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PubMed2003

Comparison of the catabolic effects of fibronectin fragments in human knee and ankle cartilages.

OBJECTIVE: To compare the response of knee and ankle cartilages to fibronectin fragments (Fn-f) in terms of kinetics of matrix proteoglycan (PG) degradation and synthesis, since previous data had shown that knee was more sensitive to Fn-f in terms of steady-state PG content. DESIGN: Human knee and ankle cartilage explants were treated with the 29kDa Fn-f, and its effects on PG-degradation kinetics, on the half-lives of 35S-sulfate-labeled PG, on PG synthesis suppression and on matrix metalloproteinase -3 (MMP-3) were compared. Cultures were also treated with the interleukin (IL) receptor antagonist protein (IRAP) in order to determine whether IL-1 is involved in the Fn-f effect. RESULTS: The Fn-f enhanced PG-degradation rates in both human knee and ankle cartilages. Knee cartilage showed a greater effect of Fn-f on half-lives of newly synthesized 35S-labeled PG than ankle. The extent of release of MMP-3 was similar for human ankle and knee cartilages. However, PG synthesis in knee cartilage was sensitive to 10- to 100-fold lower concentrations of Fn-f than was ankle cartilage. IRAP partially reversed Fn-f activity in ankle cartilages. CONCLUSIONS: The role of Fn-f in proteolysis leading to cartilage damage appears to be minor in human cartilages than had previously been shown for bovine. This decreased proteolysis is true for both knee and ankle. The major difference between human ankle and knee cartilage appears to be greater sensitivity to PG synthesis suppression in knee cartilage. A further indication that IL-1 is involved in the pathway was provided by the partial reversal with IRAP.

Adolescent↗
PubMed1997

An investigation of the stress distribution generated in articular cartilage by crystal aggregates of varying material properties.

Several joint diseases are associated with the deposition of crystals within the articular cartilage. A variety of crystal aggregates have previously been identified throughout the thickness of the cartilage. A linear elastic finite element model representing instantaneous, or short-term, loading conditions has been developed of a large crystal aggregate surrounded by articular cartilage. The material properties of the aggregate and the cartilage were varied and the resultant shear stress and equivalent strain distribution in the surrounding cartilage studied in order to provide some indication of the relative potential of various types of crystal aggregate to cause damage to the articular cartilage. Results indicated that aggregates with a Young's modulus either much less, or much greater, than that of the surrounding cartilage generated the maximum shear stress and equivalent strain concentrations at the interface between the aggregate and the cartilage. Also, that highly compressible aggregates, with a very low Poisson's ratio, generated higher shear stress and equivalent strain concentrations in the surrounding cartilage than aggregates of a more incompressible nature. Under conditions of short-term loading these results suggest that crystal aggregates present within the cartilage layer will increase the shear stress and equivalent strain concentrations in the surrounding cartilage, and therefore have the potential to cause damage to the cartilage.

Biomechanical Phenomena↗
PubMed1998

Permeability of articular cartilage to matrix metalloprotease inhibitors.

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

Animals↗
PubMed1999

Expression of type VI collagen in normal and osteoarthritic human cartilage.

OBJECTIVE: This study was undertaken in order to study the expression of type VI collagen in normal and osteoarthritic human knee cartilage. METHODS: Seventy-two osteoarthritic cartilage/bone samples were obtained form 29 patients with primary OA undergoing surgery for a total knee replacement. Normal cartilage was collected from five human knees at the time of autopsy. Type VI collagen protein was localized using a polyclonal anti human type VI collagen antibody, the corresponding mRNA was detected with an 310 base antisense probe, specific for the alpha2(VI) collagen chain. RESULTS: In normal cartilage, type VI collagen protein is concentrated pericellularly around the chondrocytes of all cartilage zones. In the middle and deep zones, type VI collagen was also found in the interterritorial matrix. Type VI collagen mRNA expression was detected in chondrocytes of all cartilage zones. In moderately affected osteoarthritic cartilage, type VI collagen expression was increased. An intensive immunohistological interterritorial staining for type VI collagen was observed in the middle and deep cartilage zones. Specific mRNA signals were also increased especially in the middle and deep cartilage zone. In the superficial zone and calcified cartilage of these samples, type VI collagen mRNA expression was restricted to focal areas. In severe osteoarthritic cartilage, an intensive staining for type VI collagen mRNA was found in clusters of proliferating chondrocytes and in the deep cartilage zone. Type VI collagen was localized pericellularly and in the matrix of chondrocyte clusters. Furthermore, chondrocytes from the deep zone showed a territorial distribution of type VI collagen. CONCLUSIONS: These results demonstrate that in normal and osteoarthritic cartilage, type VI collagen is expressed in a zone specific pattern. The observed increase of type VI collagen expression in osteoarthritis suggests a potential role in the disease process.

