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PubMed2005

Quantitative ultrasound imaging of spontaneous repair of porcine cartilage.

OBJECTIVE: Arthroscopy offers qualitative means to evaluate the surface of articular cartilage. However, possible degeneration of the deep cartilage and subchondral bone remains undetected. High frequency ultrasound imaging is an advanced cartilage evaluation method which is conceivable to arthroscopic use and brings diagnostic information also from deeper cartilage and subchondral bone. DESIGN: In this study, we characterized spontaneous repair of porcine cartilage in situ with quantitative 2D-ultrasound imaging. At the age of 7-8 months, a cartilage lesion (diameter 6mm, not penetrating into subchondral bone) was created on the lateral facet of the right femoral trochlea (n=8). The animals were sacrificed 3 months after the surgery. The lesion site, adjacent cartilage and the corresponding control area at the contralateral (left) knee were imaged in situ with 20 MHz ultrasound. Ultrasound reflection coefficients were determined from the cartilage surface (R) and from the cartilage-bone interface (R(bone)). Microtopography of the articular surface was quantified by calculating ultrasound roughness index (URI) parameter from the ultrasonically determined surface profile. RESULTS: Lesion site was spontaneously filled with visually cartilage-like soft tissue with smooth surface. However, ultrasonic images and histological analyses revealed erosion of subchondral bone under the lesion site. Ultrasound reflection (R) at the surface of the spontaneously repaired tissue was significantly lower (-73.5+/-7.6%, P<0.05) than at the surface of intact cartilage. R(bone) was lowest at the lesion site. The surface roughness of spontaneously repaired cartilage was significantly higher than that of the intact tissue (44.0+/-26.0 microm vs 7.5+/-2.3 microm, P<0.05). CONCLUSIONS: Quantitative ultrasound parameters offered diagnostic information revealing impaired structural integrity of the spontaneously repaired porcine cartilage and subchondral bone. These changes are not detectable by traditional arthroscopic means.

Animals↗
PubMed2006

Magnetic resonance imaging (MRI) of articular cartilage in knee osteoarthritis (OA): morphological assessment.

OBJECTIVE: Magnetic resonance imaging (MRI) is a three-dimensional imaging technique with unparalleled ability to evaluate articular cartilage. This report reviews the current status of morphological assessment of cartilage with quantitative MRI (qMRI), and its relevance for identifying disease status, and monitoring progression and treatment response in knee osteoarthritis (OA). METHOD: An international panel of experts in MRI of knee OA, with direct experience in the analysis of cartilage morphology with qMRI, reviewed the existing published and unpublished data on the subject, and debated the findings at the OMERACT-OARSI Workshop on Imaging technologies (December 2002, Bethesda, MA) with scientists and clinicians from academia, the pharmaceutical industry and the regulatory agencies. This report reviews (1) MRI pulse sequence considerations for morphological analysis of articular cartilage; (2) techniques for segmenting cartilage; (3) semi-quantitative scoring of cartilage status; and (4) technical validity (accuracy), precision (reproducibility) and sensitivity to change of quantitative measures of cartilage morphology. RESULTS: Semi-quantitative scores of cartilage status have been shown to display adequate reliability, specificity and sensitivity, and to detect lesion progression at reasonable observation periods (1-2 years). Quantitative assessment of cartilage morphology (qMRI), with fat-suppressed gradient echo sequences, and appropriate image analysis techniques, displays high accuracy and adequate precision (e.g., root-mean-square standard deviation medial tibia=61 microl) for cross-sectional and longitudinal studies in OA patients. Longitudinal studies suggest that changes of cartilage volume of the order of -4% to -6% occur per annum in OA in most knee compartments (e.g., -90 microl in medial tibia). Annual changes in cartilage volume exceed the precision errors and appear to be associated with clinical symptoms as well as with time to knee arthroplasty. CONCLUSIONS: MRI provides reliable and quantitative data on cartilage status throughout most compartments of the knee, with robust acquisition protocols for multi-center trials now being available. MRI of cartilage has tremendous potential for large scale epidemiological studies of OA progression, and for clinical trials of treatment response to structure modifying OA drugs.

