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PubMed1992

Effects of loading on the synthesis of proteoglycans in different layers of anatomically intact articular cartilage in vitro.

The anatomically intact articular cartilage (approximately equal to 2.5 cm2) of whole bovine sesamoid bones was cultured on its bone support. A load of 5 kg was applied intermittently at 0.3 Hz by a specially designed loading apparatus for 7 days. [35S]-sulfate was added during the last 17 h of the experiment. Loading induced a 40% increase in [35S]-sulfate incorporation into aggrecans and an almost 3-fold increase in the synthesis of small proteoglycans. The loading effects occurred mainly in the upper half of the articular cartilage. Samples left unloaded for 7 days and then loaded for 7 days likewise showed an increase in [35S]-sulfate incorporation compared with unloaded controls.

Animals↗
PubMed1987

Thinning of articular cartilage in the domestic fowl.

Thinning of articular cartilage was identified in pelvic limb joints of broiler and Leghorn-type fowls. Almost all of 100 fowls examined showed cartilage thinning or loss in hip and knee joints. Particular attention was paid to proximal femora; in these, the principal mechanism of cartilage loss involved processes described as "peripheral remodelling". From the edge of cartilage sheets, fibrovascular tissue removed articular cartilage by two mechanisms. Either a pannus of fibrovascular tissue covered the articular surface or non-osseous tissue invaded through discontinuities in the bone plate. As in man, peripheral remodelling appears to be age-related and unrelated to regressive or destructive cartilage loss.

Animals↗
PubMed2006

Safety and efficacy of ultraviolet-a light-activated gene transduction for gene therapy of articular cartilage defects.

BACKGROUND: Gene therapies for articular cartilage defects are limited by the absence of an in vivo delivery system that can mediate site-specific transduction restricted to within the margins of the defect during routine arthroscopy. We have proposed the use of ultraviolet light to stimulate gene expression following infection by recombinant adeno-associated virus (rAAV). However, research has demonstrated that short-wavelength ultraviolet light (ultraviolet C), while effective, is neither safe nor practical for this purpose. We evaluated the safety and efficacy of long-wavelength ultraviolet light (ultraviolet A) from a laser to induce light-activated gene transduction in articular chondrocytes in vitro and in vivo. METHODS: The effects of ultraviolet A from a 325-nm helium-cadmium laser, delivered through a fiberoptic cable, on cytotoxicity, mutagenesis, intracellular reactive oxygen species, and light-activated gene transduction of human articular chondrocytes were evaluated in dose-response experiments of primary cultures. Cytotoxicity was determined by trypan blue exclusion. The presence of pyrimidine dimers in purified genomic DNA was determined by enzyme-linked immunosorbent assays. Intracellular reactive oxygen species levels were determined by flow cytometry at one hour and twenty-four hours. In vitro light-activated gene transduction with rAAV vectors expressing the green fluorescent protein (eGFP) or beta-galactosidase (LacZ) was determined by fluorescence microscopy and bioluminescence assays, respectively. In vivo light-activated gene transduction was quantified by stereotactic immunohistochemistry for beta-galactosidase in rabbit articular cartilage defects in the patellar groove that had been irradiated with +/-6000 J/m2 of ultraviolet A one week after direct injection of 10(7) transducing units of rAAV-eGFP. RESULTS: Ultraviolet A failed to induce significant cytotoxicity at all fluencies below 6000 J/m2. Dose-dependent cytotoxicity was observed at greater fluencies. In contrast to ultraviolet C, which induced significant (p < 0.05) pyrimidine dimer formation at all fluencies in a dose-dependent manner, ultraviolet A failed to induce DNA modifications. Conversely, ultraviolet C proved to be a poor inducer of intracellular reactive oxygen species, while ultraviolet A immediately induced high levels of intracellular reactive oxygen species, which were completely resolved twenty-four hours later. Ultraviolet A demonstrated significant light-activated gene transduction effects in vitro, which were dose-dependent (p < 0.05). In vivo, ultraviolet A mediated a tenfold increase in transduction in which 40.8% of the superficial chondrocytes adjacent to the defect stained positive for green fluorescent protein compared with 5.2% in the knees treated with no ultraviolet A (p < 0.006). CONCLUSIONS: These results provide what we believe is the first formal demonstration of an agent that can induce rAAV transduction in the complete absence of cytotoxicity and DNA modification. They also suggest that the mechanism by which long-wavelength ultraviolet light mediates site-specific gene expression is by means of the induction of intracellular reactive oxygen species. Finally, laser-derived ultraviolet A can be readily transferred through a fiberoptic cable to mediate light-activated gene transduction in vivo.

