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PubMed2003

Articular cartilage lesions in the symptomatic anterior cruciate ligament-deficient knee.

PURPOSE: The goal of the study was to report the prevalence of the lesions of the articular cartilage of the femoral condyles and tibial plateau in patients with a symptomatic anterior cruciate ligament (ACL)-deficient knee undergoing day-case arthroscopy. TYPE OF STUDY: Case series study. METHODS: We studied 378 skeletally mature patients (average age, 27.3 years; range, 16-50 years; 282 men and 84 women), part of a sample of 1,978 patients undergoing a primary knee arthroscopy between January 1986 and August 1993. The articular cartilage lesions were classified according to Outerbridge by a single observer. We assessed the relationship between time of injury and articular cartilage lesions and between meniscal lesions and articular cartilage lesions. RESULTS: A complete ACL tear was found in all 378 knees. Of these, 157 showed at least one lesion of the articular cartilage. The medial femoral condyle (MFC) showed the highest frequency of articular cartilage lesions, especially in the weight-bearing portion. Patients with a bucket-handle tear of the medial meniscus had greater degeneration of the MFC than those with other meniscal tears. A meniscal tear was associated with a greater degree of articular damage. The second most common lesion was a combined lesion of the medial and lateral compartments, followed by isolated lateral compartment lesion. A time-dependent pattern of development of articular cartilage lesions was identified. CONCLUSIONS: In patients with more advanced degenerative changes, the time from injury to arthroscopy was significantly longer than in patients with lesser articular surface abnormalities, and the presence of a meniscal tear was associated with a greater degree of articular cartilage damage. Patients with a symptomatic ACL-deficient knee and an associated tear of the medial meniscus are at high risk of having a lesion of the articular surface of the weight bearing area of the knee.

Adolescent↗
PubMed1993

A scanning electron microscopic study of the degenerative cartilage in patellar chondropathy.

Patellar chondropathy as cartilage degeneration localized in patellar cartilage in young persons is characterized by cartilaginous changes, such as softening, swelling, and fissuring. With a view to structural characterization of early cartilaginous degeneration before erosion, the morphology of affected cartilage was studied under a scanning electron microscope. The surface network of cartilage constituting fibrils had an edematous change, presenting with fibrillation on the medial facet, whereas many fibrils of the central ridge had a collagen bundle, and fissuring of varying size was observed. It appeared that a mechanical force (shearing) acting on the site of the central ridge was associated with the formation of a collagen bundle and its destruction. On the lateral facet, fibrils were arranged perpendicular to the joint surface; the superficial layer of fibrils was worn by hyper-pressure acting on the lateral facet. On the fractured surface, the coarseness of collagen fibrils showed changes that varied with the site and stage of cartilage degeneration. Frequent changes were signs of fibril loosening (coarsening), such as reduction in fibril density (i.e., edematous change), collagen fibril aggregation, and fissuring, and longitudinal restructuring of fibrils. The patellar cartilage in the patients of this series showed a structure adapted to the mechanical force. The initial structural changes of cartilage consisted of collagen fibril aggregation and reduction in fibril density. These changes give rise to matrix rarefaction, which in turn causes cartilage degeneration to progress. These changes were concurrent in both the superficial and middle layers and were not localized as basal degeneration.

Adolescent↗
PubMed2002

Age-related changes in cartilage endogenous osteogenic protein-1 (OP-1).

