An ultrastructural study of degeneration of articular cartilage caused by experimental articular mechanical changes.
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Animals↗
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Characterization of the macromolecular components of the articular cartilage surface.
The intact surface of articular cartilage is a highly organized structure composed of a variety of macromolecules. The studies reported here deal with a partial characterization of the non-covalently bound components of the outermost layer of articular cartilage. Normal bovine and human cartilage articular surfaces were extracted for 5 min with 4-M guanidine HCl solution. Analysis and quantitation of small proteoglycans in the extract were carried out by PAGE (polyacrylamide gel electrophoresis), Western blot, and radioimmunoassays. The present studies indicate that the major proteins extracted from the articular surface of bovine and human cartilage are the collagen-binding small proteoglycans designated as fibromodulin and albumin. Fibronectin, decorin, and biglycan were also detected in smaller amounts. Immunoblotting of the surface material developed with a monoclonal antibody with keratan sulfate specificity confirmed the presence of fibromodulin coinciding with the major protein band of approximately 70-100-kDa molecular mass. Gel filtration chromatography of the surface material confirmed the previous results. Additional in vitro assays showed that the collagen-binding material extracted from the cartilage surface contained the small proteoglycans. Anti-human fibromodulin antibodies bound in significantly greater amounts to the intact articular surfaces than to cut surfaces of normal human cartilage. It is concluded that small, non-aggregating proteoglycans constitute the major proteoglycan species non-covalently bound to macromolecules at the articular surface of cartilage partially responsible for the interference of anti-collagen type II antibody binding and for the inhibition of cell adhesion to the intact surface.
Adolescent↗
Lipid composition of the tissues of human knee joints. I. Observations in normal joints (articular cartilage, meniscus, ligaments, synovial fluid, synovium, intra-articular fat pad and bone marrow).
The composition and lipid profiles of the following tissues of the human knee joint were determined: articular cartilage, meniscus, ligaments, synovial fluid, synovium, intra-articular fat pad and bone marrow. The tissues were obtained from fresh cadavers and from surgical specimens. The lipid profiles of articular cartilage, meniscus and ligaments were similar to reported analyses of other tissues that are also rich in collagen. The lipid profiles for the remaining tissues were more like the profiles found in the fat depots and fatty tissues of the human body. Both the phospholipid and fatty acid patterns of these tissues were similar within statistical deviation. These results suggest that the per cent compositions of fatty acids and the phospholipid family profile ratios have limited range variability in the "normal" tissues of the human knee. On the other hand, the per cent neutral lipid compositions and their individual profiles showed great variations among the different tissue tissues of the knee.
Adipose Tissue↗
Modified osteochondral autograft implantation for full- thickness articular cartilage lesions.
Full-thickness articular cartilage defects have been difficult to treat in patients with nonarthritic knees. A procedure is described to treat articular cartilage full-thickness lesions. Graft sites are chosen after appropriate treatment of the base of a grade IV lesion. Articular cartilage and bone are replaced into the graft site, promoting mesenchymal stem cell growth and cartilaginous coverage of the defect. Pathology, postoperative protocol, and some postoperative arthroscopic illustrations are included. This technique is simple and is associated with minimal donor-site morbidity.
Arthroscopy↗
Xeno-implantation of pig chondrocytes into rabbit to treat localized articular cartilage defects: an animal model.