Cartilage, Articular↗
PubMed2000

Age-associated changes in decorin in rat mandibular condylar cartilage.

The small proteoglycan decorin strongly binds the fibrils of collagen types I and II; this interaction is thought to play a part in the maintenance of tissue integrity and biomechanical properties. In limb articular cartilage, there is evidence that decorin synthesis increases with age and that it is elevated in response to increased loading or in osteoarthritic cartilage. The aim here was to characterize the presence and relative amount of decorin in the condylar cartilage of the temporomandibular joint (TMJ) with maturation by Western blotting, and to assess its tissue localization by immunohistochemistry. Comparative data were obtained from tibial articular cartilage, which has been extensively studied. Cartilage from the mandibular condyle and tibial plateau was harvested from 24-day-old (growing) and 161-day-old (young adult) female Sprague-Dawley rats. In growing animals, decorin appeared slightly more abundant in the mandibular condylar cartilage than in articular cartilage, whereas in young adult animals the decorin content in the TMJ cartilage was noticeably less than in limb articular cartilage. Although there was an increase in decorin abundance with age at the TMJ, the increase in decorin with age in limb articular cartilage was considerably more pronounced. These data indicate that, although decorin is present in mandibular condylar cartilage, its abundance in adults is less than in limb articular cartilage; thus, maturation-associated changes may be dissimilar in magnitude from those documented for limb articular cartilage.

Aging↗
PubMed2001

An in situ calibration of an ultrasound transducer: a potential application for an ultrasonic indentation test of articular cartilage.

A change in mechanical properties of articular cartilage would be considered one of the most reliable signs of cartilage degeneration. While an indentation method has the potential to measure the cartilage properties in vivo, an accurate measurement of cartilage thickness in situ is technically difficult. An ultrasound transducer has often been used to measure the cartilage thickness. However, its accuracy is limited by the lack of an accurate measurement of the ultrasound speed of cartilage, for the ultrasound speed varies according to the pathological conditions of the tissue. Therefore, the objective of this study is to develop an in situ calibration method of predicting the true ultrasound speed of cartilage and thus allow the ultrasound transducer to measure the thickness of the tissue with great accuracy. By simultaneously implementing an indentation testing protocol using the ultrasound transducer as an indenter, this method can also provide an indentation stiffness measurement of cartilage. The feasibility of the proposed method was examined using normal and proteoglycan-depleted cartilage specimens. It was found that the true ultrasound speed measured by the in situ calibration method was sensitive to the proteoglycan depletion (1735+/-35 m/s for normal, and 1598+/-28 m/s for proteoglycan-depleted cartilage), and that the measured cartilage thickness was consistently accurate regardless of the tissue condition. The measured indentation stiffness of articular cartilage was also sensitive to the tissue condition. Thus, this study demonstrates that the proposed ultrasonic indentation technique can be used to accurately identify the abnormality of articular cartilage in situ.

Animals↗
PubMed2001

A new in vivo model for testing cartilage grafts and biomaterials: the 'rabbit pinna punch-hole' model.

In this study an animal model was developed for evaluation of the feasibility of cartilage grafts. In the cartilage of the external ear of the rabbit multiple holes, 6 mm in diameter, were punched, leaving the adherent skin intact. Different experimental groups were evaluated. First, the punch-hole model was validated under various conditions to study spontaneous or perichondrial initiated regeneration of the cartilage defect. When both cartilage and perichondrium was excised no spontaneous repair of the cartilage defect was observed. When perichondrium is present, variable patch-like closure of the punch hole was found. As 'golden standard' a punched out piece of cartilage was reimplanted directly. This condition showed adequate closure of the punch hole, however, no perfect integration of graft and surrounding cartilage was observed. Secondly, to evaluate the 'punch-hole model' a biomaterial, trabecular demineralized bovine bone matrix (DBM), was implanted and tested as a scaffold for tissue engineering techniques in vivo and in vitro. Direct implantation of DBM did not lead to any cartilage formation to close the defect. In vivo engineered cartilage, generated by enveloping DBM in perichondrium for 3 weeks, could adequately close the punch hole. When DBM was seeded with isolated chondrocytes in vitro before implantation in the defect, a highly fragmented graft, with some islets of viable cells was seen. To promote an efficient and reliable evaluation of cartilage grafts a semi-quantitative grading system was developed. Items such as quality, quantity and integrity of the cartilage graft were included in a histomorphological grading system to provide information about the properties of a specific cartilage graft. To validate the grading system, all conditions were scored by two independent observers. An excellent reliability (R = 0.96) was seen between the observers. In summary, the rabbit pinna punch-hole model is a reliable and efficient method for first evaluation of cartilage grafts. The results can be easily analyzed using a semi-quantitative grading system.