Articular cartilage has a poor reparative capacity. This feature is exacerbated with aging and during degenerative joint conditions, contributing to loss of motion and impairment of quality of life. This study focused on osteogenic protein-1 (OP-1) and its ability to serve as a repair-stimulating factor in articular cartilage. The purpose of this work was to develop a quantitative method for the assessment of the content of OP-1 protein in extracts from human articular cartilage and to investigate the changes in OP-1 mRNA expression and protein levels with aging of normal adult cartilage. Full thickness cartilage was dissected from femoral condyles of donors with no history of joint disease within 24 h of death. Levels of OP-1 mRNA expression were measured by a semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) method; concentration of OP-1 protein was detected by new sandwich enzyme-linked immunosorbent assay (ELISA); qualitative changes in OP-1 forms were evaluated by Western blots with various anti-OP-1 antibodies. The sensitivity of the ELISA method allowed the detection of picogram quantities of OP-1 in cartilage extracts. We found that (1) concentration of OP-1 in normal cartilage is within the range of biological activity of OP-1 in vitro; and (2) during aging of human adult, articular cartilage, levels of OP-1 protein and message are dramatically reduced (more than 4-fold; p<0.02). The major qualitative changes affected primarily mature OP-1. The results of the current study suggest the possibility that OP-1 may be critical for chondrocytes to maintain their normal homeostasis and could also serve as a repair factor during joint disease or aging.

Adult↗
PubMed1996

Fibronectin fragment mediated cartilage chondrolysis. II. Reparative effects of anti-oxidants.

In an accompanying manuscript, it was shown that the cartilage chondrolytic activities of fibronectin fragments (Fn-f), which are mediated through catabolic cytokines such as TNF-alpha, IL-1 and IL-6, could be suppressed by anti-oxidants (AOs). The AOs neutralized reactive oxygen species (ROS) which are known to mediate catabolic cytokine action. The objective in this work was to test whether AOs would promote restoration of proteoglycan (PG) in Fn-f treated cartilage, since under normal culturing conditions, PG is not restored after removal of the Fn-f. Cartilage was first cultured with an amino-terminal 29-kDa Fn-f to cause loss of about half of the total PG and then treated with NAC (1 and 10 mM) or glutathione (10 microM) or DMSO (0.1 or 1%). Treatment with NAC and glutathione maximally caused restoration of PG within 14 days to normal or supernormal levels, while DMSO was less effective. Catalase, but not superoxide dismutase, enhanced PG content to a small but significant extent. The restoration of PG in Fn-f treated cartilage occurred throughout the full depth of the cartilage slices as shown by histochemical analysis. However, removal of the AO allowed a subsequent decrease in PG content suggesting that the AOs had not blocked cytokine expression but had merely suppressed cytokine activities. Addition of NAC to IL-1 treated cartilage promoted a restoration of PG, while addition to chymopapain or trypsin treated cartilage was not very effective, suggesting that the effect of AOs requires a cytokine driven damage system. We conclude that the AOs promote a restoration of PG in the Fn-f treated cartilage by suppressing the effects of catabolic cytokines. The data suggest a potential for AOs in reversing tissue damage caused by cytokines.

Acetylcysteine↗
PubMed1993

Amplification of cDNAs for human cartilage-specific types II, IX and XI collagens from chondrocytes and Epstein-Barr virus-transformed lymphocytes.

The identification of mutations in cartilage-specific collagen genes in inherited forms of osteoarthritis (OA) and other heritable cartilage diseases has been hampered by the difficulty in obtaining sufficient tissue to isolate RNA and by the loss of the cartilage phenotype during in vitro chondrocyte culture. To overcome these limitations we employed RNA Polymerase Chain Reaction (PCR) to amplify cDNAs for the cartilage-specific collagens types II, IX and XI from mRNA obtained from small numbers of chondrocytes. We also amplified cDNAs for these collagens from "illegitimate transcripts" from Epstein-Barr virus (EBV)-transformed lymphocytes. Total RNA was obtained from freshly isolated human fetal and adult chondrocytes and from long-term (90 days) chondrocyte cultures. The RNA was reverse transcribed to cDNA and the cDNA amplified in the same tube with oligonucleotide primers specific for types II, IX and XI collagens. The amplified double-stranded products were cloned and sequenced. Successful amplification of the entire 4.4 kb of the type II procollagen cDNA was obtained from as little as 6 ng of RNA from freshly isolated fetal human chondrocytes. Seven hundred and eighty base pairs of the alpha 1 (IX) collagen cDNA and the entire published sequence of alpha 2 (XI) collagen cDNA, were also amplified from these cells. We were also able to amplify cDNAs for the three cartilage-specific collagens from "illegitimate transcripts" from EBV-transformed lymphocytes. Thus, these methods will allow the identification of mutations in cartilage-specific collagen genes in patients with inherited OA and other heritable cartilage diseases from small amounts of cartilage or chondrocyte RNA or from non-cartilaginous sources.

