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PubMed1998

Diffusive properties of immature articular cartilage.

The diffusive properties of immature bovine articular cartilage were determined using two different-sized, uncharged solutes (glucose 180 Da, and dextran 10k Da). Radioactively tagged glucose and dextran were diffused into the cartilage for transport times of 5, 15, and 60 min, and the diffusion and partition coefficients were calculated by fitting the experimental data to a one-dimensional diffusion model. The diffusion and partition coefficients for the two solutes averaged 6.08 +/- 2.19 and 5.09 +/- 2.51 (x 10(-6) cm2/s) and 0.712 +/- 0.149 and 0.615 +/- 0.120, respectively. Both coefficients were significantly greater for glucose compared to the larger dextran. While no statistical differences could be found in the diffusive properties of these solutes in immature cartilage compared to their diffusive properties in mature cartilage, there was some evidence that the larger dextran solute might diffuse faster in the earlier time periods. Finally, the bulk fluid contents between the two types of cartilage were not different even though the immature tissue was significantly thicker (1.6 times) than the mature tissue. Our results indicate that the solute diffusion properties of articular cartilage, at least with respect to uncharged solutes, do not change during skeletal maturation.

Animals↗
PubMed2001

A review of articular cartilage pathology and the use of glucosamine sulfate.

OBJECTIVE: To refresh the athletic trainer's knowledge of articular cartilage biomechanics, physiology, and structure and explore the role of glucosamine sulfate in treating articular cartilage pathologic conditions, including supplementation methods and clinical outcomes. DATA SOURCES: We searched MEDLINE from 1989 through 2000 and SPORT Discus from 1975 through 2000 using the following key words: glucosamine sulfate, articular cartilage, osteoarthritis, and proteoglycans. DATA SYNTHESIS: Articular cartilage functions as a wear-resistant, smooth, nearly frictionless, load-bearing surface. Glucosamine sulfate can be thought of as a building block that helps restore the proteoglycan-rich extracellular matrix and thus balance articular cartilage catabolism and anabolism. Beneficial clinical effects of glucosamine sulfate in the osteoarthritic population have been documented. However, the use of glucosamine sulfate for athletic articular cartilage injuries is unproved. CONCLUSIONS/RECOMMENDATIONS: Clinical studies indicate that glucosamine sulfate has been shown to be a safe and relatively effective treatment for osteoarthritis. However, no evidence to date supports or refutes a carryover effect to the athletic population and the injuries that occur in sport.

Journal Article↗
PubMedDate not supplied

Dependence of electrical conductivity on fixed charge density in articular cartilage.

A new system for measuring the resistivity of articular cartilage is based on the four-point probe technique. The system measures resistivity as a function of depth from the articular surface. The measurements obtained showed that the conductivity, kappa, of articular cartilage equilibrated in Ringer's solution (pH, 7.4) is constant in all zones, with a value of 6-10 X 10(-3) mho/cm. Conversely, kappa of articular cartilage equilibrated in distilled water varies distinctly, being low in the superficial zone (about 0.7 X 10(-3) mho/cm) and high in the middle to deep zone (about 3 X 10(-3) mho/cm). This is almost the same variation shown by the fixed charge density, FCD, which was measured by the tracer cation method; a linear correlation between kappa and the FCD was found (correlation coefficient, 0.88). These observations were well understood based on the Donnan equilibrium; the mobility of Na+ in cartilage was thought to be independent of FCD.

Cartilage, Articular↗
PubMed2003

Chondromodulin-I expression in rat articular cartilage.

The localization and expression of chondromodulin-I (ChM-I), an angiogenesis inhibitor, in the rat articular cartilage during maturation from 2 to 10 weeks of age were examined by immunohistochemistry, Western blot analysis and ribonuclease protection assay, and the results were compared with those in the epiphyseal cartilage. ChM-I was found to be diffusely immunostained in the inter-territorial space of the cartilage matrix from the intermediate to the deep layers at the immature stage. As the articular cartilage matured, the immunoreactivity was localized around the hypertrophic chondrocytes in the deep layer and the immunoreactivity became weak after maturation. In contrast, the ChM-I immunoreactivity was intense in the epiphyseal cartilage at all ages examined. ChM-I was detected by Western blotting as a broad band or occasionally as a cluster of multiple bands (approximately 25 kDa) in both the articular and the epiphyseal cartilage. The intensity of the bands decreased gradually with age in the articular cartilage, but was unchanged in the epiphyseal cartilage at all ages. Ribonuclease protection assay revealed that ChM-I mRNA also decreased gradually with age in the articular cartilage in parallel with the maturation of the articular cartilage, while no decrease in ChM-I mRNA was found in the epiphyseal cartilage. The expression of ChM-I mRNA in the articular cartilage was less than that in the epiphyseal cartilage at all ages. The decrease in amount of ChM-I in the mature articular cartilage suggests that ChM-I plays a more important role in the maintenance of avascularity in the immature articular cartilage than in the mature one. The avascular condition may be preserved by angiogenic inhibitors or mechanisms other than ChM-I in the mature articular cartilage.

