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PubMed2002

[Experimental study on laryngeal cartilage defects repair with differently preserved allogeneic cartilages transplantation].

OBJECTIVE: To study the effect of laryngeal cartilage defect repair with differently preserved allogeneic cartilage grafts. METHODS: 16 New Zealand white rabbits were used and divided into two groups. A 6 mm x 3 mm x 1 mm whole thickness cartilage defect was made in each side of the thyroid cartilage of each rabbit. In group one, the tissue-cultured cartilage grafts, preserved in RPMI-1640 medium for 30 days, were implanted in the left defects and the 4% formaldehyde preserved cartilage grafts for 30 days were implanted in the right defects. Fresh autogenous and allogeneic grafts were seprately transplanted into the right and left thyroid cartilage defects of the other group. Thyroid cartilages were taken out at 7, 30, 180 and 360 days after implantation. Samples were observed by macroscopy and prepared for hematoxylin and eosin (H&E) staining and immunohistochemical examination. RESULTS: No marked changes in form and volume were found in the fresh allografts and RPMI-1640 cultured cartilage grafts. The same as the autogenous cartilages, the defects of thyroid cartilage were successfully repaired by the fresh allografts and RPMI-1640 cultured cartilages. Whereas 4% formaldehyde preserved cartilage grafts were completely absorbed and replaced by cicatricial tissues in the thyroid cartilage defects. Histological observation showed that severe inflammatory cellular infiltration in the formaldehyde preserved cartilages at 7 and 30 days. The cartilage matrixes were resorpted and the chondrocytes showed degenerative change. Finally they were replaced by fibrous connective tissue at 360 days. In the RPMI-1640 cultured and fresh allogeneic cartilages only a little inflammatory cellular infiltration was observed and the cartilage matrixes were almost normal from 7 to 360 days. CONCLUSION: It is clinically feasible to use allogeneic grafts stored in RPMI-1640 medium or fresh allogeneic cartilage grafts for repairing laryngeal cartilage defects.

Animals↗
PubMed1999

Vascularization and cartilage mineralization of the thyroid cartilage of Munich minipigs and domestic pigs.

Thyroid cartilages of Munich minipigs and domestic pigs were investigated by polychrome sequential labeling, radiography, intravascular injections, histologic examination and scanning electron microscopy in order to gain further insight into the process of vascularization and cartilage mineralization. The relationship between vascularization and cartilage mineralization has only been studied in chondroepiphyses of long bones. Vessels branch off the perichondrial vascular network and enter parts of the thyroid cartilage with a large transverse diameter. Cartilage canals, which are perichondral invaginations, contain an arteriole, a venule, a capillary network and connective tissue. The capillaries form a glomerulus-like structure deep in the matrix of the cartilage. Neighbouring cartilage canals do not display any anastomoses. Cartilage mineralization occurs in large areas of the thyroid cartilage. It is only found in the interterritorial extracellular matrix. Mineralization of the cartilage is evident in areas supplied with cartilage canals as well as in non-supplied areas. Mineralized interterritorial matrix is composed of circular structures of different sizes fusing to form plaques. In scanning electron microscopy circular structures appear as globules. It is possible to visualize the dynamic process of cartilage mineralization with polychrome sequential labeling; it proceeds up to 4 microm per week. Distribution of cartilage canals reveals their nutritional role for the cartilage. According to investigations in chondroepiphyses, cartilage mineralization starts adjacent to the glomerular end of cartilage canals. In contrast, no correlation between cartilage vascularization and the beginning of cartilage mineralization of the thyroid cartilage of Munich minipigs and of domestic pigs has been found.

Animals↗
PubMed1998

Cartilage damaging activities of fibronectin fragments derived from cartilage and synovial fluid.