Cartilage, Articular↗
PubMed1979

Calcification of aging articular cartilage in man.

Calcification of the articular cartilage was studied ultrastructually using normal femoral heads obtained from necropsies of persons ranging in age from 11 months to 80 years. Mineral crystals which appeared during the initial stages of deposition were morphologically divided into two types. Type A crystals were slender, twisted and curved, measuring from 100 nm to 360 nm in length. Type B crystals were short, needle-like and slightly curved, measuring from 30 nm to 160 nm in length. Type A crystals were found mainly in the developing epiphysis during childhood. Type B crystals were generally found in the calcified zone of adult articular cartilage. Both types of crystals initially appeared in close proximity to extracellular membrane-invested electron dense particle called "matrix vesicles", and gradually increased in number to form calcified cartilage matrix. The morphological differences between type A and B crystals might be caused by biochemical alterations of the cartilage matrices and/or biomechanical changes in the joints of children and adults.

Adolescent↗
PubMed2006

Articular cartilage collagen: an irreplaceable framework?

Adult articular cartilage by dry weight is two-thirds collagen. The collagen has a unique molecular phenotype. The nascent type II collagen fibril is a heteropolymer, with collagen IX molecules covalently linked to the surface and collagen XI forming the filamentous template of the fibril as a whole. The functions of collagens IX and XI in the heteropolymer are far from clear but, evidently, they are critically important since mutations in COLIX and COLXI genes can result in chondrodysplasia syndromes. Here we review what is known of the collagen assembly and present new evidence that collagen type III becomes covalently added to the polymeric fabric of adult human articular cartilage, perhaps as part of a matrix repair or remodelling process.

Amino Acid Sequence↗
PubMed1980

Dibutyryl cyclic AMP affects hyaluronate synthesis and macromolecular organization in normal adult articular cartilage in vitro.

When normal adult dog articular cartilage was cultured in the presence of dibutyryl cyclic AMP a higher proportion than normal of newly synthesized 35S-labeled glycosaminoglycans was released from the tissue into the culture medium, although their net synthesis was not affected. In conjunction with this release of sulfated glycosaminoglycans, 24 times more [3H]glucosamine-labeled hyaluronic acid was released from the cartilage into the medium, and net hyaluronate synthesis was enhanced 3-fold. Virtually all of the newly synthesized hyaluronic acid in the medium was associated with proteoglycans. The proteoglycans in the medium of the dibutyryl cyclic AMP treated cultures were normal in hydrodynamic size and interacted normally with hyaluronic acid to form large aggregates. These results suggest that the increase in hyaluronate synthesis caused by dibutyryl cyclic AMP mayt have destabilized the interaction of proteoglycans with the collagen meshwork of the cartilage. The changes seen in normal adult articular cartilage after incubation with dibutyryl cyclic AMP, therefore, are similar to those which are observed in cartilage of osteoarthritic joints.

Animals↗
PubMed1994

Structural differences between two populations of articular cartilage proteoglycan aggregates.

To determine if articular cartilage contains structurally distinct populations of proteoglycan aggregates, we extracted and purified proteoglycans from canine knee cartilage under associative conditions. Equilibrium density gradient centrifugation separated three proteoglycan populations, on the basis of differences in sedimentation velocity, into groups of 21, 106, and 270 S. Electron microscopic examination showed that the 21 S samples contained free aggrecan molecules and clusters of aggrecan molecules, with a mean of five aggrecan molecules per cluster. The 106 and 270 S samples contained proteoglycan aggregates consisting of central hyaluronan filaments with multiple attached aggrecan molecules. The two populations of aggregates did not differ in mean aggrecan length or in the spacing of aggrecan molecules along the hyaluronan filaments, but the slower sedimenting aggregates (106 S) had significantly shorter hyaluronan filaments as measured by electron microscopy (mean hyaluronan length, 400 compared with 1,162 nm) and one-third as many aggrecan molecules per aggregate (mean number of aggrecan molecules per aggregate, 15 compared with 44). This study shows that articular cartilage contains aggrecan clusters and two structurally distinct populations of proteoglycan aggregates. The differences between the two types of aggregate, in particular the number of aggrecan molecules per aggregate, may reflect differences in their assembly, stability, or turnover and give them different mechanical and biological properties.

