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Results for “CARTILAGE, ARTICULAR”

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At least 73 records · Page 4Linked to original sources

PubMed2002

Influence of hypoxia and reoxygenation on cytokine-induced production of proinflammatory mediators in articular cartilage.

OBJECTIVE: Articular cartilage is an avascular tissue that functions at a lower oxygen tension than do most tissues. With mobilization, arthritic joints may undergo cycles of hypoxia and reoxygenation. The goal of this study was to determine the effects of hypoxia and reoxygenation on cytokine-induced nitric oxide (NO) and prostaglandin E(2) (PGE(2)) production in articular cartilage. METHODS: Porcine cartilage explants were incubated at 37 degrees C for 72 hours in either 1% O(2) (hypoxia) or 20% O(2) (normoxia) in media supplemented with interleukin-1alpha (IL-1alpha) or tumor necrosis factor alpha (TNFalpha), with or without the NO synthase 2 (NOS2) selective inhibitor 1400W. Culture media were then removed and replaced with freshly prepared media and incubated for a further 24 hours in normoxia. RESULTS: NO levels were significantly higher in explants supplemented with IL-1alpha and TNFalpha compared with controls, in both hypoxia and normoxia. Compared with normoxia, hypoxia decreased IL-1alpha- and TNFalpha-induced NO production significantly. Reoxygenation of hypoxic explants resulted in sustained significant NO production in response to either cytokine. However, comparably high levels of NO production were not sustained in explants cultured continuously in normoxia. Although IL-1alpha alone did not significantly increase PGE(2) production, significant PGE(2) superinduction occurred in cartilage stimulated with IL-1alpha and the NOS2 inhibitor 1400W compared with stimulation with IL-1alpha alone in hypoxia, but not in normoxia. CONCLUSION: Oxygen tension significantly affects cytokine-induced proinflammatory mediator production in articular cartilage. Furthermore, hypoxia alters NO mediation of PGE(2) production. Hypoxia and reoxygenation can affect cytokine-induced proinflammatory mediator production, suggesting that oxygen tension may influence inflammation associated with cartilage injury and disease.

Animals↗

PubMed1998

Age-related changes in the structure of the keratan sulphate chains attached to fibromodulin isolated from articular cartilage.

Bovine articular cartilage fibromodulin has been isolated from animals aged 3 months to 8 years, and the attached keratan sulphate (KS) chains digested with keratanase II. The oligosaccharides generated have been reduced, examined by high-pH anion-exchange chromatography and their structures identified by comparison with standards. It has been shown that in fibromodulin from young articular cartilage, the KS chains do not possess either non-reducing terminal (alpha2-6)-linked N-acetylneuraminic acid or fucose (alpha1-3)-linked to sulphated N-acetylglucosamine residues. However, an age-related increase has been observed in the abundance of both (alpha2-6)-linked N-acetylneuraminic acid and (alpha1-3)-linked fucose, neither of which is found in KS isolated from non-articular cartilage, irrespective of the age of the source. Interestingly, the KS chain length remains constant as a function of age, which possibly relates to a role in collagen fibril assembly. In addition, no significant age-related changes were identified in levels of galactose sulphation.

Acetylglucosaminidase↗

PubMed2001

Functional tissue engineering: the role of biomechanics in articular cartilage repair.

Articular cartilage shows little or no intrinsic capacity for repair in response to injury or disease, and even minor lesions or injuries may lead to progressive damage and joint degeneration. Tissue engineering is a relatively new but rapidly growing field that has sought to use combinations of implanted cells, biomaterials, and biologically active molecules to repair or regenerate injured or diseased tissues. Despite many advances, tissue engineers have faced significant challenges in repairing or replacing tissues that serve a predominantly biomechanical function, such as articular cartilage. An evolving discipline termed functional tissue engineering seeks to address these challenges by emphasizing and evaluating the role of biomechanical factors in the intrinsic and engineered repair of tissues and organs. In the current study, the authors describe some of the fundamental issues involving the interaction of biomechanical stresses in vivo and in vitro with native and repair articular cartilage and with other biomechanically functional tissues. A more thorough and formal investigation of these issues may provide a basis for developing rational design principles for tissue engineered replacement or repair of load-bearing structures in the body.

