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PubMed1998

Magnetic resonance imaging of articular cartilage: ex vivo study on normal cartilage correlated with magnetic resonance microscopy.

The aims of this study were (a) to compare the MR appearance of normal articular cartilage in ex vivo MR imaging (MRI) and MR microscopy (MRM) images of disarticulated human femoral heads, (b) to evaluate by MRM the topographic variations in articular cartilage of disarticulated human femoral heads, and subsequently, (c) to compare MRM images with histology. Ten disarticulated femoral heads were examined. Magnetic resonance images were obtained using spin-echo (SE) and gradient-echo (GE) sequences. Microimages were acquired on cartilage-bone cylindrical plugs excised from four regions (superior, inferior, anterior, posterior) of one femoral head, using a modified SE sequence. Both MRI and MRM images were obtained before and after a 90 degrees rotation of the specimen, around the axis perpendicular to the examined cartilage surface. Finally, MRM images were correlated with histology. A trilaminar appearance of articular cartilage was observed with MRI and with a greater detail with MRM. A good correlation between MRI and MRM features was demonstrated. Both MRI and MRM showed a loss of the trilaminar cartilage appearance after specimen rotation, with greater evidence on MRM images. Cartilage excised from the four regions of the femoral head showed a different thickness, being thickest in the samples excised from the superior site. The MRM technique confirms the trilaminar MRI appearance of human articular cartilage, showing good correlation with histology. The loss of the trilaminar appearance of articular cartilage induced by specimen rotation suggests that this feature is partially related to the collagen-fiber orientation within the different layers. The MRM technique also shows topographic variations in thickness of human articular cartilage.

Aged↗
PubMed1997

Requirement of fibroblast growth factor signaling for regeneration of epiphyseal morphology in rabbit full-thickness defects of articular cartilage.

The involvement of fibroblast growth factor-2 (FGF-2) during the repair process in rabbit full-thickness defects of articular cartilage was studied. Fibroblast growth factor-2 (50 pg/h) was administered for 2 weeks in a 5 mm defect of articular cartilage, which is large enough not to repair spontaneously. The administration of FGF-2 resulted in the regeneration of the articular cartilage and the subchondral bone within 8 weeks. In these defects, undifferentiated mesenchymal cells initiated chondrogenic differentiation coupled with replacement by subchondral bone, resulting in the resurfacing of the defects with hyaline cartilage and the recovery of subchondral bone up to the original bone-articular cartilage junction. In rabbits, full-thickness defects are capable of regenerating articular cartilage as long as the defect size is limited to < or = 3 mm in diameter. In the defects, strong immunoreactivity for FGF-2 was observed in the granulation tissue filling the defects in the early stage of repair, in association with the expression of FGF-2 mRNA shown by in situ hybridization. Once the undifferentiated mesenchymal cells had differentiated into chondrocytes, both the immunoreactivity and the in situ hybridization signal declined significantly. Upon the local administration of a monoclonal antibody against FGF-2 (bFM-1, 50 ng/h), the defects were filled with fibrous tissue and no resurfacing hyaline cartilage was formed. Compared to the non-treated defects, there were marked increases in FGF-2 immunoreactivity and the overexpression of FGF-2 mRNA in the reparative tissue in the bFM-1-treated defects. This rebound phenomenon indicates that the autocrine FGF-2 signaling is critically important for the regeneration of articular cartilage.

3T3 Cells↗
PubMed1988

Lectin-binding in normal and osteoarthrotic articular cartilage from STR/1N-mouse knee joints.