Adult↗
PubMed2000

Activation of annexin II and V expression, terminal differentiation, mineralization and apoptosis in human osteoarthritic cartilage.

OBJECTIVE: To test the hypothesis that terminal differentiation of chondrocytes in human osteoarthritic cartilage might lead to the failure of repair mechanisms and might cause progressive loss of structure and function of articular cartilage. DESIGN: Markers for terminally differentiated chondrocytes, such as alkaline phosphatase, annexin II, annexin V and type X collagen, were detected by immunohistochemical analysis of human normal and osteoarthritic knee cartilage from medial and lateral femoral condyles. Apoptosis in these specimens was detected using the TUNEL labeling. Mineralization and matrix vesicles were detected by alizarin red S staining and electron microscopic analysis. RESULTS: Alkaline phosphatase, annexin II, annexin V and type X collagen were expressed by chondrocytes in the upper zone of early stage and late stage human osteoarthritic cartilage. However, these proteins, which are typically expressed in hypertrophic and calcifying growth plate cartilage, were not detectable in the upper, middle and deep zones of healthy human articular cartilage. TUNEL labeling of normal and osteoarthritic human cartilage sections provided evidence that chondrocytes in the upper zone of late stage osteoarthritic cartilage undergo apoptotic changes. In addition, mineral deposits were detected in the upper zone of late stage osteoarthritic cartilage. Needle-like mineral crystals were often associated with matrix vesicles in these areas, as seen in calcifying growth plate cartilage. CONCLUSION: Human osteoarthritic chondrocytes adjacent to the joint space undergo terminal differentiation, release alkaline phosphatase-, annexin II- and annexin V-containing matrix vesicles, which initiate mineral formation, and eventually die by apoptosis. Thus, these cells resume phenotypic changes similar to terminal differentiation of chondrocytes in growth plate cartilage culminating in the destruction of articular cartilage in osteoarthritis.

Adult↗
PubMed2002

Articular cartilage degradation and de-differentiation of chondrocytes by the systemic administration of retinyl acetate-ectopic production of osteoblast stimulating factor-1 by chondrocytes in mice.

OBJECTIVE: Vitamin A derivatives are widely used therapeutic agents for the treatment of dermatological and rheumatological disorders. Long-standing administration of these drugs, in turn, causes skeletal changes including ossification of ligaments, premature fusion of epiphyses and abnormalities of modeling. Recent in vitro experiments have further suggested that retinoid treatment of cultured chondrocytes may cause apoptotic cell death. The present study aims to address detailed cartilage changes associated with in vivo administration of vitamin A derivatives. METHODS: Retinyl acetate was administrated to experimental mice, C3H-Heston, for more than 12 months. Modified morphometry on the articular cartilage and fluorescent labeling of the subchondral bone were carried out to address the changes in the articular cartilage and subchondral bone. In order to address the detailed chondrocytes phenotypes, electron microscopy was carried out. Since findings of these studies suggested that biological properties of the cartilage matrix might be altered, the present study also immunolocalized functional matrix molecules, type I collagen and osteoblast-stimulating factor-1 (OSF-1). RESULTS: Histomorphometry demonstrated that retinoid administration lead to progressive atrophy of the articular cartilage with concomitant proliferation of subchondral bone. Furthermore, detailed light and electron microscopy suggested that the subchondral bone proliferates into the degenerating cartilage. The affected articular cartilage also resembled that of osteoarthritis in terms of ectopic type I collagen production. Furthermore, the affected articular cartilage produced a developmentally regulated matrix molecule, osteoblast-stimulating factor-1 (OSF-1) that is normally expressed in both the fetal cartilage and the epiphyseal growth plate cartilage but not in the articular cartilage. CONCLUSION: The present results indicate that the systemic retinoid administration may alter the biological properties of the articular cartilage.

