Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CARTILAGE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1976

Degradation of cartilage proteoglycan by human leukocyte granule neutral proteases--a model of joint injury. I. Penetration of enzyme into rabbit articular cartilage and release of 35SO4-labeled material from the tissue.

The present work was undertaken to explore the effect of two purified neutral proteases derived from human peripheral blood polymorphonuclear leukocytes (PMN) on articular cartilage as a model of joint injury. Human leukocyte elastase and chymotrypsin-like enzyme, purified by affinity chromatography, released 32SO4 from labeled rabbit articular cartilage slices in vitro. Release of isotope was initially delayed, suggesting that either a lag in enzyme penetration occurs or that size of degradation fragments is a limiting factor in diffusion of label out of the tissue. The release of 35SO4 was inhibited by preincubation of elastase and chymotrypsin-like enzyme with human alpha 1-anti-trypsin, or with their specific chloromethyl ketone inactivators, and the action of elastase was also inhibited by a monospecific antiserum to PMN elastase, freed of major serum proteinase inhibitors. Immunohistochemical staining procedures revealed the presence of PMN elastase inside the matrix of cartilage slices after a 20-min exposure of tissue to either the pure enzyme or crude PMN granule extract. Serum alpha 1-antitrypsin failed to penetrate into the cartilage slices under identical in vitro conditions. In association with the results reported in the accompanying paper, these findings suggest a model of cartilage matrix degradation by PMN neutral proteases in which local protease-antiprotease imbalance, coupled with different rates of penetration of protease and antiprotease into target tissue, plays a key role in accounting for matrix damage.

Animals↗
PubMed1976

Degradation of cartilage proteoglycan by human leukocyte granule neutral proteases--a model of joint injury. II. Degradation of isolated bovine nasal cartilage proteoglycan.

Extracts of human peripheral blood polymorphonuclear leukocyte granules, and two purified proteases derived from such extracts, an elastase and a chymotrypsin-like enzyme, degrade isolated bovine nasal cartilage proteoglycan at neutral pH. Viscosity studies indicate that the leukocyte granule extracts lack hyaluronidase activity and that their degradative effect on proteoglycan at physiological pH is due entirely to proteolytic action. Sepharose 4B gel chromatography and SDS-polyacrylamide gel electrophoresis of proteoglycan fractions treated with leukocyte granule enzymes at pH 7.0 indicate that they degrade one of the proteoglycan link proteins, release a fragment from the hyaluronic acid-binding portion of the proteoglycan subunit core protein, and break down the remainder of the proteoglycan subunit molecule into peptide fragments with varying numbers of chondroitin sulfate chains. Immunodiffusion studies indicate that the antigenic determinants of the proteoglycan subunit core protein and the link proteins survive treatment with granule proteases. Similar degradation of human articular cartilage proteoglycan by granule neutral proteases can be presumed to occur, in view of the similarity of structure of human articular and bovine nasal cartilage proteoglycans. The release of granule enzymes in the course of neutrophil-mediated inflammation can thus result in the degradation of cartilage matrix proteoglycan, leading to cartilage destruction and joint injury.

Animals↗
PubMed1996

Transmission of rapidly applied loads through articular cartilage. Part 1: Uncracked cartilage.

An elastostatic model of rapidly loaded articular cartilage is presented. It is assumed that the cartilage experiences little volumetric change or interstitial fluid flow while loaded instantaneously. Subchondral bone compliance and articular surface friction are incorporated. Integral representations of the stress distributions within cartilage are derived using Fourier transform techniques and the integrals are solved numerically. Localized tensile stresses are found and occur in regions close to the cartilage-bone interface as well as at the articular surface, outside the embrace of the load. The qualitative similarity between the results and those of previous investigations is explained by an elementary equilibrium analysis. The stress distributions suggest that the splits and cracks observed in diseased cartilage may be initiated, or propagated, by tensile stress.

Cartilage, Articular↗
PubMed2005

Effects of radial shock waves on membrane permeability and viability of chondrocytes and structure of articular cartilage in equine cartilage explants.