Base Sequence↗
PubMed1991

Autogenous auricular cartilage graft for temporomandibular joint repair. A comparison of technique with and without temporary silastic implantation.

Four Macaca fascicularis monkeys underwent bilateral temporomandibular joint surgery including disc removal, condyle recontouring and disc replacement using autogenous auricular cartilage grafts. One side was treated with the cartilage graft alone while the other side was treated with a cartilage graft combined with a temporarily implanted 0.02 inch dacron-reinforced silastic sheet. The silastic sheeting was removed at twelve weeks after the initial surgery. The monkeys were sacrificed at fourteen, twenty-four, thirty-six and fifty-two weeks after the initial disc removal and cartilage grafting. The joints treated with cartilage grafts alone showed significant fibrous connective tissue adhesions which had formed between the inferior surface of the graft and the articulating surface of the condyle. In the joints treated with a cartilage graft and silastic sheeting a joint space was clearly maintained between the cartilage graft and condylar surface without the formation of fibrous connective tissue adhesions. It appears that temporary implantation of a thin silastic sheet combined with autogenous cartilage grafting may prevent the formation of fibrous connective tissue adhesions within the joint.

Animals↗
PubMed2003

The volume and morphology of chondrocytes within non-degenerate and degenerate human articular cartilage.

OBJECTIVE: Cartilage swelling is an early event in osteoarthritis (OA). However, the response of chondrocytes to increased tissue hydration is unknown. This work studied the volume and morphology of living in situ human chondrocytes as a function of cartilage degeneration. METHODS: The tibial plateaus from knee joints of 40 patients were obtained following above-knee amputations or knee arthroplasty, and degree of cartilage degeneration from 0 (non-eroded) to 3 (extensive fibrillations) was assessed using several criteria. In situ chondrocytes were labeled with fluorescent indicators (calcein for living cells, propidium iodide for dead cells) permitting the quantification of volume and visualisation of morphology of cells within the cartilage zones by confocal scanning laser microscopy (CLSM). RESULTS: Chondrocyte volume within superficial and mid-zones, but not of deep zone cells, increased significantly (P<0.05 and P<0.02, respectively; one-way analysis of variance), with degree of cartilage hydration and degeneration. The volume increase ( approximately 90% for mid-zone chondrocytes, grade 3 cartilage) was greater than that which might occur following loss/excision of sub-chondral bone (<15% swelling). The CLSM technique utilised here revealed that approximately 40% of chondrocytes within all cartilage grades exhibited at least one cytoplasmic processes of <8 microm. The presence of these processes did not indicate a cell body of larger volume than cells without processes, and did not contribute to cell volume. CONCLUSIONS: The volume of in situ chondrocytes within the superficial and mid-zones increased with cartilage degeneration. Cell swelling was greater than that expected from the increased hydration in OA, suggesting that an increase in chondrocyte volume might play a role in the changes to matrix metabolism occurring in OA.

Aged↗
PubMed1994

Abnormal occurrence of a large chondroitin sulfate proteoglycan, PG-M/versican in osteoarthritic cartilage.