Animals↗

PubMed1979

Changes with age in the glycosaminoglycans of human articular cartilage.

Human articular cartilage was obtained post mortem from the lateral femoral condyles of 30 subjects aged from under 1 to 70 years. Cryostat sections taken 0--100 micrometers and 900--100 micrometers deep to the cartilage surface were exhaustively extracted to recover the glycosaminoglycans (GAG). After fractionation by cellulose acetate electrophoresis and enzyme depolymerisation individual GAG were determined by alcian blue -0.05 M MgCl2 and disaccharide microassay procedures. Changes with age were observed in GAG concentration and in the proportion of individual GAG. Large alterations occurred during the period of skeletal growth (0--16y). At birth GAG formed about 50% of the dry weight of cartilage, a value that decreased to about 15% in adult cartilage. Chondroitin sulphates (ChS) formed the principal GAG of articular cartilage and accounted for almost all of the GAG of the infant material. The ChS decreased with age and were partially replaced by keratan sulphate (KS), so the KS eventually comprised 12% of the GAG. Hyaluronic acid (HA) was identified and was found to increase linearly with age to form 6% by weight of the cartilage GAG by 60y.

Adolescent↗

PubMed2002

In vitro studies of a photo-oxidized bovine articular cartilage.

Bovine articular cartilage was photo-oxidized and cultured with native articular bovine cartilage and synovial membrane to study the interaction between these tissues mimicking the physiological situation in the joint. The photo-oxidation was applied as a pretreatment of cartilage for future use in cartilage resurfacing procedures in joints. Properties of the transplant were assessed by testing the production of local mediators, such as nitric oxide (NO) and prostaglandin E2 (PGE2), and neutral metalloproteinase activities under normal conditions and after stimulation with various stimulants representative of inflammatory changes in pathophysiological conditions. Unlike normal cartilage photo-oxidized cartilage did not release significant amounts of NO and PGE2 and showed less gelatinolytic and caseinolytic activity compared to native bovine articular cartilage. Enzyme activity of the combined cultures was at a level intermediate between that of photo-oxidized cartilage and native cartilage cultures alone. In contrast to normal cartilage, living chondrocytes were not visible in photo-oxidized cartilage using live/dead staining. These results indicate, that the photo-oxidized cartilage may have a beneficial effect on adjacent native host cartilage and therefore be a suitable transplant for use in in vivo experiments.

Animals↗

PubMed2025

Localisation-Dependent Variations in Articular Cartilage ECM: Implications for Tissue Engineering and Cartilage Repair.

Articular cartilage (AC) is a specialised connective tissue covering joint surfaces. It enables smooth movement, distributes mechanical loads, and protects the underlying bone. In response to loading, AC adapts by modifying both its thickness and composition. AC is organised in different zones, with low cellularity and a high abundance of extracellular matrix (ECM). Mechanical overloading or immobilisation can lead to structural changes, potentially resulting in osteoarthritis (OA), for which no causal treatment currently exists. However, smaller defects can be treated using chondrocyte/cartilage transplantation or tissue engineering. A better understanding of the molecular composition of AC at different locations is essential to improve such therapeutic approaches. For this purpose, we performed a comprehensive analysis of porcine femoral knee cartilage at eight defined anatomical sites. Cartilage thickness and proteoglycan (PG) content were analysed histologically, while specific ECM proteins were assessed by proteomics and validated by immunohistochemistry and Western blot. Significant differences were identified, particularly between medial and lateral compartments, in terms of cartilage thickness, PG abundance, and ECM composition. Some proteins also showed zone-specific localisation patterns. These structural differences likely reflect adaptation to mechanical loading and should be considered to optimise future cartilage repair and tissue engineering strategies.

