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High-resolution immunolocalization of osteopontin and osteocalcin in bone and cartilage during endochondral ossification in the chicken tibia.

The ultrastructural distribution of two noncollagenous proteins, osteopontin (OPN) and osteocalcin (OC), originally extracted from bone matrix and proposed to play an important role in bone formation, was examined in the matrices of bone and cartilage from embryonic and postnatal chicken tibial growth plates by high-resolution immunocytochemistry using the colloidal gold technique. In bone, immunolabeling patterns using polyclonal antibodies against chicken OPN and OC were generally similar in that both showed an intense, but regionally variable, labeling of mineralized bone matrix and small mineralization loci dispersed throughout the osteoid and containing prominent condensed organic material. Unmineralized osteoid showed weak-to-moderate labeling. In the mineralized bone matrix proper, labeling was predominantly associated with amorphous, electron-dense patches of organic material among the collagen fibrils. In growth plate cartilage, both proteins first appeared related to calcified cartilage in the hypertrophic zone, although the labeling patterns were somewhat different. For OPN, gold particles were mostly associated with an organic lamina limitans-like density containing condensed, filamentous organic matrix at the periphery of small nodules and large masses of calcified cartilage, with additional moderate labeling throughout the interior of the calcified cartilage. For OC, labeling was observed over filamentous structures throughout the calcified cartilage matrix, with some, but less, labeling at the periphery. In the lowermost zones of the growth plate, the major reaction using both antibodies was found over a layer of dense, amorphous organic material at the periphery of the calcified cartilage at the future bone/calcified cartilage interface, a labeling pattern that persisted following bone deposition at these sites. OPN and to a lesser extent OC were also concentrated in cement (resting, reversal) lines. Throughout the bone and cartilage of the tibia, cells of both the osteoblastic and the osteoclastic lineages were found directly apposed to labeled surfaces and lamina limitans of organic matrix containing OPN and OC. In summary, it is concluded from the immunocytochemical data presented here that the association of OPN and OC with mineralized regions of the extracellular matrices of bone and cartilage and the accumulation of these proteins at tissue surfaces and interfaces are consistent with the hypotheses that they play a role in the extracellular mineralization process per se and/or that they may mediate cell adhesion and dynamics.

Animals↗

Comparison of tibial cartilage volume and radiologic grade of the tibiofemoral joint.

OBJECTIVE: To compare tibial cartilage volume as measured by magnetic resonance imaging (MRI) with radiologic assessment of the tibiofemoral joint. METHODS: The MRI-determined tibial cartilage volume was compared with the radiologic grade of individual features of osteoarthritis (osteophytes and joint space narrowing [JSN]) in 252 subjects (mean +/- SD age 60.2 +/- 10 years, 62% female) who were participating in studies of knee cartilage. RESULTS: JSN seen on both medial and lateral radiographs of the tibiofemoral joint was inversely associated with the respective tibial cartilage volume. This inverse relationship was strengthened with adjustment for age, sex, body mass index (BMI), and bone size. After adjustment for these confounders, for every increase in JSN grade (0-3), the medial tibial cartilage volume was reduced by 257 mm(3) (95% confidence interval [95% CI] 193-321) and the lateral tibial cartilage volume by 396 mm(3) (95% CI 283-509). The relationship between mean cartilage volume and radiologic grade of JSN was linear. Based on results in the subgroup of subjects with normal radiographic findings, we have proposed a model to estimate average "normal" cartilage volume in men and women for a given age, BMI, and bone size. CONCLUSION: The results of this study demonstrate a strong negative, linear association between medial and lateral tibial cartilage volume and increasing grade of JSN. Using data from radiographically normal subjects, we have proposed a simple model for estimating "normal" cartilage volume. However, larger studies will be needed to confirm these findings and to determine whether they are valid in younger subjects.

Aged↗

Human rheumatoid arthritic cartilage and its neutral proteoglycan-degrading proteases. The effects of antirheumatic drugs.