Articular cartilage has only a limited ability to regenerate. The transplantation of autologous chondrocytes is currently used to treat focal defects in human articular cartilage, although use of organs, tissues, or cells from different species is being investigated as an alternative treatment. The object of this study was to use xeno-transplantation of cultured pig chondrocytes for the repair of rabbit chondral defects, and to analyze the significance of tissue rejection in this animal model. Partial chondral defects, including removal of cartilage tissue and a part of the subchondral bone, were created in the lateral femoral condyles of 30 adult New Zealand White rabbits. A periosteal flap was sutured to the native cartilage with the cambium layer facing the defect. As a control, culture medium was injected into the defect void of one group of rabbits while in a treatment group, chondrocytes, isolated from normal femoral pig cartilage, were injected into the defect void. All rabbits were killed by 24 weeks. Macroscopic changes of the cartilage were analyzed using Mankin's score. The distal femoral portion was studied histologically using hematoxylin and eosin, alcian blue, toluidine blue, and Mason's trichrome. Pig cells and pig genetic material were detected in the neo-synthesized tissue by immunohistochemical detection of SLA-II-DQ and polymerase chain reaction analysis of the gene SLA-II-DQB. The synovial membrane was studied histologically by hematoxylin and eosin staining. In the control group, on average, less than 25 percent of the chondral defect was filled. The repair tissue had an irregular surface with few cells similar to chondrocytes or fibroblasts and a minimal formation of extracellular matrix. In the treatment group, the chondral defect was approximately 90 percent filled with good integration between the neo-synthesized cartilage and the native cartilage. The repair tissue had a smooth surface with cells similar to chondrocytes and a hyaline-like extracellular matrix. The neo-synthesized cartilage was morphologically similar to hyaline cartilage. Importantly, there were no signs of graft-vs.-host rejections or infiltration by immune cells. In the neo-synthesized tissue, pig genetic material was detected in 27 +/- 5 percent of all cells. These cells containing pig genetic material were distributed throughout the neo-synthesized cartilage. We conclude that the xeno-transplantation of chondrocytes could be an alternative method for the repair of articular cartilage defects.
Animals↗
Expression of a stable articular cartilage phenotype without evidence of hypertrophy by adult human articular chondrocytes in vitro.
Chondrocytes that were isolated from adult human articular cartilage changed phenotype during monolayer tissue culture, as characterized by a fibroblastic morphology and cellular proliferation. Increased proliferation was accompanied by downregulation of the cartilage-specific extracellular matrix proteoglycan, aggrecan, by cessation of type-II collagen expression, and by upregulation of type-I collagen and versican. This phenomenon observed in monolayer was reversible after the transfer of cells to a suspension culture system. The transfer of chondrocytes to suspension culture in alginate beads resulted in the rapid upregulation of aggrecan and type-II collagen and the downregulation of expression of versican and type-I collagen. Type-X collagen and osteopontin, markers of chondrocyte hypertrophy and commitment to endochondral ossification, were not expressed by adult articular chondrocytes cultured in alginate, even after 5 months. In contrast, type-X collagen was expressed within 2 weeks in a population of cells derived from a fetal growth plate. The inability of adult articular chondrocytes to express markers of chondrocyte hypertrophy has underscored the fundamental distinction between the differentiation pathways that lead to articular cartilage or to bone. Adult articular chondrocytes expressed only hyaline articular cartilage markers without evidence of hypertrophy.
Adolescent↗
Expression of proteoglycan epitopes in articular cartilage repair tissue.