Fluorescein-isothiocyanate (FITC) labeled lectins were used to study the distribution pattern of specific binding-sites in histological sections of normal and osteoarthrotic articular cartilage from the mouse knee joint. Male inbred mice of the STR/1N-strain develop spontaneous arthrotic articular cartilage lesions on the medial condyle of tibia and femur. The varus-deformity of the knee joint leads to a recurrent medial patellar luxation with osteoarthrotic defects on the medial part of the facies patellaris femoris. It was demonstrated that the lectin staining pattern of osteoarthrotic articular cartilage, especially on the facies patellaris femoris, was different from that of normal articular cartilage. The differences in lectin staining corresponded to those observed between normal and fibrillated articular cartilage from human patellae. The normal articular cartilage of the mouse knee joint possessed lectin binding-sites for Concanavalin A (ConA) and wheat germ agglutinin (WGA), but not for Ulex europaeus agglutinin (UEA), soy bean agglutinin (SBA) and peanut agglutinin (PNA). In addition to the completely changed distribution pattern of ConA and WGA in osteoarthrotic cartilage, SBA, PNA and UEA developed distinct staining patterns particular to the fibrillated areas of arthrotic cartilage. The increased lectin-binding to arthrotic articular cartilage may be due to unmasking of sugars in the course of bondage breakdown in fibrillated cartilage or the production of pathological glycoproteins. It is evident that lectins can demonstrate minute differences between normal and arthrotic cartilage and it is concluded, therefore, that lectins are sensitive and specific tools for the study of degenerative joint diseases.

Animals↗
PubMed1996

The structure of the keratan sulphate chains attached to fibromodulin isolated from articular cartilage.

Fibromodulin has been isolated from bovine and equine articular cartilage and the attached keratan sulphate chains subjected to digestion by keratanase II. The oligosaccharides generated have been reduced and subsequently isolated by strong anion-exchange chromatography. Their structures have been determined by high-field 1H-NMR spectroscopy and high-pH anion-exchange chromatography. Both alpha(2-6)- and alpha(2-3)-linked N-acetylneuraminic acid have been found in the capping oligosaccharides, and, fucose which is alpha(1-3)-linked to N-acetylglucosamine has been found as a branch in both repeat region and capping oligosaccharides. These data demonstrate that there are fundamental differences between the structures present in the N-linked keratan sulphate chains attached to fibromodulin from articular cartilage and those from tracheal cartilage, which lack both alpha(2-6)-linked N-acetylneuraminic acid and alpha(1-3)-linked fucose. It has been confirmed that the keratan sulphate chains are short, being only eight or nine disaccharides in length. Very significant differences in the levels of galactose sulphation have been identified at the non-reducing end of the chain. The galactose residue adjacent to the non-reducing cap is sulphated in only 1-3% of chains, compared with a sulphation level of over 40% closer to the reducing end. This highlights the difference between the chain termini and the repeat region in terms of structure and points to the potential for functional importance. The repeat region and capping fragments of the N-linked keratan sulphates from bovine and equine articular cartilage fibromodulin have been found to have the following general structure: NeuAc-(alpha 2-3/6)Gal[6SO3-](beta 1-4)GlcNAc6SO3-(beta 1-3)Gal[6SO3-] (beta 1-4)¿[Fuc(alpha 1-3)]0-1GlcNAc6SO3-(beta 1-3)Gal-[6SO3-](beta 1-4)¿ 6-7GlcNAc6SO3-.

Acetylglucosaminidase↗
PubMed1995

Immunohistochemical demonstration of fibronectin in the most superficial layer of normal rabbit articular cartilage.

OBJECTIVE: To locate fibronectin ultrastructurally in the most superficial layer of normal articular cartilage of rabbits, in order to clarify its role in joint physiology. METHODS: Articular cartilage was obtained from the femoral condyle of seven normal adult rabbits and prepared by a method that included tannic acid fixation. Polyclonal antibodies against rabbit fibronectin were used in an immunohistochemical electron microscopic study, without any enzymic digestion but with a pre-embedding method for the transmission electron microscopy. RESULTS: The cartilage surface was successfully preserved by tannic acid fixation. The most superficial layer in electron photomicrographs was approximately 200-300 nm thick, cell free, and appeared to have two parallel components: the more superficial lamina and the deeper lamina. Gold labelled fibronectin lined this layer in immunohistochemical electron photomicrographs. CONCLUSIONS: Fibronectin covering the surface of the articular cartilage may have a role in joint lubrication and protection of the cartilage by binding with the collagenous matrix and hyaluronic acid in synovial fluid. Chondroitin sulphates may act as a charge barrier in close relationship with the collagen fibrils in the deeper lamina. Significant alteration in these functions may be one of the first causal steps leading to destruction of the articular cartilage.

