Articular Cartilage Of Knee Joint Research Articles

Original Functional Rehabilitation Programme Based on Healing Physiology After Reconstruction of Articular Cartilage in Knee Joint

Objectives:The evaluation of the quality of articular cartilage remodelling by means of arthroscopy findings and MRI imaging in a patient, who completed the original rehabilitation program.Methods:The rehabilitation program was conducted according to the Carolina Medical Center rehabilitation protocol. The patient was a 46 years old woman with fourth-degree cartilage damage (Outerbridge classification) located on the right medial femoral condyle of the following size: 1.5x2cm and 1x1.5cm. An arthroscopic micro-fracture repair of the cartilage was performed on the medial femoral condyle of the right knee. After the surgery the original rehabilitation program has been divided into 4 stages based on biological aspects of the physiology of cartilage tissue healing and biomechanics of the knee joint. 18 months after the reconstruction and a complete rehabilitation program, the patient underwent another right knee arthroscopy. During the surgery cartilage was been reevaluated in vivo. A pre-operative MRI was made, as well as a post-operative one after the second arthroscopy. The aim of the MRI examination was to objectify the treatment’s results.Results:The applied surgical treatment and following rehabilitation resulted in the remodelling of the cartilage-like tissue, which was observed in, both, the arthroscopy and the MRI imaging. The MRI evaluation of the quality of the cartilage tissue 18 months after the reconstruction gave very good results according to the MOCART scale (magnetic resonance observation of cartilage repair tissue).Conclusion:The positive results of the cartilage remodelling process recorded after the application of the original rehabilitation programme encourages to continue the study on a larger group of patients.

Acute Rejection of Knee Joint Articular Cartilage in a Rat Composite Tissue Allotransplantation Model.

Osteochondral allograft transplantation is used to treat severe cartilage injury or chondral defects, with good outcomes in clinical studies. However, allograft chondrocyte death due to apoptosis may occur during storage or as a result of implantation stress. We investigated a third possible cause, chondrocyte apoptosis resulting from an immune response, by means of composite tissue allografting, thus eliminating the role of storage and implantation stresses on osteochondral grafts. Vascularized composite tissue allotransplantation (from Fisher 344 to Lewis rat strains) and isotransplantation (from Lewis to Lewis strains) of rat hind limbs were performed. Immunohistochemistry was performed with use of caspase-3 and TUNEL (terminal deoxynucleotidyl transferase mediated dUTP nick end labeling) assays. Analyses were performed immediately after perfusion (day zero) and on postoperative days one, three, seven, twelve, and eighteen (n = 5 for immunohistochemistry). Transmission electron microscopy was used for detection of chondrocyte apoptosis. Laser capture microdissection followed by quantitative real-time polymerase chain reaction assays was used for analysis of postoperative caspase-3 gene expression. Caspase-3 immunochemistry was increasingly positive in allograft chondrocytes from postoperative day seven onward. In contrast, caspase-3 gene expression decreased in all allografts. TUNEL assays showed increasing apoptosis of allograft chondrocytes, and electron microscopy also revealed evidence supporting the development of apoptosis. Immunorejection of chondrocytes in transplanted cartilage has been thought to be unlikely, but our data reveal that chondrocytes can undergo apoptosis in allotransplantation. This apoptosis involves the caspase-3 cascade and indicates that chondrocytes may induce acute rejection.

Viscoelastic properties of bovine knee joint articular cartilage: dependency on thickness and loading frequency.

BackgroundThe knee is an incongruent joint predisposed to developing osteoarthritis, with certain regions being more at risk of cartilage degeneration even in non-osteoarthrosed joints.At present it is unknown if knee regions prone to cartilage degeneration have similar storage and/or loss stiffness, and frequency-dependent trends, to other knee joint cartilage. The aim of this study was to determine the range of frequency-dependent, viscoelastic stiffness of articular cartilage across the bovine knee joint. Such changes were determined at frequencies associated with normal and rapid heel-strike rise times.MethodsCartilage on bone, obtained from bovine knee joints, was tested using dynamic mechanical analysis (DMA). DMA was performed at a range of frequencies between 1 and 88 Hz (i.e. relevant to normal and rapid heel-strike rise times). Viscoelastic stiffness of cartilage from the tibial plateau, femoral condyles and patellar groove were compared.ResultsFor all samples the storage stiffness increased, but the loss stiffness remained constant, with frequency. They were also dependent on cartilage thickness. Both the loss stiffness and the storage stiffness decreased with cartilage thickness. Femoral condyles had the thinnest cartilage but had the highest storage and loss stiffness. Tibial plateau cartilage not covered by the meniscus had the thickest cartilage and lowest storage and loss stiffness.ConclusionDifferences in regional thickness of knee joint cartilage correspond to altered frequency-dependent, viscoelastic stiffness.