To determine if expression of specific proteoglycan epitopes distinguishes articular cartilage repair tissue from normal articular cartilage, we used seven monoclonal antibodies to examine normal articular cartilage and cartilage repair tissue from osteochondral defects 3.2 mm in diameter and 4.0 mm deep in the medial femoral condyles of 27 New Zealand white rabbits and seven cynomolgus monkeys. Following creation of the osteochondral defects, one limb of each animal was treated with cast immobilization while the other limb was treated with passive motion for two weeks. Rabbit knees were examined at eight (13 animals, 26 knees) and 36 weeks (14 animals, 28 knees) and monkey knees at eight weeks (seven animals, 14 knees) following surgery. Staining for six of the antibodies did not differ between repair cartilage and normal articular cartilage, but an antibody that recognizes atypical glycosaminoglycan structures in developing tissues (MAb 7D4) consistently distinguished repair cartilage from normal cartilage in rabbits and monkeys. Repair tissue consisting of hyaline toluidine blue-staining matrix containing chondrocytic cells uniformly showed strong 7D4 staining. In contrast, normal articular cartilage and fibrous repair tissue showed inconsistent weak 7D4 staining. At eight weeks following surgery, rabbit cartilage repair tissue stained more intensely for 7D4 than monkey cartilage repair tissue; in rabbits, cartilage repair tissue stained more intensely for 7D4 at eight weeks than at 36 weeks following surgery. Repair tissue staining for 7D4 did not differ between osteochondral defects treated with passive motion and those treated with immobilization in rabbits and monkeys. These results indicate that expression of a high level of proteoglycan epitope 7D4 distinguishes hyaline articular cartilage repair tissue from normal articular cartilage and fibrous cartilage repair tissue in the early stages of osteochondral healing, and that as hyaline articular cartilage repair tissue matures expression of 7D4 decreases. The ability to characterize repair cartilage proteoglycans with monoclonal antibodies may aid in the evaluation of the quality and maturity of cartilage repair tissue and thereby facilitate improvements in procedures for resurfacing joints.
Animals↗
Bipolar and monopolar radiofrequency treatment of osteoarthritic knee articular cartilage: acute and temporal effects on cartilage compressive stiffness, permeability, cell synthesis, and extracellular matrix composition.
The cellular, biochemical, biomechanical, and histologic effects of radiofrequency-generated heat on osteoarthritic cartilage were assessed. Articular cartilage explants (n=240) from 26 patients undergoing total knee arthroplasty were divided based on Outerbridge grade (I or II/III) and randomly assigned to receive no treatment (controls) or monopolar or bipolar radiofrequency at 15 or 30 W. Both potentially beneficial and harmful effects of radiofrequency treatment of articular cartilage were noted. It will be vital to correlate data from in vitro and in vivo study of radiofrequency thermal chondroplasty to determine the clinical usefulness of this technique.
Biomechanical Phenomena↗
Effects of sodium hyaluronate and methylprednisolone acetate on proteoglycan synthesis in equine articular cartilage explants.
OBJECTIVE: To determine effects of sodium hyaluronate (HA) on corticosteroid-induced cartilage matrix catabolism in equine articular cartilage explants. SAMPLE POPULATION: 30 articular cartilage explants from fetlock joints of 5 adult horses without joint disease. PROCEDURE: Articular cartilage explants were treated with control medium or medium containing methylprednisolone acetate (MPA; 0.05, 0.5, or 5.0 mg/mL), HA (0.1, 1.0, or 1.5 mg/mL), or both. Proteoglycan (PG) synthesis was measured by incorporation of sulfur 35-labeled sodium sulphate into PGs, and PG degradation was measured by release of radiolabeled PGs into the medium. Total glycosaminoglycan (GAG) content in media and explants and total explant DNA were determined. RESULTS: Methylprednisolone acetate caused a decrease in PG synthesis, whereas HA had no effect. Only the combination of MPA at a concentration of 0.05 mg/mL and HA at a concentration of 1.0 mg/mL increased PG synthesis, compared with control explants. Methylprednisolone acetate increased degradation of newly synthesized PGs into the medium, compared with control explants, and HA alone had no effect. Hyaluronate had no effect on MPA-induced PG degradation and release into media. Neither MPA alone nor HA alone had an effect on total cartilage GAG content. Methylprednisolone acetate caused an increase in release of GAG into the medium at 48 and 72 hours after treatment. In combination, HA had no protective effect on MPA-induced GAG release into the medium. Total cartilage DNA content was not affected by treatments. CONCLUSIONS AND CLINICAL RELEVANCE: Our results indicate that HA addition has little effect on corticosteroid-induced cartilage matrix PG catabolism in articular cartilage explants.
Animals↗
[Involvement in morphological changes of the articular cartilage of rat temporomandibular joint induced by experimental malocclusion].