Aging↗
PubMed2006

Repairing articular cartilage defects with tissue-engineering cartilage in rabbits.

OBJECTIVE: To investigate the effect of cancellous bone matrix gelatin (BMG) engineered with allogeneic chondrocytes in repairing articular cartilage defects in rabbits. METHODS: Chondrocytes were seeded onto three-dimensional cancellous BMG and cultured in vitro for 12 days to prepare BMG-chondrocyte complexes. Under anesthesia with 2.5% pentobarbital sodium (1 ml/kg body weight), articular cartilage defects were made on the right knee joints of 38 healthy New Zealand white rabbits (regardless of sex, aged 4-5 months and weighing 2.5-3 kg) and the defects were then treated with 2.5% trypsin. Then BMG-chondrocyte complex (Group A, n=18), BMG (Group B, n=10), and nothing (Group C, n=10) were implanted into the cartilage defects, respectively. The repairing effects were assessed by macroscopic, histologic, transmission electron microscopic (TEM) observation, immunohistochemical examination and in situ hybridization detection, respectively, at 2, 4, 8, 12 and 24 weeks after operation. RESULTS: Cancellous BMG was degraded within 8 weeks after operation. In Group A, lymphocyte infiltration was observed around the graft. At 24 weeks after operation, the cartilage defects were repaired by cartilage tissues and the articular cartilage and subchondral bone were soundly healed. Proteoglycan and type II collagen were detected in the matrix of the repaired tissues by Safranin-O staining and immunohistochemical staining, respectively. In situ hybridization proved gene expression of type II collagen in the cytoplasm of chondrocytes in the repaired tissues. TEM observation showed that chondrocytes and cartilage matrix in repaired tissues were almost same as those in the normal articular cartilage. In Group B, the defects were repaired by cartilage-fibrous tissues. In Group C, the defects were repaired only by fibrous tissues. CONCLUSIONS: Cancellous BMG can be regarded as the natural cell scaffolds for cartilage tissue engineering. Articular cartilage defects can be repaired by cancellous BMG engineered with allogeneic chondrocytes. The nature of repaired tissues is closest to the normal cartilage. Local administration of trypsin can promote the adherence of repaired tissues to host tissues. Transplantation of allogeneic chondrocytes has immunogenicity, but the immune reaction is weak.

Animals↗
PubMed2003

Strain-rate dependent stiffness of articular cartilage in unconfined compression.

The stiffness of articular cartilage is a nonlinear function of the strain amplitude and strain rate as well as the loading history, as a consequence of the flow of interstitial water and the stiffening of the collagen fibril network. This paper presents a full investigation of the interplay between the fluid kinetics and fibril stiffening of unconfined cartilage disks by analyzing over 200 cases with diverse material properties. The lower and upper elastic limits of the stress (under a given strain) are uniquely established by the instantaneous and equilibrium stiffness (obtained numerically for finite deformations and analytically for small deformations). These limits could be used to determine safe loading protocols in order that the stress in each solid constituent remains within its own elastic limit. For a given compressive strain applied at a low rate, the loading is close to the lower limit and is mostly borne directly by the solid constituents (with little contribution from the fluid). In contrast, however in case of faster compression, the extra loading is predominantly transported to the fibrillar matrix via rising fluid pressure with little increase of stress in the nonfibrillar matrix. The fibrillar matrix absorbs the loading increment by self-stiffening: the quicker the loading the faster the fibril stiffening until the upper elastic loading limit is reached. This self-protective mechanism prevents cartilage from damage since the fibrils are strong in tension. The present work demonstrates the ability of the fibril reinfored poroelastic models to describe the strain rate dependent behavior of articular cartilage in unconfined compression using a mechanism of fibril stiffening mainly induced by the fluid flow.

Animals↗
PubMed1986

Characterization of the proteoglycans recovered under nondissociative conditions from normal articular cartilage of rabbits and dogs.