OBJECTIVE: To investigate whether fibronectin fragments (Fn-fs), shown to damage cultured cartilage, can be found in cartilage from patients with osteoarthritis (OA) or rheumatoid arthritis, or can be generated from fibronectin (Fn) within synovial fluids or from Fn in the matrix of cultured cartilage. To also determine whether cartilage or synovial fluid Fn-fs are active and, thus, could contribute to cartilage damage in vivo. METHODS: Fn-fs were immunochemically identified in cartilage extracts from patients with OA or rheumatoid arthritis or in bovine cartilage cultured with IL-1 alpha or in bovine synovial fluids treated with stromelysin-1 (MMP-3). The effect of removal of Fn-fs from OA synovial fluids was tested by passing fluids over an anti-Fn column and adding the resultant fluids to bovine cartilage cultures to measure proteoglycan (PG) degradation. Gelatin-Sepharose purified Fns from bovine plasma, synovial fluid or cartilage were digested with MMP-3 and the Fn-fs tested for degradation of PG in cultured cartilage. RESULTS: Extracts of cartilage from patients with rheumatoid arthritis or with OA contained a range of Fn-fs. Removal of Fn-fs from OA synovial fluids significantly reduced the resultant damage when the fluids were added to cultured cartilage. Addition of IL-1 alpha to cultured cartilage or of MMP-3 to synovial fluids enhanced generation of Fn-fs. Fn-fs, whether derived from bovine plasma or synovial fluid or cartilage Fns, damaged cartilage. CONCLUSIONS: These data demonstrate that although Fn-fs could be generated in vivo within synovial fluids and Fn-fs found in OA synovial fluid may contribute to cartilage damage in vivo, Fn-fs could also be generated within cartilage and amplify cartilage damage. Thus, Fn-fs may be both autocrine and paracrine regulators of cartilage metabolism.

Animals↗
PubMed2002

In situ hybridization and immunohistochemistry of bone sialoprotein and secreted phosphoprotein 1 (osteopontin) in the developing mouse mandibular condylar cartilage compared with limb bud cartilage.

Mandibular condylar cartilage is often classified as a secondary cartilage, differing from the primary cartilaginous skeleton in its rapid progress from progenitor cells to hypertrophic chondrocytes. In this study we used in situ hybridization and immunohistochemistry to investigate whether the formation of primary (tibial) and secondary (condylar) cartilage also differs with respect to the expression of two major non-collagenous glycoproteins of bone matrix, bone sialoprotein (BSP) and secreted phosphoprotein 1 (Spp1, osteopontin). The mRNAs for both molecules were never expressed until hypertrophic chondrocytes appeared. In the tibial cartilage, hypertrophic chondrocytes first appeared at E14 and the expression of BSP and Spp1 mRNAs was detected in the lower hypertrophic cell zone, but the expression of BSP mRNA was very weak. In the condylar cartilage, hypertrophic chondrocytes appeared at E15 as soon as cartilage tissue appeared. The mRNAs for both molecules were expressed in the newly formed condylar cartilage, although the proteins were not detected by immunostaining; BSP mRNA in the condylar cartilage was more extensively expressed than that in the tibial cartilage at the corresponding stage (first appearance of hypertrophic cell zone). Endochondral bone formation started at E15 in the tibial cartilage and at E16 in the condylar cartilage. At this stage (first appearance of endochondral bone formation), BSP mRNA was also more extensively expressed in the condylar cartilage than in the tibial cartilage. The hypertrophic cell zone in the condylar cartilage rapidly extended during E15-16. These results indicate that the formation process of the mandibular condylar cartilage differs from that of limb bud cartilage with respect to the extensive expression of BSP mRNA and the rapid extension of the hypertrophic cell zone at early stages of cartilage formation. Furthermore, these results support the hypothesis that, in vivo, BSP promotes the initiation of mineralization.

Animals↗
PubMed1996

Cartilage canals in human thyroid cartilage characterized by immunolocalization of collagen types I, II, pro-III, IV and X.

In this study the collagenous composition of cartilage canals in human thyroid cartilage, which are perichondral invaginations of blood vessels and connective tissue, and the surrounding cartilage matrix were investigated by immunolabelling with specific antibodies against type I, II, pro-III, IV and X collagen. During childhood and early adolescence no cartilage canals were detected in thyroid cartilage, and immunolabelling for type IV collagen was restricted to basal lamina components of blood vessels in the perichondrium. First immunolabelling for type IV collagen, belonging to blood vessels in cartilage canals, in both sexes was detected about the end of the second decade; it was localized in the dorsal part of the thyroid cartilage plate. At this time thyroid cartilage has already reached its final form and size. As revealed by von Kossa staining, vascularization preceded mineralization and ossification. In contrast to the male thyroid cartilage plate, no immunostaining for type IV collagen and no ossification was detected in the ventral half of female thyroid cartilage even in advanced age. The extracellular matrix of cells in cartilage canals showed positive immunostaining for collagen types I and pro-III as well as for collagen type II, indicating that the cells in the canal possess fibroblastic and chondrogenic properties. The extracellular matrix of hypertrophic chondrocytes adjacent to cartilage canals showed strong immunoreactivity for type X collagen. First mineralization was detected close to cartilage canals, suggesting that mineralization in human thyroid cartilage starts in the extracellular matrix adjacent to cartilage canals.

