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At least 1,225 records · Page 68Linked to original sources
PubMed2005

Validation of magnetic resonance imaging for measurement of equine articular cartilage and subchondral bone thickness.

OBJECTIVE: To validate use of magnetic resonance images (MRIs) for measurement of equine articular cartilage and subchondral bone thickness by comparison with measurements in histologic specimens. SAMPLE POPULATION: 32 cadaveric carpal joints from 16 horses. PROCEDURE: Magnetic resonance imaging was performed by use of 3-dimensional fast spoiled gradient echo (SPGR) and T2* 3-dimensional fast gradient echo (GRE) pulse sequences with and without fat saturation. Standard sites on the medial and lateral facets of the intermediate, radial, and third carpal bones were used for subchondral bone and articular cartilage thickness measurements. Digital image analysis software was used for MRI measurements 10 mm from the dorsal extent and perpendicular to the articular surface. Histomorphometric measurements of hyaline, calcified cartilage, and subchondral bone thickness were obtained at selected sites. Comparisons between histomorphometric and MRI measurements and between magnetic resonance pulse sequences were evaluated. RESULTS: There were significant correlations between GRE and SPGR and SPGR and histologic measurements of articular cartilage, with no significant difference between measurements and good agreement. When calcified cartilage was excluded from the histologic measurement, MRI measurements were significantly greater than histologic measurements. For subchondral bone thickness, there was significant correlation between GRE and SPGR but GRE was significantly greater than SPGR measurements. Histomorphometric and MRI measurements were strongly correlated and not significantly different. CONCLUSIONS AND CLINICAL RELEVANCE: Magnetic resonance imaging provides a good representation of cartilage and subchondral bone thickness, supporting its use in the study and clinical diagnosis of osteochondral structure and alteration.

Animals↗
PubMed1976

The distribution of serum albumin in human normal and degenerate articular cartilage.

A method for studying the distribution of a high molecular weight solute (serum albumin) between physiological saline and human articular cartilage is described. Samples of normal and fibrillated articular cartilage from both femoral condyles and femoral heads have been studied. Limited studies have also been performed where the glycosaminoglycan content of normal cartilage has been reduced by chemical or enzymic methods. With naturally occurring cartilage a wide range of partition coefficients (0.3 to less than 0.002) was obtained. The partition coefficients are very dependent upon proteoglycan concentration, with the partition coefficient decreasing with increasing fixed charge density. An attempt is made to interpret the observed partitioning in terms of the steric exclusion by the proteoglycans.

Binding Sites↗
PubMed1992

Intra-articular injections and articular cartilage metabolism. An experimental study in rabbits.

We studied the effects of repeated intra-articular injections of sterile 140 mM NaCl solution on articular cartilage in adult rabbits. After 20 injections into the knee joints over a period of 4 weeks, chondrocyte glucosaminoglycan synthesis was evenly reduced in all cartilage layers, accompanied by a significant proteoglycan depletion of the matrix which was most marked in the superficial half of the cartilage. These and other changes only partially reversed during a further 4-week period after the injections had been stopped. Our data underline the need for a clear-cut indication for intra-articular injections. The microtrauma caused by injection, in conjunction with the introduction of a carrier solution into the joint, may, at least when repeated at short intervals, lead to measurable damage to the articular cartilage.

Animals↗
PubMed1995

Articular cartilage repair using allogeneic perichondrocyte-seeded biodegradable porous polylactic acid (PLA): a tissue-engineering study.

Efforts to expand treatment options for articular cartilage repair have increasingly focused on the implantation of cell-polymer constructs. The purpose of this study is to determine the suitability of porous D,D-L,L-polylactic acid as a carrier for delivering repair cells obtained from rib perichondrium into full-thickness articular cartilage defects. In vitro characterization of perichondrocyte-polylactic acid composite grafts was combined with in vivo assessment of the early articular cartilage repair in a clinically relevant model. Using a fluorescent double-stain protocol to visualize live and dead cells in situ, primary cells cultured from perichondrium were found to be capable of attaching to and surviving within a porous D,D-L,L-polylactic acid matrix. These perichondrocyte-polylactic acid composite grafts were then implanted within osteochondral defects drilled into the left medial femoral condyles of 16 adult New Zealand white rabbits. Experimental animals were sacrificed 6 weeks after implantation and the repair tissue was evaluated grossly, histologically, and biochemically. Grossly, 96% (15/16) of the experimental animals demonstrated repairs consisting of a smooth, firm neocartilage which appeared similar in color and texture to the surrounding articular surface. Matrix staining for cartilaginous protein was seen surrounding chondrocyte-like cells in the cartilage regions of the repair. Cellular alignment was found to be related to scaffold architecture. These results suggest that scaffolds composed of porous D,D-L,L-polylactic acid support the growth of cartilaginous repair tissue and are compatible with both in vitro and in vivo survival of chondrogenic cells.