Pretreatment of articular cartilage with a highly purified collagenase in the presence of selected protease inhibitors allowed the extraction under nondissociative conditions of 65% of the tissue hexuronate. Extracted proteoglycans were purified by two successive equilibrium centrifugations in Cs2SO4 and CsCl, respectively, and then characterized by their sedimentation properties. The use of labeled proteoglycan preparations demonstrated that no detectable degradation was introduced by the new extraction procedure. When applied to growth cartilage of rachitic rats the sedimentation profile of the purified proteoglycans was practically identical to that of the proteoglycan molecules recovered by micropuncture-aspiration. Proteoglycans were extracted from normal articular cartilage of rabbits and dogs with either the new procedure or 4.0 M guanidine HCl. The purified aA1 and A1 preparations were characterized by their sedimentation properties. The aA1 contained a higher proportion of aggregates which sedimented as two distinctive populations of molecules. This bimodal distribution of the aggregates was never observed in the A1 preparations even when the dissociative extraction was performed after collagenase pretreatment of cartilages. The two extraction procedures, however, extracted the same proteoglycan monomers since the aA1-D1 and A1-D1 preparations had similar biochemical composition and g(s) distribution functions. These observations and additional in vitro aggregation studies suggested that the differences in the size and proportion of aggregates between the aA1 and A1 preparations result from a more efficient recovery of link glycoproteins in nondissociative extractions that could have determined two structurally different hyaluronate molecules.

Animals↗
PubMed1993

The effect of naproxen and interleukin-1 on proteoglycan catabolism and on neutral metalloproteinase activity in normal articular cartilage in vitro.

The events in inflammatory and degenerative joint diseases involve major changes in the metabolic events in the articular cartilage. The effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on articular cartilage metabolism remain unclear, however. The objective of this catabolism of proteoglycans in articular cartilage explants maintained in culture. Release of proteoglycan from the cartilage was compared with release of neutral metalloproteinase activity. The effect of the drug also was determined on the IL-1-stimulated release of proteoglycan and neutral metalloproteinase activity from the explants. At concentrations that included those present in synovial fluids of patients treated with the drug, naproxen sodium was found to suppress the release of proteoglycan and neutral metalloproteinase activity from the articular cartilage extracts. This is in contrast to the well-documented effect of interleukin-1 (IL-1), which was shown to stimulate release of proteoglycan and neutral metalloproteinase activity from articular cartilage. The effect of naproxen sodium on the IL-1-stimulated release was to suppress, but not totally overcome, the increased release of proteoglycan and neutral metalloproteinase activity. In summary, these in vitro studies of cartilage metabolism indicate that naproxen sodium has the potential to suppress catabolic activities in articular cartilage, including those that are motivated by IL-1.

Animals↗
PubMed2004

Assessment of cellular, biochemical, and histologic effects of bipolar radiofrequency treatment of canine articular cartilage.

OBJECTIVE: To assess the cellular, biochemical, and histologic effects of bipolar radiofrequency-generated heat on canine articular cartilage. SAMPLE POPULATION: Articular cartilage explants (n = 72) from 6 canine cadavers and cultured articular chondrocytes from 5 canine cadavers. PROCEDURE: Cartilage explants were randomly assigned to receive no treatment or treatment with focal (3 seconds) or diffuse bipolar radiofrequency. Following treatment, methylene blue permeability assay was performed (n = 12) and remaining samples (60) were cultured. Immediately and 5, 10, and 20 days after treatment, cultured explants were assessed for glycosaminoglycan (GAG) and collagen contents, type II collagen and matrix metalloproteinase (MMP)-13 immunoreactivity, and modified Mankin histologic scores. Liquid culture media were collected every 4 days and GAG content measured. Additionally, cultured chondrocytes were exposed for 3 seconds to media preheated to 37 degrees, 45 degrees, or 55 degrees C. Cell viability was determined via 2 different assays immediately and 24 hours after treatment. RESULTS: Radiofrequency-treated cartilage had reduced permeability and considerable histologic damage, compared with control samples; most treated samples had reduced collagen II staining and increased MMP-13 immunostaining. Compared with other treatments, less GAGs were released from cartilage after diffuse radiofrequency treatment throughout the study period. Cell viability was significantly different between controls and cells treated at 55 degrees C immediately and 24 hours after heat treatment. CONCLUSIONS AND CLINICAL RELEVANCE: In this study, bipolar radiofrequency treatment had detrimental effects on normal articular cartilage cells and extracellular matrix with probable long-term clinical consequences. The usefulness of radiofrequency for treatment of osteoarthritic articular cartilage requires further investigation.