Adolescent↗
PubMed2005

Knee cartilage defects: association with early radiographic osteoarthritis, decreased cartilage volume, increased joint surface area and type II collagen breakdown.

OBJECTIVE: To generate hypotheses regarding the associations between knee cartilage defects and knee radiographic osteoarthritis (ROA), cartilage volume, bone size and type II collagen breakdown in adults. METHODS: A cross-sectional convenience sample of 372 male and female subjects (mean age 45 years, range 26-61) was studied. Knee cartilage defect score (0-4) and prevalence (a defect score of > or =2), cartilage volume, and bone surface area were determined using T1-weighted fat saturation MRI. Urinary levels of C-terminal crosslinking telopeptide of type II collagen (U-CTX-II) were measured by enzyme-linked immunosorbent assay. Height, weight and ROA were measured by standard protocols. RESULTS: In multivariate analysis, the severity and prevalence of knee cartilage defects were significantly and independently associated with tibiofemoral osteophytes (regression coefficient (beta): +0.86 to +1.31/unit, odds ratio (OR): 2.97-3.68/unit, all P<0.05 with the exception of OR in lateral tibiofemoral compartment) and tibial bone area (beta: +0.11 to +0.25/cm2; OR: 1.33-1.58/cm2, all P<0.01). Knee cartilage defects were inconsistently associated with joint space narrowing after adjustment for osteophytes but consistently with knee cartilage volume (beta: -0.27 to -0.70/ml; OR: 0.16-0.56/ml, all P<0.01 except for OR at lateral tibial cartilage site P=0.06). Lastly, knee cartilage defect severity was significantly associated with U-CTX-II (Partial r=+0.18, P<0.001 for total cartilage defect score). CONCLUSION: Osteophytes and increasing knee bone size may be causally related to knee cartilage defects. Furthermore, knee cartilage defects may result in increased cartilage breakdown leading to decreased cartilage volume and joint space narrowing suggesting an important role for knee cartilage defects in early knee OA.

Adult↗
PubMed2002

Repairing large porcine full-thickness defects of articular cartilage using autologous chondrocyte-engineered cartilage.

Large full-thickness defects of articular cartilage remain a major challenge to orthopedic surgeons because of unsatisfactory results of current therapy. Many methods, such as chondrectomy, drilling, cartilage scraping, arthroplasty, transplantation of chondrocytes, periosteum, perichondrium, as well as cartilage and bone, have been tried to repair articular cartilage defects. However, the results are far from satisfactory. In this study, we applied a tissue-engineering approach to the repair of articular cartilage defects of knee joints in a porcine model. Using isolated autologous chondrocytes, polyglycolic acid (PGA), and Pluronic, we have successfully in vivo-engineered hyaline cartilage and repaired articular cartilage defects. The surface of the repaired defects appeared smooth at 24 weeks postrepair. Histological examination demonstrated a typical hyaline cartilage structure with ideal interface healing between the engineered cartilage and the adjacent normal cartilage and underlying cancellous bone. In addition, glycosaminoglycan (GAG) levels in the engineered cartilage reached 80% of that found in native cartilage at 24 weeks postrepair. Biomechanical analysis at 24 weeks demonstrated that the biomechanical properties of the tissue-engineered cartilage were improved compared with those at an earlier stage. Thus, the results of this study may provide insight into the clinical repair of articular cartilage defects.

Animals↗
PubMed2001

ADAM-10 protein is present in human articular cartilage primarily in the membrane-bound form and is upregulated in osteoarthritis and in response to IL-1alpha in bovine nasal cartilage.