Animals↗
PubMed1997

The normal stress effect and equilibrium friction coefficient of articular cartilage under steady frictional shear.

During creep or stress relaxation, articular cartilage exhibits a time-dependent friction coefficient which has been shown to reach an equilibrium value, mu eq, as the tissue deformation equilibrates. This study investigates the frictional properties of articular cartilage explants under steady frictional shear and constant compressive strain after the tissue reaches stress-relaxation equilibrium. The two parameters measured are the normal force and frictional torque, from which the friction coefficient was then calculated. It is shown in this experimental study that: (1) Under a prescribed infinitesimal compressive strain, cartilage supports higher compressive normal stress under steady shear than it does in the absence of frictional shear. Furthermore, the normal stress increases with increasing sliding velocity, resulting in a velocity-dependent value of mu eq. The observed normal stress effectively increases the compressive stiffness of cartilage by a factor up to 3.1. (2) Under a prescribed steady frictional shear both the normal stress and frictional shear stress increase, though not proportionally, with increasing compressive strain, producing a decreasing friction coefficient. (3) This velocity-dependent normal stress effect is also shown to result, at least partly, from intrinsic properties of cartilage. The normal stress effect has not been previously reported for articular cartilage, and represents an intriguing mechanical response not commonly encountered in solids, though common in non-Newtonian fluids.

Animals↗
PubMed2005

Functional adaptation of articular cartilage from birth to maturity under the influence of loading: a biomechanical analysis.

REASONS FOR PERFORMING STUDY: The concept of functional adapatation of articular cartilage during maturation has emerged from earlier biochemical research. However, articular cartilage has principally a biomechanical function governed by joint loading. OBJECTIVES: To verify whether the concept of functional adaptation can be confirmed by direct measurement of biomechanical properties of cartilage. HYPOTHESIS: Fetuses have homogeneous (i.e. site-independent) cartilage with regard to biomechanical properties. During growth and development to maturity, the biomechanical characteristics adapt according to functional (loading) demands, leading to distinct, site-dependent biomechanical heterogeneity of articular cartilage. METHODS: Osteochondral plugs were drilled out of the surface at 2 differently loaded sites (Site 1: intermittent impact-loading during locomotion, Site 2: low-level constant loading during weightbearing) of the proximal articular cartilage surface of the proximal phalanx in the forelimb from stillborn foals (n = 8), horses of age 5 (n = 9) and 18 months (n = 9) and mature horses (n = 13). Cartilage thickness was measured using ultrasonic, optical and needle-probe techniques. The osteochondral samples were biomechanically tested in indentation geometry. Young's modulus at equilibrium, dynamic modulus at 1 Hz and the ratios of these moduli values between Sites 1 and 2 were calculated. Age and site effects were evaluated statistically using ANOVA tests. The level of significance was set at P<0.05. RESULTS: Fetal cartilage was significantly thicker compared to the other ages with no further age-dependent differences in cartilage thickness from age 5 months onwards. Young's modulus stayed constant at Site 1, whereas at Site 2 there was a gradual, statistically significant increase in modulus during maturation. Values of dynamic modulus at both Sites 1 and 2 were significantly higher in the fetus and decreased after birth. Values for both moduli were significantly different between Sites 1 and 2 from age 18 months onwards. The ratio of values between Sites 1 and 2 for Young's modulus and dynamic modulus showed a gradual decrease from approximately 1.0 at birth to 0.5-0.6 in the mature horse. At age 18 months, all values were comparable to those in the mature horse. CONCLUSIONS: In line with the concept of functional adaptation, the neonate is born with biomechanically 'blank' or homogeneous cartilage. Functional adaptation of biomechanical properties takes place early in life, resulting in cartilage with a distinct heterogeneity in functional characteristics. At age 18 months, functional adaptation, as assessed by the biomechanical characteristics, has progressed to a level comparable to the mature horse and, after this age, no major adaptations seem to occur. POTENTIAL RELEVANCE: Throughout life, different areas of articular cartilage are subjected to different types of loading. Differences in loading can adequately be met only when the tissue is biomechanically adapted to withstand these different loading conditions without injury. This process of functional adaptation starts immediately after birth and is completed well before maturity. This makes the factor of loading at a young age a crucial variable, and emphasises the necessity to optimise joint loading during early life in order to create an optimal biomechanical quality of articular cartilage, which may well turn out to be the best prevention for joint injury later in life.