Analysis of Variance↗
PubMed2001

Preferential incorporation of glucosamine into the galactosamine moieties of chondroitin sulfates in articular cartilage explants.

OBJECTIVE: To determine the metabolic fate of glucosamine (GlcN) in intact articular cartilage tissue. METHODS: Intact articular cartilage explants were cultured for up to 13 days in Dulbecco's modified Eagle's medium supplemented with 1) 1-13C-labeled GlcN, 2) 1-13C-labeled glucose (Glc), or 3) no labeling. Every 3-4 days, samples were removed and frozen in liquid nitrogen for carbon-13 magnetic resonance spectroscopic (MRS) analysis. The metabolic products of the labeled precursors were determined from the MRS data based on resonance positions and comparison with known standards and published values. RESULTS: GlcN was taken up by the chondrocytes and incorporated selectively into the hexosamine, but not the hexuronic acid, components of the glycosaminoglycan chains of articular cartilage proteoglycan. The data also demonstrated that GlcN is the substrate of choice for the galactosamine moieties of the chondroitin sulfates, incorporating at levels 300% higher than with an equivalent amount of labeled Glc. CONCLUSION: The results indicate that GlcN facilitates the production of proteoglycan components that are synthesized through the hexosamine biochemical pathway.

Animals↗
PubMed1993

Age-related changes in glycosaminoglycan distribution in different anatomical sites on the surface of knee-joint articular cartilage in young rabbits.

In spite of the fact that the various anatomical regions of a given articular cartilage surface are subjected to different degrees of stress, the present observations strongly suggest that there exists a topographical homogeneity in the distribution of glycosaminoglycans in the same articular cartilage. In contrast to this age-related changes in the proportion of the different types of glycosaminoglycan species in articular cartilage are remarkable. Non-sulphated chondroitin could only be detected in very young articular cartilage. Dermatan sulphate, which has already been detected in young adult rabbits, was followed by the appearance of keratan sulphate in older rabbits. Chondroitin 4-6-sulphates were detected in all articular cartilages studied, the proportion of the 6-sulphated variably increasing with age. The present report suggests that the distribution of glycosaminoglycans in articular cartilage varies with species and age, and the data can further vary, depending on the methods used. It is therefore concluded that generalizations against the results reported in the literature should be considered skeptically.

Aging↗
PubMed1990

The effects of exposure of articular cartilage to air. A histochemical and ultrastructural investigation.

The effects of exposure of articular cartilage to air and the potential for reversibility of the histological and ultrastructural changes that were produced by this exposure were investigated in the knee joint of the rabbit. After a medial parapatellar arthrotomy and lateral dislocation of the patella, the surface of the articular cartilage was exposed to air for one, two, and three hours in forty-five rabbits. Reversibility of the changes was assessed in fifteen rabbits after exposure of the cartilage to air for three hours, closure of the joint, and six weeks of recovery. Histochemical and ultrastructural changes were evaluated, with use of the contralateral non-exposed knee joint as a control. Depletion of glycosaminoglycans in the matrix of articular cartilage, as indicated by a loss of surface staining with toluidine blue, occurred after one hour of exposure to air. Ultrastructural changes occurred in chondrocytes throughout the full thickness of articular cartilage after one hour of exposure. Increases in the time of exposure to air resulted in more pronounced ultrastructural abnormalities in chondrocytes throughout the entire thickness of the articular cartilage, but there was no apparent irreversible cellular injury. Six weeks after arthrotomy, the chondrocytes had fully recovered from the changes that had been noted immediately after exposure to air, and they were devoid of degenerative changes. The cells showed ultrastructural evidence of increased metabolic activity in the nucleus and cytoplasm. In addition, the chondrocytes had partially restored the depleted glycosaminoglycans.

Air↗
PubMed1985

Triamcinolone hexacetonide protects against fibrillation and osteophyte formation following chemically induced articular cartilage damage.