The effect of malocclusion induced by increase in unilateral occlusal vertical dimension on the articular cartilage of rat mandibular condyle was histologically and immunohistologically examined. WKA rats (8 weeks) were divided into three group A: untreated (control) rats, group B: rats forced to mouth open just for 20 min, and group C: rats given malocclusion by putting the 1 mm diameter wire on the right upper molar continuously. After treatment, each rat was sacrificed periodically up to 9 weeks, and the morphological changes of condylar cartilage (articular, embryonic and transitional zones of cartilage layer) were histologically investigated. The thickness of articular cartilage in all groups was decreased in a time-dependent manner (up to 9 weeks after treatment). In group C rats, whose articular cartilage was thinnest in three groups, the reduced thickness of cartilage in the non-treated side (the left side) was same as that in the treated side which was presented with excessive molar contact. But, its occurrence in the treated side was seen 2 weeks earlier than that in the non-treated side. Even in group B rats which were only forced to open the mouth for 20 min without setting of permanent malocclusion, the thickness of condylar cartilage was decreased more than that of group A rats. When the condylar cartilages of all three groups were immunohistologically examined with anti-interleukin-1 (IL-1) antibody in order to investigate the pathophysiological involvement of IL-1, which is well-known catabolic factor to cartilage, some chondrocytes in articular cartilage were positively stained. The ratio of IL-1 positive cells increased time-dependently. IL-1-producing cells in group B and the non-treated side of group C reached to the maximal ratio at the same time when the condylar cartilage markedly decreased in thickness. However, the ratio of IL-1-positive chondrocytes in the treated side of group C was maximal four weeks after the decrease of cartilage thickness. In respect with the size of cells in cartilage, the occurrence of decreased thickness in condylar cartilage corresponded to that of the reduction of cellular size, especially in the embryonic zone of group C. These results described above suggest that malocclusion, unilateral immature occlusion, can induce the thinning of condylar cartilage which may result from the reducing size of articular chondrocytes (differentiated chondrocytes) and the accompanying decreased cartilage matrix. This change of cartilage may be caused by IL -1 that articular chondrocyte seemed to produce.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Healing of articular cartilage in intra-articular fractures in rabbits.
Intra-articular fractures were created in the distal end of the femur in adult rabbits. Fractures were then reduced in three different fashions: incomplete reduction, adequate reduction without compression of the fregments, and ideal reduction, which consisted of reduction with strong compression of the fracture fragments. Animals were killed at intervals ranging from seven weeks to one year, and the cartilage fractures were studied by light, transmission, and scanning electron microscopy, using proteoglycan stains. Cartilage fractures that were inadequately reduced or were adequately reduced without compression healed by fibrocartilage only. Fractures that were reduced with compression across the fragments healed with a tissue which, by light and electron microscopy, appeared to be hyaline cartilage, which showed the collagen and proteoglycan orientation and relationships of normal hyaline cartilage. The healing of these defects appears to be the result of a proliferation of cells emanating from the region of the tidemark, and perhaps of migration of chondrocytes from the surface into the lesion. We postulate that compression of the cartilage surfaces either creates a physical environment that allows certain chondrocytes to heal the defect with hyaline cartilage, or, by coapting the surfaces, prevents ingrowth of granulation tissue from the subchondral bone that might interfere with repair by hyaline cartilage. This study suggests a hitherto unappreciated capacity for hyaline cartilage to repair structural defects.
Animals↗
Rabbit articular cartilage defects treated by allogenic chondrocyte transplantation.