OBJECTIVE: To investigate in vitro effects of radial shock waves on membrane permeability, viability, and structure of chondrocytes and articular cartilage. SAMPLE POPULATION: Cartilage explants obtained from the third metacarpal and metatarsal bones of 6 horses. PROCEDURE: Equine cartilage was subjected to radial shock waves and then maintained as explants in culture for 48 hours. Treatment groups consisted of a negative control group; application of 500, 2,000, and 4,000 impulses by use of a convex handpiece (group A); and application of 500, 2,000, and 4,000 impulses by use of a concave handpiece (group B). Effects on explant structure were evaluated by use of environmental scanning electron microscopy (ESEM). Membrane permeability was determined by release of lactate dehydrogenase (LDH). Chondrocyte viability was assessed by use of vital cell staining. Comparisons of LDH activity and nonviable cell percentages were performed by ANOVA. RESULTS: Cell membrane permeability increased significantly after application of 2,000 and 4,000 impulses in groups A and B. A significant decrease in cell viability was observed for application of 4,000 impulses in explants of group A. There was no detectable damage to integrity of cartilage explants observed in any treatment group by use of ESEM. CONCLUSIONS AND CLINICAL RELEVANCE: Radial shock waves do not appear to structurally damage articular cartilage but do impact chondrocyte viability and membrane permeability. Caution should be exercised when extremely high periarticular pulse doses are used until additional studies can determine the long-term outcome of these effects and appropriate periarticular treatment regimens can be validated.

Analysis of Variance↗
PubMed1987

[Antigenicity of the auricular cartilage and its modification by vital preservation. 1. Xenogeneic transplantation of human auricular concha cartilage to the rabbit].

By means of xenotransplantation of human auricular cartilage to rabbits tests were carried out to see, if antigenicity is reduced through storing elastic cartilage either in a nutrient solution (Ham F 12) at 4 degrees C above zero or in a tissue culture (Ham F 12 + 10% serum of a calf-foetus) at 37 degrees C above zero, and if vital preservation prevents degeneration- and resorption processes of cartilage. The results were compared to transplants of fresh, not treated cartilages, and those preserved with cialit and merthiolate. It turned out that these vital preservation methods seem to cause an extensive loss of the cartilages characteristic qualities and that they keep degeneration- and resorption processes at a minimal level. Big differences between storage in nutrient solution and tissue culture could not be observed.

Animals↗
PubMed1987

Topographical variation of glycosaminoglycan content and cartilage thickness in canine knee (stifle) joint cartilage. Application of the microspectrophotometric method.

A recently developed microspectrophotometric method was used to measure local changes of thickness and glycosaminoglycan (GAG) content in articular cartilage. The intensity of the GAG stain was recorded from the superficial, intermediate, deep and calcified zones of articular cartilage. At each site of analysis, both the average stain concentration and the total stain content were determined. Of the 10 predefined locations of the Beagle knee (stifle) joint, the thickest cartilage was observed in the medial condyle of the tibia, which also possessed the highest GAG concentration. In the femur, the summits of the condyles had 33% thicker cartilage than the peripheral parts, while the GAG concentration was about equal in both of these regions. The thinnest cartilage and smallest GAG concentration was at the posterior end of the lateral condyle of the femur. The GAG content in the medial condyle and in the patellar surface of the femur was slightly greater than that in its lateral condyle.

Animals↗
PubMed1997

Mechanisms of cartilage destruction and novel nonsurgical therapeutic strategies to retard cartilage injury in rheumatoid arthritis.

Although there are excellent rationales for the use of biologic agents, no published novel therapeutic strategy in patients with early or late rheumatoid arthritis has thus far been proven in controlled clinical studies to prevent or retard cartilage destruction. Although T-cell-specific therapies in chronic rheumatoid arthritis have some success, the percentage of patients responding and the degree of clinical improvement are disappointing, and cartilage injury can neither be prevented nor retarded. Similarly, attempts to interrupt the cytokine loops and inhibit adhesion molecules are only modestly successful. The alternative approach of solely controlling the effector side by direct or indirect metalloproteinase inhibition seems attractive because it would circumvent the cytokine networks while theoretically still preventing the final consequences of inflammation on cartilage. One therapeutic strategy that inhibits metalloproteinses-tetracyclines or chemically transformed tetracyclines-cannot be considered a breakthrough with respect to either reduction of disease activity or prevention or retardation of cartilage injury in rheumatoid arthritis. It is likely that combination therapy will be further developed in the future. The most promising agents today, such as the anti-tumor necrosis factor-alpha antibodies, must be combined with other current strategies as well as with newly developed disease-specific biologic agents. To affect multiple sites in the underlying inflammatory process and to target the delivery of the agents could be one of the goals. The efficacy and effectiveness of any new strategy depends on its ability to alter the function of the aggressive and transformed synovial fibroblasts within the pannus and to protect the articular chondrocytes and early cartilage injury.