Measurements were made of the neutral proteoglycan-digesting protease activity in the cartilage matrix breakdown observed in the rheumatoid arthritic process. Normal knee (tibial plateau) cartilage specimens were obtained from 7 fresh cadavers and 29 cartilage specimens were obtained from 23 patients diagnosed as having rheumatoid arthritis (RA). The total neutral metalloproteoglycan-degrading enzyme (NMPE) activity in RA cartilages exhibited roughly an eightfold elevation over that of control subjects. The active form of the NMPE for diseased cartilage was higher than that observed for normal cartilage, but was not statistically different. A very low level of activity was detected for serine proteases and no variation was observed between normal and diseased cartilages. Data obtained from RA cartilages were also analyzed with respect to the relationship between enzyme activities and the patients' medications. Four groups of patients were then selected according to their drug treatments: S + G patients received steroid and gold therapy; S patients received steroids only; NS + NG patients did not receive steroid or gold therapy; G patients received gold therapy alone. The total NMPE activity for each of these groups remained at a very high level. The active enzyme activity measured in S + G and S patients was decreased to a level not different from that of normal controls. Specimens from NS + NG patients presented a significantly higher level of the active form of the enzyme (P less than 0.05) when compared with either normal controls, S + G, or S patients. No significant difference was noted in the level of serine protease activity between the RA cartilage and normal cartilage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Rheumatoid synovial fibroblast adhesion to human articular cartilage. Enhancement by neutrophil proteases.

OBJECTIVE: To determine if preexposure of human articular cartilage to activated neutrophils alters rheumatoid synovial fibroblast adhesion to human articular cartilage. METHODS: Human articular cartilage was exposed to either activated neutrophils, interleukin-1, or supernatants obtained from activated neutrophils that had been treated with different protease inhibitors. Radiolabeled rheumatoid synovial fibroblasts were then incubated with the cartilage and the number of counts associated with the cartilage was determined. RESULTS: Pretreatment of human articular cartilage with either activated neutrophils or supernatants obtained from activated neutrophils enhanced subsequent rheumatoid synovial fibroblast adhesion. In contrast, interleukin-1 treatment of cartilage did not alter the adhesion of synovial fibroblasts. The enhanced adhesion could be attenuated by pretreatment of the neutrophil supernatants with either diisopropylfluorophosphonate or EGTA and almost completely abolished by using both inhibitors. CONCLUSION: This study demonstrates that adhesion of rheumatoid synovial fibroblasts to human articular cartilage can be enhanced by exposing the cartilage to proteases released by neutrophils. These results suggest that neutrophil products may play a role in enhancing adhesion of rheumatoid synovium to cartilage in vivo.

Adult↗

Increased apoptosis in human osteoarthritic cartilage corresponds to reduced cell density and expression of caspase-3.

OBJECTIVE: Chondrocyte apoptosis has been described in both human and experimentally induced osteoarthritis (OA), but its importance in the etiopathogenesis of OA is uncertain. The aims of this study were to determine the rate of chondrocyte apoptosis using different methods, and to investigate the relationship between this process and cartilage cellularity, expression of proapoptotic molecules, and expression of antiapoptotic molecules in articular cartilage obtained from patients with OA and from nonarthritic controls. METHODS: We examined the extent of apoptosis in OA and nonarthritic control cartilage using expression of caspase-3, an enzyme that mediates the final stage of cell death by apoptosis, as well as the TUNEL method. We used immunohistochemistry to analyze the expression of a panel of proapoptotic and antiapoptotic molecules that regulate apoptosis in articular cartilage, in order to determine whether the rate of apoptosis is associated with the expression of these molecules. RESULTS: The median (range) percentage of TUNEL-positive chondrocytes in knee OA cartilage (n = 10 specimens), hip OA cartilage (n = 9), and control cartilage (n = 7) was 3.11 (1.67-3.67), 1.86 (1.22-2.89), and 0.39 (0.00-1.78), respectively. When all cartilage samples were pooled, apoptosis showed a strong inverse correlation with cellularity (r = -0.74, P < 0.0001). The percentage (range) of cells expressing caspase-3 in the 3 groups was 15.70 (7.40-20.50), 15.77 (7.42-20.5), and 7.40 (5.90-8.00), respectively. One-way analysis of variance showed that the differences between groups for both TUNEL-positive cells and expression of caspase-3 were statistically significant (P < 0.0001). There was a significant positive correlation between TUNEL-positive cells and expression of caspase-3 (r = 0.654, P< 0.01). CONCLUSION: The data suggest that apoptosis is increased, on average, 2-4-fold in OA cartilage. Considering that OA develops over many years, such an increase in the rate of apoptosis in the articular cartilage could play an important role in the disease process.