Adjuvants, Immunologic↗
PubMed1999

[Allogenic heterotopic cartilage transplantation for primary corneal replacement in a rabbit model].

BACKGROUND: Aim of the present study was to investigate woundhealing after allogen heterotopic cartilage transplantation in a rabbit model. MATERIAL AND METHODS: Cartilage discs were transplanted by central lamellar keratoplasty (diameter 5.0 mm) in eleven New Zealand White Rabbits. Cartilage was harvested of the ears of rabbits at the day of transplantation. The cartilage discs 0.5-0.6 mm thick were prepared with 5.2 mm diameter and transplanted within 12 hours. Fixation was performed by eight 10-0 nylon sutures. Postoperatively, dexamethasone ointment containing gentamicin was applied three times a day for three weeks. Clinical course was documented by photographs. For histological examinations the transplanted eyes were enucleated after one day or three days, and after 3, 6 or 12 months. RESULTS: Allogen cartilage healed firmly in the cornea within two months. During the course of observation the cartilage grafts thinned and were replaced by normal appearing collagen fibrills. In one case neovascularisation of the cornea occurred and reached the cartilage graft, but did not invate. Histologically, in all cases no leukocytes could be seen in the cartilage or its neighbourhood. The cartilage grafts did not proliferate and remained avascular. The intraocular structures showed no inflammatory reaction. CONCLUSIONS: Allogen cartilage grafts to a clear corneal pounch do not induce an inflammatory reaction. Therefore, autologous cartilage prepared of ears seems to be useful biological material in ophthalmologic surgical procedures, for example to fill up corneal defects. To investigate if cartilage grafts will be helpful to stop neovascularisation in keratoplasty further studies with vascularisized corneas are necessary.

Animals↗
PubMed2003

Immunohistochemical distribution patterns of collagen type II, chondroitin 4-sulfate, laminin and fibronectin in human nasal septal cartilage.

Collagen type II, chondroitin 4-sulfate, laminin and fibronectin are major components of cartilage matrix. It is important to know their distribution patterns to evaluate relationships between cartilage cells and surrounding cartilage matrix. In the present study, we investigated localization patterns of these macromolecules in human nasal septal cartilage by immunohistochemical methods. Samples of human nasal septal cartilage were obtained from patients with nasal septum deviations who underwent septoplastic operation and were prepared for immunohistochemical examination. Distribution patterns of cartilage matrix macromolecules correlated with those found in other cartilage tissues. Diffuse staining of collagen type II was found in the cartilage matrix, chondroitin 4-sulfate immunostaining was present in the cytoplasm and like a pericellular ring around chondrocytes. Laminin immunostaining was found in the cytoplasm of chondrocytes, and fibronectin was localized in the pericellular matrix and in capsules of human nasal septal cartilage. Moreover, fibronectin was also detected at high levels in the interconnecting segments between adjacent chondrons. In conclusion, similar localisation patterns of the components investigated in human septal cartilage as in other tissues indicate that these macromolecules may play a role in both cell-matrix adhesion and matrix-matrix cohesion in the pericellular microenvironment surrounding nasal septal cartilage chondrocytes as in other cartilage tissues.

Adult↗
PubMed1986

Correction of abnormal matrix formed by cmd/cmd chondrocytes in culture by exogenously added cartilage proteoglycan.

