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PubMed2005

Colonies in engineered articular cartilage express superior differentiation.

In view of poor regeneration potential of the articular cartilage, in-vitro engineering of cartilage tissue offers a promising option for progressive joint disease. This study aims to develop a biologically engineered articular cartilage for autologous transplantation. The initial work involved determination of chondrocyte yield and viability, and morphological analysis. Cartilage was harvested from the knee, hip and shoulder joints of adult New Zealand white rabbits and chondrocytes were isolated by enzymatic digestion of the extra-cellular matrix before serial cultivation in DMEM/Ham's F12 media as monolayer cultures. No differences were noted in cell yield. Although chondrocytes viability was optimal (>93%) following harvest from native cartilage, their viability tended to be lowered on passaging. Chondrocytes aggregated in isogenous colonies comprising ovoid cells with intimate intracellular contacts and readily exhibited Safranin-O positive matrix; features typically associated with articular cartilage in-vivo. However, chondrocytes also existed concurrently in scattered bipolar/multipolar forms lacking Safranin-O expression. Therefore, early data demonstrated successful serial culture of adult chondrocytes with differentiated morphology seen in established chondrocyte colonies synthesizing matrix proteoglycans.

Animals↗
PubMed1973

Isolation and characterization of cyanogen bromide peptides from the collagen of bovine articular cartilage.

Significant amounts of native collagen can be extracted from bovine articular cartilage after removal of the acid mucopolysaccharides by controlled proteolysis. The fraction thus solubilized upon denaturation gives rise to three identical alpha chains. Cleavage of these chains with CNBr generated nine peptides, all of which contain glycine as one-third of their total amino acid residues. Two of the smaller peptides CB-1 and CB-2 contain partially hydroxylated proline. A similar CNBr digest of intact cartilage also gives a series of peptides identical with those obtained from the soluble cartilage collagen. The absence of cross-linking peptides, the fact that only few beta components are seen in articular cartilage collagen and the similarity in peptide pattern between the two collagen fractions investigated, suggests that this collagen is stabilized by a different cross-linking mechanism, possibly involving an association with the tissue proteoglycans.

Amino Acids↗
PubMed1987

A histological study of human femoral condylar articular cartilage.

Paraffin sections cut both parallel to and perpendicular to the surface were used to study the histological structure of the articular cartilage of the lateral femoral condyle of infants, children and adults. Two main cell types were present--fusiform chondrocytes lying in swirling patterns were the predominant cell type of the cartilage up to and including two years, while a more rounded cell, randomly arranged, was commoner in the older specimens. Evidence suggests that these cells represent two distinct populations of chondrocyte, the round cells being derived from the earlier fusiform cells. Cartilage canals were a feature of the deeper regions of the presumptive articular cartilage in young specimens in which the epiphysis was still cartilaginous. The basophilic tidemark which marks the junction between the calcified and uncalcified cartilage in perpendicular sections was not seen in parallel sections. The calcified cartilage layer contained numerous processes of vascular bone which extended up from the subchondral bone and were a characteristic feature of the cartilage-bone interface. This layer of the articular cartilage cannot therefore be considered to be truly avascular.

Adult↗
PubMed2006

Maturation-dependent change and regional variations in acoustic stiffness of rabbit articular cartilage: an examination of the superficial collagen-rich zone of cartilage.

OBJECTIVE: The purpose of the study was to investigate maturation-dependent changes of acoustic (ultrasound) stiffness and other ultrasound features of articular cartilage in healthy rabbit knees. METHODS: Five groups of rabbits of various ages (3 weeks, 8 weeks, 6 months, 1 year, 2.5 years) consisting of five rabbits per group were examined. Signal intensity (index of stiffness), signal duration (index of surface irregularity) and interval between signals (index of thickness) of the ultrasound reflection from articular cartilage were examined at four sites: posterior lateral femoral condyle, posterior medial femoral condyle, lateral tibial plateau, and medial tibial plateau. The sites were observed macroscopically and microscopically with a light microscope and a polarized light microscope. RESULTS: At the lateral and medial condyles and the lateral tibial plateau, signal intensity was least in 3-week-old specimens. The intensity increased until 6 months or 1 year of age. At these sites, the signal durations and intervals between signals were least at the ages of 6 months or 1 year. At the medial tibial plateau, the intensity was the least at 2.5 years of age and the interval between signals was least at 3 weeks of age; there was no effect of age on signal duration. Cartilage surfaces of all specimens were smooth and no degenerative changes were macroscopically or microscopically evident. The surface brightness of cartilage under the polarized light microscope was consistent with signal intensity values. CONCLUSIONS: The response of articular cartilage to ultrasound was maturation-dependent. Acoustic properties differed from mechanical stiffness properties, which were determined using indentation. Ultrasound may detect properties of the surface collagen of the articular cartilage.