Aggrecans↗
PubMed2004

Arthroscopic evaluation of the articular cartilage after anterior cruciate ligament reconstruction: a short-term prospective study of 105 patients.

PURPOSE: Several reports have shown the progression of degenerative osteoarthritis after anterior cruciate ligament (ACL) reconstruction. No report has been published about early cartilage change after ACL reconstruction. The purpose of this study was to evaluate the articular cartilage after ACL reconstruction in a short postoperative period by arthroscopy. TYPE OF STUDY: Case series. METHODS: We examined the status of articular cartilage of 105 patients who received ACL reconstruction and second-look arthroscopy. Cartilage lesion was evaluated arthroscopically in the 6 articular surfaces independently, and these features were classified by modified Outerbridge's classification. We compared the articular cartilage at reconstruction and at second-look arthroscopy. RESULTS: A significant worsening of the status of the articular cartilage was seen after ACL reconstruction. This worsening was seen at all articular surfaces except the lateral femoral condyle. Most of the change involved softening or fibrillation. Anterior laxity and meniscal lesion had no correlation with a progression of degenerative change of articular cartilage. Patient's age influenced the progression of articular cartilage damage after reconstruction significantly in our cases. CONCLUSIONS: The status of articular cartilage was significantly worsened after ACL reconstruction. Potent risk factors causing articular cartilage damage include female gender and age of 30 years or older. LEVEL OF EVIDENCE: Level IV.

Adolescent↗
PubMed2002

Ectopic mineralization of articular cartilage in the bullfrog Rana catesbeiana and its possible involvement in bone closure.

Mineralization of the articular cartilage is a pathological condition associated with age and certain joint diseases in humans and other mammals. In this work, we describe a physiological process of articular cartilage mineralization in bullfrogs. Articular cartilage of the proximal and distal ends of the femur and of the proximal end of the tibia-fibula was studied in animals of different ages. Mineralization of the articular cartilage was detected in animals at 1 month post-transformation. This mineralization, which appeared before the hypertrophic cartilage showed any calcium deposition, began at a restricted site in the lateral expansion of the cartilage and then progressed to other areas of the epiphyseal cartilage. Mineralized structures were identified by von Kossa's staining and by in vivo incorporation of calcein green. Element analysis showed that calcium crystals consisted of poorly crystalline hydroxyapatite. Mineralized matrix was initially spherical structures that generally coalesced after a certain size to occupy larger areas of the cartilage. Alkaline phosphatase activity was detected at the plasma membrane of nearby chondrocytes and in extracellular matrix. Apoptosis was detected by the TUNEL (TDT-mediated dUTP-biotin nick end-labeling) reaction in some articular chondrocytes from mineralized areas. The area occupied by calcium crystals increased significantly in older animals, especially in areas under compression. Ultrastructural analyses showed clusters of needle-like crystals in the extracellular matrix around the chondrocytes and large blocks of mineralized matrix. In 4-year-old animals, some lamellar bone (containing bone marrow) occurred in the same area as articular cartilage mineralization. These results show that the articular cartilage of R. catesbeiana undergoes precocious and progressive mineralization that is apparently stimulated by compressive forces. We suggest that this mineralization is involved in the closure of bone extremities, since mineralization appears to precede the formation of a rudimentary secondary center of ossification in older animals.

Age Factors↗
PubMed1978

Articular cartilage degradation and the pathology of haemophilic arthropathy.

Synovial membrane and specimens of articular cartilage, obtained from the affected knee joints of 5 haemophilic patients at the time of surgical synovectomy, were studied. All the synovial specimens showed villous proliferation and multiplication of synovial cells. Haemosiderin granules were present within synovial cells and in macrophages. There was congestion and capillary proliferation. An inflammatory infiltrate of plasma cells and lymphocytes was seen in some instances. Articular cartilage changes were classified into the following 4 grades according to severity: 1--an increase in the number of surface chondrocytes with fibrous metaplasia, and the appearance of superficial fissures; 2--a fibrous vascularized overgrowth, resembling rheumatoid pannus; 3--deep fissuring and necrosis of cartilage; 4--erosion and disappearance of articular cartilage with exposure of subchondral bone. In the first 3 grades, deep nests of chondrocytes containing haemosiderin were present. These cell aggregates became larger and more degenerate as cartilage degradation progressed. Damaged articular cartilage was deficient in glycosaminoglycan (acid mucopolysaccharide). No excess enzyme activity could be demonstrated within the cartilage matrix. Immunofluorescent studies were not helpful. Electron microscopical examination revealed siderosomes within degenerate chondrocytes and synovial cells. Granules resembling haemosiderin were also present in the cartilage matrix. It is considered that iron products affect both chondrocytes and matrix adversely and play a part in articular cartilage destruction in haemophilia.