The cartilage matrix deficiency (cmd/cmd) mouse fails to synthesize the core protein of cartilage-characteristic proteoglycan (cartilage PG). Chondrocytes from the cmd/cmd cartilage cultured in vitro produced nodules with greatly reduced extracellular matrix. Immunofluorescence staining revealed that the nodules of mutant cells differed from the normal in lacking cartilage PG and in uneven and reduced deposition of type II collagen. Exogenously added cartilage PG prepared from either normal mouse cartilage or Swarm rat chondrosarcoma to the culture medium was incorporated exclusively into the extracellular matrices of the nodules, with a concurrent correction of the abnormal distribution pattern of type II collagen. The incorporation of cartilage PG into the matrix was disturbed by hyaluronic acid or decasaccharide derived therefrom, suggesting that the incorporation process involves the interaction of added proteoglycan with hyaluronic acid. Both the hyaluronic acid-binding region and the protein-enriched core molecule prepared from rat chondrosarcoma cartilage PG could also be incorporated but, unlike the intact cartilage PG, they were distributed equally in the surrounding zones where fibroblast-like cells predominate. The results indicate that the intact form of cartilage PG is required for specific incorporation into the chondrocyte nodules, and further suggest that cartilage PG plays a regulatory role in the assembly of the matrix macromolecules.

Animals↗
PubMed1960

Comparison of the effects of papain and vitamin A on cartilage. II. The effects on organ cultures of embryonic skeletal tissue.

The effects of papain protease and of vitamin A on explanted limb bone rudiments from 7- and 13-day chick embryos and fetal mice have been studied and compared. The incubation of cartilaginous rudiments from 7-day chick embryos in a solution containing papain and cysteine resulted in complete loss of the metachromasia of the cartilage matrix within 1 hour; explants treated in this fashion recovered normal metachromatic staining properties when grown in normal medium for 4 days. The incubation of 7-day chick cartilage rudiments in a solution containing papain without cysteine resulted in partial loss of metachromasia from cartilage within 1 hour; the addition of vitamin A to the solution did not enhance the effect of papain during this period. The addition of papain to the culture medium in which 7-day chick embryo cartilage rudiments were grown resulted in uniform loss of the metachromasia of the cartilage matrix; similar explants grown in the presence of excess vitamin A also showed loss of the metachromasia of cartilage, but certain regions of the cartilage were affected earlier and more severely than others. Changes in cartilage cells, including loss of glycogen, occurred when the rudiment was grown in medium containing excess vitamin A, but not when it was grown in the presence of papain. Bone rudiments from 13-day chick embryos showed changes in cartilage similar to those seen in 7-day chick embryo rudiments when grown in the presence of papain or of excess vitamin A; the existing bone was not affected under these conditions. When grown in the presence of papain or excess vitamin A, the cartilage of late fetal mouse bone underwent changes similar to those already described in chick embryo rudiments. In contrast to the chick embryo rudiments, those from the fetal mouse showed rapid resorption of bone when grown in the presence of excess vitamin A. Papain had no effect on bone from either source. The changes seen in cartilage of explants grown in the presence of vitamin A and papain together were greater than those seen with either agent alone. The changes seen in fetal mouse bone grown in the presence of vitamin A were not enhanced by the additional presence of papain. On the basis of these observations, it is suggested that the changes in cartilage seen in experimental hypervitaminosis A may be the result of activation of a proteolytic enzyme or enzymes with properties similar to papain.

Animals↗
PubMedDate not supplied

Repair of osteochondral defects in rabbits with ectopically produced cartilage.

Cartilage has poor regenerative capacity. Donor site morbidity and interference with joint homeostasis should be considered when applying the autologous chondrocyte transplantation technique. The use of ectopically produced cartilage, derived from periosteum, might be a novel method to heal cartilage defects. Ectopic cartilage was produced by dissecting a piece of periosteum from the tibia of rabbits. After 14 days the reactive tissue at the dissection site was harvested and a graft was cored out and press-fit implanted in an osteochondral defect in the medial condyle of the femur with or without addition of hyaluronan. After 3 weeks and 3 months the repair reaction was evaluated by histology. Thionine- and collagen type II-stained sections were evaluated for graft viability, ingrowth of the graft, and joint surface repair. Empty defects remained empty 3 weeks after implantation, ectopic cartilage filled the defect to the level of the surrounding cartilage. Histologically, the grafts were viable, consisting mainly of cartilage, and showed a variable pattern of ingrowth. Three months after implantation empty defects with or without hyaluronan were filled primarily with fibrocartilaginous tissue. Defects treated with ectopic cartilage contained mixtures of fibrocartilaginous and hyaline cartilage. Sometimes a tidemark was observed in the new articular cartilage and the orientation of the cells resembled that of healthy articular cartilage. Subchondral bone repair was excellent. The modified O'Driscoll scores for empty defects without and with hyaluronan were 12.7 +/- 6.4 and 15.3 +/- 3.2; for treated defects scores were better (15.4 +/- 3.9 and 18.2 +/- 2.9). In this conceptual study the use of ectopic cartilage derived from periosteum appears to be a promising novel method for joint surface repair in rabbits.