Development of a Non-Invasive Bio-Acoustics Measurement System for Assessing Articular Cartilage Knee Joint Problem

A technique in measuring and recording of bio-acoustics signals for the assessment of physiological of knee joint articular cartilage conditions has been developed. Currently, invasive technique such as knee arthroscopy and imaging modalities methods are widely been applied in determining problems related to the knee joint. However, these methods are uncomfortable to the patient, performing in static condition, costly instrumentation and maintenance and most of the times it could not reveal the early symptoms of knee articular cartilage problems. Knee acoustical is used to overcome the current practice limitation and could assist physicians to diagnose at the early stage. The measurement system is developed which consists of a high-sensitivity acoustical piezoelectric transducer with frequency response ranges from 2.5 to 5000Hz, the signal conditioning circuit, and real-time signal visualization and analyzed using a short time Fourier transform technique. The knee cartilage produced an acoustic signals are measured non-invasively during a dynamic cycle of flexion-extension and sit-stand-sit movements. This paper also describes the details of hardware components and software used in this system. Six volunteers with normal and injured cartilage involved in this study. The normal conditions of the knee articular cartilage produced a lower frequency component which is less than 120Hz, and abnormal signal shows frequency more than 200Hz is generated. It has been demonstrated that, the developed system prototype could be used to differentiate between normal and abnormal knee articular cartilage acoustic signal using frequency spectral which could be beneficial in the early detection of the problem.

Mechanical motion promotes expression of Prg4 in articular cartilage via multiple CREB-dependent, fluid flow shear stress-induced signaling pathways

Lubricin is a secreted proteoglycan encoded by the Prg4 locus that is abundantly expressed by superficial zone articular chondrocytes and has been noted to both be sensitive to mechanical loading and protect against the development of osteoarthritis. In this study, we document that running induces maximal expression of Prg4 in the superficial zone of knee joint articular cartilage in a COX-2-dependent fashion, which correlates with augmented levels of phospho-S133 CREB and increased nuclear localization of CREB-regulated transcriptional coactivators (CRTCs) in this tissue. Furthermore, we found that fluid flow shear stress (FFSS) increases secretion of extracellular PGE2, PTHrP, and ATP (by epiphyseal chondrocytes), which together engage both PKA- and Ca(++)-regulated signaling pathways that work in combination to promote CREB-dependent induction of Prg4, specifically in superficial zone articular chondrocytes. Because running and FFSS both boost Prg4 expression in a COX-2-dependent fashion, our results suggest that mechanical motion may induce Prg4 expression in the superficial zone of articular cartilage by engaging the same signaling pathways activated in vitro by FFSS that promote CREB-dependent gene expression in this tissue.

Similar Hyaline-Like Cartilage Repair of Osteochondral Defects in Rabbits Using Isotropic and Anisotropic Collagen Scaffolds

Lesions in knee joint articular cartilage (AC) have limited repair capacity. Many clinically available treatments induce a fibrous-like cartilage repair instead of hyaline cartilage. To induce hyaline cartilage repair, we hypothesized that type I collagen scaffolds with fibers aligned perpendicular to the AC surface would result in qualitatively better tissue repair due to a guided cellular influx from the subchondral bone. By specific freezing protocols, type I collagen scaffolds with isotropic and anisotropic fiber architectures were produced. Rabbits were operated on bilaterally and two full thickness defects were created in each knee joint. The defects were filled with (1) an isotropic scaffold, (2) an anisotropic scaffold with pores parallel to the cartilage surface, and (3) an anisotropic scaffold with pores perpendicular to the cartilage surface. Empty defects served as controls. After 4 (n=13) and 12 (n=13) weeks, regeneration was scored qualitatively and quantitatively using histological analysis and a modified O'Driscoll score. After 4 weeks, all defects were completely filled with partially differentiated hyaline cartilage tissue. No differences in O'Driscoll scores were measured between empty defects and scaffold types. After 12 weeks, all treatments led to hyaline cartilage repair visualized by increased glycosaminoglycan staining. Total scores were significantly increased for parallel anisotropic and empty defects over time (p<0.05). The results indicate that collagen scaffolds allow the formation of hyaline-like cartilage repair. Fiber architecture had no effect on cartilage repair.