Absorption↗
PubMed1996

In vitro effects of methotrexate on human articular cartilage and bone-derived osteoblasts.

Conflicting data have been published on whether low-dose methotrexate (MTX) treatment of rheumatoid arthritis (RA) is able to slow down radiological joint damage, i.e. retard the destruction of articular cartilage and (subchondral) bone. We studied the effects of MTX on proteoglycan (PG) turnover and interleukin-1 (IL-1)- and RA mononuclear cell (RA-MNC)-induced cartilage damage in human articular cartilage tissue cultures, and the effects of MTX on basal and RA-MNC-influenced proliferation and differentiation of osteoblasts in cultures of human bone-derived osteoblasts. MTX exerted no direct effect on cartilage nor did MTX influence IL-1- or RA-MNC-induced cartilage damage, despite strong suppression of basal as well as mitogen- and antigen-induced RA-MNC proliferation. MTX induced strong inhibition of osteoblast proliferation, but did not significantly interfere with osteoblast differentiation (i.e. alkaline phosphatase activity). RA-MNC-enhanced proliferation and differentiation of osteoblasts were abolished by MTX. These results suggest that if MTX is able to induce retardation of radiological progression in RA, this is not based on an initial direct effect of MTX on cartilage as measured by PG turnover, nor on an initial inhibition of IL-1- or RA-MNC-induced cartilage damage. However, longstanding MTX-induced inhibition of RA-MNC proliferation may lead to reduction of the catabolic activity involved in cartilage destruction. On the other hand, long-term inhibition of osteoblast proliferation may eventually lead to decreased bone formation and osteopenia. Whether this will turn out to be a problem of clinical importance in the treatment of RA has to be established.

Adult↗
PubMed1997

Immunohistochemical localization of type II and type I collagens in articular cartilage of the femoral head of dexamethasone-treated rats.

The immunohistochemical localization of type II and type I collagens was examined in the articular cartilage of the femoral head of growing rats injected systemically with 5 mg kg-1 dexamethasone for 2 weeks every other day. The intensities of immunostaining for type II collagen, measured by microphotometry, was highest in the flattened cell layer and high in the hypertrophic cell layer, moderate in the proliferative cell and transitional cell layers and low in the superficial layer. After dexamethasone administration, the intensities decreased markedly in the flattened cell layer and slightly in the hypertrophic cell layer, although the decreases in other layers were negligible. The staining intensities for type I collagen were highest in the flattened cell layer, low in the superficial and transitional cell layers and very low in the proliferative and hypertrophic cell layers. After dexamethasone administration, the intensities increased markedly in the flattened cell layer and slightly in the superficial and proliferative cell layers, but did not change in the transitional and hypertrophic cell layers. Thus, dexamethasone administration caused a decrease in type II collagen and an increase in type I collagen in the matrix of the surface portion of articular cartilage. The composition of isoforms of collagen in the matrix changed after the steroid administration. The results strongly that the shift in collagen composition from type II to type I predominance is a cause of the degeneration of the articular cartilage after glucocorticoid administration.

Animals↗
PubMed1987

Replacement of femoral head using endoprosthesis (alumina ceramics vs metal)--an experimental study of canine articular cartilage.

In two groups of adult dogs with a femoral head prosthesis of either metal or ceramic implanted in the hip joint, the implanted prostheses were compared in terms of the associated gross, histologic changes of the articular cartilage. At 1 or 3 months after implantation the resulting damage to the articular cartilage was minimal in both groups. However, at 6 months a marked difference was noted between the groups: the articular cartilage was almost completely lost in the metallic group, whereas a considerable portion of the cartilage remained intact in the ceramic group.

Animals↗
PubMed2005

Toxic effects of povidone-iodine on synovial cell and articular cartilage.