Adaptation, Physiological↗
PubMed2002

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

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

Adjuvants, Immunologic↗
PubMed2003

Localization of insulin-like growth factor binding protein-2 in chondrocytes of bovine articular cartilage.

PURPOSE: Previous work indicated that transforming growth factor (TGF-beta) treatment of bovine articular cartilage resulted in an accumulation of insulin-like growth factor binding protein-2 (IGF-BP-2). The purpose of the work presented in this paper was to define the localization of the IGF-BP-2 in freshly excised articular cartilage and in slices cultured in the presence and absence of TGF-beta. METHOD: Newborn calf articular cartilage was dissected and immediately fixed or maintained in organ culture for five days under basal conditions (media without added serum or growth factors) or with basal media containing 15 ng/ml of TGF-beta1. Frozen or paraffin embedded sections were prepared, and immunohistochemistry using anti-IGF-BP-2 performed. RESULTS: The paraffin sections provided the best preservation of morphology and consistency of immunohistochemical staining patterns. In fresh cartilage slices, IGF-BP-2 was associated with most of the chondrocytes. The basal cultured cartilage showed positive immunostaining in some areas, but not others: the most consistently stained area was the upper radial zone. In all cases where a positive reaction was observed, it was associated mostly with chondrocytes. On the other hand, all the TGF-beta treated samples that were examined in this study were evenly stained, and most chondrocytes were positive in all areas from superficial to deep zones, thus closely resembling the pattern of fresh tissue. CONCLUSIONS: It is concluded that IGF-BP-2 is closely cell associated in bovine articular cartilage. Following culture of cartilage slices, TGF-beta increases the number of cells with positive immunostaining. These data help to support the postulate that TGF-beta exerts at least some of its actions in articular cartilage via cross-talk mechanisms involving the IGF-BP-2 system.

Animals↗
PubMed1979

[An experimental study on the influences of artificial socket upon articular cartilage of the femoral head (author's transl)].

In order to investigate the influences of artificial socket made of stainless-steel, pure titanium, high-density polyethylene (HDP), and polycrystal ceramics upon the articular cartilage of the femoral head, experimental artificial sockets were developed. This artificial socket was inserted into the hip joint in a dog, and the changes in the articular cartilage of the femoral head were studied at varying intervals after insertion of the socket. The results revealed that both the stainless-steel and the ceramic sockets caused slight atrophy and degeneration in the articular cartilage of the femoral head since one month after the operation, and these changes were increasingly more appreciable as time advanced. Any changes were hardly noted in the articular cartilage of the femoral head by titanium socket at the end of one month after the operation, whereas the HDP socket caused substantial changes. At the end of one year after the operation, marked degeneration was noted in the articular cartilage of the femoral head by socket made of stainless-steel, titanium, and HDP, and also the femoral head developed deformity. On the basis of the scanning electron microscopic findings on the surface of the articular cartilage of the femoral head affected by each of these artificial socket, and of the metal microscopic examinations of the surface of the artificial sockets, and furthermore on the basis of the findings of gradual deformation of femoral heads due to the artificial sockets, it was shown that articular cartilage of the femoral head was mainly influenced in the case of metallic socket and that both sides of the artificial socket and the articular cartilage of the femoral head were worn out in the case of HDP socket. The ceramic socket was found cracked, developing a loosening in some cases. In summary, it was concluded that the articular cartilage of the femoral head is affected by the artificial socket at a relatively early stage after its application despite materials of the sockets.

Animals↗
PubMed1992

Calcium phosphate crystal distribution in the superficial zone of human femoral head articular cartilage.