Induction of high temperature requirement A1, a serine protease, by TGF-beta1 in articular chondrocytes of mouse models of OA.

The goal of this study is to determine whether transforming growth factor beta 1 (Tgf-β1) induces the high temperature requirement A1 (HtrA1) in articular chondrocytes of two mouse models of osteoarthritis (OA). Early onset articular cartilage degeneration in the mouse models was characterized by histology. Expression profiles of Tgf-β1, p-Smad1, p-Smad2/3 and HtrA1 in knee joints of the mouse models were examined by immunofluorescene. By in vitro and ex vivo experiments, human primary chondrocytes and articular cartilages from femoral condyles of mice were treated with recombinant human TGF-β1 and an ALK5 chemical inhibitor, SB431542. The level of HTRA1 mRNA in human and mouse articular chondrocytes was examined by real-time PCR. Chondrocyte clusters were present in the articular cartilage of knee joints in the mouse models. Increased expressions of Tgf-β1, p-Smad2/3 and HtrA1 were detected in the articular chondrocyte of knee joints in the mouse models. The increased expressions of p-Smad2/3 and HtrA1 were co-localized in the articular chondrocyte of the knee joints. The expression of p-Smad1 was hardly detectable in the mouse models and their corresponding wild-type littermates. The level of HTRA1 mRNA was increased in human and mouse articular chondrocytes treated with TGF-β1, compared with that in chondrocytes without the treatment of TGF-β1. The TGF-β1-induced expression of HTRA1 in human and mouse articular chondrocytes was inhibited by SB431542. These results suggest that the Tgf-β1 canonical signaling was activated to induce HtrA1 in the articular chondrocytes of the mouse models of OA.

Experimental correlation study of lumbar spinal stenosis and knee joint degeneration

To explore the correlation of lumbar stenosis and knee osteoarthritis by establishing a rabbit lumbar spinal stenosis model and observing the hind limb movement function and pathological change of articular cartilage of knee joint. A total of 36 healthy adult rabbits were randomly divided into model group and control group. In the model group, spinal canal was filled with bone pieces to make lumbar spinal stenosis; in the control group, sham operation was performed and materials were inserted into spinal canal. Movement function was evaluated by Tarlov method and pathological features were observed by Mankin's scores under light microscope at 4, 8 and 12 weeks. Early degenerative changes of knee cartilage were observed in the model group at 4 and 8 weeks post-operation. There were synovial hyperemia and hyperplasia, increased synovial fluid effusion and lightly-stained cartilage. The Mankin score was 3.3 - 4.5 and Tarlov score 3 - 4. Intermediate stage changes of osteoarthritis were found in the model group at 12 weeks post-operation, showing synovial hyperplasia, decreased synovial fluid, fissure in cartilage surface, tangled cartilage cells and unevenly stained matrix. The Mankins score was 7 - 9 and Tarlov score 2 - 3. Most of articular cartilage was normal in the control group with Mankin score of 0 - 1 and Tarlov score of 4. Lumbar stenosis may be correlated with knee joint degeneration.

Effects of aging and exercise training on the histological and mechanical properties of articular structures in knee joints of male rat

The impact of aging on joints can have a profound effect on an individual's functioning. Our objectives were to assess the histological and mechanical properties of the knee joint capsule and articular cartilage with aging, and to examine the effects of exercise on age-related changes in the knee joint. 2-year-old Wistar rats were divided into a sedentary control group and an exercise-trained group. 10-week-old animals were used to investigate the changes with aging. The joint capsule and cartilage were evaluated with histological, histomorphometric, immunohistochemical, and mechanical analyses. Severe degenerative changes in articular cartilage were observed with aging, whereas exercise apparently did not have a significant effect. The articular cartilage of aged rats was characterized by damage to the cartilage surface, cell clustering, and an abnormal cartilage matrix. Histomorphometric analysis further revealed changes in cartilage thickness as well as a decreased number of chondrocytes. Aging led to stiffness of the articular cartilage and reduced the ability to dissipate the load and distribute the strain generated within the joint. Joint stiffness with aging was independent of capsular stiffness and synovitis was not a characteristic feature of the aging joint. This study confirms that aging alone eventually leads to joint degeneration in a rat model. The lack of recovery in aging joint changes may be due to several factors, such as the duration of the intervention and the regeneration ability of the cartilage.