Aging↗
PubMedDate not supplied

Mesenchymal progenitor cells in adult human articular cartilage.

The transmembrane receptor Notch-1 regulates cell fate and differentiation and was suggested to identify a cell type with progenitor characteristics in newborn bovine articular cartilage. We show that Notch-1 is expressed on > 70% of BM-MSC in early passage monolayer culture. We also demonstrate that normal articular cartilage contains Notch-1+ cells and that the frequency is increased in OA. Most Notch-1+ cells in OA cartilage are located in the clusters of proliferating cells. These findings indicate that multipotential mesenchymal progenitor cells are present in articular cartilage from adult humans and that their frequency is increased in OA. This observation has implications for understanding the intrinsic repair capacity of articular cartilage and raises the possibility that these progenitor cells might be involved in the pathogenesis of arthritis.

Adult↗
PubMed1979

[Chronic polyarthritis: role of polymorphonuclear leukocytes in the destruction of pannus-free articular cartilage].

The synovial fluid (SF) of RA patients contains large amounts of PMN which are well equipped with neutral enzymes to degrade articular cartilage: elastase and cathepsin G, which both destroy proteoglycans and native collagen, as well as 2 types of collagenoases. Indirect evidence suggests that PMN might be important in the destruction of RA articular cartilage. In 19 SF of RA patients no free elastase or collagenase was found. Using immune histochemical methods, we observed that PMN and macrophages of SF contain both elastase and alpha 1-anti-trypsin and alpha 2-macroglobulin. Peripheral PMN - but not monocytes - contain elastase, however both types of cells lack alpha 1-antitrypsin and alpha 2-macroglobulin. Elastase is demonstratable in the superficial layer of pannus free RA articular cartilage. These findings suggest that neutral proteinases from PMN in RA SF are generally neutralized by physiologic inhibitors and removed by phagocytes. The enzyme-inhibitor interaction might be bypassed during "frustrated phagocytosis" so that enzymes like PMN elastase can damage RA articular cartilage.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Proteoglycan metabolism in isolated chondrocytes from human cartilage and in short-term tissue-cultured human articular cartilage.

The effect of piroxicam on proteoglycan metabolism of human cartilage cells was investigated in two in vitro models. Cells or tissue samples were obtained from six different donors. Piroxicam levels used in the test systems ranged from 2 to 6 micrograms r/ml and were comparable with serum concentrations in humans after oral intake. Piroxicam increased the synthesis rates of proteoglycan in some batches of isolated and monolayer-cultured chondrocytes and in tissue-cultured articular cartilage. The fact that this increase in the synthesis of proteoglycan was restricted to some of the donors whereas isolated cells or tissue samples from other individuals remained unaffected illustrates the heterogeneity of different human donors. Depression of proteoglycan synthesis in the presence of the drug was not observed.

Cartilage↗
PubMed1989

The use of the contact Nd:YAG laser in arthroscopic surgery: effects on articular cartilage and meniscal tissue.