Adrenal Cortex Hormones↗
PubMed1986

Uncalcified cartilage resorption in human fetal cartilage canals.

In the human fetus, epiphyses appear as a solid avascular cartilaginous mass until the eleventh week of development. Around the third fetal month of development, vascular canals coming from the perichondrium are recognized in the mineralized epiphyseal cartilage. Whether cartilage canals develop by passive inclusion or active chondrolysis is still a matter of controversy. We studied the relationships between the intracanalar cells and the surrounding matrix on human fetal epiphyses embedded in glycol methacrylate. At the blind end of canals both stellate fibroblast-like cells and vacuolated macrophages are observed. These cellular foci show all characteristics of active chondrolysis (loss of metachromasia, lacunae containing cells intimately associated with matrix, and presence of granular debris). Similar resorptive foci have been observed in the pannus of rheumatoid joints and in the embryonic chick growth plate composed of uncalcified cartilage. A cellular cooperation (fibroblast/macrophage) is necessary for uncalcified cartilage breakdown. In the human fetus, monocytes/macrophages have been recognized in the peripheral blood as early as the twelfth week of gestation. Our observations support the view that chondrolysis due to both fibroblasts (of mesenchymal origin) and macrophages is the basic mechanism for cartilage canal development.

Abortion, Spontaneous↗
PubMed2004

The potential and limitations of cartilage-specific (V+C)(-) fibronectin and cartilage oligomeric matrix protein as osteoarthritis biomarkers in canine synovial fluid.

OBJECTIVE: To determine if levels of the cartilage-specific (V+C)(-) fibronectin isoform in the synovial fluid is associated with cartilage change during osteoarthritis. DESIGN: Synovial fluid was collected from 26 healthy dogs presenting to the Orthopedic Surgery Clinic with unilateral cranial cruciate rupture, 22 control dogs, and 13 dogs from a colony maintained for the study of canine hip dysplasia. Total fibronectin, (V+C)(-) fibronectin, and cartilage oligomeric matrix protein (COMP) were quantitated by ELISA assays. Statistical analysis used Wilcoxon's signed-rank and rank-sum tests and Spearman's rank correlation. RESULTS: The concentration of total fibronectin was increased in affected (P<0.0001) and contralateral (P=0.0005) knees of the clinic population (compared to unaffected knees in colony controls). Both (V+C)(-) fibronectin and COMP concentrations were elevated in the contralateral knees in clinical patients relative to unaffected knees in the colony controls (P=0.03 and P=0.04, respectively), and relative to the affected knees (P=0.003); however, corrections for joint effusions suggest elevated totals in the affected knees. (V+C)(-) fibronectin and COMP concentrations were correlated (r(sp)=0.74; P<0.0001) in 30 unaffected knees of patients and colony controls. Total fibronectin was correlated negatively with months since the initial injury (r(sp)=-0.44; P=0.03) in the affected joints. The intraoperative lesion severity score did not correlate with total fibronectin or (V+C)(-) fibronectin (P>or=0.35). CONCLUSIONS: Concentration of total fibronectin in synovial fluid might be a useful biomarker for cross-sectional studies in osteoarthritis, but only (V+C)(-) fibronectin provides information specifically about cartilage damage. Elevated concentrations of (V+C)(-) fibronectin and COMP seen in the contralateral knees of patients with cranial cruciate rupture might indicate cartilage changes early in the disease process (pre-clinical). However, the wide range of values obtained limits the diagnostic value for any one individual. Joint effusions obscure the total amount of biomarkers in affected synovial joints.

Animals↗
PubMed2003

[The biomarker assey for cartilage destruction in rheumatoid arthritis. -Which molecules can reflect cartilage breakdown in RA?-].

Rheumatoid arthritis (RA) is characterized as inflammatory disease associated with cartilage degradation and subchondral bone erosion. RA is an autoimmune disease that has genetic and environmental backgrounds. The preservation of a functional articular cartilage enables the survival of a tissue that covers articulating surfaces in affected joints. The extracellular matrix of articular cartilage provides this tissue with its gprimary strength, resistance to deformation, and ability to dissipate load in the joint. Many research had been designed for trying to measure the remodeling and pathologic events in RA caritlage. The many matrix molecules, and their degradation products, are released from cartilage and bone and can be detected biochemically and immunologically in the serum and Joint fluids. Before evaluating the data of biomarkers revealed in pathologic conditions such as RA and OA, our skeletal system is built and maintained by a balance between synthesis and degradation. Furthermore this balance varies considerably from one person to another. It is nortworhy that the off-balance between synthesis and degradation lead to cartilage destruction. The use of many of the biomarker assays for matrix turnover offers the evidences to evaluate whether the treatments designed to inhibit the joint damage may successfully work in specific RA patients.