Aged↗

Differential acoustic properties of early cartilage lesions in living human knee and ankle joints.

OBJECTIVE: Although numerous studies have been performed to determine whether there are histologic, biochemical, biomechanical, and metabolic differences between knee and ankle cartilage, none have investigated the presence of such differences in living human cartilage. We previously developed an ultrasonic evaluation system for articular cartilage that analyzes the A-mode echogram using wavelet transformation. The current study was undertaken to determine whether the acoustic properties of living human cartilage differ between knee and ankle joints. METHODS: Twenty-eight patients were subjected to ultrasonic evaluation under arthroscopy. After arthroscopic grading, the cartilage was measured using an ultrasonic probe. Two quantitative parameters were used, i.e., the maximum magnitude and the echo duration at the 95% interval of the maximum magnitude. RESULTS: In intact cartilage, the maximum magnitude and echo duration did not differ between the knee and the ankle. In lesional cartilage, in contrast, the maximum magnitude was higher, and the echo duration was shorter, in the ankle than in the knee. These differences were statistically significant. CONCLUSION: Ultrasound findings could be used to judge the degree of early cartilage degeneration in vivo on the basis of objective data such as the maximum magnitude and echo duration. Because we were unable to quantitatively analyze the biochemical and biomechanical properties of the cartilage in this study, our biochemical and biomechanical findings are based only on qualitative assessment. Nevertheless, the results indicate that this ultrasonic evaluation system may be useful for elucidating the processes of articular cartilage degeneration in osteoarthritis.

Acoustics↗

Effects of ovariectomy and estrogen therapy on type II collagen degradation and structural integrity of articular cartilage in rats: implications of the time of initiation.

OBJECTIVE: To investigate how the time of initiation influences the effects of estrogen therapy on type II collagen (CII) turnover and the structural integrity of articular cartilage in ovariectomized rats and to determine whether estrogen exerts direct effects on the catabolic function of chondrocytes ex vivo. METHODS: A total of 46 Sprague-Dawley rats were distributed into 1 of the following treatment groups: 1) ovariectomy, 2) ovariectomy plus early estrogen therapy, 3) ovariectomy plus delayed estrogen therapy, or 4) sham operation. Cartilage turnover was estimated by measuring the serum levels of C-telopeptide of type II collagen (CTX-II). Cartilage lesions at week 9 were quantified using a published scoring technique. The presence of the CTX-II epitope in articular cartilage was assessed by immunohistochemistry. The effects of estrogen (1-100 nM) on chondrocytes were investigated in bovine cartilage explants subjected to catabolic cytokines (tumor necrosis factor alpha [TNFalpha] and oncostatin M [OSM]). RESULTS: In ovariectomized rats, estrogen therapy evoked significant decreases in serum CTX-II independently of the time of initiation; yet, delayed initiation resulted in diminished efficacy in terms of preventing cartilage lesions. CTX-II fragments were present in articular cartilage, colocalizing with early lesions at the cartilage surface. In untreated animals, the early relative increases in serum CTX-II were proportional to the severity of cartilage lesions at week 9 (r = 0.73, P < 0.01). Estrogen significantly and dose-dependently countered CTX-II release from TNFalpha plus OSM-stimulated cartilage explants ex vivo. CONCLUSION: Our results suggest that estrogen counters the acceleration of CII degradation and related structural alterations, and these benefits can be maximized by early initiation after menopause. The protective effect of estrogen seems to involve direct inhibition of the catabolic function of chondrocytes.

Animals↗

Tetraspanin CD151 is expressed in osteoarthritic cartilage and is involved in pericellular activation of pro-matrix metalloproteinase 7 in osteoarthritic chondrocytes.