The objective of our study was to determine the tissue distribution and localization of ADAM-10 protein in human and bovine cartilage and the changes it undergoes with cartilage degeneration seen in osteoarthritis (OA) and under the influence of interleukin-1 (IL-1). Human normal and OA articular cartilage and bovine nasal cartilage cultured in the presence of IL-1alpha were processed for histology and immunohistochemistry. ADAM-10 protein was extracted from human cartilage and analyzed by Western blotting using anti-ADAM-10 antibodies. Fluor S Image analyzer and Quantity One software program were applied to quantify the total amount of ADAM-10. ADAM-10 protein was detected in both human and bovine cartilage. The strongest immunostaining was found in the cytoplasm and/or cell membranes of the superficial and upper middle layer of normal adult human cartilage, in the clusters and fibrillated areas of OA cartilage, and in IL-1alpha-stimulated bovine nasal cartilage. The distribution of ADAM-10 protein in bovine nasal cartilage was dependent on the length of exposure to IL-1alpha and corresponded to the areas of proteoglycan depletion. By Western blotting analysis of human cartilage, ADAM-10 was primarily detected in the membrane-enriched fraction and its levels were increased in degenerated and OA cartilage compared to normal cartilage. The results of this study suggest that ADAM-10 might be an important factor associated with cartilage degenerative processes. (J Histochem Cytochem 49:1165-1176, 2001)

ADAM Proteins↗
PubMed2003

Pathways of load-induced cartilage damage causing cartilage degeneration in the knee after meniscectomy.

Results of both clinical and animal studies show that meniscectomy often leads to osteoarthritic degenerative changes in articular cartilage. It is generally assumed that this process of cartilage degeneration is due to changes in mechanical loading after meniscectomy. It is, however, not known why and where this cartilage degeneration starts. Load induced cartilage damage is characterized as either type (1)--damage without disruption of the underlying bone or calcified cartilage layer--or type (2), subchondral fracture with or without damage to the overlying cartilage. We asked the question whether cartilage degeneration after meniscectomy is likely to be initiated by type (1) and/or type (2) cartilage damage. To investigate that we applied an axisymmetric biphasic finite element analysis model of the knee joint. In this model the articular cartilage layers of the tibial and the femoral condyles, the meniscus and the bone underlying the articular cartilage of the tibia plateau were included. The model was validated with data from clinical studies, in which the effects of meniscectomy on contact areas and pressures were measured. It was found that both the maximal values and the distributions of the shear stress in the articular cartilage changed after meniscectomy, and that these changes could lead to both type (1) and type (2) cartilage damage. Hence it likely that the cartilage degeneration seen after meniscectomy is initiated by both type (1) and type (2) cartilage damage.

Anisotropy↗
PubMed1997

Cartilage canals in equine articular/epiphyseal growth cartilage and a possible association with dyschondroplasia.

Cartilage canals have been described in most mammals and contain the vascular elements necessary for the maintenance of epiphyseal growth cartilage. The presence and longevity of cartilage canals in developing articular/epiphyseal cartilage of horses is described for the first time. Growth cartilages from 30 normal horses (from 130 days gestation to age 2 years) and 6 cases of dyschondroplasia (age < 15 months) were examined. Cartilage canals were located in the epiphyses of fetuses as early as 130 days gestation. The secondary centres of ossification had developed by 250 days gestation and, at full term (approximately 340 days), the articular/epiphyseal cartilage was highly vascularised. Cartilage canals were closely surrounded by small round chondrocytes even when present in the zone of hypertrophic chondrocytes. From late gestation until at least age 10 weeks, blood vessels surrounded by cartilage were found extending beyond the zone of hypertrophic chondrocytes into the secondary centre of ossification. Cartilage canals were absent from normal articular/epiphyseal cartilage of animals age > 6 months. Cartilage canals were associated with retained cartilage of dyschondroplastic lesions found in animals age < 15 months. The presence of cartilage canals in association with dyschondroplastic lesions suggests they may have a role in the pathogenesis of this important disease.

Animals↗
PubMed1991

Mechanisms of disruption of the articular cartilage surface in inflammation. Neutrophil elastase increases availability of collagen type II epitopes for binding with antibody on the surface of articular cartilage.