Knee Joint Articular Cartilage Segmentation, Visualization and Quantification using Image Processing Techniques: A Review

is a complex and articulated joint of the body. Cartilage is a smooth hyaline spongy material between the tibia and femur bones of knee joint. Cartilage morphology change is an important biomarker for the progression of osteoarthritis (OA). Magnetic resonance imaging (MRI) is the modality widely used to image the knee joint because of its hazard free and high resolution soft tissue contrast. Cartilage thickness measurement and visualization is useful for early detection and progression of the disease in case of OA affected patients. A wide variety of algorithms are available for knee joint image segmentation. They are classified as pixel based and model based methods. Based on the human intervention required, segmentation methods are also classified as manual, semi-automatic and fully automatic methods. This paper reviews knee joint articular cartilage segmentation methods, visualization, thickness measurement, volume measurement and validation methods.

Oxidant damage in Kashin‐Beck disease and a rat Kashin‐Beck disease model by employing T‐2 toxin treatment under selenium deficient conditions

Kashin-Beck disease (KBD) is an endemic degenerative osteoarthropathy, but the mechanisms underlying its pathogenesis remains unclear. This study compares antioxidant capacity and lipid peroxidation using a novel model, in which rats were administered a selenium-deficient diet for 4 weeks prior to their exposure to T-2 toxin for 4 weeks. Changes in cell morphology and empty chondrocyte lacunae indicative of cell death, as well as cartilage proteoglycan loss in the deep zone of articular cartilage of knee joints were observed in rats with selenium-deficient diet plus T-2 toxin treatment. These changes were similar to those observed previously in KBD. The levels of thiobarbituric acid reactive substances (TBARS), indicative of lipid peroxidation in serum and cartilage, were significantly increased in all experimental groups compared to the normal diet group, while the levels of antioxidants, measured as total antioxidant capacity (T-AOC), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidases (GPX), in serum and cartilage were significantly lower than that in the normal diet group. The mRNA expression of those antioxidants in cartilage tissue was significantly reduced by T-2 toxin alone or by selenium-deficient diet plus T-2 toxin treatment. These results indicate that increasing TBARS and decreasing antioxidants in serum and cartilage by T-2 toxin treatment with a selenium-deficient nutritional status may alter oxidative stress in joint tissues and contribute to the pathological process of cartilage damage in KBD.

Histopathology of chondronecrosis development in knee articular cartilage in a rat model of Kashin–Beck disease using T-2 toxin and selenium deficiency conditions

The objective of this study is to observe pathogenic lesions of joint cartilages in rats fed with T-2 toxin under a selenium deficiency nutrition status in order to determine possible etiological factors causing Kashin-Beck disease (KBD). Sprague-Dawley rats were fed selenium-deficient or control diets for 4 weeks prior to their being exposed to T-2 toxin. Six dietary groups were formed and studied 4 weeks later, i.e., controls, selenium-deficient, low T-2 toxin, high T-2 toxin, selenium-deficient diet plus low T-2 toxin, and selenium-deficient diet plus high T-2 toxin. Selenium deficiencies were confirmed by the determination of glutathione peroxidase activity and selenium levels in serum. The morphology and pathology (chondronecrosis) of knee joint cartilage of experimental rats were observed using light microscopy and the expression of proteoglycans was determined by histochemical staining. Chondronecrosis in deep zone of articular cartilage of knee joints was seen in both the low and high T-2 toxin plus selenium-deficient diet groups, these chondronecrotic lesions being very similar to chondronecrosis observed in human KBD. However, the chondronecrosis observed in the rat epiphyseal growth plates of animals treated with T-2 toxin alone or T-2 toxin plus selenium-deficient diets were not similar to that found in human KBD. Our results indicate that the rat can be used as a suitable animal model for studying etiological factors contributing to the pathogenesis (chondronecrosis) observed in human KBD. However, those changes seen in epiphyseal growth plate differ from those seen in human KBD probably because of the absence of growth plate closure in the rat.