Adolescent↗
PubMed2002

Transforming growth factor-beta in calcium alginate beads for the treatment of articular cartilage defects in the rabbit.

PURPOSE: Articular cartilage has only limited capability for intrinsic repair. The use of growth factors has been suggested to improve the repair of cartilage after injury. Reliable delivery systems for these agents are needed. In this study we tested calcium alginate for the delivery of TGF-beta in the treatment of osteochondral defects in the rabbit knee. TYPE OF STUDY: Randomized trial animal study and basic science study. METHODS: In vitro, to establish the kinetics of TGF-beta release from the alginate, 125I- labeled TGF-beta was suspended in 1.2% sodium alginate at concentrations of 1 microg/mL and 10 microg/mL. Beads were formed from 50 microL aliquots and placed into standard culture medium by immersion in calcium chloride solution and incubated at 37 degrees C. A gamma counter was used to measure the amount of TGF-beta that was released into the medium at various time points. In vivo, osteochondral defects were created in the trochlear grooves of 32 New Zealand White rabbits. Defects were treated with plain alginate or with alginate containing TGF-beta at 20 ng/mL or 2,000 ng/mL. Untreated defects served as a control. Animals were killed after 6 and 12 weeks. Knee joints were evaluated grossly with a 12-point grading scale. Histologic sections of the repair tissue were stained with Safranin O and evaluated using a 24-point grading scale by 2 independent blinded observers. Mean scores and standard deviations were calculated. P values were determined using the Student t test. RESULTS: The TGF-beta was released at a surprisingly slow but steady rate. Release rates extrapolated from the gamma counter measurements were 0.25% per hour and 0.33% per hour, for the 1 microg/mL and 10 microg/mL beads, respectively. Gross analysis scores at 6 and 12 weeks resulted in higher scores for both TGF-beta groups without reaching statistical significance. The lower TGF-beta concentration reached the highest scores, whereas the higher concentration (2,000 ng/mL) resulted in increased osteophyte formation. Histologic analysis at 6 weeks resulted in average scores ranging from 14.5 for empty defects and 18.1 for alginate-treated defects, to 20.0 and 20.3 for the 2,000 ng/mL and 20 ng/mL TGF-beta groups, respectively (P <.05). At 12 weeks, histologic scores ranged from 14.9 for empty and 14.5 for alginate to 20.1 and 20.5 for the 2,000 ng/mL and 20 ng/mL TGF-beta groups, respectively (P <.05). These results indicate a significant improvement of the quality of the repair tissue at 6 and 12 weeks with TFG-beta treatment, especially at the lower concentration. CONCLUSIONS: The use of alginate allows the controlled delivery of TGF-beta selectively to the site of injury, potentially avoiding systemic side effects. Furthermore, treatment with TGF-beta appears to improve the repair of articular cartilage defects. Longer-term studies are needed to assess whether the benefits of the TGF-beta treatment can be sustained.

Alginates↗
PubMed2006

The effects of intermittent hydrostatic pressure on self-assembled articular cartilage constructs.

To date, static culture for the tissue engineering of articular cartilage has shown to be inadequate in conferring functionality to constructs. Various forms of mechanical stimuli accompany articular cartilage development in vivo, and one of these is hydrostatic pressure. This study used histology, biochemistry, and biomechanics to examine the effects of intermittent hydrostatic pressure, applied at 10 MPa and 1 Hz for 4 h per day for 5 days per week for up to 8 weeks on self-assembled chondrocyte constructs. The self-assembling process is a novel approach that allows engineering of articular cartilage constructs without the use of exogenous scaffolds. The self-assembled constructs were found to be capable of enduring this loading regimen. Significant increases in collagen production were only observed in pressurized samples. Intermittent hydrostatic pressure prevented a significant decrease in total GAG, which was significant in controls. Aside from the beneficial effects intermittent hydrostatic pressure may have on ECM synthesis, its effects on mechanical properties may require longer culture periods to manifest. This study demonstrates the successful use of the self-assembling process to produce articular cartilage constructs. It also shows for the first time that long-term culture of tissue-engineered articular cartilage construct benefits from intermittent hydrostatic pressure.