OBJECTIVE: The proenzyme of matrix metalloproteinase 7 (proMMP-7), which can degrade various extracellular matrix (ECM) and non-ECM molecules after being activated, is overexpressed in osteoarthritic (OA) articular cartilage, but the process of its activation in the cartilage remains unknown. The present study was undertaken to investigate the expression of tetraspanin CD151 in OA cartilage and its involvement in proMMP-7 activation. METHODS: The expression of CD151 in articular cartilage was examined by reverse transcription-polymerase chain reaction (RT-PCR), real-time PCR, immunohistochemistry, in situ hybridization, and immunoblotting. Chondrocytes were used to study the interaction between CD151 and proMMP-7, and activation of proMMP-7. RESULTS: RT-PCR revealed expression of CD151 messenger RNA in all OA cartilage samples, but in only 30% of normal control cartilage samples. Immunohistochemistry and in situ hybridization findings indicated that CD151 was coexpressed with proMMP-7 in chondrocytes, mainly in the superficial and transitional zones of OA cartilage. CD151 immunoreactivity directly correlated with the Mankin score (r = 0.757, P < 0.0001 [n = 30]) and the degree of chondrocyte cloning (r = 0.83, P < 0.0001 [n = 30]) in the cartilage samples. Complexes CD151 and proMMP-7 and their colocalization on the cell membranes were demonstrated by immunoprecipitation and double fluorescence immunostaining of the OA chondrocytes. In situ zymography indicated that chondrocytes exhibit pericellular proteolytic activity, which was abolished by treatment with MMP inhibitors, anti-MMP-7 antibody, or anti-CD151 antibody. CONCLUSION: These data demonstrate that CD151 is overexpressed in OA cartilage and suggest that CD151 plays a role in the pericellular activation of proMMP-7, leading to cartilage destruction and/or chondrocyte cloning.

Aged↗

Crucial role of macrophages in matrix metalloproteinase-mediated cartilage destruction during experimental osteoarthritis: involvement of matrix metalloproteinase 3.

OBJECTIVE: To explore the involvement of synovial macrophages in early cartilage damage in osteoarthritis (OA), and to identify the role of matrix metalloproteinase 3 (MMP-3) in the pathology of early and late OA. METHODS: The role of synovial macrophages in MMP-mediated damage in OA was studied by depleting synovial macrophages prior to elicitation of a collagenase-induced instability model of OA. The expression of MMP in synovium and cartilage was monitored using TaqMan analysis. In spontaneous and induced OA, cartilage pathology was scored in MMP-3-knockout mice and control mice, by histologic assessment and VDIPEN staining. RESULTS: On day 14 following induction of OA, MMP-mediated neoepitopes were detected in cartilage from mice with mild experimental OA (mean +/- SD positively stained surface area 20 +/- 3.2%). Remarkably, by depleting synovial macrophages prior to induction of OA, the generation of MMP-induced neoepitopes was largely prevented (mean +/- SD positively stained surface area 5 +/- 1%; P< 0.001), indicating an important role for synovial macrophages in the occurrence of MMP-mediated cartilage damage. We observed a strong decrease in MMP-3 and MMP-9 expression in synovial but not cartilage tissue in macrophage-depleted joints. Among 2-year-old mice, spontaneous OA-like changes in the lining layer were significantly decreased in MMP-3-knockout mice compared with control mice. Even more striking was the 67% reduction in the occurrence of severe cartilage damage in MMP-3-knockout mice. In addition, MMP-mediated VDIPEN expression was significantly decreased, indicating reduced MMP-mediated cartilage breakdown. CONCLUSION: The results of this study prove that MMP-3 is involved in the generation of severe cartilage damage in murine OA. Synovial macrophages are crucial in early MMP activity and appear to mediate MMP production in synovium rather than cartilage.

Animals↗

Effect of IL-1beta-induced macromolecular depletion on residual quadrupolar interaction in articular cartilage.