Articular cartilage glycosaminoglycan in the rat knee joint after strenuous running exercise

Objective To study the influences of the strenuous running training program on the knee joint articular cartilage. Methods At the age of 16 weeks, 5 male Wistar rats started running on a horizontal treadmill. Thereafter, the rats were trained for 45 days continuously. The rats ran 1 km/day at the speed of 20 m/min. Five matched male rats served as controls. Knees of the rats were studied by whole-mounted section, Hematoxylin and Eosin (HE) stain, safranin O stain. Results The cartilage surfaces were intact after the running exercise. The glycosaminoglycan concentration was decreased by an average of 66% in the superficial zone, 56% on the middle zone, but no difference was found in the deep zone. The glycosaminoglycan concentration was increased by 38% in the calcified cartilage. Conclusion Strenuous running induced marked decrease of proteoglycan in the uncalcified cartilage, but induced no osteoarthritis in this rat strenuous running model. Key words: Knee; Articular cartilage; Running exercise; Glycosaminoglycan

Numerical analysis of cartilage surfaces for osteoarthritis diagnosis using field and feature parameters

Osteoarthritis (OA) is one of the most common degenerative wear diseases of knee joints worldwide. Within knee joint articular cartilage (AC), collagen structure losing integrity is a major symptom of OA. Based on the development of laser scanning confocal microscopy (LSCM), AC images containing three-dimensional (3D) surface texture information could be obtained for quantitative analysis using numerical parameters. Numerical analysis results could be applied for OA diagnosis and progression assessment. Unique to existing numerical analysis techniques, two surface texture parameter sets named field and feature parameters have been used to study wear features in this study. Field parameters are statistically applied to consecutive surface of each scale-limited surface portion while feature parameters are statistically used for a sub-set of pre-defined topographic features. In this study, the feature parameters are for the first time innovatively used for numerical analysis of wear testing AC samples. This project has also selected critical parameters from the field and feature parameter sets to study the correlation between the AC surface changes and OA development. The results presented in the paper have demonstrated that the selected field parameters describe the wear trait of the surfaces for the study of OA progression and the selected feature parameters characterise surface features and their relationship for the study of the functional performance of the surfaces. By utilizing the proposed analysis approach, it is possible to enhance the current numerical analysis techniques for both OA status monitoring and problem diagnosis.

In vitro growth and activity of chondrocytes on three dimensional polycaprolactone/chitosan scaffolds

Porous polycaprolactone/chitosan blend scaffolds with various compositional proportions were prepared using a particulate-leaching method. The pore parameters of resultant scaffolds were found to be mainly modulated by porogen. The compressive mechanical properties and hydrophilicity of scaffolds were examined by measuring their compressive modulus and stress strength as well as swelling index. Selected chondrocytes isolated from articular cartilage of knee joints of rabbits were seeded on these scaffolds, and further in vitro cultured for various periods. The growth and activity of seeded cells were estimated by counting numbers of cells proliferated on scaffolds and measuring the amounts of proteoglycans and type II collagen synthesized by the seeded cells. It was found that some scaffolds composed of proper component ratios and having appropriate pore parameters exhibited promising characteristics for the adhesion and proliferation of seeded cells while maintaining the phenotype and activity of the cells. Copyright © 2010 John Wiley & Sons, Ltd.

Role of HTRA1, a serine protease, in the progression of articular cartilage degeneration.

This study is to investigate the possible role of high temperature requirement A 1 (HtrA1) in the articular cartilage degeneration. Paraffin sections were prepared from the knee and temporomandibular (TM) joints of four mouse OA models; two of the models had a genetic mutation (type IX collagen-deficient and type XI collagen-haploinsufficient) and two were surgically induced (destabilization of the medial meniscus of knee joint and discectomy of TM joint). The HtrA1 protein expression profiles of the prepared sections were examined by immunohistostaining. The level of HtrA1 mRNA in the articular cartilage taken from the knee joints of one of the genetically mutated OA models was determined by real-time PCR. Double immunohistostaining was used to examine the expression of co-localization of HtrA1 with type VI collagen and HtrA1 with discoidin domain receptor 2 (Ddr2) in the articular cartilage of knee joints from the genetically mutated OA model. The expression of HtrA1 was found to be increased in the knee and TM joints of these four models at early stages of the disease. An examination of the knee joint of a mutant mouse indicated an 8-fold increase in the level of HtrA1 mRNA, when compared to the levels observed in the knee joints of its wild-type littermates. Pericellular type VI collagen was not present in chondrocytes expressing HtrA1. Meanwhile, the expression of HtrA1 was associated with the expression of Ddr2 in the chondrocytes. Results indicate that HtrA1 may disrupt the pericellular matrix network, resulting in alteration of chondrocyte metabolisms. This eventually leads to OA.

