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PubMed1978

Degradation of proteoglycan in articular cartilage.

Adult rabbit articular cartilage was labelled in vivo over 48 h with [35S]sulphate and was then incubated in organ culture at pH 7.2. Approx. 65% of the tissue content of [35S]proteoglycan was released into the culture medium during the first 48 h of incubation. The average molecular size of the released proteoglycans, as assessed by fractionation on Sepharose 2B/CL and 4B/Cl, was only slightly smaller than that of the proteoglycans extracted from non-cultured cartilage with 4 M guanidine HCl. The percentage of released proteoglycans and extracted proteoglycans which formed aggregates with hyaluronic acid was approx. 25% and 75%, respectively. The results indicate that proteoglycan degradation in adult articular cartilage is initiated by a limited proteolysis of subunit core protein, with the production of non-aggregating species which diffuse readily from the tissue.

Animals↗
PubMed2006

Synthetic biodegradable microparticles for articular cartilage tissue engineering.

Articular cartilage tissue engineering procedures require the transplantation of chondrocytes that have been expanded in vitro. The expansion is carried out for a considerable time and can lead to a modulation of cell phenotype. However, microcarrier cultures have been shown to allow cell expansion while maintaining the phenotype. Here, we have used the biodegradable polyester poly(lactide-co-glycolide) (PLGA) in the form of microspheres and irregular shaped microparticles with a diameter between 47 and 210 microm. Surface modification of particles was carried out by ammonia plasma treatment and subsequent adsorption of collagen. Alternatively, particles were modified by partial hydrolysis and subsequent immobilization of an amine-terminated dendrimer. Each surface modification step was characterized by X-ray photoelectron spectroscopy. The effectiveness of the surface modification procedures was demonstrated by in vitro cell culture experiments using sheep articular cartilage chondrocytes. A significant influence of both the particle shape and the surface chemistry on the proliferation rate was observed while the phenotype was maintained independent of the surface chemistry or particle shape. Chondrocytes cultured on PLGA microspheres were further assessed for cartilage tissue formation in collagen type I gels in nude mice. The tissue that were formed showed the appearance of a hyaline-like cartilage and the presence of the microspheres substantially reduced the degree of collagen gel contraction over 1-2 months.

Animals↗
PubMed2005

A nonlinear biphasic viscohyperelastic model for articular cartilage.

Experiments on articular cartilage have shown nonlinear stress-strain curves under finite deformations as well as intrinsic viscous effects of the solid phase. The aim of this study was to propose a nonlinear biphasic viscohyperelastic model that combines the intrinsic viscous effects of the proteoglycan matrix with a nonlinear hyperelastic constitutive equation. The proposed equation satisfies objectivity and reduces for uniaxial loading to a solid type viscous model in which the actions of the springs are represented by the hyperelastic function proposed by Holmes and Mow [1990. J. Biomechanics 23, 1145-1156.]. Results of the model, that were efficiently implemented in an updated Lagrangian algorithm, were compared with experimental infinitesimal data reported by DiSilverstro and Suh [2001. J. Biomechanics 34, 519-525.] and showed acceptable fitting for the axial force (R(2)=0.991) and lateral displacement (R(2)=0.914) curves in unconfined compression as well as a good fitting of the axial indentation force curve (R(2)=0.982). In addition, the model showed an excellent fitting of finite-deformation confined compression stress relaxation data reported by Ateshian et al. [1997. J. Biomechanics 30, 1157-1164.] and Huang et al. [2005. J. Biomechanics 38, 799-809.] (R(2)=0.993 and R(2)=0.995, respectively). The constitutive equation may be used to represent the mechanical behavior of the proteoglycan matrix in a fiber reinforced model of articular cartilage.

Animals↗
PubMed2000

[The possibility of isolation, culture and storage of articular cartilage cells].