PURPOSE: Sodium multiple-quantum filtered (MQF) NMR spectroscopy may potentially be used to measure proteoglycan (PG) depletion in cartilage caused by osteoarthritis (OA). The purpose of this work was to quantify the effect of interleukin-1 (IL-1beta)-induced macromolecule depletion on the residual quadrupolar interaction (RQI) of sodium in bovine cartilage plugs. MATERIALS AND METHODS: Fifteen 8-mm-diameter cartilage plug specimens were cored from the articular surface of fresh bovine patellae. All plugs were kept in culture media and nine of the plugs were subjected to interleukin-1 (IL-1beta)-induced degeneration of cartilage for 4, 6, and 7 days. Sodium NMR spectra were obtained from each sample with a 1-cm-diameter solenoid coil in a 2T whole-body magnet interfaced to a custom-built spectrometer. We employed a previously described theoretical model to analyze triple-quantum filtered (TQF) and double-quantum filtered magic angle (DQFMA) spectra obtained from normal cartilage and cartilage treated with IL-1beta. The model assumes a static Gaussian distribution of the RQI frequency, omega(Q), in the sample. TQF and DQFMA spectra from each sample were fitted with the appropriate signal expressions to determine sigma (the root mean square (RMS) omegaQ), T2f, and T2s. An inversion-recovery sequence was used to determine T1 of each plug. A spectrophotometric assay was used to determine the amount of PG depleted from each plug. Histology was performed to visualize the PG loss in cartilage plugs. We defined sigma as the measure of changes in macroscopic order in the tissue. RESULTS: Simulated spectra from the theoretical model were in excellent agreement with the experimental data. We were able to determine the relaxation times as well as sigma of each specimen from their corresponding fits. T2f ranged between 2.26-3.50 msec, decreasing with increased PG loss. Over the range of PG depletion investigated, T2s increased from 12.3 msec to 14.9 msec, and T1 increased from 16 msec to 21 msec, while sigma decreased from 180 Hz to 120 Hz. The order of macromolecules in the cartilage tissue decreased substantially with PG loss. Histology sections clearly showed qualitative visualization of the PG loss in cartilage following treatment with IL-1beta. CONCLUSION: We demonstrated that IL-beta-induced macromolecule depletion in cartilage not only changes the relaxation characteristics of sodium but also changes RQI of the tissue. Using MQF sodium spectroscopy we quantified the changes in sigma and showed that loss of macromolecules reduces the degree of order in the tissue.

Animals↗

Driven equilibrium magnetic resonance imaging of articular cartilage: initial clinical experience.

PURPOSE: To evaluate three-dimensional driven equilibrium Fourier transform (3D-DEFT) for image quality and detection of articular cartilage lesions in the knee. MATERIALS AND METHODS: We imaged 104 consecutive patients with knee pain with 3D-DEFT and proton density (PD-FSE) and T2-weighted (T2-FSE) fast spin echo. Twenty-four went on to arthroscopy. Signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR) efficiency were measured. Subjective image quality, fat suppression, and cartilage thickness visibility were assessed. Cartilage lesions on 3D-DEFT and T2-FSE were compared with findings outlined in operative reports. RESULTS: SNR efficiency was higher for 3D-DEFT and PD-FSE than for T2-FSE (P < 0.02). 3D-DEFT and PD-FSE showed superior cartilage thickness visibility compared with T2-FSE (P < 0.02). T2-FSE showed better fat suppression and fewer image artifacts than 3D-DEFT (P < 0.04). 3D-DEFT had similar sensitivity and similar specificity for cartilage lesions compared with PD-FSE and T2-FSE. CONCLUSION: 3D-DEFT provides excellent synovial fluid-to-cartilage contrast while preserving signal from cartilage, giving this method a high cartilage SNR. 3D-DEFT shows the full cartilage thickness better than T2-FSE. T2-FSE had superior fat saturation and fewer artifacts than 3D-DEFT. Overall, 3D-DEFT requires further technical development, but is a promising method for imaging articular cartilage.

Arthroscopy↗

Correlation of histopathology and sulfated proteoglycans in human osteoarthritic hip cartilage.

The histopathologic characteristics, in vitro proteoglycan and glycosaminoglycan biosynthesis, and proteoglycan content of osteoarthritic (OA) cartilage tissue types from human femoral heads obtained at the time of total joint replacement were compared. Articular cartilage from fibrillated or discolored cartilage surfaces demonstrated overlapping histopathologic patterns, while cartilage from osteophytic areas was distinct. 35SO4 from each of these three tissue types was found in two peaks of radioactivity on a Sepharose CL-2B column. The average partition coefficient (Kav) of the first peak (peak I) was 0.07, while that of the second (peak II) was 0.63. Proteoglycan monomer predominated in discolored, fibrillated, and osteophytic OA cartilage in peak I. The hydrodynamic size on Sepharose CL-2B of the synthetic proteoglycan monomer was the same for discolored, fibrillated, and osteophytic samples (Kav, 0.25-0.28). Discolored and fibrillated tissues showed a similar percentage of proteoglycan monomer in peak II, whereas osteophyte was reduced in proteoglycan monomer content in peak II. In addition, the endogenous proteoglycans extracted from each cartilage area were generally of a smaller hydrodynamic size than the newly synthesized peak I or proteoglycan monomer. Glycosaminoglycans were predominantly chondroitin 6-sulfate. These results indicated that OA discolored and fibrillated cartilage tissue types from defined topographical areas of human femoral heads possessed neither unique histopathologic nor synthetic or endogenous proteoglycan characteristics. Osteophytic cartilage appeared more histopathologically distinct than either discolored or fibrillated OA cartilage, but synthesized proteoglycan monomer with similar hydrodynamic size to the other cartilage tissue types.