Animals↗
PubMed2003

Alterations in endogenous osteogenic protein-1 with degeneration of human articular cartilage.

A synchronized balance between synthesis and breakdown of extracellular matrix (ECM) molecules in normal articular cartilage is disturbed in osteoarthritis (OA). The focus of our study is the anabolic factor, osteogenic protein-1 (OP-1) that is expressed in articular cartilage and is able to induce the synthesis of ECM components. The major aim was to investigate both qualitatively and quantitatively endogenous OP-1 in normal, degenerative, and OA cartilage. Normal and degenerative cartilage was obtained at autopsies from femoral condyles of human organ donors with no documented history of joint disease; OA cartilage was obtained from patients undergoing joint arthroplasty. Appearance of donor cartilage was evaluated by Collins scale, where normal cartilage is assigned grades 0-1, and degenerated cartilage is assigned grades 2-4. OP-1 mRNA expression was assessed by RT-PCR; OP-1 protein (pro- and active forms) was qualitatively analyzed by Western blotting and quantified by OP-1 ELISA. The highest levels of OP-1 expression (mRNA and protein) were detected in normal cartilage of grade 0. The concentration of OP-1 protein was about 50 ng per gram cartilage dry weight. With the progression of cartilage degeneration (increased Collins grades and OA) OP-1 protein was down-regulated up to 9-fold. These changes affected primarily the active form of OP-1. OP-1 message also declined in cartilages with the increase of degenerative changes. In conclusion, an overall decrease in endogenous OP-1 in degenerated and OA tissue suggests that OP-1 could be one of the factors responsible for normal homeostasis and matrix integrity in cartilage.

Adult↗
PubMed2003

Topographic and zonal distribution of tenascin in human articular cartilage from femoral heads: normal versus mild and severe osteoarthritis.

OBJECTIVE: The extracellular matrix glycoprotein tenascin (TN) is upregulated in articular cartilage with severe osteoarthritis (OA). This study gives a detailed description of TN expression in areas of articular cartilage from femoral heads with mild OA showing structural lesions and in structurally normal areas of the same femoral heads compared with normal cartilage and cartilage with severe OA. METHODS: Immunohistochemical evaluation was performed on cryosections stained with antibodies against TN. Sections were selected as follows: from each macroscopically normal femoral head (n=6) a normal central and peripheral biopsy; from each femoral head with macroscopically mild OA (n=8) a central biopsy that showed structural lesions and a peripheral normal biopsy; from each femoral head with severe OA (n=9) a central and a peripheral biopsy with structural lesions. Central biopsies represent load bearing areas, whereas peripheral biopsies are non-load bearing. RESULTS: Central cartilage with mild OA contains significantly higher levels of TN in the superficial zone than structurally normal, peripheral cartilage from the same femoral heads. Normal cartilage and cartilage with severe OA do not display this topographic variation. Central cartilage with mild OA shows significantly higher levels of TN than normal, central cartilage. Peripheral, normal cartilage with mild OA shows significantly less TN than peripheral cartilage with severe OA. CONCLUSIONS: In femoral heads with mild OA, TN is accumulated in areas displaying structural damage. This proposes mild OA to be a localized disorder. Extreme caution is necessary for sampling of articular cartilage, especially from joints with mild OA.