The distribution of cuboid crystals in articular cartilage was examined by image analysis of electron micrographs. The specimens were considered to be functionally normal articular cartilage from femoral heads resected either because of femoral neck fracture or tumour in the distal femur. The study was restricted to the superficial region between 0 and 50 microns depth. Crystals were present in all specimens regardless of the age of the patient. The crystal profile area density was significantly greater in superior region samples than inferior region samples and this difference was less in older specimens. A band of microcrystals 10-20 microns below the articular surface was observed in superior samples. A significant correlation between mean individual crystal profile area and age was observed. It is noted that crystals are present in regions of cartilage subject to high mechanical stress.

Adolescent↗
PubMed2000

The insulin-like growth factors (IGFs) I and II bind to articular cartilage via the IGF-binding proteins.

Bovine articular cartilage discs (3 mm diameter x 400 micrometer thick) were equilibrated in buffer containing (125)I-insulin-like growth factor (IGF)-I (4 degrees C) +/- unlabeled IGF-I or IGF-II. Competition for binding to cartilage discs by each unlabeled IGF was concentration-dependent, with ED(50) values for inhibition of (125)I-IGF-I binding of 11 and 10 nM for IGF-I and -II, respectively, and saturation by 50 nM. By contrast, an analog of IGF-I with very low affinity for the insulin-like growth factor-binding proteins (IGF-BPs), des-(1-3)-IGF-I, was not competitive with (125)I-IGF-I for cartilage binding even at 100-400 nM. Binding of the (125)I-labeled IGF-II isoform to cartilage was competed for by unlabeled IGF-I or -II, with ED(50)s of 160 and 8 nM, respectively. This probably reflected the differential affinities of the endogenous IGF-BPs (IGF-BP-6 and -2) for IGF-II/IGF-I. Transport of (125)I-IGF-I was also measured in an apparatus that allows diffusion only across the discs (400 micrometer), by addition to one side and continuous monitoring of efflux on the other side. The time lag for transport of (125)I-IGF was 266 min, an order of magnitude longer than the theoretical prediction for free diffusion in the matrix. (125)I-IGF-I transport then reached a steady state rate (% efflux of total added (125)I-IGF/unit time), which was subsequently accelerated approximately 2-fold by addition of an excess of unlabeled IGF-I. Taken together, these results indicate that IGF binding to cartilage, mostly through the IGF-BPs, regulates the transport of IGFs in articular cartilage, probably contributing to the control of their paracrine activities.

Animals↗
PubMedDate not supplied

The acute effects of radiofrequency energy in articular cartilage: an in vitro study.

SUMMARY: The purpose of this investigation was to determine the acute effect of radiofrequency (RF) energy on articular cartilage. Six fresh human articular cartilage specimens were obtained from patients undergoing total knee arthroplasty for unicompartmental osteoarthritis. A jig was used as the RF-energy was delivered to 2 designated treatment areas. These areas included a normal and a diseased area of articular cartilage tested at 3 voltage settings (kilohertz per voltage root mean square), 133 to 147 (setting 2), 161 to 179 (setting 4), and 190 to 210 (setting 6) for 3 seconds. The designated testing areas were marked with tissue dye and processed using standard histological techniques. A scalloped concave excavation with a smooth surface remains at each treatment site. The chondrocytes are viable at the RF-treated sites without alterations in nuclear cytoplasmic nor lacunae structure when compared with collateral untreated areas. In conclusion, chondrocytes remain viable, no collagen abnormalities are detected, and diseased areas are smoothed without further evidence of fibrillation. RF-energy appears to be safe for use on articular cartilage.

Cartilage, Articular↗
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↗
PubMed1985

Demonstration of chondroitin sulphate and glycoproteins in articular cartilage matrix using periodic acid-Schiff (PAS) method.