The contact Nd:YAG laser's small size, tip variety, fiberoptic application, and suitability for use in a saline medium make it a particularly appealing tool for use in arthroscopic procedures. This study was performed to investigate the laser's effects on articular cartilage and meniscal tissue with respect to depth of damage (canine cadaver model) and healing response (rabbit model). Depth of damage in the canine cadaver model was greater in meniscal tissue than in articular cartilage at each wattage level. In the presence of a saline bath, depth damage in both tissues was diminished. Scalpel articular cartilage lesions showed no response over time. Electrocautery lesions uniformly showed significant wide margins of hyaline cartilage necrosis which increased over time. Laser articular cartilage lesions showed vigorous healing responses characterized by fibrocartilage healing by 6 weeks. Scalpel meniscectomies showed characteristic fibrocartilagenous remodeling by 6 weeks, while electrocautery meniscectomies showed wide margins of necrosis with no specimen showing remodeling capability. Laser meniscectomies showed an intermediate response with a small number of menisci remodeling in a normal fashion. This article represents the first comprehensive look at the effects of the Nd:YAG laser on articular cartilage and meniscal tissue in terms of depth of damage and healing response over time, and indicates this laser's biological advantage over scalpel and electrocautery in arthroscopic procedures.

Animals↗
PubMed2004

Zonal and directional variations in tensile properties of bovine articular cartilage with special reference to strain rate variation.

UNLABELLED: THE AIMS of this study were: (i) to investigate the variation in the tensile properties of articular cartilage with depth through cartilage thickness and fibre orientation; (ii) to determine the effect of strain rate on tensile properties of articular cartilage. MATERIALS AND METHOD: All experimental work was performed on cartilage specimens taken from two bovine knee joints. Osteochondral plugs 12 mm in diameter were harvested with a special reamer from the femur and the tibial plateaux of each knee. Slices (0.2 mm thick), of articular cartilage were cut from the plug with a microtome. The predominant orientation of the collagen fibres on the cartilage surface was determined using the pinpricking technique. Each specimen used for the tensile test was cut, so as to produce a dumbbell shape, with a gauge length of 6 mm. Uniaxial tensile tests were performed on each specimen in order to determine the tensile Young's modulus, and ultimate tensile strength (UTS). In this investigation, these tensile tests were carried out at different strain rate: 1, 20, 50 and 70%/sec. RESULTS: As regards the zonal properties, it was found that tensile stiffness was greater in the superficial layer than in deep layer. However, a few specimens from the deep layer displayed similar or greater stiffness compared to the superficial layer. With respect to the directional properties, the specimens oriented parallel to the predominant alignment of collagen, were stiffer than those, which were perpendicular to it in each layer. However, only the results regarding the deep layer can be considered statistically significant. In regard to the variation of modulus with the strain-rate, the results showed that there is no significant increase of the modulus with increasing strain rate from 20 to 50% per second. However, at 70% per second, articular cartilage stiffness considerably increased by up to one order of magnitude greater than that determined at lower strain rates in both the superficial and deep layer. Moreover, the UTS of cartilage specimens tested at 70% per second showed a significant rise, reaching values of four to five times that of those measured at 1, 20 or 50% per second. CONCLUSION: The steep increases in both the stiffness and ultimate tensile strength of cartilage at high strain rates point to the existence in cartilage of a mechanism for its protection from damage by stresses arising in trauma, which are usually applied at high rates. This mechanism needs to be elucidated. The reduced anisotropy found in the present study pointed out that collagen is likely to be less organized in bovine cartilage than in the human and therefore, a study of its ultra-structure would be appropriate.

Adaptation, Physiological↗
PubMed2002

Cyclosporin A inhibition of aggrecanase-mediated proteoglycan catabolism in articular cartilage.

OBJECTIVE: To determine the effect of cyclosporin A (CSA) on aggrecanase- and matrix metalloproteinase (MMP)-mediated catabolism of proteoglycan (aggrecan) in articular cartilage explants stimulated with interleukin-1 (IL-1) in a culture system that mimics early pathologic processes associated with arthritic disease. METHODS: Proteoglycan (glycosaminoglycan) and lactate quantification, Western immunoblot analyses of aggrecan degradation products, reverse transcription-polymerase chain reaction analyses of aggrecanase-1, aggrecanase-2 (ADAM-TS4, ADAM-TS5, respectively), MMP-1, MMP-3, MMP-13, tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-2, and TIMP-3 messenger RNA (mRNA) expression in articular cartilage explant cultures, and electrophoretic mobility shift assay analysis of nuclear factor of activated T cells (NF-AT) transcription factor activation were used. RESULTS: CSA inhibited, in a dose-dependent and noncytotoxic manner, aggrecanase-mediated proteoglycan catabolism and loss from IL-1-stimulated cartilage explants. There was no evidence of MMP-mediated aggrecan catabolism in this in vitro model. Treatment of articular cartilage explant cultures with 10 ng/ml of IL-1alpha up-regulated the expression of mRNA for ADAM-TS4, ADAM-TS5, MMP-1, MMP-3, and MMP-13. The expression of ADAM-TS4, ADAM-TS5, and MMP-13 was abrogated by the inclusion of 10 microM CSA in the culture medium. NF-AT activation was observed in chondrocytes but could not be inhibited by preincubation with 10 microM CSA. CONCLUSION: CSA can inhibit IL-1-induced aggrecanase-mediated proteoglycan catabolism in articular cartilage explants maintained in culture for 4 days, thus demonstrating molecular mechanisms whereby CSA may be an effective therapy for degenerative joint disease.