Lesions of articular cartilage are a common problem and concern millions of people world-wide. A decrease in physical activity and pain symptoms among patients resulting from damage to articular cartilage have prompted research concerning new methods allowing cartilage regeneration. State-of-the-art treatment of articular damage depends very much on genetic engineering techniques. The aim of this paper was to determine the authors' own way of isolation, proliferation and storage of chondrocytes of articular cartilage. The material consisted of 30 rabbits, from which fragments of articular cartilage were taken. The study consisted of the following stages: isolation, chondrocyte proliferation, cell and matrix identification, storage and MTT tests. Matrix digestion was achieved using the following solutions: 0.1% type IA collagenase; 0.025% trypsin, a mixture of collagenase and trypsin. The greatest amount of cells were found after digestion of the basic matter of cartilage by 0.1% solution of type IA collagenase. When ascorbic acid was added to the medium, a 25% increase in cellularity was observed. A cumulation of procollagen mRNA was noted in the isolated cells. After about 21 days the isolated cells formed a multilayer structure, with the space between the cells filled with a substance that showed typical traits for cartilage matrix. Storing the isolated cells for less than 48 hours at room temperature gave a 90% survival rate. Most cells died after less than 12 hours when stored at 4 degrees C. The described method of chondrocyte isolation proved to be effective in preparing material for treatment of articular cartilage lesion.

Cartilage, Articular↗
PubMed2000

Up-regulation of cartilage oligomeric matrix protein at the onset of articular cartilage degeneration in a transgenic mouse model of osteoarthritis.

OBJECTIVE: To investigate the suitability of cartilage oligomeric matrix protein (COMP) as a marker for articular cartilage degeneration in a transgenic mouse model of osteoarthritis (OA). METHODS: Northern blot analysis of total RNA extracted from the knee joints of transgenic Del1 mice, which harbor a short deletion in a type II collagen transgene, and of their nontransgenic littermates was used to monitor changes in COMP messenger RNA (mRNA) levels during cartilage degeneration. Immunohistochemistry was used to determine the distribution of COMP in articular cartilage, and serum levels of COMP were measured by immunoassay. RESULTS: Transient up-regulation of COMP mRNA was seen in articular cartilage of transgenic Del1 mice at the onset of OA lesions at the age of 3 months. Compared with nontransgenic controls, COMP immunostaining of articular cartilage in 3-9-month-old transgenic mice was increased, especially at the border of uncalcified and calcified cartilage. There was also a change from predominantly interterritorial to pericellular/territorial deposition of COMP. This difference persisted until the age of 15 months, when the nontransgenic controls also demonstrated articular cartilage degeneration and increased COMP immunostaining. Increased serum levels of COMP were seen in Del1 mice at the age of 4 months, correlating temporally with the onset of cartilage degeneration. CONCLUSION: These findings suggest that upregulation of COMP mRNA and redistribution of the protein are characteristic of the early stages of articular cartilage degeneration in the transgenic mouse model in which OA results from a dominant-negative mutation in the type II collagen gene. The data provide additional support for the notion that COMP is a useful marker for altered cartilage metabolism in developing OA.

Animals↗
PubMed2005

Expression profile of genes related to osteoclastogenesis in mouse growth plate and articular cartilage.

Based on developmental fate and function, cartilage tissue is broadly classified into transient cartilage (e.g. growth plate, GP) and permanent cartilage (e.g. articular cartilage, AC). The former eventually disappears and is replaced by bone during the endochondral ossification process, whereas the latter retains its permanency. Osteo(chondro)clasts, multinucleated giant cells of the monocyte/macrophage lineage, are selectively induced in the GP during endochondral ossification and play central roles in the resorption of cartilagenous matrices. The aim of this study was to investigate the factors determining the GP-specific recruitment of osteo(chondro)clasts. We especially focused on the expression pattern of the receptor activator of NF-kappaB ligand (RANKL), an essential factor for osteo(chondro)clast differentiation, and on that of epigenetic and transcriptional factors affecting RANKL gene expression. Knee joints of male BALB/c mice aged 8 weeks were dissected and subjected to immunohistochemical analysis using anti-RANKL, Runx2, Dlx5 and Msx2 antibodies. The methylation status of the mouse RANKL gene promoter in both the GP and the AC was analyzed by sodium bisulfite mapping using microdissected mouse tissue. The expression of BMP-2, -3, -4, -6 and type X collagen mRNA was examined by in situ hybridization (ISH). At the boundary between the calcifying cartilage and the hypertrophic chondrocytes of the GP, RANKL-expressing chondrocytes overlapped those expressing Runx2, Dlx5 and Msx2, near numerous osteo(chondro)clasts. Although similar BMP-2 and -4 expression was observed in chondrocytes in both the GP and the AC as well as in maturing osteoblasts, a rather restricted BMP-6 expression pattern was observed in resting and proliferating chondrocytes in the GP. On the other hand, sodium bisulfite mapping showed that mostly non-CpG methylation was similarly scattered in a non-specific manner in chondrocytes in the GP and the AC. Taken together with the fact that putative Runx2 binding elements are located in the RANKL promoter, our data suggest that Runx2, an essential transcription factor for skeletal development, is also a key regulator of RANKL expression in chondrocytes in the GP. Furthermore, a selective and sequential expression of a subset of BMP and of transcription factors may define the expression pattern of RANKL through Runx2.

