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PubMed1996

Integrins on joint cartilage chondrocytes and alterations by ofloxacin or magnesium deficiency in immature rats.

Recently, we showed that magnesium deficiency induces lesions in knee joint cartilage from 5-week-old rats that are very similar to ofloxacin-induced cartilage defects. We concluded that quinolone-induced arthropathy is probably due to chelation of magnesium and thus a deficit in functionally available magnesium in joint cartilage (Stahlmann et al. 1995). As magnesium deficiency in joint cartilage could impair chondrocyte-matrix interaction which is mediated by cation-dependent integrin receptors of the beta 1-subfamily, we investigated integrin expression in joint cartilage from untreated, ofloxacin-treated and magnesium-deficient Wistar rats. With immunohistochemical methods using monoclonal and polyclonal antibodies, we showed that the integrin pattern in joint cartilage from rats corresponded largely to integrin expression described for human cartilage tissue: beta 1, alpha 1, alpha 3 and alpha v subunits and the alpha 5 beta 1 and alpha v beta 3 heterodimers were consistently expressed. Joint cartilage lesions were detected in ofloxacin-treated and magnesium-deficient rats. Lesions were more pronounced in the quinolone-treated group. Expression of several integrins was reduced in the vicinity of lesions after oral treatment with 2 x 600 mg ofloxacin/kg for 1 day. Gross-structural lesions (e.g., cleft formation, unmasked collagen fibres) in magnesium-deficient rats were very similar but changes in integrin expression were less pronounced. On the other hand, changes in cartilage matrix composition showed similar alterations in ofloxacin-treated and magnesium-deficient rats: fibronectin deposition in the cartilage matrix increased in both groups while glycosaminoglycan content decreased. In summary, similar defects occur in ofloxacin-treated and magnesium-deficient rats and with immunohistochemical methods subtle differences are demonstrable.

Animals↗
PubMed1999

The effects of NSAID on the matrix of human articular cartilages.

The present paper presents data obtained over a 12 year period, on the matrix synthesis and turnover in some 650 arthritic and 180 non-arthritic (N) human cartilages using a standardised in vitro method. When the relative metabolic (synthetic/repair activity) of these human cartilages was compared, it was demonstrated that in osteoarthritis (OA) and rheumatoid arthritis (RA) cartilages synthetic activity was diminished by approximately 50% as compared with N cartilages. However, the turnover rate of matrix was not significantly different between Non-arthritic and OA, but was very substantially increased in RA cartilages compatible with the activity of inflammatory cells and proteolytic enzymes released from pannus. The action of 13 NSAIDs was compared in terms of their effect on cartilage GAG synthesis. 3 of these NSAIDs were also studied in terms of their effect on cartilage collagen synthesis. Consideration of the results in this study and from published material, led to the suggestion that NSAIDs may be divided into 3 categories in respect of their in vitro action on the extracellular matrix of human arthritic cartilages: 1. Those such as Aceclofenac, Tenidap and Tolmetin which can stimulate matrix synthesis 2. Those such as Piroxicam, Tiaprofenic Acid and Aspirin which appear to be without significant effect on matrix synthesis and, 3. Those like Naproxen, Ibuprofen, Indomethacin, Nimezulide which significantly inhibit matrix synthesis. It is suggested that the stimulatory action of group 1 NSAID is due to inhibition of locally produced IL1 and consequent expression of growth factor activity. Other NSAIDs may also inhibit IL1 synthesis or release, but probably do not have a beneficial effect on chondrocyte synthetic activity as they have toxic effects on cartilage metabolism. These experiments led to the suggestion that NSAIDs such as Aceclofenac would be appropriate for long-term treatment of arthritic conditions provided that one is prepared to extrapolate between in vitro experiments on human cartilage and what may be happening in vivo.

Adult↗
PubMed1999

Functional analysis of articular cartilage deformation, recovery, and fluid flow following dynamic exercise in vivo.