We recently observed that specific antibodies to type II collagen do not bind in appreciable amounts to the intact surface of articular cartilage, whereas antibodies to the minor collagen types V, VI, and IX do. These results suggest that the outermost cartilage surface layer prevented interaction of the antibodies with the major collagen type in articular cartilage. The present studies were designed to investigate the pathogenic mechanisms involved in the disruption of the cartilage surface layer in inflammatory arthritis. Articular cartilage obtained from rabbits undergoing acute antigen-induced arthritis of 72 h duration showed a significant increase in binding of anti-type II antibody to cartilage surfaces compared with normal control cartilage (P less than 0.01). Augmentation of anti-type II binding was also observed upon in vitro incubation of bovine articular slices or intact rabbit patellar cartilage for 1 h with human polymorphonuclear neutrophils (PMN), PMN lysates, or purified human PMN elastase. This increase was not inhibited by sodium azide, nor was it enhanced by incubation of cartilage with the strong oxidant hypochlorous acid. Chondrocyte-mediated matrix proteoglycan degradation in cartilage explants cultured in the presence of cytokines failed to increase antibody binding appreciably. The augmentation in antibody binding seen with PMN lysates was inhibited by the nonspecific serine-esterase inhibitor PMSF, but not by the divalent metal chelator EDTA. The elastase-specific inhibitor AAPVCMK also inhibited most of the PMN-induced increase in antibody binding, whereas the cathepsin G-specific inhibitor GLPCMK was much less effective. Incubation of intact cartilage with purified human PMN elastase indicated that this serine esterase could account for the increase in anti-type II collagen antibody binding to intact cartilage surfaces. These studies suggest that in an inflammatory response, PMN-derived elastase degrades the outer layer of articular cartilage, exposing epitopes on type II collagen. They also help clarify the pathogenic mechanisms involved in early articular cartilage damage in inflammatory joint diseases.

Animals↗
PubMed1992

Human osteoarthritic cartilage is synthetically more active but in culture less vital than normal cartilage.

The proteoglycan turnover of human osteoarthritic (OA) cartilage was compared to that of normal (N) cartilage. The cartilage was obtained postmortem from human femoral knee condyles. Short term cultures were compared to longterm cultures, and proteoglycan synthesis rate, content and release determined. Proteoglycan synthesis rate, determined shortly after collection of the cartilage, was higher in OA cartilage than in N cartilage. After longterm culture, the initially higher proteoglycan synthesis rate of OA cartilage became lower than that of N cartilage. An increased percentage release of proteoglycans from OA cartilage compared to N cartilage was apparent both shortly after collection of the cartilage and after culture. Thus, although OA cartilage in vivo is synthetically more active, in vitro it has an increased catabolic and a decreased anabolic activity, from which we conclude that OA cartilage is less vital than N cartilage.

Aged↗
PubMed2001

[Fabrication of allogeneic cartilage with tissue engineering technique and repair of laryngeal cartilage defects in rabbits].

OBJECTIVE: To investigate the fabrication of allogeneic tissue engineered cartilage in predetermined shapes and its ability to repair laryngeal cartilage defects. METHODS: Tissue engineering technique was used to make allogeneic tissue engineered cartilage in predetermined shapes, and then some of them were utilized to repair cartilage defects in the rabbit larynges(n = 12). Finally, the chondrogenesis and reparative effect were studied grossly and histologically at various periods. RESULTS: 1. The gross specimens of 4 weeks after implantation revealed the presence of new hyaline cartilage of approximately the same shapes as original predetermined shapes, which had fair elasticity and support ability. Histological evaluation showed the characteristics of cartilage tissue. 2. Laryngeal cartilage defects were well repaired using allogeneic tissue engineered cartilage in different periods after operation. A few chondrocytes were observed between the reparative areas with tissue engineered cartilage and normal cartilage. Abundant matrices were also detected in the reparative and interfacial areas. No inflammatory cells were found. CONCLUSION: It is possible to regenerate new cartilage in predetermined shapes using tissue engineering technique in allograft animals with immunity. Allogeneic tissue engineered cartilage can be used as reparative material to repair cartilage defect of rabbit larynx.

Animals↗
PubMed1999

Localization and expression of cartilage oligomeric matrix protein by human rheumatoid and osteoarthritic synovium and cartilage.