Animals↗
PubMed2006

The mechanical behaviour of chondrocytes predicted with a micro-structural model of articular cartilage.

The integrity of articular cartilage depends on the proper functioning and mechanical stimulation of chondrocytes, the cells that synthesize extracellular matrix and maintain tissue health. The biosynthetic activity of chondrocytes is influenced by genetic factors, environmental influences, extracellular matrix composition, and mechanical factors. The mechanical environment of chondrocytes is believed to be an important determinant for joint health, and chondrocyte deformation in response to mechanical loading is speculated to be an important regulator of metabolic activity. In previous studies of chondrocyte deformation, articular cartilage was described as a biphasic material consisting of a homogeneous, isotropic, linearly elastic solid phase, and an inviscid fluid phase. However, articular cartilage is known to be anisotropic and inhomogeneous across its depth. Therefore, isotropic and homogeneous models cannot make appropriate predictions for tissue and cell stresses and strains. Here, we modelled articular cartilage as a transversely isotropic, inhomogeneous (TI) material in which the anisotropy and inhomogeneity arose naturally from the microstructure of the depth-dependent collagen fibril orientation and volumetric fraction, as well as the chondrocyte shape and volumetric fraction. The purpose of this study was to analyse the deformation behaviour of chondrocytes using the TI model of articular cartilage. In order to evaluate our model against experimental results, we simulated indentation and unconfined compression tests for nominal compressions of 15%. Chondrocyte deformations were analysed as a function of location within the tissue. The TI model predicted a non-uniform behaviour across tissue depth: in indentation testing, cell height decreased by 43% in the superficial zone and between 11 and 29% in the deep zone. In unconfined compression testing, cell height decreased by 32% in the superficial zone, 25% in the middle, and 18% in the deep zones. This predicted non-uniformity is in agreement with experimental studies. The novelty of this study is the use of a cartilage material model accounting for the intrinsic inhomogeneity and anisotropy of cartilage caused by its microstructure.

Animals↗
PubMed1994

Restoration of Injured or Degenerated Articular Cartilage.

Intra-articular fractures, ligamentous and meniscal injuries, and articular cartilage breakdown are major causes of degenerative joint disease. Lesions on the articular surface seem to have a limited capacity for repair and often progress inexorably toward osteoarthritis. Recent studies on joint immobilization and cartilage atrophy, however, have shown that repair and remodeling of articular cartilage may be possible. Currently used clinical methods of stimulating cartilage repair and remodeling include alteration of the loading on degenerated joints (primarily by using osteotomies), introduction of new cartilage-forming cells by perforation of subchondral bone, and soft-tissue arthroplasty. These procedures provide temporary relief in selected patients, but they often do not predictably restore long-term joint function. Experimentally, cartilage repair has been stimulated successfully with the use of allografts of periosteum and perichondrium, which serve as sources of cells with chondrogenic potential; introduction of cells grown in culture (stem cells or chondrocytes); stimulation by fibrin clot formation; artificial collagen matrices combined with cell transplants; and chondrogenic growth factors. The long-term success of all these methods has not been explored thoroughly, even in animal studies. Nevertheless, some research results are sufficiently encouraging to suggest that repair of the degenerating articular cartilage may be possible in the future.

Journal Article↗
PubMed2001

Articular cartilage. Anatomy, injury, and repair.