The function of articular cartilage depends on the interaction between the tissue matrix and the interstitial fluid bound to the proteoglycan molecules. Mechanical loading has been shown to be involved in both the metabolic regulation of chondrocytes and in matrix degeneration. The purpose of the present study was therefore to analyze the deformation, recovery, and fluid flow in human articular cartilage after dynamic loading in vivo. The patellae of 7 volunteers were imaged at physical rest and after performing knee bends, with a specifically optimized fat-suppressed FLASH-3D magnetic resonance (MR) sequence. To measure cartilage deformation, the total volume of the patellar cartilage was determined, employing 3D digital image analysis. Patellar cartilage deformation ranged from 2.4 to 8.6% after 50 knee bends, and from 2.4% to 8.5% after 100 knee bends. Repeated sets of dynamic exercise at intervals of 15 min did not cause further deformation. After 100 knee bends, the cartilage required more than 90 min to recover from loading. The rate of fluid flow during relaxation ranged from 1.1 to 3.5 mm(3)/min (0.08 to 0.22 mm(3)/min per square centimeter of the articular surface) and was highly correlated with the individual degree of deformation after knee bends. The data provide the first quantification of articular cartilage recovery and of the rate of fluid flow between the cartilage matrix and surrounding tissue in intact joints in vivo. Measurement in the living opens the possibility of relating interindividual variations of mechanical cartilage properties to the susceptibility of developing joint failure, to assess the load-partitioning between the fluid phase and solid cartilage matrix during load transfer, and to determine the role of mechanically induced fluid flow in the regulation of the metabolic activity of chondrocytes.

Adult↗
PubMed2001

The development of articular cartilage: evidence for an appositional growth mechanism.

It is well-established that cartilage grows by a combination of matrix secretion, cell hypertrophy and cell proliferation. The extent to which this growth is by appositional, as opposed to interstitial mechanisms, however, remains unclear. Using the knee joints of the marsupial Monodelphis domestica to study cartilage growth, we have combined an immunohistochemical study of the TGF-beta family of cartilage growth and differentiation factors between 30 days postpartum to 8 months, together with a stereological analysis of cartilage morphology during growth. Furthermore, to gain an insight into the generation of the characteristic zones within cartilage, we have examined the effects of intra-articular administration of bromodeoxyuridine, an agent that is incorporated into DNA during cell division and blocks further cell cycling. During early growth, TGF-beta2 and -beta3 were widely expressed but TGF-beta1 was less so. After the formation of the secondary centre of ossification, all isoforms became more restricted to the upper half of the tissue depth and their distribution was similar to that previously described for IGFs, and PCNA-positive cells. Stereological analysis of tissue sections from the femoral condylar cartilage at 3 and 6 months showed that there was a 17% increase in total cartilage volume but a 31% decrease in cell density on a unit volume basis. Finally, cell-cycle perturbation with BrDU, which was injected into the knee joints of 3-month-old animals and analysed 1 and 4 months post-injection, revealed that the chondrocytes occupying the transitional zone were depleted 1 month post-injection, resulting in thinning of the articular cartilage. This effect was reversed 4 months post-injection. Immunohistochemical analysis revealed that BrDU-treatment altered the expression patterns of all TGF-beta isoforms, with a marked reduction in labelling of TGF-beta1 and -beta3 isoforms in the upper half of the cartilage depth. Overall, the data lends further support to the notion of articular cartilage growing by apposition from the articular surface rather than by interstitial mechanisms.

Animals↗
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↗
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↗
PubMed2002

Ultrasound detection of trypsin-treated articular cartilage: its association with cartilaginous proteoglycans assessed by histological and biochemical methods.

We studied the correlation between histological imaging quantification and the biochemical assessment of proteoglycan (PG) content in articular cartilage in vitro, which served as a basis for the validation of ultrasound detection as a noninvasive tool in the assessment of PG changes in full-thickness articular cartilage. Articular cartilage of 14 intact fresh bovine femoral condyles was used for trypsin digestion. Full-thickness articular cartilage cylinders, 3 mm in diameter, were harvested at time intervals of 0.5, 1, 2, and 3 h after trypsin digestion. Each cartilage cylinder was then cut into two equal parts for either histomorphometric quantification of the PG area fraction stained with Safranine O or conventional biochemical assessment of uronic acid content. In addition, five fresh mature bovine patellae were used for the validation of an ultrasound compression system developed for testing the potential layered biomechanical properties of articular cartilage, including the equilibrium compressive modulus, i.e., the slope of the linear regression of the equilibrium stress-strain curve. Results showed that PG content in the articular cartilage was significantly decreased with increasing time of trypsin digestion, both histologically and biochemically, with a significant correlation of r = 0.502 ( P < 0.001). Ultrasound measurements demonstrated differences in the equilibrium compressive moduli of the digested zone, the undigested zone, and the entire articular cartilage layer, as well as a characteristically large ultrasound reflection signal detected in the interface of the trypsin digestion front of articular cartilage. The results of this study suggested that the histomorphometric quantification of PG content could be used to reflect not only PG quantity but also its spatial distribution; also, the ultrasound compression system might have potential for the non-invasive detection of pathological changes in articular cartilage.