Cartilage, Articular↗
PubMed1993

Alterations of proteoglycan synthesis in rabbit articular cartilage induced by intra-articular injection of papain.

In order to investigate the biochemical alteration of proteoglycan (PG) synthesis during cartilage repair, reversible destruction was induced by injecting papain into the knee joint cavity of rabbits. The PG synthesis in the cartilage was examined using Na2 35SO4 and high performance liquid chromatography (HPLC). PGs labeled with 35SO4(2-) (35S-PGs) were extracted from normal and papain-treated cartilage, and the amount of synthesis, ability to aggregate with hyaluronan (HA), and the composition of glycosaminoglycan and chondroitin sulfate isomer labeled with 35SO4(2-) (35S-GAG and 35S-CS isomer) were analyzed. Synthesis of 35S-PGs, especially those that were unable to aggregate with HA (nonaggregating 35S-PGs), increased in papain-treated cartilage compared with that in normal cartilage. The acceleration and qualitative change in PG synthesis in the papain-treated cartilage are considered to be responses to the supplementation of the loss of cartilage PGs induced by papain. The compositions of 35S-GAG and 35S-CS isomer of the nonaggregating 35S-PGs differed from those of 35S-PGs which were able to aggregate with HA (aggregating 35S-PGs) in the papain-treated cartilage as well as in the normal cartilage. However, the compositions of both nonaggregating and aggregating 35S-PGs in the papain-treated and normal cartilage were similar. These results indicate that most of the nonaggregating 35S-PGs in papain-treated cartilage have properties similar to those in normal cartilage and are not simple degradation products of aggregating 35S-PGs; they also suggest that the supplementary reaction for PG content in the cartilage during its repair process is not simple acceleration in PG turn-over but the enhancement of PG synthesis accompanied by alterations in aggregating ability and the compositions of GAG and CS isomer.

Animals↗
PubMed2002

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

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

Animals↗
PubMed2000

Incomplete restoration of immobilization induced softening of young beagle knee articular cartilage after 50-week remobilization.

The aim of this study was to characterize the biomechanical and structural changes in canine knee cartilage after an initial 11-week immobilization and subsequent remobilization period of 50 weeks. Cartilage from the immobilized and remobilized knee was compared with the tissue from age-matched control animals. Compressive stiffness, in the form of instant shear modulus (ISM) and equilibrium shear modulus (ESM) of articular cartilage, was investigated using an in situ indentation creep technique. The local variations in cartilage of glycosaminoglycan (GAG) concentration were measured with a microspectrophotometer after safranin O staining of histological sections. Using a computer-based quantitative polarized light microscopy method, collagen-related optical retardation, gamma, of cartilage zones were performed to investigate the collagen network of cartilage. Macroscopically, cartilage surfaces of the knee joint remained intact both after immobilization and remobilization periods. Immobilization caused significant softening of the lateral femoral and tibial cartilages, as expressed by ESM (up to 30%, p < 0.05). Remobilization restored the biomechanical properties of cartilage in the lateral condyle of tibia, but in the lateral condyle of femur ESM remained 15% below the control level (p = 0.05). The instant shear modulus was not changed either after immobilization or remobilization. The GAG content of the cartilage was slightly decreased after immobilization, especially in the superficial zone of cartilage, but the change was not statistically significant. After remobilization the intensity of safranin O content rose to control level. Neither immobilization nor remobilization had any effect on the gamma value of collagen fibril network either in the superficial or the deep zone at any of the test points. The changes of ESM were positively correlated with the alterations in GAG content of the superficial and deep zones after immobilization and remobilization. This confirms the key role of protoglycans in the regulation of the equilibrium stiffness of articular cartilage. As a conclusion, immobilization of the joint of a young individual may cause long-term, if not permanent, alterations of cartilage biomechanical properties. This may predispose joint to degenerative changes later in life.

Age Factors↗
PubMed2004

Proteomic analysis of articular cartilage shows increased type II collagen synthesis in osteoarthritis and expression of inhibin betaA (activin A), a regulatory molecule for chondrocytes.