Articular cartilage plays a vital role in joint morphology. An understanding of articular cartilage anatomy and physiology will enable the physician to more fully appreciate its function and necessity. Articular cartilage is made up of four basic biological layers or zones. Each zone possesses attributes necessary to make articular cartilage as a whole strong, durable, and more able to withstand shear and axial forces through a joint. Cartilage metabolism is relatively slow in comparison with other tissues; hence, it is much more difficult for defects in cartilage to heal spontaneously. There are many ways in which articular cartilage can incur damage. Mechanical injury, be it acute or insidious, causes cartilage to fissure and fracture. This results in painful and inflamed joints along with disruption of the cartilage. Metabolic diseases also can produce joint destruction, inflammation, and pain. The resultant defects fail to heal spontaneously because of slow metabolism of cartilage. These chondral defects eventually may penetrate subchondral bone. Disruption of the layers of cartilage eventually will cause collapse and loss of integrity of the entire joint apparatus as a whole. More than 250 years ago, Hunter stated, "Ulcerated cartilage is a troublesome thing--once [it is] destroyed it is not repaired." Articular cartilage defects are very difficult to repair effectively. Cartilage defects can heal spontaneously, if the defect extends to subchondral bone. The reparative substance, fibrocartilage, is less durable and much less smooth. There are many techniques and procedures in which chondral or osteochondral defects can be filled. Promoting subchondral bleeding is the method most commonly used clinically. This allows pleuripotent cells to fill the defect with eventual fibrocartilage. Implants are gaining favor as a method of inducing a more pure, hyaline-like cartilage into cartilage defects. Gene therapy and tissue engineering are at the forefront of cartilage research today. Cartilage injury and repair remains today a very difficult topic of study. Understanding the anatomy of articular cartilage, the pathomechanics of injury, and methods available for cartilage repair, will help the physician more adequately approach treatment options.

Animals↗
PubMed1997

Effect of impact load on articular cartilage: development of an intra-articular fracture model.

OBJECTIVES: To investigate the biological and mechanical effects of a single-impact load on articular cartilage. DESIGN: An in vitro laboratory study was performed using mature bovine cartilage and bone, and isolated cartilage explants. Each specimen was impacted with a single load applied with a specially designed impactor and materials test machine. Chondrocyte metabolic activity and cartilage structural integrity was investigated using force displacement curves, radionuclide labeling, histology, and changes in water content. SETTING: Laboratory for Soft Tissue Research, New York, New York, U.S.A. SPECIMENS: Viable mature bovine cartilage and cartilage and bone explants. MAIN OUTCOME MEASUREMENTS: Mechanical failure, proteoglycan synthesis, water content, histology, radiography, and scanning electron microscopy changes occurring during the twenty-four-hour period immediately following impact. RESULTS: Force/displacement curves for the cartilage and bone explants demonstrated two failure-stress peaks, the first at fifty megapascals, representing cartilage failure, and a second peak at seventy-five megapascals, representing bone failure. Fine grain radiographs, histology, and scanning electron microscopy all confirmed the destruction of the cartilage in the area of direct impact (zone I) and subchondral bone failure and the detachment of the cartilage within the lesser impacted area (zone II). Proteoglycan synthesis was reduced significantly (p < 0.05) in the areas of direct impact (zone I) compared with areas with less or no impact (zones II and III, respectively). Significantly greater water content (p < 0.05) was found within the cartilage of zone I compared with zones II and III. CONCLUSIONS: Significant and possibly irreversible articular cartilage damage occurs after a single high-energy impact load.

Animals↗
PubMed2001

A noncontacting method for material property determination for articular cartilage from osmotic loading.