Extracellular Matrix↗

PubMed1976

The fate of the articular cartilage in intracapsular fracture of the femoral neck (articular cartilage in femoral neck fracture).

The fate of the articular cartilage of the hip joint with intracapsular neck fracture was studied by histological, histochemical and autoradiographic techniques and by using a polarized microscope and a scanning electron microscope. Cartilage specimens from 93 femoral heads and 7 acetabula were obtained from fractured hips 2 days to 4 1/3 years postfracture and from control hips with various disorders. The cartilage degeneration appeared 2 weeks after fracture and advanced steadily with time. The matrix was covered, invaded and ultimately replaced by the fibrous tissue. Chondrocyte viability, though it was lost from the surface, was recognized in the deep matrix even in the oldest fracture examined. It is concluded that the humoral factor directly caused by the injury as well as the biomechanical impairment, i.e. a loss of physical stress, may play an essential role in the pathogenesis of the degeneration. The possibility of regeneration was discussed.

Acetabulum↗

PubMed2003

Clinical applications of growth factors for articular cartilage repair.

Articular cartilage injuries and degeneration present a challenge for orthopedic surgeons. Chondrocytes have limited regenerative and reparative abilities. Healing of a defect results in a fibrocartilaginous repair tissue that lacks the structural and biomechanical properties of hyaline cartilage and that degrades over time. Polypeptide growth factors have an important role in regulating the behavior of all cells, including articular chondrocytes. Our understanding of growth factor effects on and interactions with chondrocytes is progressing rapidly. The most prominent growth factors identified for articular cartilage include insulin-like growth factor, fibroblast growth factor, the transforming growth factor-beta superfamily, hepatocyte growth factor, platelet-derived growth factor, Indian hedgehog and parathyroid hormone-related peptide, bone morphogenetic proteins, and the interleukin-1 receptor antagonist. Orthopedic surgeons need to be familiar with the properties of these growth factors, as they hold great therapeutic promise. In-progress clinical studies are examining how growth factors may have applications in treatments of bone.

Cartilage, Articular↗

PubMed1981

Staining of demineralized cartilage. II. Quantitation of articular cartilage proteoglycan after fixation and rapid demineralization.

Safranin O in the orthochromatic form stains articular cartilage proteoglycan quantitatively in histological sections of demineralized cartilage. This was shown by scanning microdensitometry of stained sections of undemineralized and demineralized articular cartilage and by biochemical analysis of 35S labelled cartilage subjected to demineralization. In contrast, Alcian Blue staining is affected by unknown factors other than simply the amount of proteoglycan present. Alcoholic formalin fixes articular cartilage proteoglycan more successfully than formol Zenker for subsequent rapid demineralization. Alcoholic formalin does not preserve cellular appearance as well as formol Zenker. Staining of articular cartilage with PAS appears unaffected by demineralization.

Aged↗

PubMedDate not supplied

Articular cartilage biology.

Articular cartilage is a complex tissue maintained by chondrocytes, which undergo metabolic changes as a result of aging, disease, and injury. These changes may hinder tissue maintenance and repair, resulting in accelerated loss of articular surface and leading to end-stage arthritis. Researchers are investigating both normal and pathologic cellular and molecular processes as well as the development of chondroprotective agents to improve the metabolic function of articular cartilage. Current research is helping to clarify the mechanisms by which a variety of agents, such as glucosamine, chondroitin sulfate, hyaluronic acid, green tea, glucocorticoids, and nonsteroidal anti-inflammatory drugs, can modify the symptoms and course of osteoarthritis. Also under investigation are methods of stimulating repair or replacing damaged cartilage, such as matrix metalloproteinase inhibitors, gene therapy, growth factors, cytokine inhibitors, and artificial cartilage substitutes. Tissue engineering, the combining of artificial matrices with cells and growth factors or genes, offers great potential for improving patient care.

Cartilage, Articular↗

PubMed1999

The effect of continuously applied cyclic mechanical loading on the fibronectin metabolism of articular cartilage explants.