Animals↗
PubMed1996

Localization of insulin-like growth factor-1 receptor in human normal and osteoarthritic cartilage in relation to proteoglycan synthesis and content.

Insulin-like growth factor-1 (IGF-1) plays a key role in the regulation of chondrocyte proteoglycan (PG) metabolism. We investigated whether chondrocyte PG synthetic activity correlates with the presence of chondrocyte IGF-1 receptor in the surface, middle and deeper zones of normal human articular cartilage and in cartilage known to display a shift in chondrocyte metabolism, i.e. cultured cartilage or osteoarthritic (OA) cartilage. Cartilage specimens were obtained post mortem from human knees within 18 h after death from donors without known clinical OA history. The samples were taken from macroscopically normal looking regions as well as from damaged regions with osteoarthritic appearance, yielding a range of OA grades from mild to moderate and severe OA. We examined chondrocyte PG synthesis by in situ autoradiography of incorporated [35S]sulphate and chondrocyte IGF-1 receptor localization by immunohistochemistry, followed by confocal laser scanning microscopical (CLSM) analysis in the same cartilage samples. In normal cartilage, both the amount of chondrocyte PG synthesis and the level of chondrocyte IGF-1 receptor localization are at low levels in the surface zone chondrocytes, but both are high in middle and deeper zone chondrocytes. Furthermore, after culture, the increase in chondrocyte PG synthesis in the surface layer coincides with increase in IGF-1 receptor expression. However, in mild OA particularly high levels of chondrocyte synthetic activity were found in the upper cartilage layer, whereas IGF-1 receptor expression was low in this layer, suggesting that factors other than IGF-1 are involved. High chondrocyte PG synthetic activity and chondrocyte IGF-1 receptor staining were found in the upper and deeper layers of moderate OA cartilage, whereas both low levels of chondrocyte activity as well as IGF-1 receptors were observed in cases of severe OA. Our data indicate that IGF-1 displays cellular heterogeneity in chondrocyte stimulation in the various cartilage zones in normal cartilage. Clear zonal correlation is lost in OA cartilage, and patterns of chondrocyte IGF-1 receptor expression and PG synthesis vary with the stage of OA.

Aged↗
PubMed2005

Factors affecting progression of knee cartilage defects in normal subjects over 2 years.

OBJECTIVES: Cartilage defects are present in subjects with knee osteoarthritis (OA). Although they are often present in healthy subjects, there is little data on the natural history of cartilage defects. The aim of this study was to examine the change in cartilage defects over 2 yr and to identify factors associated with this change. METHODS: One hundred and twenty-four healthy subjects underwent magnetic resonance imaging of their dominant knee at baseline and follow-up. Cartilage defects were scored (0-4) at five sites. Bone size was determined at medial and lateral tibial plateau and patella. Height, weight, body mass index and physical activity were measured by standard protocols. RESULTS: Eighty-six subjects completed the study. The mean cartilage defect score of each tibiofemoral compartment increased over time. However, medial and lateral tibiofemoral defect score decreased in 5% of the subjects. Cartilage defects were more likely to progress in males than females in each individual compartment (P<0.001 for medial tibiofemoral, P=0.005 for lateral tibiofemoral and P=0.01 for patellar cartilage). Baseline cartilage defect score was negatively associated with the progression of cartilage defects in each compartment (all P<0.001). CONCLUSION: Although knee cartilage defects progressed over time in the majority of normal subjects, those of the highest severity tended to regress. Male gender and baseline cartilage defect score were the main factors associated with the progression of cartilage defects. Larger studies will be required to identify factors associated with the progression and regression of lesions.