The expression of PG-M in osteoarthritic cartilage was investigated. Cartilage from five hip joints with osteoarthritis (OA) and control cartilage from five knee joints with post-traumatic injury were obtained and analyzed with anti-PG-M antibodies. Control cartilage showed no staining, but in osteoarthritic cartilage there was strong staining of the cytoplasm of chondrocytes with abnormal morphology. The cytoplasm of inflammatory cells invading the osteoarthritic cartilage matrix was also strongly stained which led to determining the sequence of PG-M core protein. The deduced amino acid sequence and homology analysis indicated that PG-M had a complement regulatory protein-like domain, a lectin-like domain, two EGF-like domains from the carboxyl-terminal with an extremely high homology to the respective domains of versican, a large proteoglycan expressed by human fibroblasts. The anti-PG-M antibodies cross-reacted with Ver-27b fusion protein which was expressed by a cDNA clone coding the N-terminal portion of versican core protein. Thus, the immunological and sequencing data suggest that PG-M is a molecule similar to or identical with human versican, and that the material in cartilage reactive to the anti-PG-M antibodies is versican. These findings suggest the PG-M/versican is expressed in osteoarthritic cartilage.

Base Sequence↗
PubMed1995

Topographical variation within the articular cartilage and subchondral bone of the normal ovine knee joint: a histological approach.

Topographical variation in the articular cartilage and subchondral bone of the normal ovine knee was examined using histological techniques. The articular cartilage was examined grossly, then histological sections were cut and the cartilage thickness and chondrocyte density were measured. Bone mineral density, thickness of the subchondral bone plate (SBP) and volume and surface histomorphometrical parameters and mineral apposition rate were calculated for the subchondral bone. It was found that the articular cartilage on the tibial plateaux was thicker, less cellular, and overlay a thicker SBP than that on the femoral condyles. Similarly, the cartilage in the medial joint compartments was thicker, less cellular and overlying a thicker less dense SBP than that in the lateral joint compartments. There was no variation in bone histomorphometric parameters or mineral apposition rate between regions. Biomechanical testing has shown that loading is not uniform throughout the normal human knee joint. The present results suggest that loading within the ovine knee is also nonuniform, with the central regions of the tibial plateaux bearing greater loads than the femoral condyles, and the medial joint compartment being loaded more than the lateral one. The articular cartilage and subchondral bone have adapted in order to best withstand these variations in loading. These histological findings, plus the topographical variations in cartilage biochemistry reported by Read et al. (Topographical variation in composition, PG-biosynthesis and swelling pressure of cartilages of loaded tibio-femoral joints (Abstract). Proceedings of the Combined Meeting of the Orthopaedic Research Societies of USA, Japan and Canada.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Articular cartilage proteoglycans in osteoarthritic STR/Ort mice.

Compared to controls, the lateral and medial tibial articular cartilage chondroitin sulfate (CS) content in male STR/Ort mice was elevated between 8 and 19 weeks of age, fell at 24-26 weeks and increased again thereafter. The CS cartilage content of CBA mice remained relatively unchanged. Cartilage CS content was measured in female CBA and STR/Ort mice and in male and female Balb C mice, all at 18 weeks of age. In every case the content was much lower than that found in male STR/Ort mice. CS unsaturated disaccharides were analysed by capillary electrophoresis after digestion of the glycosaminoglycans with chondroitinase ABC. Chondroitin-4-sulfate (C4S) was the predominant isomer at all ages in both strains. The C4S:C6S isomer ratio in CBA mice was much higher in the lateral than the medial cartilage. This difference was much less marked in STR/Ort knee joints: these mice have relatively more C6S than CBA mice. Proteoglycans, extracted from STR/Ort and CBA male mouse cartilage, were characterized by large pore gel electrophoresis and Western blotting. All cartilages contained two slow mobility bands identified as aggrecan by the reactivity with the mab 1C6. Both bands contained C4S and C6S chains. A third band of faster mobility contained only C4S and was 1C6 negative. It was present in both strains. Thus the STR/Ort cartilage contained a normal spectrum of murine articular cartilage proteoglycans.