Aggrecans↗
PubMed1999

Tensile properties of articular cartilage are altered by meniscectomy in a canine model of osteoarthritis.

Loss of or damage to the meniscus alters the pattern of loading in the knee joint and frequently leads to cartilage degeneration and osteoarthritis. The mechanical properties of articular cartilage have been shown to reflect the extent of cartilage degeneration in human osteoarthritis and in experimental models of joint disease, but there is little experimental data documenting changes in cartilage mechanics following meniscectomy. We hypothesized that the tensile properties of the surface zone of articular cartilage are altered following total medial meniscectomy. Twelve mongrel dogs underwent complete resection of the medial meniscus in the right knee, and the femoral cartilage was studied 12 weeks after the operation. We performed uniaxial, tensile stress-relaxation tests to determine the equilibrium tensile modulus of surface-zone cartilage. Water and glycosaminoglycan content were also measured at site-matched locations. The tensile moduli of the cartilage decreased significantly following meniscectomy. The linear region modulus decreased by 40%, from 25.5 +/- 7.7 to 15.3 +/- 7.2 MPa. There was a weak (r = -0.45), but significant, correlation between the linear region modulus and the gross morphological grade for cartilage damage. Water and glycosaminoglycan content did not change following meniscectomy. Composition was not correlated with mechanical properties or morphological grade, suggesting that cartilage structure may play a more important role than composition in determining the mechanical properties. The observed decrease in cartilage material properties provides a quantitative measure of the loss of cartilage function following meniscectomy and reflects a pattern of change that is consistent with damage to the collagen-proteoglycan solid network.

Animals↗
PubMed1986

The effect of salicylate on anatomically intact articular cartilage is influenced by sulfate and serum in the culture medium.

The established, suppressive effect of salicylate on sulfated glycosaminoglycan (sGAG) synthesis by normal articular cartilage was reinvestigated using anatomically intact articular cartilage of the whole mouse patella. Employing the physiological murine sulfate concentration (1.0 mM) sodium salicylate (1-5 X 10(-3) M) caused a dose dependent inhibition of 35S-sGAG synthesis (10-35%). At a lower sulfate concentration (0.4 mM) this inhibition was increased (15-45%) and the suppression was even more pronounced in sulfate deprived medium. This observation stresses the need of using physiological sulfate concentrations in cartilage culture studies. In the presence of 100% serum the therapeutic drug concentration (1-2 X 10(-3) M) had no longer any suppressive effect, either at 1.0 mM or at any lower sulfate concentration. Our data suggest that salicylate has no direct effect on sGAG metabolism in normal articular cartilage in vivo and that adverse effects may be due to the observed salicylate induced lowering of the endogenous sulfate level.

Animals↗
PubMed1996

Plasminogen modulation of IL-1-stimulated degradation in bovine and human articular cartilage explants. The role of the endogenous inhibitors: PAI-1, alpha 2-antiplasmin, alpha 1-PI, alpha 2-macroglobulin and TIMP.