Body Mass Index↗
PubMed2000

Cartilage shaping using the Er:YAG laser: preliminary report.

Cartilage grafts have been widely used for reconstruction of congenital or acquired deformities. Reshaping and preserving the new shape of the cartilage grafts have been a problem. In this in vitro experimental study the authors studied the effect of the Er:YAG laser on cartilage reshaping in comparison with scalpel stripping and suture holding. The study consisted four groups (n = 9): group I, untouched cartilage; group II, the short edges of the cartilage were sutured to each other; group III, cartilage was incised using a scalpel; and group IV, Er:YAG laser stripping was applied to the cartilage. Changes in the shape of cartilage were evaluated at 15 minutes, and days 1, 4, and 10. The majority of cartilage in the scalpel-stripped group returned to the initial shape by day 10, whereas the laser-stripped cartilage showed progressive warping day by day, and almost all cartilage formed a circle by day 10. The Er:YAG laser enhanced cartilage warping by a mechanical effect of stripping and a thermal effect of laser radiation resulting in ultrastructural changes.

Animals↗
PubMed2004

Microtia chondrocytes as a donor source for tissue-engineered cartilage.

OBJECTIVES/HYPOTHESIS: Current surgical techniques for the correction of microtia are challenging. Research in the field of tissue engineering is providing insight into chondrocyte behavior for a possible future treatment of microtia. The authors wished to evaluate the biological potential of chondrocytes isolated from microtia cartilage as compared with normal auricular cartilage as a source of tissue-engineered cartilage. STUDY DESIGN: A comparative research design to study the potential of microtia cartilage chondrocytes with normal auricular chondrocytes as a source of tissue-engineered cartilage. METHODS: Cartilage specimens from 12 pediatric patients (six normal auricular specimens and six auricular specimens with microtia) were obtained. The chondrocytes were isolated and cultured in vitro; chondrocyte number was increased by passaging. Each type of cell was implanted in nude mice to generate tissue-engineered cartilage. Eight weeks after implantation the specimens were dissected and removed. Results were compared between the normal auricular and microtia specimens in regard to cell number expansion in vitro and generation of tissue-engineered cartilage in vivo. RESULTS: An initial mean cell number of 150,000 cells in each group (normal and microtia) increased to an average cell number of 120 million cells/mL in the normal and 130 million cells in the microtia subgroups, respectively, at the end of the second passage. Histologically, both types of chondrocytes generated normal elastic cartilage. CONCLUSION: The study demonstrated the potential of cells isolated from microtia cartilage to generate tissue-engineered cartilage. Microtia cartilage represents an important additional donor source for the possible generation of a human tissue-engineered auricle.

Case-Control Studies↗
PubMedDate not supplied

Xeno-implantation of pig chondrocytes into rabbit to treat localized articular cartilage defects: an animal model.

Articular cartilage has only a limited ability to regenerate. The transplantation of autologous chondrocytes is currently used to treat focal defects in human articular cartilage, although use of organs, tissues, or cells from different species is being investigated as an alternative treatment. The object of this study was to use xeno-transplantation of cultured pig chondrocytes for the repair of rabbit chondral defects, and to analyze the significance of tissue rejection in this animal model. Partial chondral defects, including removal of cartilage tissue and a part of the subchondral bone, were created in the lateral femoral condyles of 30 adult New Zealand White rabbits. A periosteal flap was sutured to the native cartilage with the cambium layer facing the defect. As a control, culture medium was injected into the defect void of one group of rabbits while in a treatment group, chondrocytes, isolated from normal femoral pig cartilage, were injected into the defect void. All rabbits were killed by 24 weeks. Macroscopic changes of the cartilage were analyzed using Mankin's score. The distal femoral portion was studied histologically using hematoxylin and eosin, alcian blue, toluidine blue, and Mason's trichrome. Pig cells and pig genetic material were detected in the neo-synthesized tissue by immunohistochemical detection of SLA-II-DQ and polymerase chain reaction analysis of the gene SLA-II-DQB. The synovial membrane was studied histologically by hematoxylin and eosin staining. In the control group, on average, less than 25 percent of the chondral defect was filled. The repair tissue had an irregular surface with few cells similar to chondrocytes or fibroblasts and a minimal formation of extracellular matrix. In the treatment group, the chondral defect was approximately 90 percent filled with good integration between the neo-synthesized cartilage and the native cartilage. The repair tissue had a smooth surface with cells similar to chondrocytes and a hyaline-like extracellular matrix. The neo-synthesized cartilage was morphologically similar to hyaline cartilage. Importantly, there were no signs of graft-vs.-host rejections or infiltration by immune cells. In the neo-synthesized tissue, pig genetic material was detected in 27 +/- 5 percent of all cells. These cells containing pig genetic material were distributed throughout the neo-synthesized cartilage. We conclude that the xeno-transplantation of chondrocytes could be an alternative method for the repair of articular cartilage defects.

