weeks on the stiffness of the articular cartilage in the canine knee were investigated. Stiffness was determined for femoral, tibial, and patellar articular cartilages with nine, eight, and three test points, respectively, in the form of elastic moduli. Immobilization, without causing any macroscopic changes on cartilage surface, influenced the quality and quantity of articular cartilage. Immobilization caused significant softening of the femoral and tibial cartilages. The rate of deformation under the test load increased (42%) and the average thickness of the cartilage decreased (9%) as compared with the controls. Normal cartilage stiffness remained in the contact area between the patella and patellar surface of the femur, probably as a consequence of the sustained, but not forceful, loading between the femur and the patella produced by the flexion of the knee joint.

Animals↗
PubMed2002

The effect of thymosin beta4 on articular cartilage chondrocyte matrix metalloproteinase expression.

Mechanical loading is paramount in regulating both the anabolic and catabolic activities of articular cartilage chondrocytes, essential for the matrix to retain its functional integrity. We have identified thymosin beta(4) as a putative mechanically regulated gene that may mediate load-enhanced synthesis and activation of matrix metalloproteinases (MMPs) 2 and 9 in articular cartilage. The objective of this study was to confirm the mechanical regulation of thymosin beta(4) and determine its effect on cartilage chondrocyte MMP production. Thymosin beta(4) mRNA expression, analysed by quantitative PCR, revealed a significant 20-fold increase in cartilage loaded for 10 min which was still evident after 30 min of loading. Treatment of primary chondrocytes with 2 and 4 micro x ml(-1) thymosin beta(4) peptide for 4 h significantly increased pro-MMP 9 expression and activation. We postulate a functional role for load-induced thymosin beta(4) in modulating the cytoskeletal organization of articular cartilage chondrocytes to affect MMP expression.

Animals↗
PubMed2006

Ultrasound elastomicroscopy using water jet and osmosis loading: potentials for assessment for articular cartilage.

Research in elasticity imaging typically relies on 1-10 MHz ultrasound. Elasticity imaging at these frequencies can provide strain maps with a resolution in the order of millimeters, but this is not sufficient for applications to skin, articular cartilage, or other fine structures. In this paper, we introduced two methods of ultrasound elastomicroscopy using water jet and osmosis loading for imaging the elasticity of biological soft tissues with high resolutions. In the first system, the specimens were compressed using water jet compression. A water jet was used to couple a focused 20 MHz ultrasound beam into the specimen and meanwhile served as a "soft" indenter. Because there was no additional attenuation when propagating from the ultrasound transducer to the specimen, the ultrasound signal with high signal-to-noise ratio could be collected from the specimens simultaneously with compressing process. The compression was achieved by adjusting the water flow. The pressure measured inside the water pipe and that on the specimen surface was calibrated. This system was easily to apply C-scan over sample surfaces. Experiments on the phantoms showed that this water jet indentation method was reliable to map the tissue stiffness distribution. Results of 1D and 2D scanning on phantoms with different stiffness are reported. In the second system, we used osmotic pressure caused by the ion concentration change in the bathing solutions for the articular cartilage to deform them. When bovine articular cartilage specimens were immerged in solutions with different salt concentration, a 50 MHz focused ultrasound beam was used to monitor the dynamic swelling or shrinkage process. Results showed that the system could reliably map the strain distribution induced by the osmotic loading. We extract intrinsic layered material parameters of the articular cartilage using a triphasic model. In addition to biological tissues, these systems have potential applications for the assessment of bioengineered tissues, biomaterials with fine structures, or some engineering materials. Further studies are necessary to fully realize the potentials of these two new methods.

Algorithms↗