Articular cartilage defects have a poor capacity for repair. Most of the current treatment options result in the formation of fibro-cartilage, which is functionally inferior to normal hyaline articular cartilage. We studied the effectiveness of allogenic chondrocyte transplantation for focal articular cartilage defects in rabbits. Chondrocytes were cultured in vitro from cartilage harvested from the knee joints of a New Zealand White rabbit. A 3 mm defect was created in the articular cartilage of both knees in other rabbits. The cultured allogenic chondrocytes were transplanted into the defect in the right knees and closed with a periosteal flap, while the defects in the left knees served as controls and were closed with a periosteal flap alone, without chondrocytes. Healing of the defects was assessed at 12 weeks by histological studies. Allogenic chondrocyte transplantation significantly increased the amount of newly formed repair tissue (P=0.04) compared with that found in the control knees. The histological quality score of the repair tissue was significantly better (P=0.05), with more hyaline characteristics in the knees treated with allogenic chondrocytes than in the control knees. Articular cartilage defects treated with allogenic chondrocyte transplantation result in better repair tissue formation with hyaline characteristics than those in control knees.
Animals↗
The interrelationship of cell density and cartilage thickness in mammalian articular cartilage.
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Anatomy, Comparative↗
Optical and mechanical determination of Poisson's ratio of adult bovine humeral articular cartilage.
The equilibrium stiffness of articular cartilage is controlled by flow-independent elastic properties (Young's modulus, ES, and Poisson's ratio, v(s)) of the hydrated tissue matrix. In the current study, an optical (microscopic) method has been developed for the visualization of boundaries of cylindrical bovine humeral head articular cartilage disks (n = 9), immersed in physiological solution, and compressed in unconfined geometry. This method allowed a direct, model-independent estimation of Poisson's ratio of the tissue at equilibrium, as well as characterization of the shape changes of the sample during the nonequilibrium dynamic phase. In addition to optical analyses, the equilibrium behavior of cartilage disks in unconfined and confined ramp-stress relaxation tests provided a direct estimation of the aggregate modulus, H(a) and Young's modulus and, indirectly, Poisson's ratio for the articular cartilage. The mean value for Poisson's ratio obtained from the optical analysis was 0.185 +/- 0.065 (mean +/- S.D., n = 9). Values of elastic parameters obtained from the mechanical tests were 0.754 +/- 0.198 MPa, 0.677 +/- 0.223 MPa, and 0.174 +/- 0.106 for H(a), ES, and v(s), respectively (mean +/- S.D., n = 7). The similar v(s)-values obtained with optical and mechanical techniques imply that, at equilibrium for these two tests, the isotropic model is acceptable for mechanical analysis. However, the microscopic technique revealed that the lateral expansion, especially during the initial phase of relaxation, was inhomogeneous through the tissue depth. The superficial cartilage zone expanded less than the radial zone. The zonal differences in expansion were attributed to the known zonal differences in the fibrillar collagen architecture and proteoglycan concentration.
Analysis of Variance↗
A self-assembling process in articular cartilage tissue engineering.
Current therapies for articular cartilage defects often result in fibrocartilaginous tissue. To achieve regeneration with hyaline articular cartilage, tissue-engineering approaches employing cell-seeded scaffolds have been investigated. However, limitations of scaffolds include phenotypic alteration of cells, stress-shielding, hindrance of neotissue organization, and degradation product toxicity. This study employs a self-assembling process to produce tissue-engineered constructs over agarose in vitro without using a scaffold. Compared to past studies using various meshes and gels as scaffolding materials, the self-assembly method yielded constructs with comparable GAG and collagen content. By 12 weeks, the self-assembling process resulted in tissue-engineered constructs that were hyaline- like in appearance with histological, biochemical, and biomechanical properties approaching those of native articular cartilage. Overall, constructs contained two thirds more GAG per dry weight than calf articular cartilage. Collagen per dry weight reached more than one third the level of native tissue. IHC and gel electrophoresis showed collagen type II production and absence of collagen type I. More importantly, self-assembled constructs reached well over one third the stiffness of native tissue.
Animals↗
The interaction between retinoic acid and the transforming growth factors-beta in calf articular cartilage organ cultures.