Articular cartilage is one of several biological tissues in which swelling effects are important in tissue mechanics and function, and may serve as an indicator of degenerative joint disease. This work presents a new approach to quantify swelling effects in articular cartilage, as well as to determine the material properties of cartilage from a simple free-swelling test. Samples of nondegenerate and degenerate human patellar cartilage were subjected to osmotic loading by equilibrating the tissue in solutions of varying osmolarity. The resulting swelling-induced strains were measured using a noncontacting optical method. A theoretical formulation of articular cartilage in a free-swelling configuration was developed based on an inhomogeneous, triphasic mechano-chemical model. Optimization of the model predictions to the experimental data was performed to determine two parameters descriptive of material stiffness at the surface and deeper cartilage layers, and a third parameter descriptive of thickness of the cartilage surface layer. These parameters were used to determine the thickness-averaged uniaxial modulus of cartilage, H(A). The obtained values for H(A) were similar to those for the tensile modulus of human cartilage reported in the literature. Degeneration resulted in an increase in thickness of the region of "apparent cartilage softening," and a decrease in the value for uniaxial modulus at this layer. These findings provide important evidence that collagen matrix disruption starts at the articular surface and progresses into the deeper layers with continued degeneration. These results suggest that the method provides a means to quantify the severity and depth of degenerative changes in articular cartilage. This method may also be used to determine material properties of cartilage in small joints in which conventional testing methods are difficult to apply.

Adult↗
PubMed2003

Experimental model for cartilage tissue engineering to regenerate the zonal organization of articular cartilage.

OBJECTIVE: Regeneration of the zonal organization of articular cartilage may be an important advancement for cartilage tissue engineering. The first goal of this study was to validate our surgical technique as a method to selectively isolate chondrocytes from different zones of bovine articular cartilage. The second goal was to confirm that chondrocytes from different zones would have different proliferative and metabolic activities in two-dimensional (2-D) and 3-D cultures. Finally, to regenerate the zonal organization, we sought to make multi-layered constructs by encapsulating chondrocytes from different zones of articular cartilage. DESIGN: Cartilage slices were removed from three (upper, middle, and lower) zones of articular cartilage of young bovine legs. Histology and biochemical composition of the cartilage slices were analyzed to confirm that they had been obtained from the proper zone. Growth kinetics and gene expression in monolayer culture and matrix formation in photopolymerizing hydrogels were evaluated. Multi-layered photopolymerizing hydrogels were constructed with chondrocytes from each zone of native cartilage encapsulated. Cell viability and maintenance of the cells in the respective layer were evaluated using the Live/Dead Viability kit and cell tracking protocols, respectively. After 3 weeks, the multi-layered constructs were harvested for histologic examination including immunohistochemistry for type II collagen. RESULTS: Analysis of histology and biochemical composition confirmed that the cartilage slices had been obtained from the specific zone. Chondrocytes from different zones differed in growth kinetics and gene expression in monolayer and in matrix synthesis in 3-D culture. Cells encapsulated in each of the three layers of the hydrogel remained viable and remained in the respective layer in which they were encapsulated. After 3-week culture, each zone of multi-layered constructs had similar histologic findings to that of native articular cartilage. CONCLUSION: We present this as an experimental model to regenerate zonal organization of articular cartilage by encapsulating chondrocytes from different layers in multi-layered photopolymerizing gels.

Animals↗
PubMed2001

[Preliminary trial of three-dimensional water-excitation magnetization transfer contrast MR imaging of articular cartilage].

MR images of articular cartilage were evaluated with a three-dimensional (3D) water-excitation sequence (repetition time/echo time/flip angle = 28 msec/14 msec/20 degrees) with and without on-resonance magnetization transfer contrast (MTC) pulse in-vitro and in-vivo. 3D water-excitation images with MTC pulse showed a significantly higher contrast-to-noise ratio between normal saline or joint effusion and articular cartilage than images without MTC pulse. In 2 patients with osteoarthritis of the knee, joint effusion showed higher signal intensity than cartilage (arthrogram-like effect) on 3D water-excitation MTC images. The contrast between joint effusion and articular cartilage on 3D water-excitation MTC images was similar to that on fat-suppressed 2D protondensity-weighted fast spin echo images. In conclusion, 3D water-excitation MTC imaging is a promising method by which to evaluate articular cartilage in osteoarthritis and cartilage defect with thin sections and a reasonable scan time.

Adult↗
PubMed1991

Phospholipase A2 is a major component of the salt-extractable pool of matrix proteins in adult human articular cartilage.