Animals↗
PubMed2006

High-impact athletics after knee articular cartilage repair: a prospective evaluation of the microfracture technique.

BACKGROUND: Knee articular cartilage injuries in athletes present a therapeutic challenge and have been identified as an important cause of permanent disability because of the high mechanical joint stresses in athletes. PURPOSE: To determine whether microfracture treatment of knee articular cartilage injuries can return athletes to high-impact sports and to identify the factors that affect the ability to return to athletic activity. STUDY DESIGN: Case series; Level of evidence, 4. METHODS: Thirty-two athletes who regularly participated in high-impact, pivoting sports before articular cartilage injury were treated with microfracture for single articular cartilage lesions of the knee. Functional outcome was prospectively evaluated with a minimum 2-year follow-up by subjective rating, activity-based outcome scores, and the ability for postoperative participation in high-impact, pivoting sports. RESULTS: At last follow-up, 66% of athletes reported good or excellent results. Activity of daily living, Marx activity rating scale, and Tegner activity scores increased significantly after microfracture. After an initial improvement, score decreases were observed in 47% of athletes. Forty-four percent of athletes were able to regularly participate in high-impact, pivoting sports, 57% of these at the preoperative level. Return to high-impact sports was significantly higher in athletes with age <40 years, lesion size <200 mm(2), preoperative symptoms <12 months, and no prior surgical intervention. CONCLUSION: Microfracture is an effective first-line treatment to return young athletes with short symptomatic intervals and small articular cartilage lesions of the knee back to high-impact athletics.

Activities of Daily Living↗
PubMed1997

The proteoglycan metabolism, morphology and viability of articular cartilage treated with a synthetic matrix metalloproteinase inhibitor.

Matrix metalloproteinases (MMP) are among the key enzymes responsible for the proteolytic destruction of articular cartilage during chronic rheumatic diseases. Articular cartilage is one potential target for drugs designed to inhibit the activity of MMPs in order to stop or to slow down the proteolytic destruction of the extracellular matrix of cartilage. The purpose of this study was to investigate the effect of the synthetic inhibitor of MMPs U-24522 for its ability (1) to inhibit in vitro the activity of MMP-proteoglycanases; (2) to modulate the morphology and viability of cartilage explants; and (3) to modify the biosynthesis and release of proteoglycans from articular cartilage explants. U-24522 dose-dependently inhibited the activity of MMP-proteoglycanases and significantly reduced the release of proteoglycans from interleukin-1 treated bovine articular cartilage explants when tested at concentrations ranging from 10(-4) to 10(-9) M. This hydroxamic acid derivative proved not to be harmful to chondrocyte viability and cartilage morphology. In addition, U-24522 had no effect on the rate of proteoglycan biosynthesis of interleukin-1 treated cartilage explants and increased the percentage of newly synthesized proteoglycans to form macromolecular aggregates. Thus U-24522 combines direct inhibitory potential on the activity of MMP-proteoglycanases with the inhibition of interleukin-1 stimulated proteoglycan loss from articular cartilage explants without affecting the morphology, viability and biosynthesis of proteoglycans of bovine articular cartilage explants.

Animals↗
PubMed1998

Permeability of articular cartilage to matrix metalloprotease inhibitors.

PURPOSE: To develop an in vitro cartilage permeation model for cartilage permeability study and to evaluate the effects of molecular hydrophilicity and cartilage location on the permeability of articular cartilage to matrix metalloprotease inhibitors. METHODS: An in vitro cartilage permeation model was developed and utilized to determine the permeability of articular cartilage to the matrix metalloprotease inhibitors of different hydrophilicity. Permeability coefficients were obtained by measuring the steady-state flux of the inhibitor compounds. HPLC methods were also developed and employed for the analysis of drug levels in assay media. RESULTS: The relationship between permeability and hydrophilicity of drug molecules was examined. Results indicated that the permeability coefficient increased with increasing hydrophilicity of the molecule. Additionally, the relationship between the permeability and the location of the cartilage section within the animal joint was investigated. Our results showed that the drug molecules penetrated faster in the surface layer cartilage than in the deep layer cartilage. CONCLUSIONS: Increasing the hydrophilicity of a molecule would increase its permeability across articular cartilage. The in vitro cartilage permeation model developed could be used to rank order drug compounds according to their cartilage permeability profiles and to aid in drug selection and development.