The objective of this study was to investigate the toxic effects of povidone-iodine (PVI). A series of MTT assay of cultured synovial cells stimulated by PVI have been made. Test for assay of membrane-toxic effect of PVI and lactate dehydrogenase (LDH) has also been carried out. After making intraarticular injection into rats' hind knee joints with 0.1 ml of PVI every day for 1 week, we have extracted the knee joints and blood from rats in four divided groups on the 0, 1st, 3rd, and 7th day. Our microscopic analysis was performed that cartilage and synovium membrane were stained with hematoxylin, toluidine blue, and safranin O. Iodine, glutamic oxaloacetic transminase, creatine phosphokinase (CPK), and LDH in rat sera have been measured. We were able to confirm cytotoxicity in the synovial cells placed in PVI concentration of more than 6.25 x 10(-2)%. In comparison with the positive control, LDH, in this case, was released at the concentration level of 33.3%. Independent of period of stimulation, LDH was released the most in the PVI concentration of 6.25 x 10(-2). The histopathological analysis of articular cartilage has indicated clear morphological alterations in rats' synovium; especially, toluidine blue staining and safranin O staining were seen in the metachromasia of articular cartilage. However, no fissures or erosive changes in the articular cartilage, which were usually observable in the case of osteoarthritis, were observed. In the synovium inflammatory cells, which were mainly plasma cells and lymphoid cells, no neutrophils were infiltrated. The degree of infiltration has increased steadily day by day. Fibrin deposition has been observed even in the synovium of 1-day stimulation. On the 7th day, a serum total iodine concentration has been 544 microg/dl, 4,440 IU/ml for CPK concentration, and 2,049 IU/ml for LDH concentration, while the control concentrations have been 7.1 microg/dl, 491 IU/ml, and 700 IU/ml, respectively. Our experiment has disclosed that PVI preparation is strongly cytotoxic to synovial cell and articular cartilage.

Animals↗
PubMed1989

Optical verification of a technique for in situ ultrasonic measurement of articular cartilage thickness.

Several investigators have used pulse-echo ultrasonics to measure the thickness of articular cartilage in situ. The underlying assumption in all measurements was that the second reflection used in thickness calculations was from the calcified-cartilage/cartilage boundary (tidemark). To investigate this assumption, the thickness of 24 cartilage plugs excised from a human femoral head was measured both ultrasonically and optically. Measurements established that the second reflection was from the tidemark and validated the ultrasonic technique as a method of mapping the thickness distribution of articular cartilage in synovial joints in situ.

Acetabulum↗
PubMed2005

Morphological studies on the ageing and osteoarthritis of the articular cartilage in C57 black mice.

PURPOSE: To study the cause and mechanism of joint degeneration in osteoarthritis, through histopathological and ultrastructural-histochemical experiments on the articular cartilage of the knees of the C57 black mouse. METHODS: 192 C57 black mice and a control group of 64 C57BL/6J mice were used in this study. The left and right knee articular capsules of the joints were removed and stained. Each articular cartilage sample was examined and osteoarthritic changes were assessed using a transmission electron microscope. The severity of osteoarthritis in the knee joint cartilage of C57 black mice was histologically assessed using a classification system described by Okabe, based on Maier's system. RESULTS: The incidence and the severity of osteoarthritis gradually increased with age; the incidence increased from 20% at 2 months to 80% at 16 months. Irreversible changes appeared at an advanced stage, and the process of degeneration was quite similar to that in human osteoarthritis. Through transmission electron microscopy, we observed poorly developed Golgi apparatus, markedly increased intracellular microfilaments, decreased proteoglycan granules, and broken collagen networks in all stages of osteoarthritis. By contrast, Golgi apparatus and other organelles were well developed in histologically normal mice of all ages. Proteoglycan granules, which mainly consisted of keratan sulphate, were observed; collagen networks were maintained. CONCLUSION: Disturbed protein transport and sugar synthesis in chondrocytes, caused by the deficient development of the Golgi apparatus, could result in degenerative changes in articular cartilage. The structure and function of the matrix were maintained mainly because of the continued presence of keratan sulphate.

Aging↗
PubMed1993

Elevation in urinary levels of pyridinium cross-links of collagen following chymopapain-induced degradation of articular cartilage in the rabbit knee provides evidence of metabolic changes in bone.