The studies described here examine the involvement of the fibrinolytic cascade and its endogenous inhibitors in the regulation of activity of matrix metalloproteinases and cartilage degradation related to non-inflammatory joint disease, like osteoarthritis. An interleukin-1-induced model of degradation using [35S]-labeled bovine and human articular cartilage explants was utilized. One goal of these studies was to compare the responses of bovine and human articular cartilage. Degradation was not inhibited by alpha 1-PI, PAI-1, alpha 2-macroglobulin, alpha 2-antiplasmin or TIMP-2, when IL-1 alone was added. Addition of human plasminogen to bovine explants, at concentrations found in human synovial fluid, increased degradation by three to four-fold. Under these conditions, the degradation was inhibited effectively by all of the endogenous inhibitors tested, indicating the presence of a cascade where activated chondrocytes are a source of u-PA. Plasminogen activated by u-PA gives plasmin, which is known to further activate pro-stromelysin. Stromelysin is essential for activation of collegenase. Not only TIMP, but also inhibitors at earlier steps of activation like PAI-1, alpha 2-antiplasmin, alpha 1-PI and alpha 2-macroglobulin inhibited degradation, and could provide cartilage protection in vivo. An experiment with human articular cartilage explants showed that very little or no degradation occurred when human articular cartilage explants were stimulated with interleukin-1 alone. Addition of human plasminogen (at physiologically relevant concentrations) resulted in significant degradation, which was inhibited in the same manner as in bovine explants, by inhibitors of the fibrinolytic cascade and TIMP. TIMP is much more efficient in human explants, indicating the limited participation of human plasmin in the degradation of human cartilage. Although speculative, it is possible that in vivo, cartilage degradation could be promoted not only by TIMP/MMP imbalance, but also accelerated by decreased levels of certain serpins in synovial fluid (e.g. PAIs, alpha 2-antiplasmin and alpha 1-PI).

Animals↗
PubMedDate not supplied

Relationship between articular cartilage damage and bone density in the first metatarsal.

It is well known that bone changes occur in relationship to the articular cartilage damage seen in osteoarthritis. Numerous studies have shown a relationship between bone density and articular cartilage damage in knee and hip joints, but it is controversial as to whether or not an increased subchondral bone density results in greater cartilage damage. We studied 49 pairs of cadaveric first metatarsals in an attempt to correlate the level of cartilage damage seen on the distal articular surface with areal and volumetric density and other parameters such as bone geometry. A positive correlation was detected between articular cartilage damage and bone density by peripheral quantitative computed tomography in five of eight frontal slices in the head of the left metatarsal in the male sample only. The more extensive subchondral cysts found in the right male metatarsal may have contributed to the lack of correlation between the two variables on the right side. In addition, females displayed significantly greater osteophytosis than males at a given grade of cartilage damage, thus, possibly leading to a painful, apropulsive gait and a disuse osteopenia which would neutralize any subchondral bone density increase associated with cartilage damage. Microscopic investigations are, therefore, warranted to detect bone changes on a more discreet level, particularly within the subchondral plate.

Adult↗
PubMed2000

Inhibition of chondrogenesis by parathyroid hormone in vivo during repair of full-thickness defects of articular cartilage.

We studied the effects of parathyroid hormone (PTH) on differentiation of chondroprogenitor cells during the repair of full-thickness articular cartilage defects. Three-millimeter cylindrical full-thickness articular cartilage defects, which are small enough to be resurfaced spontaneously by hyaline cartilage, were created in the femoral trochlea of the rabbit knee. Recombinant human PTH(1-84) (hPTH[1-84]) (25 ng/h) then was administered into the joint cavity with an osmotic pump, or in control animals, saline alone was administered. The animals were killed at 1, 2, 4, and 8 weeks. At 1 week, the defects were filled with undifferentiated cells, regardless of the PTH treatments. By 8 weeks, well-developed cartilage covered the defects with reconstitution of subchondral bone up to the original bone-articular cartilage junction. In contrast, no evidence of chondrogenic differentiation was seen at any time during the experimental period in the defects treated with PTH. The reparative tissues also were examined immunohistochemically using anti-proliferating cell nuclear antigen (PCNA) and anti-PTH/PTH-related peptide (PTHrP) receptor antibodies. Interestingly, the chondroprogenitor cells that filled the defects expressed PTH/PTHrP receptor, suggesting that these cells are capable of responding to PTH/PTHrP signaling before overt chondrogenesis. Application of PTH did not interfere with proliferation but inhibited chondrogenic differentiation of the cells resulting in the formation of fibrous tissue that lost the expression of PTH/PTHrP receptor within 4 weeks.