Aged↗

Steindler lecture. Binding sites in fetal and growth plate cartilage.

In addition to genetic and nutritional factors, linear growth during the prenatal and postnatal periods is controlled by peptide, steroid, and thyroid hormones interacting with the receptors present on the membrane or in the cytosol and nuclei of growth plate cartilage. Using standard procedures, insulin and "nonsuppressible insulin-like activity" (a somatomedin) showed significant binding in 600, 15,000, and 105,000 g membrane fractions of epiphyseal cartilage of immature animals. The binding of growth hormone and prolactin was small and probably not significant. Specific uptake of glucocorticoid was demonstrated in viable canine chondrocytes, but not of androgen, estrogen, or vitamin D3 metabolite. A triiodothyronine receptor was present in nuclei from dog epiphyseal cartilage. Hormones that lack binding may affect cartilage only indirectly. Hormone receptors were studied in those portions of fetal growth cartilage that will later evolve into an ossification center, articular cartilage, and epiphyseal cartilage. Cytosol fractions contained a receptor for glucocorticoid but not for androgen or estrogen. Zonal analysis showed a higher level in the peripheral and central sections than in the palisade section. Triiodothyronine binding was also detected in nuclei prepared from whole fetal cartilage. Heterogeneity of cell function was obvious in fetal cartilage. Cell division was high in the central and peripheral zones as well as the upper half of the palisade zone, but low in the lower palisade section. Proline and sulfate incorporation predominated in the palisade section compared with the central and peripheral sections. Disease states with changes of metabolic activities in the cartilage may perhaps be better understood with a clearer knowledge of receptor levels and interactions.

Animals↗

Analysis of experimental immune synovitis cartilage using monoclonal antibodies reactive to rabbit proteoglycan.

This study details the macromolecular changes in cartilage involving proteoglycan molecules in an animal model of rheumatoid arthritis. In experimental chronic immune synovitis, fluorescein-conjugated mouse IgG and three monoclonal antibodies (MAbs 2G2, 2E9, and 6C9) portraying differing fine antigenic specificity for rabbit cartilage proteoglycan monomer were utilized to detail alterations in cartilage proteoglycan. In normal and IgG-immune animals, fluorescein isothiocynate (FITC)-conjugated MAbs 2G2 and 2E9 stained cellular/pericellular (C/PC) region intensely. FITC-MAb 2G2 stained cartilage interterritorial matrix as well. FITC-MAb 6C9 stained only C/PC area lightly but did not stain matrix. A marked decrease in staining intensity with FITC-MAb 2G2 was noted in cartilage sections derived from animals with immune synovitis. A corresponding increase in staining of cartilage was noted with FITC-MAb 6C9. The augmented staining of articular cartilage with FITC-MAb 6C9 was most prominent in femoral condyle tissue sections, which corresponded to the cartilaginous area, with the greatest severity in gross pathology. There was a slight augmentation of staining with FITC-MAb 2E9, especially in the C/PC area of medial/femoral cartilage. In addition, the animals with immune synovitis showed abortive cartilage repair exemplified by the presence of chondrocyte cloning (up to 20 cells) which correlated with increased FITC-MAb 2G2 staining. The differential MAb staining patterns of cartilaginous tissues obtained utilizing FITC-conjugated monoclonal antibodies with known fine antigenic specificity indicates a modulation of proteoglycans involving predominantly core protein epitopes in the articular cartilage of animals with chronic immune synovitis.

Animals↗

Use of a guanidine extract of demineralized bone in the treatment of osteochondral defects of articular cartilage.