Animals↗
PubMed2004

Tetrapolar measurement of electrical conductivity and thickness of articular cartilage.

A tetrapolar method to measure electrical conductivity of cartilage and bone, and to estimate the thickness of articular cartilage attached to bone, was developed. We determined the electrical conductivity of humeral head bovine articular cartilage and subchondral bone from a 1- to 2-year-old steer to be 1.14+/-0.11 S/m (mean+/-sd, n =11) and 0.306+/-0.034 S/m, (mean+/-sd, n =3), respectively. For a 4-year-old cow, articular cartilage and subchondral bone electrical conductivity were 0.88+/-0.08 S/m (mean+/-sd, n =9) and 0.179+/-0.046 S/m (mean+/-sd, n =3), respectively. Measurements on slices of cartilage taken from different distances from the articular surface of the steer did not reveal significant depth-dependence of electrical conductivity. We were able to estimate the thickness of articular cartilage with reasonable precision (<20% error) by injecting current from multiple electrode pairs with different inter-electrode distances. Requirements for the precision of this method to measure cartilage thickness include the presence of a distinct layer of calcified cartilage or bone with a much lower electrical conductivity than that of uncalcified articular cartilage, and the use of inter-electrode distances of the current injecting electrodes that are on the order of the cartilage thickness. These or similar methods present an attractive approach to the non-destructive determination of cartilage thickness, a parameter that is required in order to estimate functional properties of cartilage attached to bone, and evaluate the need for therapeutic interventions in arthritis.

Animals↗
PubMed2005

In vivo cartilage deformation after different types of activity and its dependence on physical training status.

BACKGROUND: Knowledge of the deformational behaviour of articular cartilage in vivo is required to understand the pathogenesis of osteoarthritis and the mechanical target environment of prospective cartilage transplant recipients. OBJECTIVES: To study the in vivo deformational behaviour of patellar and femorotibial cartilage for different types of physiological activities; and to test the hypothesis that in vivo deformation of cartilage is modified by intense physical exercise. METHODS: Magnetic resonance imaging and 3D digital image analysis were used to determine cartilage volume before and after physical activity in the patella of 12 volunteers (knee bends, squatting, normal gait, running, cycling). Deformation of femorotibial cartilage was investigated in 10 subjects (knee bends, static compression, high impact loading). Patellar cartilage deformation after knee bends was compared in seven professional weight lifters, seven sprinters, and 14 untrained volunteers. RESULTS: Patellar cartilage deformation was -5.9% after knee bends, -4.7% after squatting, -2.8% after normal walking, -5.0% after running, and -4.5% after cycling. The pattern of patellar cartilage deformation corresponded to the range of motion involved in the particular activity. Tibial cartilage deformation was greatest under high impact loading (-7%), but small for other activities. No significant difference was found between athletes and non-athletic controls. CONCLUSIONS: Patellar cartilage deformation shows a "dose dependent" response, where more intense loading leads to greater deformation. Relatively little deformation was observed in the femorotibial joint, except during high impact activities. The findings provide no evidence that adult human cartilage properties are amendable to training effects in vivo.

Adult↗