Animals↗
PubMed1995

Splicing patterns of fibronectin mRNA from normal and osteoarthritic human articular cartilage.

Fibronectin, a large extracellular glycoprotein, mediates the interaction of cells with the extracellular matrix. Heterogeneity in the structure of fibronectin is largely due to the alternative splicing of three exons (IIIB, IIIA and V) during processing of the fibronectin primary transcript. Osteoarthritis, a degenerative disease of synovial joints, is characterized by a progressive loss of the articular cartilage eventually resulting in pain and loss of joint function. In contrast to the loss of most cartilage matrix proteins accompanying this process, osteoarthritic cartilage contains more fibronectin than disease-free cartilage. We examined the splicing patterns of fibronectin mRNA from adult human articular cartilage of normal and osteoarthritic joints by RNase protection (exon IIIA and exon IIIB) and reversed transcription-polymerase chain reaction (exon V) assays to determine whether or not the increased fibronectin content in osteoarthritic cartilage is also associated with differences in the splicing patterns of these three alternatively spliced exons. The results revealed no gross differences in splicing of these exons between the fibronectin mRNA isolated from adult human articular normal and osteoarthritic cartilage. Thus alterations in the structure of cartilage fibronectin do not appear to correlate with the increased level of fibronectin protein associated with osteoarthritis.

Adult↗
PubMed1996

Effect of high molecular weight hyaluronan on cartilage degeneration in a rabbit model of osteoarthritis.

The effects of high molecular weight hyaluronan (HA) on cartilage degeneration were investigated in a partial menisectomy model of osteoarthritis (OA) in the rabbit knee. This study compared HA80 (0.8 x 10(6) Da, 1%), HA190 (1.9 x 10(6) Da, 0.01-1%) and saline. HA (0.1 ml/kg) or saline were injected intra-articularly twice a week immediately after surgery. Degenerative changes in femoral and tibial cartilages were graded histopathologically 2 and 4 weeks after surgery. Two weeks after surgery, HA190, only when used at a 1% concentration, resulted in a dramatic inhibition of cartilage degeneration in both the femoral condyle and the tibial plateau (P < 0.01). Two weeks after surgery, the protection against cartilage degeneration was significantly (P < 0.05) greater with HA190 than with HA80. Four weeks after surgery, only the femoral cartilage degeneration was significantly and similarly inhibited with HA190 (P < 0.01) and HA80 (P < 0.05). Scanning electron micrographs of femoral cartilage showed that cartilage degeneration was less severe with HA190 than with saline. These results might suggest that, in the rabbit model, intra-articular administration of higher molecular weight HA is more effective than lower molecular weight HA in inhibiting cartilage degeneration in early OA.

Animals↗
PubMed1996

Changes with age in the structure of fibromodulin in human articular cartilage.

An anti-peptide antibody was raised in a rabbit against the carboxy terminal region of the human fibromodulin core protein. The antibody was purified from other components of the resulting antiserum by affinity chromatography using the immobilized peptide, and was used to study the structural heterogeneity of fibromodulin extracted from human articular cartilage of different ages by the use of immunoblotting following sodium dodecyl sulfate polyacrylamide gel electrophoresis analysis of the extracted macromolecules. In the fetus and neonate, fibromodulin was visualized as a diffuse component with a relative molecular weight of 70-110 kDa, whereas in the mature adult a more discrete component of smaller size was apparent with a relative molecular weight of 67 kDa. The size of the fibromodulin from mature adult cartilage could not be altered by pretreatment of the samples with keratanase II or endo-beta-galactosidase before analysis. In contrast, the size of the fibromodulin from younger cartilage could be decreased with both glycosidases, with the endo-beta-galactosidase yielding a smaller product than the keratanase. The size of the product resulting from endo-beta-galactosidase treatment of the fibromodulin from young cartilage was the same as that of the intact fibromodulin from mature adult cartilage. Thus, fibromodulin is present in human articular cartilage at all ages, but the extracted molecules only appear to exist in a proteoglycan form possessing keratan sulfate chains in the juvenile and young adult, and the size of these chains decreases with age. In the mature adult the fibromodulin does not possess either keratan sulfate or non-sulfated polylactosamine chains, though it appears to possess the same number of N-linked oligosaccharides as its counterparts from the younger tissue, but they are not modified further. The majority of the fibromodulin extracted from arthritic cartilage is of the same size as that found in the normal mature adult, although there is evidence for proteolytic processing. The degree of such processing is greater for the fibromodulin obtained from the cartilage of rheumatoid arthritic joints than osteoarthritic joints.