Synovium and cartilage from patients with osteoarthritis or rheumatoid arthritis were analyzed for expression of cartilage oligomeric matrix protein. Immunostaining of synovium with antiserum to cartilage oligomeric matrix protein demonstrated positive staining in both diseases. In osteoarthritis, there was positive staining within the synovial cells and immediately subjacent connective tissue, with less intense staining in the deeper connective tissue. In rheumatoid arthritis, there was less intense staining within the synovial cells and marked intense staining in the deeper connective tissue. In situ hybridization performed with an antisense digoxigenin-labeled riboprobe to human cartilage oligomeric matrix protein confirmed the presence of cartilage oligomeric matrix protein mRNA in the cells of the synovial lining in both types of synovium. Quantitative polymerase chain reaction with a cartilage oligomeric matrix protein MIMIC demonstrated increased cartilage oligomeric matrix protein mRNA in rheumatoid cartilage and synovium as compared with osteoarthritic cartilage and synovium, respectively; mRNA levels in rheumatoid synovium were similar to those from osteoarthritic chondrocytes. As a result of the high expression of cartilage oligomeric matrix protein from rheumatoid synovium, inflammatory synovium should be considered as a potential tissue source of cartilage oligomeric matrix protein in any investigation of biological markers of cartilage metabolism. The upregulated expression of cartilage oligomeric matrix protein in inflammatory tissues suggests its in vivo regulation by cytokines.

Arthritis, Rheumatoid↗
PubMed2001

Articular cartilage repair using a tissue-engineered cartilage-like implant: an animal study.

OBJECTIVE: Because articular cartilage has limited ability to repair itself, treatment of (osteo)chondral lesions remains a clinical challenge. We aimed to evaluate how well a tissue-engineered cartilage-like implant, derived from chondrocytes cultured in a novel patented, scaffold-free bioreactor system, would perform in minipig knees with chondral, superficial osteochondral, and full-thickness articular defects. DESIGN: For in vitro implant preparation, we used full-thickness porcine articular cartilage and digested chondrocytes. Bioreactors were seeded with 20x10(6) cells and incubated for 3 weeks. Subsequent to culture, tissue cartilage-like implants were divided for assessment of viability, formaldehyde-fixed and processed by standard histological methods. Some samples were also prepared for electron microscopy (TEM). Proteoglycans and collagens were identified and quantified by SDS-PAGE gels. For in vivo studies in adult minipigs, medial parapatellar arthrotomy was performed unilaterally. Three types of defects were created mechanically in the patellar groove of the femoral condyle. Tissue-engineered cartilage-like implants were placed using press-fit fixation, without supplementary fixation devices. Control defects were not grafted. Animals could bear full weight with an unlimited range of motion. At 4 and 24 weeks postsurgery, explanted knees were assessed using the modified ICRS classification for cartilage repair. RESULTS: After 3-4 weeks of bioreactor incubation, cultured chondrocytes developed a 700-microm- to 1-mm-thick cartilage-like tissue. Cell density was similar to that of fetal cartilage, and cells stained strongly for Alcian blue and safranin O. The percentage of viable cells remained nearly constant (approximately 90%). Collagen content was similar to that of articular cartilage, as shown by SDS-PAGE. At explantation, the gross morphological appearance of grafted defects appeared like normal cartilage, whereas controls showed irregular fibrous tissue covering the defect. Improved histologic appearance was maintained for 6 months postoperatively. Although defects were not always perfectly level upon implantation at explanation the implant level matched native cartilage levels with no tissue hypertrophy. Once in place, implants remodelled to tissues with decreased cell density and a columnar organization. CONCLUSIONS: Repair of cartilage defects with a tissue-engineered implant yielded a consistent gross cartilage repair with a matrix predominantly composed of type II collagen up to 6 months after implantation. This initial result holds promise for the use of this unique bioreactor/tissue-engineered implant in humans.

Animals↗
PubMed2000

[Experimental study on repair of cricoid cartilage defect with cartilage grafts in rabbits].