We show that proteomic analysis can be applied to study cartilage pathophysiology. Proteins secreted by articular cartilage were analyzed by two-dimensional SDS-PAGE and mass spectrometry. Cartilage explants were cultured in medium containing [35S]methionine/cysteine to radiolabel newly synthesized proteins. To resolve the cartilage proteins by two-dimensional electrophoresis, it was necessary to remove the proteoglycan aggrecan by precipitation with cetylpyridinium chloride. 50-100 radiolabeled protein spots were detected on two-dimensional gels of human cartilage cultures. Of 170 silver-stained proteins identified, 19 were radiolabeled, representing newly synthesized gene products. Most of these were known cartilage constituents. Several nonradiolabeled cartilage proteins were also detected. The secreted protein pattern of explants from 12 osteoarthritic joints (knee, hip, and shoulder) and 14 nonosteoarthritic adult joints were compared. The synthesis of type II collagen was strongly up-regulated in osteoarthritic cartilage. Normal adult cartilage synthesized little or no type II collagen in contrast to infant and juvenile cartilage. Potential regulatory molecules novel to cartilage were identified; pro-inhibin betaA and processed inhibin betaA (which dimerizes to activin A) were produced by all the osteoarthritic samples and half of the normals. Connective tissue growth factor and cytokine-like protein C17 (previously only identified as an mRNA) were also found. Activin induced the tissue inhibitor for metalloproteinases-1 in human chondrocytes. Its expression was induced in isolated chondrocytes by growth factors or interleukin-1. We conclude that type II collagen synthesis in articular cartilage is down-regulated at skeletal maturity and reactivated in osteoarthritis in attempted repair and that activin A may be an anabolic factor in cartilage.

Activins↗
PubMed2002

Meniscal and articular cartilage changes in knee osteoarthritis: a cross-sectional double-contrast macroradiographic study.

OBJECTIVE: In knee osteoarthritis (OA) damage to meniscal cartilage is associated with the changes in articular cartilage. Using double-contrast macroradiographs we determined whether the degree of meniscal cartilage damage was similar to or different from that at the corresponding regions of the articular cartilage on the tibia and femur. DESIGN: Double-contrast microfocal macroradiographs,x7-x9 magnification, were obtained of the tibio-femoral joint in 20 osteoarthritic knee patients with medial compartment disease (Kellgren and Lawrence grades I-III). The appearance of the meniscus and the femoral and tibial articular cartilage were graded separately using a 5-point scale. RESULTS: In the medial diseased compartment, articular cartilage damage on the tibia was similar to that of the meniscus, which had significantly greater (P<0.02) degenerative changes than the cartilage on the femur. In the lateral compartment, meniscal damage was significantly worse than in either tibial (P<0.04) or femoral articular cartilages (P<0.01), respectively; none was as severe as that in the medial osteoarthritic compartment. CONCLUSION: Although the cross-sectional nature of this study precluded definite aetiological inferences, this study showed that degenerative changes in the meniscal and articular cartilages were not totally variable. Because of its larger articular surface, changes in the medial femoral cartilage were less marked than at the meniscal and tibial cartilages in the osteoarthritic compartment. In the lateral compartment, meniscal damage precedes tibial and femoral articular cartilage changes. In knees with medial compartment OA, combined meniscal and articular cartilage damage would account for detection of radiographic joint space loss and not meniscal extrusion only.

Adult↗
PubMed2006

An in situ hybridization study of Runx2, Osterix, and Sox9 at the onset of condylar cartilage formation in fetal mouse mandible.