Animals↗
PubMed1997

Scanning electron microscopy of "fibrillated" and "malacic" human articular cartilage: technical considerations.

Specimens of articular cartilage from human knees with gross evidence of malacia (dull appearance and/or softness) or fibrillation (exposed fibrous strands and/or staining with India ink) were prepared for scanning electron microscopy (SEM) and compared to cartilage from apparently intact regions. Vertical cryofractures were made through the center of each specimen, so the matrix collagen structure and its relationship to surface features could be examined. Soft, dull, malacic cartilage was characterized by the presence of numerous clefts among the collagen fibers within the most superficial region of the cartilage. In one form of this condition, these clefts did not extend through the articular surface. In a second form, usually observed where the tangential zone was normally thin or absent, the free ends of radial collagen fibers were exposed, but the deeper layers were intact. Two forms of fibrillation were also identified. The first is created by separation of the superficial lamellae which curl up from the tangential layer and form frondlike projections above the normal plane of the joint surface. In the second, deep radial fibers are exposed by vertical fissures. This second form is associated with advanced damage to the joint. The early stages of cartilage failure are characterized by debonding among the major collagen fiber tracts. This process may initiate in the deep tangential zone where the radial fibers cross into the surface. The patterns of the degenerative changes are dictated by the original architecture of the collagen matrix. The microscopic findings do not correlate adequately with conventional gross grading. SEM provides useful information about injured articular cartilage.

Adolescent↗
PubMed1997

The structure of the keratan sulphate chains attached to fibromodulin from human articular cartilage.

The small keratan sulphate proteoglycan, fibromodulin, has been isolated from pooled human articular cartilage. The main chain repeat region and the chain caps from the attached N-linked keratan sulphate chains have been fragmented by keratanase II digestion, and the oligosaccharides generated have been reduced and isolated. Their structures and abundance have been determined by high pH anion-exchange chromatography. These regions of the keratan sulphate from human articular cartilage fibromodulin have been found to have the following general structure: [structure: see text]. Significantly, both alpha(2-6)- and alpha(2-3)-linked N-acetyl-neuraminic acid have been found in the capping oligosaccharides. Fucose, which is alpha(1-3)-linked as a branch to N-acetylglucosamine, has also been found along the length of the repeat region and in the capping region. The chains, which have been found to be very highly sulphated, are short; the length of the repeat region and chain caps is ca. nine disaccharides. These data demonstrate that the structure of the N-linked keratan sulphate chains of human articular cartilage fibromodulin is similar, in general, to articular cartilage derived O-linked keratan sulphate chains. Further, the general structure of the keratan sulphate chains attached to human articular cartilage fibromodulin has been found to be generally similar to that of both bovine and equine articular cartilage fibromodulin.

Acetylglucosaminidase↗
PubMed1975

In vitro wear of articular cartilage.

Seeking a reliable chemical index of the wear of articular cartilage during in vitro experiments, the contents of hydroxyproline, hexosamine, and the amino acid composition of adult bovine articular cartilage were determined as functions of depth from the surface. The hydroxyproline content, expressed as per cent of dry weight of tissue, was constant throughout the thickness of the tissue except in a surface region approximately twenty-five micrometers thick; the hexosamine content in this region was less than in the interior of the tissue; the collagen content was higher and the amino acid composition was less like that of pure collagen here than in the interior, indicating that the content of noncollagenous protein in the superficial layer of cartilage was greater than that in the interior. It was also evident that adult bovine articular cartilage contains significant amounts of collagen with a low hydroxylysine content, presumably Type I as well as Type II. Since the content of hydroxyproline is constant throughout the cartilage and the collagen and proteoglycan constituents of the intact tissue are relatively insoluble, the hydroxyproline content of the lubricant and the wear debris can be used to measure the extent of wear of articular cartilage during in vitro experiments. However, approximately 10 per cent of the hydroxyproline and 50 to 60 per cent of the glycosaminoglycans of the wear debris are dissolved in the lubricating fluid. Therefore, both the lubricant (solvent) and the solid wear debris must be analyzed to determine the amount of cartilage wear.

Amino Acids↗