In calf articular cartilage organ cultures, retinoic acid depressed proteoglycan anabolism to levels approximately 10% of control values and increased their catabolism approximately 14-fold at concentrations of 1 x 10(-8) and 1 x 10(-6) M, respectively, leading to a severe depletion of this component from the extracellular matrix (95% loss in 3 weeks). These effects were powerfully antagonized by maximal levels of transforming growth factors-beta (TGF-beta s) 1, 2, and 3, leading to preservation of matrix components. At a concentration of 1 x 10(-8) M retinoic acid, the TGF-beta s restored anabolism to control levels and lowered catabolic rates greater than 3-fold. While the TGF-beta s increased protein synthesis 2- to 3-fold over controls, retinoic acid alone did not change protein synthesis, as determined by incorporation of [3H]serine. Nevertheless, retinoic acid effectively antagonized the stimulation of protein synthesis by TGF-beta and restored control levels of synthesis at 1 x 10(-7) M. Analysis of proteins, labeled using [3H]serine and [35S]sulfate as precursors, by SDS-PAGE revealed that large molecular weight proteins (greater than 100 kDa) were not detectable in retinoic-acid-treated cultures, but treatment with the TGF-beta s restored these components in coincubation cultures, again supporting the antagonistic role of the polypeptide effectors on retinoid action. Treatment of the cultures with retinoic acid elevated levels of TGF-beta 2 synthesis, but not TGF-beta 1. While the role of the newly synthesized TGF-beta 2 in the set of events elicited by retinoic acid in articular cartilage is unclear, the results establish an intrinsic metabolic link between the isoprenoid and TGF-beta in articular cartilage. We propose that the retinoids and TGF-beta s are integral parts of a regulatory network that controls homeostasis, resorption, or growth, depending on their relative contributions.
Animals↗
Immunology of articular cartilage.
The extracellular matrix of articular cartilage is, in part, comprised of 2 macromolecular moieties, collagen and proteoglycans. This article discusses the role of an autoimmune response to these macromolecules in both inflammatory synovitis and osteoarthritis (OA). Autoimmunity to Type II collagen involving "arthrogenic epitope(s)", expressed on the Type II collagen molecule, as well as cell mediated immune responses to collagen may be relevant in the overall development of destruction of articular cartilage. In OA, a role for inflammation and the immune response to connective tissue macromolecules has been suggested by recent investigations. In this regard, autoimmunity plays a part in the progression of the degeneration of articular cartilage in OA.
Animals↗
Expression of 92-kD type IV collagenase/gelatinase (gelatinase B) in osteoarthritic cartilage and its induction in normal human articular cartilage by interleukin 1.
We report here that a 92-kD gelatinolytic metalloproteinase is expressed as protein and mRNA in human osteoarthritic cartilage, but not in normal adult articular cartilage. Western immunoblotting demonstrated that the 92-kD gelatinolytic activity corresponded to 92-kD type IV collagenase/gelatinase (gelatinase B); mRNA for gelatinase B was identified by Northern blotting. Chondrocytes from normal cartilage also exhibited mRNA for 72-kD type IV collagenase/gelatinase (gelatinase A), tissue collagenase, and stromelysin-1, and these mRNAs were increased in osteoarthritic cartilage. Regional analysis of osteoarthritic cartilage samples from four individuals revealed that gelatinase B mRNA was expressed in grossly fibrillated areas; two of four nonfibrillated cartilage samples failed to exhibit the mRNA, but did have increased levels of mRNA for other neutral metalloproteinases. IL-1 alpha treatment of normal human cartilage explants or isolated chondrocytes induced increased levels of gelatinase B and increased mRNA for tissue collagenase and stromelysin-1. Under identical conditions, mRNA levels for gelatinase A were not increased indicating that regulation of this enzyme in human articular chondrocytes is distinct from that of other metalloproteinases. Our data showing expression of gelatinase B in fibrillated cartilage suggest that it is a marker of progressive articular cartilage degradation in osteoarthritis.
Adult↗