To measure urinary levels of two pyridinium cross-links of collagens at various times, rabbits were injected in the left knee with 0.2 mg (N = 11) or 2.0 mg chymopapain (N = 11). Urinary levels of the bone-specific deoxy-pyridinoline cross-link and of the hydroxylysyl pyridinoline cross-link, found in large amounts in articular cartilage and bone, were measured by high performance liquid chromatography (HPLC). The urinary levels were correlated with histological evidence of progressive articular cartilage destruction in animals injected with 2.0 mg chymopapain and of successful repair in rabbits injected with the lower dose. Rabbits injected with 2.0 mg chymopapain showed a very large increase in urinary levels of deoxy-pyridinoline during the first 30 days after the injection. This rise was not seen in animals injected with the lower dose. A rise in urinary level of the hydroxylysyl pyridonline cross-link was observed in all rabbits but was more pronounced and lasted longer in animals receiving the higher dose. The failure of rabbits injected with 2.0 mg chymopapain to repair the damaged articular cartilage was strongly associated with a marked increase in the catabolism of the bone-specific deoxy-pyridinoline cross-link and to a lesser extent with the catabolism of the hydroxylysyl pyridinoline found in bone and in articular cartilage.

Aging↗
PubMedDate not supplied

The effect of trans-stifle external skeletal fixation and hyaluronic acid therapy on articular cartilage in the dog.

Transarticular external skeletal (TES) fixators were applied unilaterally to the stifle joints of 10 young adult dogs. After 4 weeks, the fixators were removed from all dogs. Two dogs were not allowed a remobilization period, whereas 8 dogs were provided with 4 additional weeks of weight-bearing activity in a kennel run. Four dogs were given high-molecular weight hyaluronic acid by intra-articular injection weekly during the remobilization period. Clinical gait evaluations and range of motion were determined during the remobilization period. Articular cartilage samples from both stifle joints of all dogs were evaluated histologically and histochemically. No significant differences in gait scores or range of motion were noted between treated and untreated dogs. Articular cartilage proteoglycan content was reduced after 4 weeks of trans-stifle external skeletal fixation as determined by loss of alcian blue (AB) histochemical staining. Improved homogeneity of histochemical staining was observed after remobilization. However, remobilization was associated with histological damage to the surface and tangential layers of articular cartilage. Remobilization combined with hyaluronic acid (HA) therapy improved histochemical staining and reduced structural damage to articular cartilage when compared with remobilization alone.

Animals↗
PubMed2005

Evaluation of the effect of collagen network degradation on the frictional characteristics of articular cartilage using a simultaneous analysis of the contact condition.

BACKGROUND: Superficial conditions and integrity of collagen network play an important role on the lubrication performance of articular cartilage. In this work, a technique based on the evanescent waves is used for the evaluation of contact condition during friction tests. METHODS: The frictional and superficial characteristics of the normal and degraded articular cartilages with high and low concentration of collagenase were evaluated. The optical apparatus was set in order to decrease the intensity of a light reflected at the interface between a prism and specimens when collagen fibers are found near the interface. FINDINGS: For all conditions, an increase in the attenuation of reflectance as the friction coefficient increases was observed with reasonable correlation. For the specimens degraded with collagenase, low friction and reduced attenuation of reflectance were observed at the beginning of sliding followed by a gradual increase in both friction and attenuation of reflectance. In comparison to the degraded specimens, normal specimens presented high friction at beginning and low friction at the end of test. INTERPRETATION: The superficial conditions and the presence of water at the articular surface play an important role in the lubrication of synovial joints. The ability to retain water for degraded specimens is impaired due to the loss of proteoglycan observed in the histological sections and hence, their low friction observed at the beginning of the test is not sustained for a long time. The use of evanescent waves demonstrated to be very useful in the analysis of the contact condition of articular cartilage.

Animals↗
PubMedDate not supplied

The effects of interleukin-1 on articular cartilage destruction as observed in arthritic diseases, and its therapeutic control.

At present there is substantial evidence to suggest that interleukin 1 (IL-1) may act as a key mediator in the normal physiologic regulation of cartilage as well as in the pathogenesis of cartilage destruction in arthritic disorders. IL-1 induces stimulation of chondrocyte catabolism and alters chondrocyte biosynthesis in articular cartilage. These actions of IL-1 may lead to destruction and inappropriate repair following degradation of the cartilage matrix. Moreover, IL-1 induced biological activities in chondrocytes may be influenced by growth factors (e.g. fibroblast growth factor, insulin-like growth factor, transforming growth factor-beta), guanine nucleotide proteins, or other cytokines. With respect to the widely suggested potential significance of IL-1 in arthritis, pharmacological control of IL-1 action is of important clinical relevance. Today the therapeutic control of IL-1 induced effects in articular cartilage destruction as observed in arthritic diseases can be divided into drugs which affect IL-1 production, drugs which modify or block the IL-1 effect before stimulation of the target cell, or drugs that interfere with the IL-1 induced effects, e.g. steroidal drugs, non-steroidal anti-inflammatory drugs, immunoregulatory drugs or class-specific proteinase inhibitors. However, these drugs do not specifically block IL-1 activity. For the development of therapeutic agents capable of specifically blocking IL-1 effects, a better understanding of IL-1 induced activities is needed. In conclusion, knowledge about chondrocyte metabolic and regulatory alterations would be beneficial in unraveling the events that take place in arthritic diseases and would favor therapeutic research for agents that might arrest the progressive destruction of articular cartilage in pathological conditions.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

Depth-varying density and organization of chondrocytes in immature and mature bovine articular cartilage assessed by 3d imaging and analysis.