Articular cartilage serves primarily as a load-bearing material able to regulate its own metabolic activity in response to the mechanical stimuli applied. Fibronectin plays a critical role in the organization and function of the cartilage extracellular matrix. The purpose of this study was to investigate systematically the effect of load magnitude, frequency and duration of loading on the synthesis, content and release of fibronectin and proteins by mature bovine articular cartilage explants using a novel mechanical loading system. Increasing the load magnitude, as well as the duration of loading, inhibited the synthesis and content of fibronectin and proteins; the fibronectin synthesis was more specifically affected than the overall protein synthesis indicating that fibronectin is more responsive to pressure than synthesis of other proteins. Reducing the load frequency did not modulate the inhibitory effect of a given cyclic stress on synthesis and content of fibronectin and proteins even though explants were more compressed. The release of endogenous fibronectin was significantly reduced independent of the applied loading protocols when compared with unloaded controls. This study demonstrates that the magnitude and the duration of loading influences the degree of inhibition of fibronectin and protein synthesis, while loaded explants possess an elevated but limited capacity to bind fibronectin. Compared with other studies, our present results show that the applied load function in particular has a profound effect on the metabolism of chondrocytes.

Animals↗

PubMed1979

Articular cartilage preservation and storage. II. Mechanical indentation testing of viable, stored articular cartilage.

Mature rabbit articular cartilage in the form of distal femoral condyles, composite osteoarticular structures, were incubated in the presence of alpha-tocopherol (200 micrograms/ml) over a period of time. Indentation testing and 35S uptake indicate preservation of sustained load carrying capacity and viability, respectively, in the presence of alpha-tocopherol for up to 30 days in organ culture. Condylar cartilage stored in the absence of alpha-tocopherol as well as frozen cartilage demonstrated progressive inability to resist sustained loading over time. Nonoptimal synthetic function apparently occurred in these latter two groups when compared to alpha-tocopherol stored material.

Animals↗

PubMed2006

Basic science and treatment options for articular cartilage injuries.

Articular cartilage injuries can produce significant musculoskeletal morbidity for both young and active aging patient populations. The complex and highly specialized composition of normal hyaline cartilage makes treatment of focal chondral injuries a formidable challenge for the basic scientist, surgeon, and physical therapist. The current array of surgical treatment options offers palliative, reparative, and restorative treatment strategies. Palliative options include simple arthroscopic debridement. Reparative strategies utilize marrow stimulation techniques to induce formation of fibrocartilage within the chondral defect. Restorative tactics attempt to replace damaged cartilage with hyaline or hyaline-like tissue using osteochondral or chondrocyte transplantation. Furthermore, while treatment success is obviously dependent on good surgical selection and technique, the importance of sound, compliant postoperative rehabilitation cannot be understated. The purpose of this article is to review the basic science of articular cartilage, current treatment options available, and outline the clinical decision making involved when using these procedures by presenting the algorithm used at our institution for treating focal cartilage lesions.

Arthroplasty↗

PubMed1997

Hepatocyte growth factor facilitates cartilage repair. Full thickness articular cartilage defect studied in rabbit knees.

Hepatocyte growth factor (HGF) is a multifunctional factor which promotes proliferation, motility and morphogenesis in epithelial cells. In addition, it has been found to play an important role in cartilage metabolism. To investigate articular cartilage repair using HGF in vivo, we injected HGF into rabbit knee joints, where 4 mm diameter osteochondral defects had been made, and observed the animals for 6 months. We found that HGF effectively repaired osteochondral defects. The repair process of the articular cartilage defects using HGF was shown to be much better than saline injection on all macroscopic and histologic examinations. Although the observation period in our study was short, HGF is one of the most promising candidates for repairing articular cartilage defects clinically.

Animals↗

PubMed1991

Fluorophores from aging human articular cartilage.