Animals↗
PubMed2006

Effect of compressive strain on cell viability in statically loaded articular cartilage.

Physiological loading of articulating joints is necessary for normal cartilage function. However, conditions of excessive overloading or trauma can cause cartilage injury resulting in matrix damage and cell death. The objective of this study was to evaluate chondrocyte viability within mechanically compressed articular cartilage removed from immature and mature bovine knees. Twenty-three mature and 68 immature cartilage specimens were subjected to static uniaxial confined-creep compressions of 0-70% and the extent of cell death was measured using fluorescent microscopic imaging. In both age groups, cell death was always initiated at the articular surface and increased linearly in depth with increasing strain magnitude. However, most of the cell death was localized within the superficial zone (SZ) of the cartilage matrix with the depth never greater than approximately 500 microm or 25% of the thickness of the test specimen. The immature cartilage was found to have a significantly greater (> 2 times) amount (depth) of cell death compared to the mature cartilage, especially at the higher strains. This finding was attributed to the lower compressive modulus of the immature cartilage in the SZ compared to that of the mature cartilage, resulting in a greater local matrix strain and concomitant cell surface membrane strain in this zone when the matrix was compressed. These results provide further insight into the capacity of articular cartilage in different age groups to resist the severity of traumatic injury from compressive loads.

Aging↗
PubMed2003

Fibroblast growth factor 2 in synovial fluid from an osteoarthritic knee with cartilage regeneration.

The levels of fibroblast growth factor 2 (FGF2) in synovial fluid of osteoarthritic knees were measured. The correlation between FGF2 and the severity of cartilage degeneration in varus-deformed knees with medial compartmental osteoarthritis or the articular cartilage regeneration that occurs after high tibial osteotomy (HTO) were investigated. Knees that underwent total knee arthroplasty (TKA) were categorized as either mildly or severely degenerated according to a modified Outerbridge's grading system for degeneration of articular cartilage. Regeneration of articular cartilage was observed in a biopsy specimen from the medial femoral condyle removed with the patient's consent during hardware removal approximately 2 years after HTO. The joint fluid FGF2 level was measured at that time using an enzyme-linked immunosorbent assay. Cartilage regeneration was classified as immature or mature according to the staging for regeneration of articular cartilage. The histological findings were analyzed using Pineda's evaluation method for cartilage regeneration. The mean concentration of FGF2 was 57.4 +/- 17.6 pg/ml in the joint fluid from knees with severely degenerated cartilage. This was higher than the FGF2 concentration found in the mildly degenerated group. Approximately 2 years after HTO the FGF2 level in synovial fluid was lower in knees with mature regenerated cartilage than in those with immature regeneration. Osteoarthritic knees at a more mature regeneration stage had a lower Pineda's histological score. This result suggested that the FGF2 concentration in knees with osteoarthritis was influenced by articular cartilage degeneration and regeneration, and it correlated with the histological evaluation.

Aged↗
PubMed1983

Proteoglycan extraction of sized cartilage particles.

The relationship between cartilage thickness and proteoglycan extractability was examined. Bovine nasal cartilage slices (20, 100, and 500 micron thicknesses) were extracted with low-ionic-strength buffer and 4 M guanidine hydrochloride. The extractability of proteoglycans with both solutions depended on slice thickness. Thinner slices yielded greater amounts of proteoglycans. Sixty-three percent of the total cartilage uronic acid was extracted from 20-micron cartilage slices with low-ionic-strength buffer while only 7% was extracted for 500-micron slices. Each fivefold increase in cartilage surface area led to a threefold increase in uronic acid extraction with low-ionic-strength buffer. Extraction of proteoglycan aggregates was directly proportional to the cartilage surface area whereas extraction of non-aggregated proteoglycans, per surface area, increased with increasing cartilage thickness. These data are consistent with the hypothesis that proteoglycan aggregates are extracted mainly from the cartilage surface while non-aggregated proteoglycans diffuse from deep within the cartilage. Extraction with low-ionic-strength buffer occurred in two phases. There was an initial rapid loss of proteoglycans in which 1/3 to 1/2 of all proteoglycans eluting over 6 days were extracted during the first 30 min. Subsequent extraction was much slower with decreasing amounts extracted on each consecutive day. The initial rapid loss of proteoglycans was probably due to the steep osmotic-pressure gradient existing when the cartilage was placed in the low-ionic-strength buffer.

Animals↗
PubMed1985

Histomorphometric analysis of cartilage and subchondral bone in mandibular condyles of young human adults at autopsy.