Staining of articular cartilage by the periodic acid-Schiff (PAS) method was measured using microspectrophotometry. Standard PAS technique with 2 h oxidation produced a distinct Schiff reaction in the cartilage sections. The staining increased with depth of the articular cartilage demonstrating distribution of the glycoproteins. The modified PAS method included a second, longer periodic acid treatment, which made the uronic acid of glycosaminoglycans PAS-positive. The modified PAS method proved to be highly specific for chondroitin sulphate, which was determined from the samples with gas chromatography. A statistically significant correlation between the Schiff reactivity and galactosamine content of the sections was observed. It is concluded that for articular cartilage standard and modified PAS methods are useful procedures for demonstrating local changes of glycoproteins and chondroitin sulphate, respectively.

Animals↗
PubMed2003

Analysis of rabbit articular cartilage repair after chondrocyte implantation using optical coherence tomography.

OBJECTIVE: To evaluate the utility and limitations of optical coherence tomography (OCT) for immediate, high-resolution structural analysis of rabbit articular repair tissue following chondrocyte implantation without excising or sectioning the specimen. METHODS: Full thickness articular cartilage defects were created in the patellar grooves of 30 adult rabbit knee joints. Allogenic cultured chondrocytes embedded in collagen gels were implanted into the surgical defects. A periosteal patch was then sutured over the chondrocyte-collagen composites. Six animals per time point were sacrificed at 2, 4, 8, 12 and 24 weeks after surgery. The repair tissues were sequentially analysed by arthroscopic surface imaging, OCT, and histology. The resulting images were compared to determine qualitative and quantitative features of surface roughness, repair tissue integration, and micro-architecture. Statistical analysis was performed using Student's t -testing and linear regression. RESULTS: OCT was able to identify the bone and cartilage interface in normal rabbit articular cartilage and regenerated cartilage at 24 weeks post chondrocyte implantation. OCT was able to identify hypertrophy at 4 and 8 weeks, and subtle surface fibrillations at 24 weeks, comparable with histological analysis at low magnification (20x). More importantly, OCT was able to detect embedded gaps between the repair tissue and surrounding host cartilage. CONCLUSION: Close correlation was observed between OCT and histological analysis of morphological features important to the assessment of articular cartilage repair. These results demonstrate that OCT is capable of providing immediate 'optical biopsy' of the rabbit articular cartilage repair tissue without damaging the specimen, and suggest that this new technique, if integrated with an arthroscope, can potentially be used in longitudinal studies of articular cartilage repair in vivo.

Animals↗
PubMed2001

Telomere erosion and senescence in human articular cartilage chondrocytes.

Aging and the degeneration of articular cartilage in osteoarthritis are distinct processes, but a strong association exists between age and the incidence and prevalence of osteoarthritis. We hypothesized that this association is due to in vivo replicative senescence, which causes age-related declines in the ability of chondrocytes to maintain articular cartilage. For this hypothesis to be tested, senescence-associated markers were measured in human articular chondrocytes from donors ranging in age from 1 to 87 years. These measures included in situ staining for senescence-associated beta-galactosidase activity, (3)H-thymidine incorporation assays for mitotic activity, and Southern blots for telomere length determinations. We found that senescence-associated beta-galactosidase activity increased with age, whereas both mitotic activity and mean telomere length declined. These findings indicate that chondrocyte replicative senescence occurs in vivo and support the hypothesis that the association between osteoarthritis and aging is due in part to replicative senescence. The data also imply that transplantation procedures performed to restore damaged articular surfaces could be limited by the inability of older chondrocytes to form new cartilage after transplantation.

Adolescent↗
PubMed1982

Water content of equine articular cartilage: effects of enzymatic degradation and "artificial fibrillation".

A method is described for accurate and reproducible determination of wet and dry weights of small articular cartilage samples. The water content of the articular cartilage samples before and after treatment with selective degradative enzymes and "artificial fibrillation" was determined. It was found that the water content of articular cartilage can be altered by changing the physical and chemical composition of articular cartilage. The combination of protein polysaccharide degradation and "fibrillation" causes an increase in articular cartilage water content, while collagenase and the combination of collagenase and "fibrillation" causes a decrease. The relationship between these findings and function of normal and osteoarthritic cartilage is discussed.

Animals↗