Human articular cartilages of various ages were digested with collagenase, and the fluorescence of the digests was measured as a function of age. At acidic pH, all collagenase-treated fractions were found to contain two main fluorophores with fluorescence maxima at 395 and 385 nm (excitation at 295 and 335 nm, respectively). Each fluorophore was isolated from the hydrolysate and its structure was deduced from spectral and chemical data. The 395/295 nm fluorophore was identified as pyridinoline, which is one of the non-reducible cross-linkages in collagen. The 385/335 nm fluorophore was identical to pentosidine, which was isolated from human dura mater and characterized by Sell and Monnier in 1989. Our results showed that the amount of pentosidine per collagen in human articular cartilage increases linearly with age (r = 0.929, p less than 0.005), while the amount of pyridinoline per collagen remained constant and was not correlated with age (r = 0.20). On the other hand, the amount of pentosidine per pyridinoline increased exponentially during life (r2 = 0.839, p less than 0.05).

Adult↗

PubMed1987

Drug action on articular cartilage surface. An in vitro study using mouse femoral heads labeled with cationized ferritin.

The direct effects on the cartilage articular surface of three anti-inflammatory drugs (Diclofenac, Pirprofen and acetyl-salicylic acid) and of a polysulfated glycosaminoglycan (Arteparon), were studied using an in vitro system in which BALB-c mouse femoral heads were incubated with the drugs. After incubation and labeling of the negative charges of the articular surfaces with cationized ferritin, the femoral heads were examined by electron microscopy. In addition, the effect of the drugs on the aggressive action of collagenase on the articular surface was tested using the same in vitro system. Diclofenac, Pirprofen and the polysulfated glycosaminoglycan did not alter the structure or the charge properties of the surface. Acetyl salicylic acid produced a slight disruption of the articular surface. The drugs studied had no effect on the disruptive action of collagenase.

Animals↗

PubMed1990

Articular cartilage preservation and storage. III. Quantitative zonal analysis of cytoplasmic components of stored versus in vivo articular cartilage chondrocytes.

The cytoplasmic components of chondrocytes in the various zones of articular cartilage of the medial femoral condyle of six-week-old male New Zealand white rabbits stored in tissue culture medium at 37 degrees in 5% CO2 and air were quantitated from electron micrographs, and the results were compared statistically with the cytoplasmic components of chondrocytes in the corresponding zones of in vivo articular cartilage. The major changes that occurred during storage were: (1) an increase in the amount of lipid bodies in chondrocytes in the tangential, transitional, and calcified zones; (2) a decrease in the number of holes in the cytoplasm of chondrocytes in the radial and calcified zones; (3) a decrease in the amount of endoplasmic reticulum in the radial and calcified zones; and (4) an increase in cell size and cytosol area in the tangential and transitional zones but a significant decrease in cell size and cytosol area in the calcified zone. Stored articular cartilage chondrocytes demonstrated cellular changes associated with aging, whereas in vivo articular cartilage chondrocytes demonstrated changes associated with degeneration. The matrix of stored articular cartilage in the tangential, transitional, and upper part of the radial zones showed a decrease in opacity due to a decrease in the number of collagen fibers per unit area of matrix, a condition termed "chondroporosis." This study demonstrates that articular cartilage stored in standard tissue culture medium under ideal physiological conditions is morphologically abnormal. Based on these findings, one would not expect such stored cartilage to remain functionally intact when transplanted to replace articular cartilage loss.

Animals↗

PubMed1975

Organ culture of adult human articular cartilage. II. The differential rate of glycosaminoglycan synthesis in layers of articular cartilage matrix.

Adult human articular cartilage was maintained in culture for three days and labelled with 35SO4 for the first 48 hours. The explants were sectioned horizontally on the cryostat, and the sections from the top, middle, and deep layers analyzed separately. Autoradiographs were prepared from every twentieth section. The DNA content in each of the three layers was of the same order, but the sulfate uptake and uronic acid content were considerably reduced at the surface. It is suggested that the chondrocytes synthesize matrix appropriate to the layer in which they lie.

Autoradiography↗