In order to evaluate the ability of a guanidine extract of demineralized bone to repair osteochondral defects in articular cartilage, plugs made of this extract were implanted into defects in rabbit knees. The repair tissue was examined macroscopically, histologically, and immunohistochemically at 4, 8, 12, and 30 weeks. Controls (defects that were left empty) showed no cartilage formation. Four weeks after implantation of a guanidine extract plug, histological examination showed a nonhomogeneous metachromatically stained region extending from the surface of the repair tissue down to cancellous bone. This region also was labeled by an anti-type-II collagen antibody, indicating that cartilage-like tissue had been induced. At 8 weeks, the newly formed cartilage in the subchondral and cancellous bone had been partially replaced by bone. At 12 weeks, the thickness of the newly formed cartilage layer had decreased, and most of the newly formed cartilage in the subchondral and cancellous bone had been replaced by bone. In addition, a tidemark was observed. At 30 weeks, the repair tissue was a mixture of cartilage and fibrocartilage, and there was severe degeneration of the cartilage surrounding the repaired defects. These findings indicate that osteochondral defects of articular cartilage can be partially repaired by the implantation of a guanidine extract and that the newly formed cartilage-like tissue is not permanent.

Animals↗

Reduction of residual dipolar interaction in cartilage by spin-lock technique.

The influence of radiofrequency (RF) spin-lock pulse on the laminar appearance of articular cartilage in MR images was investigated. Spin-lock MRI experiments were performed on bovine cartilage plugs on a 4.7 Tesla small-bore MRI scanner, and on human knee cartilage in vivo on a 1.5 Tesla clinical scanner. When the normal to the surface of cartilage was parallel to B0, a typical laminar appearance was exhibited in T2-weighted images of cartilage plugs, but was absent in T1rho-weighted images of the same plugs. At the "magic angle" orientation (when the normal to the surface of cartilage was 54.7 degrees with respect to B0), neither the T2 nor the T1rho images demonstrated laminae. At the same time, T1rho values were greater than T2 at both orientations throughout the cartilage. T1rho dispersion (i.e., the dependence of the relaxation rate on the spin-lock frequency omega1) was observed, which reached a steady-state value of close to 2 kHz in both parallel and magic-angle orientations. These results suggest that residual dipolar interaction from motionally-restricted water and relaxation processes, such as chemical exchange, contribute to T1rho dispersion in cartilage. Further, one can reduce the laminar appearance in human articular cartilage by applying spin-lock RF pulses, which may lead to a more accurate diagnosis of degenerative changes in cartilage.

Animals↗

Articular cartilage destruction in experimental inflammatory arthritis: insulin-like growth factor-1 regulation of proteoglycan metabolism in chondrocytes.

Rheumatoid arthritis, a disease of unknown aetiology, is characterized by joint inflammation and, in its later stages, cartilage destruction. Inflammatory mediators may exert not only suppression of matrix synthesis but also cartilage degradation, which eventually leads to severe cartilage depletion. Systemically and locally produced growth factors and hormones regulate cartilage metabolism. Alterations in levels of these factors or in their activity can influence the pathogenesis of articular cartilage destruction in arthritic joints. The main topic of the present review is the role of the anabolic factor insulin-like growth factor-1 in the regulation of chondrocyte metabolic functions in normal and in diseased cartilage. This is the most important growth factor that balances chondrocytes proteoglycan synthesis and catabolism to maintain a functional cartilage matrix. A brief overview of how chondrocytes keep the cartilage matrix intact, and how catabolic and anabolic factors are thought to be involved in pathological cartilage destruction precedes the review of the role of this growth factor in proteoglycan metabolism in cartilage.

Arthritis, Rheumatoid↗

[Behavior of artificially-induced epiphyseal groove defects. 3: Transplantation of autologous and homologous rib cartilage in Göttingen minipigs. Findings after a 16 week interval].

Drillholes of 8 mm diameter were made through the epiphyseal cartilage of the distal femora in 20 6-week-old Göttingen minipigs. The defects were filled with autologous or with homologous cartilage. This was intended to prevent epi-metaphyseal osseous bridge formation. If of appropriate size and location, the latter would lead to subsequent misgrowth. In group A (autologous costal cartilage), at all drillholes the transplanted costal cartilage can prevent ossification of the defect. An epiphyseal boundary lamella was formed over the transplant which precluded penetration of vessels into the defect. In group B (homologous costal cartilage), the transplanted costal cartilage showed a tendency to mineralization in all preparations at the 20 drillholes available. The cartilage was integrated into the primary cancellous bone developing within the defect. An epiphyseal boundary lamella had not formed in the period of the experiment (in contrast to autogenous transplantation). These investigations show that autologous costal cartilage is superior to homologous costal cartilage in the potential clinical application of costal cartilage transplants in the treatment of Brodie abscesses or post-traumatic epiphyseodeses.

Animals↗