Mandibular condylar cartilage is the principal secondary cartilage, differing from primary cartilage in its rapid differentiation from progenitor cells (preosteoblasts/skeletoblasts) to hypertrophic chondrocytes. The expression of three transcription factors related to bone and cartilage formation, namely Runx2, Osterix and Sox9, was investigated at the onset of mouse mandibular condylar cartilage formation by in situ hybridization. Messenger RNAs for these three molecules were expressed in the condylar anlage, consisting of preosteoblasts/skeletoblasts, at embryonic day (E)14. Hypertrophic chondrocytes appeared at E15 as soon as cartilage tissue appeared. Runx2 mRNA was expressed in the embryonic zone at the posterior position of the newly formed cartilage, in the bone collar and in the newly formed cartilage, but expression intensity in the newly formed cartilage was slightly weaker. Osterix mRNA was also expressed in the embryonic zone and in the bone collar, but was at markedly lower levels in the newly formed cartilage. Sox9 mRNA was continuously expressed from the embryonic zone to the newly formed cartilage. At this stage, Sox5 mRNA was expressed only in the newly formed cartilage. These results suggest that reduced expression of Osterix in combination with Sox9-Sox5 expression is important for the onset of condylar (secondary) cartilage formation.

Animals↗
PubMed1994

Effects of tenoxicam and aspirin on the metabolism of proteoglycans and hyaluronan in normal and osteoarthritic human articular cartilage.

1. As nonsteroidal anti-inflammatory drugs may impair the ability of the chondrocyte to repair its damaged extracellular matrix, we explored the changes in the metabolism of newly synthesized proteoglycan (PG) and hyaluronan (HA) molecules produced by tenoxicam and aspirin in human normal cartilage explants and in osteoarthritic (OA) cartilage from age-matched donors. 2. Explants were sampled from the medial femoral condyle and were classified by use of Mankin's histological-histochemical grading system. Cartilage specimens were normal in 10 subjects, exhibited moderate OA (MOA) in 10 and had severe OA (SOA) in 10. 3. Cartilage explants were pulsed with [3H]-glucosamine and chased in the absence and in the presence of either aspirin (190 micrograms ml-1) or tenoxicam (4-16 micrograms ml-1). After papain digestion, the labelled chondroitin sulphate ([3H]-PGs) and HA([3H]-HA) molecules present in the tissue and media were purified by anion-exchange chromatography. 4. In normal cartilage as well as in explants with MOA and SOA aspirin reduced more strongly PG and HA synthesis than the loss of [3H]-HA and [3H]-PGs. 5. In normal cartilage, tenoxicam did not affect PG metabolism whereas it reduced HA synthesis in a dose-dependent manner and did not change or even increased the net loss of [3H]-HA. In contrast, in OA cartilage, tenoxicam produced a stronger reduction in the loss of [3H]-PGs than in PG synthesis and this decrease occurred at lower concentrations in cartilage with SOA (4-8 micrograms ml-1) than in cartilage with MOA (8-16 micrograms ml-1). In cartilage with MOA, the metabolic balance of HA was unaffected by tenoxicam whereas in cartilage with SOA, the drug decreased the loss of [3H]-HA and concomitantly did not change or even increased HA synthesis.6. The data obtained in short-term in vitro cultures indicate that aspirin may produce OA-like changes in normal cartilage and is likely to worsen the disease process in OA tissue. On the other hand, although tenoxicam may reduce the HA content of normal cartilage, and, in so doing, may produce OA-like lesions, this drug should not per se accelerate joint failure in OA.

Adult↗
PubMed2005

Effects of radiofrequency energy on human articular cartilage: an analysis of 5 systems.

BACKGROUND: Previous radiofrequency work has not rigidly controlled energy application to the articular cartilage, giving uncertain results published to date. HYPOTHESIS: At minimal settings, radiofrequency probes cause cell death in measurable areas when applied to human articular cartilage. STUDY DESIGN: Controlled laboratory study. METHODS: Simulating operating room conditions, 5 commercially available radiofrequency probes were attached to a customized jig to standardize a minimal contact pressure of each probe tip to 2.0 g. Keeping all variables the same, probes were placed on specific points of fresh grade II human cartilage with treatment times of 1 and 3 seconds at the manufacturer's recommended settings. Grade III cartilage was also tested with a treatment time of 3 seconds, and grade II cartilage was studied with the probe held 1 mm off the cartilage surface. Cartilage was blindly analyzed by confocal microscopy using a live/dead cell viability assay to determine the extent of cell death. RESULTS: Radiofrequency probes produced significant cellular death in the form of a half-circle into the cartilage to variable depths. For treatment times of 1 and 3 seconds, cell death measurements ranged from 404 to 539 mum and 1034 to 1283 mum, respectively. One probe failed to show any effect, with minimal evidence of cell death or cartilage smoothing. When probes were kept a 1.0-mm distance above the cartilage, no cell death or cartilage smoothing was noted. Radiofrequency treatment of grade III cartilage penetrated to the subchondral bone. There was no statistically significant difference between the damage caused by monopolar and bipolar probes when tested under these rigidly controlled conditions. CONCLUSION: These results showed significant cellular death at these minimal conditions to the underlying chondrocytes with radiofrequency probes. Surgeons using this technology need to be aware of the power and dangerous potential these probes can have on articular cartilage.