English Abstract↗
PubMed1986

Ultrastructure of hyaline cartilage. I. A comparative study of cartilage from different species and locations, using cryofixation, freeze-substitution and low-temperature embedding techniques.

Important progress in the cryofixation of tissues has recently been made with the introduction of a new technique which permits a great reduction in the rates of ice-crystal growth and nucleation by rapid freezing under a pressure of 2 100 bar. Tissue pieces up to 0.5 mm in thickness can now be processed at a freezing rate sufficient to prevent the formation of detectable ice crystals at the ultrastructural level. In the present investigation this technique, in combination with freeze substitution and low temperature embedding was applied for ultrastructural and immunocytochemical studies of hyaline cartilage. No extraction of matrix proteoglycans was observed during the substitution procedure, and there are good reasons to believe that in preparations obtained by this technique the native state of the matrix components is preserved, since, for example, the collapse temperature of the macromolecules is not exceeded. Furthermore, no chemical fixatives or cryoprotectants are required. Ultrastructural differences in the hyaline cartilage of the growth-plate between normal rats and mice were observed, and also differences between cartilage at different locations, such as tracheal cartilage and growth-plate. Using this technique, further comparative ultrastructural studies enable us to obtain information about the macromolecular organisation of cartilage matrix under various normal and pathological conditions in vivo. In addition, using monoclonal antibodies to the main macromolecules of the matrix, it was found that this technique not only provides excellent tissue preservation but is also well suited for immunocytochemistry with colloidal gold as a marker.

Animals↗
PubMed1999

Enhancement of cell adhesion and spreading by a cartilage-specific noncollagenous protein, cartilage matrix protein (CMP/Matrilin-1), via integrin alpha1beta1.

Cartilage matrix protein (CMP; also known as matrilin-1), one of the major noncollagenous proteins in most cartilages, binds to aggrecan and type II collagen. We examined the effect of CMP on the adhesion of chondrocytes and fibroblasts using CMP-coated dishes. The CMP coating at 10-20 micrograms/ml enhanced the adhesion and spreading of rabbit growth plate, resting and articular chondrocytes, and fibroblasts and human epiphyseal chondrocytes and MRC5 fibroblasts. The effect of CMP on the spreading of chondrocytes was synergistically increased by native, but not heated, type II collagen (gelatin). The monoclonal antibody to integrin alpha1 or beta1 abolished CMP-induced cell adhesion and spreading, whereas the antibody to integrin alpha2, alpha3, alpha5, beta2, alpha5beta1, or alphaVbeta5 had little effect on cell adhesion or spreading. The antibody to integrin alpha1, but not to other subunits, coprecipitated 125I-CMP that was added to MRC5 cell lysates, indicating the association of CMP with the integrin alpha1 subunit. Unlabeled CMP competed for the binding to integrin alpha1 with 125I-CMP. These findings suggest that CMP is a potent adhesion factor for chondrocytes, particularly in the presence of type II collagen, and that integrin alpha1beta1 is involved in CMP-mediated cell adhesion and spreading. Since CMP is expressed almost exclusively in cartilage, this adhesion factor, unlike fibronectin or laminin, may play a special role in the development and remodeling of cartilage.

Animals↗
PubMed2005

The concentration, gene expression, and spatial distribution of aggrecan in canine articular cartilage, meniscus, and anterior and posterior cruciate ligaments: a new molecular distinction between hyaline cartilage and fibrocartilage in the knee joint.

The concentration, spatial distribution, and gene expression of aggrecan in meniscus, articular cartilage, and the anterior and posterior cruciate ligaments (ACL and PCL) was determined in the knee joints of five mature dogs. An anti-serum against peptide sequences specific to the G1 domain of aggrecan was employed in competitive-inhibition ELISA of guanidine HCl extracts and immunofluorescence microscopy. Gene expression was determined by Taqman real-time PCR. The concentration of aggrecan in articular cartilage (240.1 +/- 32 nMol/g dry weight) was higher than that in meniscus (medial meniscus: 33.4 +/- 4.3 nMol/g) and ligaments (ACL: 6.8 +/- 0.9 nMol/g). Aggrecan was more concentrated in the inner than the outer zone of the meniscus. Aggrecan in meniscus showed an organized, spatial network, in contrast to its diffuse distribution in articular cartilage. Thus, differences in the concentration, gene expression, and spatial distribution of aggrecan constitute another molecular distinction between hyaline cartilage and fibrocartilage of the knee.