Meniscectomy alters the dynamic deformational behavior and cumulative strain of tibial articular cartilage in knee joints subjected to cyclic loads

Meniscectomy-induced osteoarthritis may be mechanically based. We asked how meniscectomy alters time-dependent deformation of physiologically loaded articular cartilage. We hypothesized that meniscectomy alters nominal strain in tibial articular cartilage, and that meniscectomy affects cartilage thickness recovery following cessation of loading. A cyclic load simulating normal gait was applied to four sheep knees. A custom device was used to obtain MR images of cartilage at 4.7T during cyclic loading. Articular cartilage thickness and nominal strain were measured every 2.5 min during 1h of cyclic loading, and during 2.5h after cessation of loading. Following meniscectomy the loaded joints rapidly developed high strain centrally and minimal strain peripherally. Maximum nominal strains after 1h of loading were about 55% in the intact knees and 72% in the meniscectomized knees. Nominal strains in the peripheral tibial cartilage were significantly reduced in the meniscectomized knees. Strain recovery was markedly prolonged in the meniscectomized knees. With meniscectomy, tibial articular cartilage in the central load bearing region remains chronically deformed and dehydrated, even after cessation of loading. Post-meniscectomy osteoarthritis may be initiated in this region by direct damage to the cartilage matrix, or by altering the hydration of the tissue. In peripheral regions, reduced loading and strain may facilitate subchondral vascular invasion, and endochondral ossification. This is consistent with the central fibrillation and peripheral osteophyte formation seen in post-meniscectomy osteoarthritis.

Study of comparing the multiple MR sequenc in the articular cartilage of knee joint

To investigate the value of various MR imaging sequences for the assessment of articular cartilage and to determine the most optional sequence. MR sagittal scanning of knee joints were performed in nine fresh bovine models. MR scan sequences consisted of TSE-T(1)WI, TSE-T(2)WI, TSE-PDWI, 3D-FFE-T(1)WI, 3D-BFFE, TSE-T(1)WI-SPIR, TSE-T(2)WI-SPIR, TSE-PDWI-SPIR, 3D-FFE-SPIR, 3D-FFE-WATS, 3D-FFE-MTC, 3D-BFFE-WATS. The signal noise ratio (SNR) and contrast noise ratio (CNR) between cartilage and adjacent tissue were calculated and compared. The knees of fifteen healthy volunteers were imaged with the selective MR sequences and the SNR, CNR and their efficiency were calculated and analyzed statistically. In bovine knee models, the cartilage SNR was higher in the sequences which attached SPIR, WATS and MTC than that of without these techniques. There was a statistically significant difference. The CNR between cartilage and adjacent tissue was also higher in the former. In healthy volunteers, the cartilage SNR was better in 3D-FFE-SPIR, 3D-FFE-WATS, 3D-BFFE-WATS. CNR between cartilage and bone, marrow, muscle, fat were better in 3D-FFE-SPIR, 3D-FFE-WATS, 3D-BFFE-WATS; CNR between cartilage and liquid was better in 3D-FFE-WATS, TSE-T2WI-SPIR, TSE-PDWI-SPIR; CNR between cartilage and meniscus, ligament was better in 3D-FFE-SPIR, 3D-BFFE-WATS, TSE-PDWI-SPIR. The SNR and CNR efficiency were higher in 3D-FFE-WATS, 3D-BFFE-WATS, 3D-FFE-SPIR. There was a statistical difference between these sequences and others (P < 0.01). The cartilage SNR and CNR between cartilage and bone, muscle of 3D-FFE-SPIR weren't significantly higher than that of 3D-FFE-WATS (P > 0.05); CNR between cartilage and liquid, marrow, fat were higher in 3D-FFE-WATS and significantly different than that of 3D-FFE-SPIR (P < 0.01). Articular cartilage SNR and CNR between cartilage and its surrounding tissue are higher in sequences attached SPIR, WATS, so fat suppress technique should routinely be used in clinical cartilage examination. WATS has high scan speed and suppress the fat signal evenly, so it can substitute SPIR. 3D-FFE-WATS is one of the most sensitive sequences in showing cartilage shape and detecting its injury. The cartilage SNR, the CNR between cartilage and adjacent tissue and their efficiency are high in 3D-BFFE-WATS and it can be used in the clinical examination.