Aged↗
PubMed2006

The normal human chondro-osseous junctional region: evidence for contact of uncalcified cartilage with subchondral bone and marrow spaces.

BACKGROUND: The chondro-osseous junctional region of diarthrodial joints is peculiarly complex and may be considered to consist of the deepest layer of non-calcified cartilage, the tidemark, the layer of calcified cartilage, a thin cement line (between the calcified cartilage and the subchondral bone) and the subchondral bone. A detailed knowledge of the structure, function and pathophysiology of the normal chondro-osseous junction is essential for an understanding of the pathogenesis of osteoarthrosis. METHODS: Full thickness samples from human knee joints were processed and embedded in paraffin wax. One hundred serial sections (10 mum thick) were taken from the chondro-osseous junctional region of a block from the medial tibial plateau of a normal joint. They were stained with haematoxylin and eosin and photographed. For a simple physical reconstruction images of each 10th sequential tissue section were printed and the areas of the photomicrographs containing the chondro-osseous junctional region were cut out and then overlaid so as to create a three-dimensional (3D) model of this region. A 3D reconstruction was also made using computer modelling. RESULTS: Histochemical staining revealed some instances where prolongations of uncalcified cartilage, delineated by the tidemark, dipped into the calcified cartilage and, in places, abutted onto subchondral bone and marrow spaces. Small areas of uncalcified cartilage containing chondrocytes (virtual islands) were seen, in two-dimensional (2D) sections, to be apparently entombed in calcified matrix. The simple physical 3D reconstruction confirmed that these prolongations of uncalcified cartilage were continuous with the cartilage of zone IV and demonstrated that the virtual islands of uncalcified cartilage were cross-sections of these prolongations. The computer-generated 3D reconstructions clearly demonstrated that the uncalcified prolongations ran through the calcified cartilage to touch bone and marrow spaces and confirmed that the apparent entombment of chondrocytes was a 2D artefact. CONCLUSION: This study demonstrates that the chondro-osseous junctional region is more complex than previously described. The tidemark is a clearly defined boundary delineating uncalcified from calcified cartilage. It is not a straight line across a joint, but a complex three-dimensional structure that follows uncalcified cartilage prolongations dipping down through the calcified cartilage to abut onto subjacent bone or marrow spaces.

Adult↗
PubMed1990

The 25-kilodalton insulin-like growth factor (IGF)-binding protein inhibits both basal and IGF-I-mediated growth of chick embryo pelvic cartilage in vitro.