Acetylglucosaminidase↗
PubMed1997

A methodology for the quantitative assessment of articular cartilage histomorphometry.

OBJECTIVE: Traditionally, histological analysis of cartilage and cartilage repair has been performed qualitatively. While new techniques and grading systems have attempted to improve the quantitative nature of histological assessment, the advent of computer-based analysis systems have enabled development of more quantitative methodologies for cartilage repair. The objective of this study was to develop such a methodology for a more quantitative assessment of cartilage repair using a color-based image analysis system. DESIGN: Repair parameters were defined to describe the degree of cartilage restoration: repair dimensions, degree of attachment, surface roughness and repair location. This technique was experimentally applied to a cartilage repair study using cultured perichondrial cells implanted in a polylactic acid matrix in the rabbit femoral condyle. Specimens were examined and compared with the contralateral normal knee. RESULTS: Results showed increases in cartilage height, repair area, and surface roughness over controls for both 6 and 12 weeks. Surface elevation was significantly decreased at 6 weeks over 12 weeks. The percentage of repair improved between 6 and 12 weeks. Results were compared with a traditional grading system and demonstrated close correlation. Intraobserver and interobserver precision analysis were performed and demonstrated the reproducibility of the quantitative results by and between individuals. CONCLUSIONS: The methodology was deemed successful for a more objective analysis of cartilage with the added advantage of providing measured parameters that can assist in making comparisons between different studies using the same methodology.

Animals↗
PubMed1997

Chondrocyte tumor necrosis factor receptors and focal loss of cartilage in osteoarthritis.

OBJECTIVE: Osteoarthritis (OA) is characterized by focal loss of cartilage. Here we show for the first time that tumor necrosis factor (TNF) alpha can act on cartilage but only at specific sites where chondrocyte TNF alpha-receptor (R) expression is high. DESIGN: Cartilage explants from specified sites in the knee joints of both OA patients and non-arthritic (NA) subjects were cultured with and without TNF alpha for 14 days and cumulative glycosaminoglycan (GAG) release into the supernatant measured. p55 and p75 TNF-R expression was measured by flow cytometry on chondrocytes isolated from the same sites. RESULTS: Cartilage explants from different sites in knee joints from both OA patients and NA subjects varied in their susceptibility to TNF alpha. Overall, the proportion of samples that responded to TNF alpha was higher in cartilage taken from OA joints than cartilage from NA subjects. Variations in p55 and p75 TNF-R expression were found between chondrocytes from different sites. p55, but not p75 TNF-R, expression on chondrocytes was closely related to the susceptibility of explants from the same site to TNF alpha-induced GAG loss. CONCLUSION: It is considered that focal loss of cartilage will occur at sites where chondrocyte p55 TNF-R expression is high, if sufficient TNF alpha is present, and that these results identify a mechanism by which cytokine-mediated focal loss of cartilage may occur.

Adult↗
PubMed1998

Protective effect of exogenous chondroitin 4,6-sulfate in the acute degradation of articular cartilage in the rabbit.