Animals↗
PubMed2005

Biochemical and biomechanical properties of lesion and adjacent articular cartilage after chondral defect repair in an equine model.

BACKGROUND: Chondral defects may lead to degradative changes in the surrounding cartilage, predisposing patients to developing osteoarthritis. PURPOSE: To quantify changes in the biomechanical and biochemical properties of the articular cartilage adjacent to chondral defects after experimental defect repair. STUDY DESIGN: Controlled laboratory study. METHODS: Specimens were harvested from tissue within (lesion), immediately adjacent to, and at a distance from (remote area) a full-thickness cartilage defect 8 months after cartilage repair with genetically modified chondrocytes expressing insulin-like growth factor-I or unmodified, control chondrocytes. Biomechanical properties, including instantaneous Young's and equilibrium aggregate moduli, were determined by confined compression testing. Biochemical properties, such as water and proteoglycan content, were also measured. RESULTS: The instantaneous Young's modulus, equilibrium modulus, and proteoglycan content increased, whereas water content decreased with increasing distance from the repaired lesion. The instantaneous Young's and equilibrium moduli of the adjacent articular cartilage were 80% and 50% that of remote area samples, respectively, whereas water content increased 0.9% and proteoglycan content was decreased by 35%. No significant changes in biomechanical and biochemical properties were found either in the lesion tissue or in adjacent cartilage with genetic modification of the chondrocytes. CONCLUSION: Articular cartilage adjacent to repaired chondral defects showed significant remodeling 8 months after chondral defect repair, regardless of whether genetically modified or unmodified cells were implanted. CLINICAL RELEVANCE: Changes in the biochemical and biomechanical properties of articular cartilage adjacent to repaired chondral defects may represent remodeling as part of an adaptive process or degeneration secondary to an altered distribution of joint forces. Quantification of these changes could provide important parameters for assessing progress after operative chondral defect repair.

Animals↗
PubMed1997

Expression of osteonectin in articular cartilage of osteoarthritic knees.

The expression of osteonectin (ON) in osteoarthritic articular cartilage was investigated by enzyme immunohistochemistry and colloidal gold immunoelectron microscopy. A total of 96 specimens from 9 knees of 8 patients with osteoarthritis (OA) were examined. In OA cartilage, ON-positive cells varied in distribution and were not seen in all the specimens obtained from the same patient. However, in over half of the specimens (56 of 96), especially in the specimens on Mankin's grades from 4 to 9, which corresponds to relatively early stages of OA, ON was expressed in the cartilage above the calcified layer. On the other hand, ON was detected only in the calcified layer below the tidemark in normal articular cartilage. In addition, colloidal gold immunoelectron microscopy revealed ON in chondrocytes and matrix vesicles (MVs). These findings suggest that ON acts through MVs in the early stages of OA as a significant pathogenetic factor involved in intracartilage calcification, which is known to have a close relationship to the progression of OA.

Aged↗
PubMedDate not supplied

Winner of the 1996 Cabaud Award. The effect of lifelong exercise on canine articular cartilage.

The effect of long-term exercise on canine knees was studied to determine whether an increased level of lifelong weightbearing exercise causes degeneration, or changes that may lead to degeneration, of articular cartilage. Eleven dogs were exercised on a treadmill at 3 km/hr for 75 minutes 5 days a week for 527 weeks while carrying jackets weighing 130% of their body weight. Ten control dogs were allowed unrestricted activity in cages for the 550 weeks. At the completion of the study all knee joints were inspected for evidence of joint injury and degeneration. Articular cartilage surfaces from the medial tibial plateau were examined by light microscopy, the cartilage thickness was measured, and the intrinsic material properties were determined by mechanical testing. No joints had ligament or meniscal injuries, cartilage erosions, or osteophytes. Light microscopy did not demonstrate cartilage fibrillation or differences in safranin O staining of the tibial articular cartilages between the two groups. Furthermore, the tibial articular cartilage thickness and mechanical properties did not differ between the two groups. These results show that a lifetime of regular weightbearing exercise in dogs with normal joints did not cause alterations in the structure and mechanical properties of articular cartilage that might lead to joint degeneration.

Animals↗