Although corticosteroids have been shown to cause articular cartilage degeneration, recent studies of experimentally induced osteoarthritis indicate that under certain conditions they may protect against cartilage damage and osteophyte formation. The present study examines the in vivo effect of triamcinolone hexacetonide on the degeneration of articular cartilage which occurs following intraarticular injection of sodium iodoacetate. Three weeks after a single injection of iodoacetate into the knees of guinea pigs, ipsilateral femoral condylar cartilage exhibited fibrillation, loss of staining with Safranin O, depletion of chondrocytes, and prominent osteophytes. In striking contrast, when triamcinolone hexacetonide was injected into the ipsilateral knee 24 hours after the intraarticular injection of iodoacetate, fibrillation was noted in only 1 of 6 samples, osteophytes were much less prominent, pericellular staining with Safranin O persisted, and cell loss was less extensive. Knees of animals which received only one-tenth as much intraarticular triamcinolone hexacetonide after the iodoacetate injection also exhibited marked reduction in size and extent of osteophytes. However, the degree of fibrillation, loss of Safranin O staining, and chondrocyte depletion was similar to that observed in animals injected with iodoacetate but not treated with intraarticular steroid. No apparent morphologic or histochemical changes were observed after intraarticular injection of the steroid preparation alone. Thus, triamcinolone hexacetonide produced a marked, dose-dependent protective effect in this model of chemically induced articular cartilage damage.

Animals↗
PubMed2001

Up-regulation of matrix metalloproteinase expression and activation following cyclical compressive loading of articular cartilage in vitro.

Osteoarthritis (OA) results in articular cartilage degeneration and subchondral bone remodeling. Excessive or abnormal loading of the joint may contribute to matrix destruction by creating an imbalance between proteinases and their inhibitors. This study investigates whether cyclical loading regulates expression and/or activation of metalloproteinases 2 and 9 (MMPs) in articular cartilage explants. Gelatin zymography, reverse zymography, and MMP activity assays of mechanically loaded bovine cartilage explants (0.5 MPa, 1 Hz, 3 h) showed increased expression and activation of MMPs 2 and 9, whereas expression of the tissue inhibitors of MMPs was unaffected. This shows, for the first time that mechanical loading can influence tissue homeostasis generating an imbalance of proteinases and their inhibitors inducing turnover and/or catabolic events in cartilage.

Animals↗
PubMed1989

Interaction of macrophages with rheumatoid articular cartilage.

These experiments investigated the in vitro interaction of macrophages and rheumatoid articular cartilage. When rheumatoid articular cartilage samples were incubated with normal peripheral blood mononuclear cells (PBM) for 1 hour or 12 hours in vitro, there were large numbers of PBM attached to the articular surface, and some PBM invaded the cartilage during the 12 hour incubation period. Conversely, in cartilage from osteoarthritic and normal subjects in the control, only a few PBM were attached to the articular surface after incubation with PBM. Under electron microscopic observation, macrophages were tightly attached to the surface and within the eroded cartilage. Light and electron microscopic observation with immuno-peroxidase staining of the rheumatoid cartilage surfaces showed the deposition of immunoglublins adjacent to the attached macrophages, suggesting the presence of immune-complexes as chemoattractants. These results suggest that macrophages in a rheumatoid joint may play an important role in the formation of pannus, resulting in the destruction of cartilage to interact with immune-complexes trapped in the superficial region of the rheumatoid articular cartilage.

Arthritis, Rheumatoid↗
PubMed1998

Articular cartilage: injuries and potential for healing.

Impact and torsional joint loading can injure articular cartilage, causing pain, joint dysfunction and effusions, and, in some instances, progressive joint degeneration. Differences in the type of injury and the repair response distinguish three classes of articular surface injuries: 1) damage to the joint surface that leaves the articular surface intact but causes internal chondral damage and may cause subchondral bone injury, 2) mechanical disruption of the articular surface limited to articular cartilage, and 3) mechanical disruption of articular cartilage and subchondral bone. A variety of treatments has the potential to improve healing of articular surfaces, including perforation of subchondral bone, altered joint loading, periosteal and perichondrial grafts, cell transplantation, growth factors, and artificial matrices. Selection of treatment for a patient with an articular cartilage injury should be guided by an understanding of the type of injury, the potential for healing, and the effects of treatment on joint surface restoration.

Animals↗
PubMed1990

Metabolic activity in the calcified zone of cartilage: observations on tetracycline labelled articular cartilage in human osteoarthritic hips.

The tidemark is a metabolically active zone in the calcified layer of the cartilage in which it is possible to show that there is calcifying activity even over a short period of time using a tetracycline labelling technique. The tidemark slowly advances in the direction of the non-calcified cartilage and analysis of double-tetracycline labelled cartilage shows that this is not an appositional phenomenon like that occurring in bone, but that, where present, several tidemarks can be labelled at the same time. Each tidemark may therefore be metabolically active and it is not just the tidemark adjacent to hyaline cartilage which incorporates calcium.

Bone Development↗