Fragmentation of decorin, biglycan, lumican and keratocan is elevated in degenerate human meniscus, knee and hip articular cartilages compared with age-matched macroscopically normal and control tissues

IntroductionThe small leucine-rich proteoglycans (SLRPs) modulate tissue organization, cellular proliferation, matrix adhesion, growth factor and cytokine responses, and sterically protect the surface of collagen type I and II fibrils from proteolysis. Catabolism of SLRPs has important consequences for the integrity of articular cartilage and meniscus by interfering with their tissue homeostatic functions.MethodsSLRPs were dissociatively extracted from articular cartilage from total knee and hip replacements, menisci from total knee replacements, macroscopically normal and fibrillated knee articular cartilage from mature age-matched donors, and normal young articular cartilage. The tissue extracts were digested with chondroitinase ABC and keratanase-I before identification of SLRP core protein species by Western blotting using antibodies to the carboxyl-termini of the SLRPs.ResultsMultiple core-protein species were detected for all of the SLRPs (except fibromodulin) in the degenerate osteoarthritic articular cartilage and menisci. Fibromodulin had markedly less fragments detected with the carboxyl-terminal antibody compared with other SLRPs. There were fewer SLRP catabolites in osteoarthritic hip than in knee articular cartilage. Fragmentation of all SLRPs in normal age-matched, nonfibrillated knee articular cartilage was less than in fibrillated articular cartilage from the same knee joint or total knee replacement articular cartilage specimens of similar age. There was little fragmentation of SLRPs in normal control knee articular cartilage. Only decorin exhibited a consistent increase in fragmentation in menisci in association with osteoarthritis. There were no fragments of decorin, biglycan, lumican, or keratocan that were unique to any tissue. A single fibromodulin fragment was detected in osteoarthritic articular cartilage but not meniscus. All SLRPs showed a modest age-related increase in fragmentation in knee articular and meniscal cartilage but not in other tissues.ConclusionEnhanced fragmentation of SLRPs is evident in degenerate articular cartilage and meniscus. Specific decorin and fibromodulin core protein fragments in degenerate meniscus and/or human articular cartilage may be of value as biomarkers of disease. Once the enzymes responsible for their generation have been identified, further research may identify them as therapeutic targets.

Alteration in articular cartilage of rat knee joints after spinal cord injury

Mechanical forces are crucial for the maintenance of the morphologic and functional integrity of articular cartilage. The alteration of the articular cartilage after spinal cord injury (SCI) has been described in relation to a suppression of mechanical forces, since the joint is unloaded and restricted in movement. However, the morphological and biochemical characteristics of the cartilage after SCI are still poorly understood. We identified the localization of cartilage alterations after SCI and verified the influence of mechanical forces on the articular cartilage. A total of 32 Wistar rats were used. Sixteen animals underwent an SCI and 16 animals served as control. The articular cartilage of the knee joint was assessed, respectively, at 4, 8, 10, and 12 weeks after intervention by histochemical, histomorphometric, immunohistochemical, and biochemical analyses. Cartilage thickness of spinal cord-injured knees decreased at the tibial and posterior femoral (FP) regions and increased at the anterior femoral (FA) region. Spinal cord injuries decreased the number of chondrocytes at the anterior regions and decreased the cartilage matrix staining only at the tibial regions. Immunolabeling to collagen type II was noted comparably in the superficial layer but noted weakly from the middle to deep layer. Collagen type I existed excessively at the cartilage surface and the pericellular regions. Cartilage alterations after SCI would not be explained by only a suppression of mechanical forces by unloading and immobilization, but there may be influences on the cartilage in addition to the change in mechanical forces.