The injection of 2.0 mg chymopapain into the adolescent rabbit knee causes severe loss of articular cartilage proteoglycans (PG). Although chondrocytes attempt to restore lost PG, failure to repair ensues. Pure chondroitin 4,6-sulfate (Condrosulf, IBSA Lugano, Switzerland) has been used in clinical studies of human osteoarthritis (OA) as a slow-acting drug for OA (SYSADOA). Using our model of articular cartilage injury, we examined the effects of oral and intramuscular administration of Condrosulf after chymopapain-induced cartilage injury. In this study, animals received an injection of 2.0 mg chymopapain (Chymodiactin, Boots Pharmaceuticals) into the left knee and were sacrificed after 84 days. The contralateral right knee served as a noninjected control. Some animals received oral Condrosulf while others received intramuscular injections of Condrosulf. Serum keratan sulfate (KS) levels were monitored to ensure degradation of the cartilage PG. Those animals not exhibiting at least a 100% increase of serum KS following chymopapain injection were excluded from the study. At sacrifice, cartilage PG contents were markedly reduced in animals receiving an injection of 2.0 mg chymopapain with no further treatment. In contrast, oral administration of Condrosulf beginning 11 days prior to chymopapain injury resulted in significantly higher (P = 0.0036) cartilage PG contents. Intramuscular administration of Condrosulf resulted in higher, but less significantly so (P = 0.0457), cartilage PG contents. These results suggest that daily Condrosulf treatment prior to and continuing after chymopapain injury may have a protective effect on the damaged cartilage, allowing it to continue to re-synthesize matrix PG after the treatment is discontinued.

Administration, Oral↗
PubMed2003

Analysis of clones from a human cartilage cDNA library provides insight into chondrocyte gene expression and identifies novel candidate genes for the osteochondrodysplasias.

To begin to define the gene expression pattern in fetal cartilage and to identify uncharacterized candidate genes for the osteochondrodysplasias, we analyzed clones from a fetal cartilage cDNA library. Sequence analysis of 420 cDNA clones identified 210 clones derived from established genes but, for many of them, expression in cartilage had not been previously reported. Among the established genes were 14 genes known to produce skeletal abnormalities in either humans or mice when mutated. Thirty-two uncharacterized genes and their respective chromosomal positions were also identified. To further understand the expression profile of these genes in fetal cartilage, we constructed a cDNA microarray utilizing the clones. The microarray was used to determine which genes had higher expression in cartilage as compared with dedifferentiated, cultured chondrocytes. Many of the established genes, as well as five of the uncharacterized genes, had increased expression in cartilage, suggesting an important role for these genes in the differentiated state of chondrocytes. These data provide new candidate genes for the osteochondrodysplasias and demonstrate the usefulness of cartilage cDNA microarrays in expanding our understanding of the complexity of fetal cartilage gene expression.

Cartilage↗
PubMed2002

Arthroscopic assessment of human cartilage stiffness of the femoral condyles and the patella with a new tactile sensor.

We measured the stiffness of the cartilage of the human femoral condyles via an ultrasonic tactile sensor under arthroscopic control. The stiffness and the degeneration of articular cartilage were assessed in 105 knees in 74 patients (39 men, 35 women, age: 9-72 years) who underwent arthroscopic observation or surgery. Twenty-five knees suffered from traumatic cartilage injury, 14 from osteochondritis dissecans, 13 from osteoarthritis, 11 from meniscal injury and six from ligamentous injury, bipartita patellae (three knees), and symptomatic plica synovialis (two knees). The degeneration of cartilage was classified according to Outerbridge's grading system. The relationships between the stiffness and the grade of cartilage degeneration, and gender were analyzed. The stiffness of grade I (softening) and II (fissuring less than 0.5 inches in length) was significantly lower than that of intact cartilage. In contrast, the stiffness of grade IV (exposed subchondral bone) was significantly higher than that of any other group. The cartilage stiffness of the patella in women was significantly lower than that in men. The tactile sensor was useful for determining the intraoperative stiffness of healthy and diseased human cartilage in all grades.

Adolescent↗