OBJECTIVE: To investigate the effect of free cartilage fragment in repair of cricoid cartilage defect. METHOD: One-third of cricoid cartilage was cut and repaired with free thyroid cartilage fragment and pedicled cartilage in rabbits. The pathological changes of the cartilages were observed. RESULT: 1. The free thyroid cartilage fragments were absorbed in two months, and were replaced by scars. 2. The pedicled cartilage fragments were not absorbed and healed with the cricoid cartilage. 3. No evidence of growth impairment of surgery-induced cricoid cartilage was observed. CONCLUSION: In rabbits, both free cartilage fragments and pedicled cartilage fragments could repair the defect of cricoid cartilage effectively.

Animals↗
PubMed2004

VEGF expression in adult permanent thyroid cartilage: implications for lack of cartilage ossification.

Vascular endothelial growth factor (VEGF) has been shown to play an important role during endochondral bone formation in hypertrophic cartilage remodeling, ossification, and angiogenesis, but it is not expressed in normal adult articular cartilage. Thyroid cartilage undergoes only partial ossification beginning at the age of about 20. Because it never completely ossifies, we investigated a possible role of VEGF and its receptors (VEGFRs) as well as the angiogenetic inhibitor endostatin in this permanent cartilage. In analysis of cartilage samples from all specimens evaluated, VEGF121 and VEGF165 were identified as the only VEGF splice forms expressed. In addition to VEGF, VEGFR-2 (kinase domain region/fetal liver kinase 1), but not VEGFR-1 (fms-like tyrosine kinase 1), was detectable by RT-PCR in cartilage. However, VEGFR-2 expression was only detectable up to the age of 19 years. Deposition of VEGF and VEGFR was confirmed by immunohistochemistry. VEGF concentrations measured by ELISA in thyroid cartilage increased with age in males but decreased in females. Endostatin concentrations measured by ELISA in thyroid cartilage were three times lower than in articular cartilage and showed no change with age, either in females or males. VEGF was immunostained within the intra- and pericellular matrices of some but not all chondrocytes. Thus, apart from its production in hypertrophic chondrocytes of growth plates, VEGF is also produced in single chondrocytes of thyroid cartilage. The data allow us to speculate that thyroid cartilage persists in an embryological state until it has reached its final size. After reaching its final size at the end of the second decade, VEGFR-2 is downregulated and ossification starts in the posterior part of the thyroid cartilage, proceeding ventrally. Both proteins, VEGF121 and VEGF165, should contribute to this process. VEGF concentration is high and changes in an age-related and sex-specific manner. Therefore, we postulate that VEGF is at least one of the key factors that is important for the lifelong ossification in thyroid cartilage.

Base Sequence↗
PubMed1997

Differences in patellofemoral joint cartilage material properties and their significance to the etiology of cartilage surface fibrillation.

OBJECTIVE: To determine if differences in biomechanical properties and biochemical composition exist between human patellar articular cartilage and the opposing femoral articular cartilage. DESIGN: The biomechanical properties and biochemical composition of the articular cartilage of 17 knees from 13 donors were determined for four sites on the patella and three sites on the femur representing regions of contact at 30 degrees and 90 degrees of flexion. The material properties were determined by biphasic indentation testing, yielding the compressive aggregate modulus, HA, permeability, k, and Poisson's ratio, vs. The thickness of the cartilage at the indentation site, h, was also measured using a needle probe. Full-thickness samples of cartilage adjacent to each indentation site were used for wet weight, sulfated glycosaminoglycan content and hydroxyproline content determinations. RESULTS: The patellar cartilage was found to have a lower compressive aggregate modulus by 30% (P < 0.001), higher permeability to fluid flow by 66% (P < 0.001) and greater thickness by 23% (P = 0.017) than that of the opposing femoral cartilage. The Poisson's ratios for both surfaces were found to be nearly zero. The water content of the patella was higher by 5% (P = 0.031) and the proteoglycan content lower by 19% (P = 0.030) than that of the femur. However, no differences were found between the collagen contents of the cartilages. CONCLUSIONS: Significant differences were found between the intrinsic material properties of the patellar cartilage and those of the femoral-trochlear cartilage. This variability of cartilage material properties with the patellofemoral joint may help explain why patellar cartilage has been frequently observed clinically to exhibit earlier and more severe fibrillation changes than the opposing femoral cartilage.

Adolescent↗