After demineralization, sagittal sections were made from the lateral, the central and the medial parts of 33 mandibular condyles from people aged 20 to 36 years, and studied for undifferentiated mesenchymal (UM) cells, cartilage and subchondral bone, the thickness of which were measured. Two condyles showed a continuous layer of UM cells extending all over. In 13 condyles, UM cells were absent; 18 condyles showed variability in UM cell occurrence in one or more out of the nine standardized areas. In 14 condyles, non-hypertrophic cartilage was present, 10 condyles showed hypertrophic cartilage and in nine condyles hyperplastic cartilage. Hyperplastic cartilage was associated with minimal numbers of UM cells. In combination with hypertrophic cartilage the UM cell layer appeared less irregular. Of nine condyles with incongruence of the cartilage-bone interface and the articular surface, seven showed hyperplastic cartilage. Six out of these seven were free of bony changes. A negative correlation was found between the presence of UM cells and the condylar-cartilage thickness (p less than 0.05). These results suggest that condylar changes are initiated by alterations in the cartilage and that changes in the bone are secondary.

Adult↗
PubMed1976

Stimulation of cartilage macromolecule synthesis by adenosine 3',5'-monophosphate.

The role of cyclic AMP in the regulation of cartilage macromolecule synthesis in vitro was studied in pelvic cartilage from 10-12 day chick embryos. Incubation of cartilages in medium containing 0.5 mM cyclic AMP resulted in a 30% inhibition of 35SO4-2, [3H]leucine and [3H]uridine incorporation into proteoglycan, total protein and RNA, respectively. Higher concentrations of cyclic AMP had no greater effects. In contrast, butyrylated cyclic AMP derivatives (0.5-5.0 mM) added to the incubation medium stimulated (50-100%) the incorporation of these radiolabeled precursors into cartilage macromolecules. Theophylline, in concentrations (0.1-0.5 mM) which raise intracellular cyclic AMP, also increases the incorporation of radiolabeled precursors into macromolecules. The data indicate that exogenous cyclic AMP and butyrylated cyclic AMP derivatives have paradoxical effects on cartilage macromolecule synthesis. Butyrylated cyclic AMP derivatives, not exogenous cyclic AMP, mimic the effects of intracellular cyclic AMP. Incubation of embryonic chicken cartilage with exogenous cyclic AMP results in the extracellular degradation of the cyclic AMP to adenosine. Adenosine (0.125 mM) inhibits precursor incorporation into cartilage macromolecules. The metabolism of exogenous cyclic AMP generates sufficient adenosine to account for the observed inhibitory effects of exogenous cyclic AMP on cartilage macromolecule synthesis. Butyrylated cyclic AMP derivatives are not degraded during incubation with cartilage. The data indicate that cartilage is a tissue in which the effect of cyclic AMP is to stimulate anabolic processes.

Animals↗
PubMed1988

The fate of Meckel's cartilage chondrocytes in ocular culture.

Modulation of the chondrocyte phenotype was observed in an organ culture system using Meckel's cartilage. First branchial arch cartilage was dissected from fetal rats of 16- and 17-day gestation. Perichondrium was mechanically removed, cartilage was split at the rostral process, and each half was grafted into the anterior chamber of an adult rat eye. The observed pattern of development in nonirradiated specimens was the following: hypertrophy of the rostral process and endochondral-type ossification, fibrous atrophy in the midsection, and mineralization of the malleus and incus. A change in matrix composition of the implanted cartilage was demonstrated with immunofluorescence staining for cartilage-specific proteoglycan (CSPG). After 15 days of culture, CSPG was found in the auricular process but not in the midsection or rostral process. In order to mark the implanted cells and follow their fate, cartilage was labeled in vitro with [3H]thymidine [3H]TdR). Immediately after labeling 20% of the chondrocytes contained [3H]TdR. After culturing for 5 days, 20% of the chondrocytes were still labeled and 10% of the osteogenic cells also contained radioactive label. The labeling index decreased in both cell types with increased duration of culture. Multinucleated clast-type cells did not contain label. Additional cartilages not labeled with [3H]TdR were exposed to between 20000 and 6000 rad of gamma irradiation before ocular implantation. Irradiated cartilage did not hypertrophy or form bone but a fibrous region developed in the midsection. Cells of the host animal were not induced to form bone around the irradiated cartilage. Our studies suggest that fully differentiated chondrocytes of Meckel's cartilage have the capacity to become osteocytes, osteoblasts, and fibroblasts.

Animals↗
PubMed1992

An analysis of the squeeze-film lubrication mechanism for articular cartilage.