Articular cartilage is a heterogeneous tissue, with cell density and organization varying with depth from the surface. The objectives of the present study were to establish a method for localizing individual cells in three-dimensional (3D) images of cartilage and quantifying depth-associated variation in cellularity and cell organization at different stages of growth. Accuracy of nucleus localization was high, with 99% sensitivity relative to manual localization. Cellularity (million cells per cm3) decreased from 290, 310, and 150 near the articular surface in fetal, calf, and adult samples, respectively, to 120, 110, and 50 at a depth of 1.0 mm. The distance/angle to the nearest neighboring cell was 7.9 microm/31 degrees , 7.1 microm/31 degrees , and 9.1 microm/31 degrees for cells at the articular surface of fetal, calf, and adult samples, respectively, and increased/decreased to 11.6 microm/31 degrees , 12.0 microm/30 degrees , and 19.2 microm/25 degrees at a depth of 0.7 mm. The methodologies described here may be useful for analyzing the 3D cellular organization of cartilage during growth, maturation, aging, degeneration, and regeneration.

Animals↗
PubMed1997

Ultrastructure of adult human articular cartilage matrix after cryotechnical processing.

The ultrastructure of adult human articular cartilage matrix is reexamined in tissue processed according to recently improved cryotechniques [Studer et al. (1995) J. Microsc., 179:321-332]. In truely vitrified tissue, a network of fine cross-banded filaments (10-15 nm in diameter) with a periodicity characteristic of collagen fibrils is seen throughout the extracellular substance, even within the pericellular compartment, which has hitherto been deemed free of such components. Proteoglycans fill the interstices between these entities as a homogeneously distributed granular mass; they do not manifest a morphologically identifiable reticular structure. Longitudinally sectioned collagen fibrils exhibit variations in thickness and kinking; they tend to align with their periodic banding in register and are frequently seen to split or fuse along their longitudinal course. The tendency of fibrils to form bundles is greater in deeper zones than in more superficial ones. A duality in the orientation of fibrils and fibril bundles is observed within the interterritorial matrix compartment: superimposed upon the well-characterized arcade-like structure formed by one subpopulation is another, more randomly arranged one. The classical concepts of matrix organization thus need to be modified and refined to encompass these findings.

Cartilage, Articular↗
PubMed1982

Partial reversal by beta-D-xyloside of salicylate-induced inhibition of glycosaminoglycan synthesis in articular cartilage.

While net 35S-glycosaminoglycan synthesis in normal canine articular cartilage was suppressed by 10(-3)M sodium salicylate to about 70% of the control value, addition of xyloside (10(-6)M-10(-3)M) to the salicylate-treated cultures led to a concentration-dependent increase in glycosaminoglycan synthesis, which rose to 120-237% of controls. Similar results were obtained when 3H-glucosamine was used to measure glycosaminoglycan synthesis, confirming that salicylate suppresses and xyloside stimulates net glycosaminoglycan synthesis, and not merely sulfation. Salicylate (10-3)M) did not affect the activity of xylosyl or galactosyl transferase prepared from canine knee cartilage, and net protein synthesis was unaltered by either salicylate or xyloside. The proportion of newly synthesized proteoglycans existing as aggregates when cartilage was cultured with xyloside was similar to that in controls, although the average hydrodynamic size of disaggregated proteoglycans and of sulfated glycosaminoglycans was diminished.

Animals↗
PubMed1983

Surface of articular cartilage: immunohistological studies.

Using several physical techniques the surface of articular cartilage has been reported to be structurally different from the deeper layers. In this paper using immunohistochemical methods, the surface has been shown to contain a characteristically different collagen, Type I in contrast to Type II which is the major collagen of cartilage. These results support previous proposals for a surface layer, or lamina splendens, the presence of which would be of considerable importance in understanding the degradation of cartilage in arthritides.

Animals↗