Insulin-like growth factor (IGF)-I stimulates the growth of many tissues, including growth plate cartilage. However, the role of IGF-binding proteins in the growth process is controversial. We purified a 25-kDa IGF-binding protein (BP-25) from amniotic fluid. We tested the effect of this BP-25 preparation on both basal and IGF-I-stimulated growth of chick embryo pelvic cartilages maintained in serum-free organ culture. Cartilage wet weight was 4.1 +/- 0.3 mg/cartilage initially; after 3 days, BP-25 inhibited both basal and IGF-I-stimulated growth. Control cartilages weighed 7.4 +/- 0.7 mg/cartilage, while those incubated with 100 nM BP-25 weighed 5.8 +/- 0.5 mg/cartilage (P less than 0.001 vs. control); BP-25 concentrations as low as 0.2 nM significantly inhibited basal cartilage growth. Cartilages incubated with 1.25 nM IGF-I weighed 10.4 +/- 0.8 mg/cartilage (P less than 0.001 vs. control), while those incubated with both 100 nM BP-25 and 1.25 nM IGF-I weighed 8.1 +/- 0.5 mg/cartilage (P less than 0.001 vs. cartilage incubated with IGF-I alone); BP-25 concentrations as low as 0.4 nM significantly inhibited IGF-I-stimulated cartilage growth. BP-25 also inhibited basal and IGF-I-stimulated increases in cartilage dry weight, [3H]thymidine incorporation into DNA, and 35SO4 incorporation into proteoglycan. A second BP-25 preparation, which in the presence of 1% platelet-poor plasma acts synergistically with IGF-I to stimulate DNA synthesis and cell replication of fibroblasts and smooth muscle cells in tissue culture, inhibited IGF-I-stimulated cartilage growth to the same degree as did our BP-25 preparation. In separate experiments, proteins present in serum-free medium conditioned for 3 days by chick cartilages were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred to nitrocellulose, and incubated with [125I]IGF-I. This medium was found to contain two IGF-binding proteins; one appeared to be the chick equivalent of BP-25, while the other had a molecular mass similar to that of a poorly characterized human 34-kDa IGF-binding protein. We conclude that purified BP-25 inhibits the growth of chick embryo pelvic cartilage in our serum-free organ culture system. Since conditioned medium from these cartilages contains both IGF-I-like peptides and IGF-binding proteins such as BP-25, we suggest that the IGF-binding proteins present may act to down-regulate the growth-promoting effects of the local IGF peptides.

Animals↗
PubMed2004

Regeneration of defects in articular cartilage in rat knee joints by CCN2 (connective tissue growth factor).

UNLABELLED: CTGF/CCN2, a hypertrophic chondrocyte-specific gene product, possessed the ability to repair damaged articular cartilage in two animal models, which were experimental osteoarthritis and full-thickness defects of articular cartilage. These findings suggest that CTGF/CCN2 may be useful in regeneration of articular cartilage. INTRODUCTION: Connective tissue growth factor (CTGF)/CCN2 is a unique growth factor that stimulates the proliferation and differentiation, but not hypertrophy, of articular chondrocytes in vitro. The objective of this study was to investigate the therapeutic use of CTGF/CCN2. MATERIALS AND METHODS: The effects of recombinant CTGF/CCN2 (rCTGF/CCN2) on repair of damaged cartilage were evaluated by using both the monoiodoacetic acid (MIA)-induced experimental rat osteoarthritis (OA) model and full-thickness defects of rat articular cartilage in vivo. RESULTS: In the MIA-induced OA model, quantitative real-time RT-PCR assays showed a significant increase in the level of CTGF/CCN2 mRNA, and immunohistochemical analysis and in situ hybridization revealed that the clustered chondrocytes, in which clustering indicates an attempt to repair the damaged cartilage, produced CTGF/CCN2. Therefore, CTGF/CCN2 was suspected to play critical roles in cartilage repair. In fact, a single injection of rCTGF/CCN2 incorporated in gelatin hydrogel (rCTGF/CCN2-hydrogel) into the joint cavity of MIA-induced OA model rats repaired their articular cartilage to the extent that it became histologically similar to normal articular cartilage. Next, to examine the effect of rCTGF/CCN2 on the repair of articular cartilage, we created defects (2 mm in diameter) on the surface of articular cartilage in situ and implanted rCTGF/CCN2-hydrogel or PBS-hydrogel therein with collagen sponge. In the group implanted with rCTGF/CCN2-hydrogel collagen, new cartilage filled the defect 4 weeks postoperatively. In contrast, only soft tissue repair occurred when the PBS-hydrogel collagen was implanted. Consistent with these in vivo effects, rCTGF/CCN2 enhanced type II collagen and aggrecan mRNA expression in mouse bone marrow-derived stromal cells and induced chondrogenesis in vitro. CONCLUSION: These findings suggest the utility of CTGF/CCN2 in the regeneration of articular cartilage.

Aggrecans↗