Aggrecans↗
PubMed1958

Studies on cartilage: electron microscope observations on normal rabbit ear cartilage.

Normal rabbit ear cartilage studied with the light and electron microscope shows chondrocytes in which large lipide spherules, and an abundance of glycogen, a few small mitochondria, and relatively few elements of the endoplasmic reticulum can be identified. The chondrocytes contain, in addition, a material which stains strongly with acid fuchsin and appears in the electron microscope as a relatively dense felt-work. In electron micrographs, the matrix of normal rabbit ear cartilage consists of two components: a uniformly distributed moderately dense substance which appears as a fine meshwork without any particular pattern extending from cartilage cell border to cartilage cell border; and a three-dimensional anastomotic network of more dense material, which is best described as "felt-like" lying between the cells. The similarity between the felt-like material of the matrix and the elastic fibers described in previous electron microscope observations is discussed.

Animals↗
PubMed1991

Class II antigenicity of human cartilage: relevance to the use of homologous cartilage graft for reconstructive surgery.

The presence and distribution of class II transplantation antigens was studied on fresh and Merthiolate-preserved human nasal, tracheal, auricular, and rib cartilage using monoclonal antibodies in an indirect immunoperoxidase method. Substantial class II antigen expression was found on cells of the superficial area of the perichondrium of the nasal, auricle, and tracheal cartilages. In contrast, cartilage tissue lacked cells with detectable class II antigens. Our results indicate that the host response to fresh cartilage graft is induced by class II antigens presented in the perichondrium. A complete disappearance of this class II antigenicity of perichondrium can be achieved by means of an adequate Merthiolate preservation.

Cartilage↗
PubMed2000

Magnetic resonance imaging of articular cartilage and evaluation of cartilage disease.

Clinical magnetic resonance imaging of articular cartilage is possible by using techniques that offer high contrast between articular cartilage and adjacent structures in reasonable examination times. The fat-suppressed, three-dimensional, spoiled gradient-echo sequence has been reported to be accurate and reliable, and the addition of this sequence to a routine examination does not significantly compromise patient throughput. Fast spin-echo imaging also shows promise in the clinical evaluation of articular cartilage, because the newer, stronger-gradient systems allow thinner slice acquisition with two-dimensional sequences. Together, these sequences allow the evaluation of intrachondral lesions and surface defects. Furthermore, quantitative measurements of cartilage volume for follow-up studies are possible with the use of the fat-suppressed, three-dimensional, spoiled gradient-echo sequence.

Cartilage Diseases↗
PubMed2004

Comparison of cartilage self repairs and repairs with costal and articular chondrocyte transplantation in treatment of cartilage defects in rats.

In our experiment, we tried to assess the potential of repair of full-thickness defects in articular cartilages of rabbit femurs. An artificially made, full-thickness defect in the rabbit's femoral patellar groove was created. The defects were divided into six groups. The reparative tissue was evaluated by macroscopic, histological, and immunohistochemical examinations. The reparative tissues in defects with transplanted chondrocytes, had mostly a hyaline-like cartilage appearance and were firmly attached to the surrounding normal cartilage. Only in the control group with periosteal flap and broken subchondral plate, there were signs of partial repair. Self repair of rabbit articular cartilage is very limited. Transplantation of chondrocytes, costal and articular, without differences between groups, is a very potential treatment, producing hyaline-like repair tissue with good histological results.

Animals↗
PubMedDate not supplied

Overview of studies comparing human normal cartilage with minimal and advanced osteoarthritic cartilage.

A major area under study in the osteoarthritis (OA) research field is the characterization of specific molecular and biochemical changes that distinguish advanced diseased cartilage from less involved or normal tissue. This information is important to better define the pathogenic mechanisms that are operating during OA progression and to identify disease-specific markers. This review describes recent studies that have addressed changes in chondrocyte gene expression, proliferation, and apoptosis in "experimental" (more advanced OA cartilage) versus "control" (less involved or non-OA cartilage). Included is a comprehensive listing of recently published studies in this area with general findings. The review also includes a discussion of study design and the strengths and weaknesses of the various approaches. In addition, specific strategies to deal with some of the important issues are discussed. One particular model utilizing minimal and advanced OA cartilage obtained from the same patient is described in more detail.

Apoptosis↗