An asymptotic analysis of a lubrication problem is presented for a model of articular cartilage and synovial fluid under the squeeze-film condition. This model is based upon the following constitutive assumptions: (1) articular cartilage is a linear porous-permeable biphasic material filled with a linearly viscous fluid (i.e. Newtonian fluid); (2) synovial fluid is also a linearly viscous fluid. The geometry of the problem is defined by assuming that (1) cartilage is a uniform layer of thickness H; (2) synovial fluid is a very thin layer compared to H; (3) the radius R of the load-supporting area (or the effective radius of curvature of joint surface, Ri) is large compared to H. Squeeze-film action is generated in the lubricant by a step loading function applied onto the two bearing surfaces. The model assumptions and the material properties yield two small parameters in the mathematical formulation. Based on these two small parameters, two coupled nonlinear partial differential equations were derived from an asymptotic analysis of the problem: one for the lubricant (analogous to the Reynolds equation) and one for the cartilage. For known properties of normal cartilage, our calculations show: (1) the cartilage layer deforms to enlarge the load-supporting area; (2) cartilage deformation acts to reduce the lateral fluid speed in the lubricant, thus prolonging the squeeze-film time which ranges from 1 to 10 s; (3) lubricant fluid in the gap is forced from the central high-pressure region into cartilage, and expelled from the tissue at the low-pressure periphery of the load-bearing region; and (4) tensile hoop stress exists at the cartilage surface despite the compressive squeeze-film loading condition. This hoop stress results directly from the radial flow of the interstitial fluid in the cartilage layer.

Biomechanical Phenomena↗
PubMed1987

The development of tone in the smooth muscle of guinea-pig isolated tracheal preparations may be influenced by prostanoids released from the adjacent airway cartilage.

Guinea-pig tracheal strip preparations containing cartilage, placed under an applied load in vitro, develop tone spontaneously. The finding that spontaneous tone is reduced by indomethacin suggests that one or more prostanoids are involved in the development of spontaneous tone in this species. In this study we examined the effects of removing the cartilage component of the preparations on changes in tone induced by indomethacin and isoproterenol. In contrast to preparations containing cartilage, tissues devoid of cartilage, did not develop tone after the application of an initial 1 g resting load. Indomethacin (1 microM) reduced resting tone by 0.62 +/- 0.14 g in cartilage-containing tissues but, in contrast, reduced tone by only 0.03 +/- 0.01 g in tissues devoid of cartilage. Furthermore, relaxation responses (0.38 +/- 0.05 g) to isoproterenol (1 microM) could be produced in cartilage-containing preparations but not in cartilage-free preparations. Radioimmunoassays indicated that the release of PGE2, PGF2 alpha and 6-keto PGF1 alpha, the end-product of PGI2 breakdown, was diminished in preparations lacking cartilage. Thus, in guinea-pig airway preparations cartilage is apparently a source of sufficient prostanoids to induce spontaneous tone.

Animals↗
PubMed1976

The effects of proteolytic enzymes on the mechanical properties of adult human articular cartilage.

The effects of the lysosomal proteinase cathepsin D on the mechanical properties of adult human articular cartilage were examined in detail in 7 joints within the age range 21 to 72 years. The results of a preliminary study on the effects of the lysosomal proteinase cathepsin B1 and clostridial collagenase on the mechanical properties of cartilage are also presented. Cartilage which had been incubated with either cathepsin D or cathepsin B1 showed increased deformation in uniaxial compression perpendicular to the articular surface. The enzyme-treated cartilage also showed decreased tensile stiffness at low values of stress. This effect was more pronounced in specimens from the deeper zone of cartilage than in specimens from the superficial zone. It was also more pronounced in specimens which were aligned perpendicular to the predominant alignment of the collagen fibres in the superficial zone than in specimens which were parallel to the collagen fibres. At higher stresses the tensile stiffness of the treated cartilage was not significantly different from that of the untreated tissue. The tensile fracture stress of the cartilage was also not significantly reduced by the action of cathepsin D. In contrast to the effects observed with the cathepsins, the preliminary results obtained by incubating cartilage for 24 h with clostridial collagenase showed that both the tensile stiffness and the fracture stress were considerably lower than the corresponding values for the untreated tissue. Biochemical analysis of the incubation media, and the specimens, revealed that a large proportion of the proteoglycans was released from the cartilage by each of the three enzymes. The proportion of the total collagen which was released from the cartilage was different for each enzyme: cathepsin D released between 0 and 1.5 per cent, cathepsin B1 released between 2.3 and 4.3 per cent and collagenase released between 5.3 and 27.8 per cent of the collagen after 24 h.

Adult↗
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↗
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↗