Adult human articular cartilage contains a component with an apparent molecular weight of 16 kd, which is extractable with high ionic strength buffers. This protein, which, in addition to lysozyme, is one of the most prominent components in salt extracts of adult cartilage, is not detectable in cartilage from newborns. We performed N-terminal sequence analysis to identify the protein. The amino acid sequence obtained for the first 20 residues was identical to that reported for phospholipase A2 (PLA2) from human placenta and human synovial cells. The extractable PLA2 was found to be active. The lack of PLA2 in salt extracts from newborn cartilage observed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis was confirmed by the very low levels of PLA2 activity detectable in these preparations. PLA2 was clearly present in cartilage extracts from an 18-year-old subject and a 19-year-old subject, suggesting that its accumulation begins at some stage during the adolescent growth period. The enzyme does not appear to be released from cartilage matrix under normal physiologic conditions, and it is possible that the accumulation of PLA2 in maturing cartilage is a result of the decreased matrix turnover associated with the termination of skeletal growth. Whether PLA2 is active in the cartilage matrix, its precise localization, and its effects on the resident chondrocytes remain to be determined.

Adolescent↗
PubMed1978

Long term effects of myochrysine in articular cartilage.

Intra-articularly administered sodium aurothiomalate (Myochrysine) produced aurosomes containing characteristic electron dense contents (indicating the presence of gold), in the chondrocytes of rabbit articular cartilage. At first the aurosomes were bounded by a membrane but later the electron dense contents were seen lying free in the cytoplasmic matrix. Such deposits were detectable up to 14 months after injection of Myochrysine but none were found at later time intervals (18 months and 2 years). There was a reduction in the population of superficial chondrocytes (Zone I) while those in deeper zones (Zones II and III) showed an increased content of intracytoplasmic filaments. It is thought that these are regressive or degenerative changes produced by gold.

Animals↗
PubMed1975

Comparison of proteoglycans from bovine articular cartilage.

Four bovine articular cartilages have been compared with regard to the chemical composition of the whole cartilages, the amount of proteoglycan selectively extracted with 3 M MGCl2 or with 3 M guanidine-HCl, and the compositions and physical properties of the isolated proteoglycans. The whole cartilages differ but slightly in composition. Occipital condylar cartilage, a thin cartilage from the smallest joint, contains 4% more collagen and proportionately less proteoglycan than proximal humeral, the thickest cartilage from the largest joint. Each cartilage contains a pool of proteoglycan that resists extraction with 3 M MgCl2 but is extracted with 3 M guanidine-HCl. The proteoglycan extracted from each cartilage with 3 M guanidine-HCl contains a high molecular weight proteoglycan-collagen complex demonstrated by analytical ultracentrifugation and by the turbidity of its visible and ultra-violet spectra. The four cartilages appear to differ most remarkably in the fraction of total proteoglycan extracted from each as proteoglycan-collagen complex.

Animals↗
PubMed1995

Influence of various irrigation fluids on articular cartilage.

When bovine articular cartilage was incubated in Ringer's solution, considerable amounts of proteoglycan were washed out of the cartilage. Thus, 4% of the proteoglycan was lost into the medium during an incubation of 4 hours. Subsequently, it was found that ionic aqueous media like saline or Ringer's solution extracted much more proteoglycan than ion-free media like distilled water or a variety of carbohydrate containing solutions. In separate experiments, it could be shown that solutions of 20% sorbitol and 2% mannitol exhibited particularly low proteoglycan extracting properties. It was found that the extraction of proteoglycan was dependent on the ion concentration in the aqueous media. The extraction of proteoglycan by sodium chloride was negligible at NaCl concentrations of 0.1% and lower. Proteoglycan loss from cartilage was only induced at 0.9% NaCl. Using intact rat femoral heads it could be shown that the elution of proteoglycan from cartilage occurred as well when the cartilage was intact. Here, the elution occurred at a slower rate but the differences between ionic and ion-free solutions were greater. By electronmicroscopic examination of bovine cartilage incubated in different media, it was observed that Ringer's solution induced a more uneven and rougher appearance of the cartilage surface than did 10% mannitol solution, indicating that probably a denudation of collagen fibers occurs on the loss of proteoglycan from the cartilage. Because the observed proteoglycan washout occurred within rather short periods of contact of the cartilage with the medium, it is concluded that this may be of relevance for the clinical situation during arthroscopic procedures. The use of preferably isotonic carbohydrate solutions like 5% mannitol is suggested to prevent unnecessary loss of proteoglycan from hyaline cartilage.

Animals↗