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PubMed1999

MR imaging of articular cartilage using driven equilibrium.

The high incidence of osteoarthritis and the recent advent of several new surgical and non-surgical treatment approaches have motivated the development of quantitative techniques to assess cartilage loss. Although magnetic resonance (MR) imaging is the most accurate non-invasive diagnostic modality for evaluating articular cartilage, improvements in spatial resolution, signal-to-noise ratio (SNR), and contrast-to-noise ratio (CNR) would be valuable. Cartilage presents an imaging challenge due to its short T(2) relaxation time and its low water content compared with surrounding materials. Current methods sacrifice cartilage signal brightness for contrast between cartilage and surrounding tissue such as bone, bone marrow, and joint fluid. A new technique for imaging articular cartilage uses driven equilibrium Fourier transform (DEFT), a method of enhancing signal strength without waiting for full T(1) recovery. Compared with other methods, DEFT imaging provides a good combination of bright cartilage and high contrast between cartilage and surrounding tissue. Both theoretical predictions and images show that DEFT is a valuable method for imaging articular cartilage when compared with spoiled gradient-recalled acquisition in the steady state (SPGR) or fast spin echo (FSE). The cartilage SNR for DEFT is as high as that of either FSE or SPGR, while the cartilage-synovial fluid CNR of DEFT is as much as four times greater than that of FSE or SPGR. Implemented as a three-dimensional sequence, DEFT can achieve coverage comparable to that of other sequences in a similar scan time. Magn Reson Med 42:695-703, 1999.

Cartilage, Articular↗
PubMed2000

Compressive force promotes chondrogenic differentiation and hypertrophy in midpalatal suture cartilage in growing rats.

Midpalatal suture cartilage (MSC) is secondary cartilage located between the bilateral maxillary bones and has been utilized in the analysis of the biomechanical characteristics of secondary cartilage. The present study was designed to investigate the effects of compressive force on the differentiation of cartilage in midpalatal suture cartilage in rats. Forces of various magnitudes were applied to the midpalatal suture cartilage in 4-week-old male Wistar rats for 1, 2, 4, 7, or 14 days, mediated through the bilateral 1st molars using orthodontic wires. The differentiation pathways in the MSC cells were examined by immunohistochemistry for the differentiation markers type I, type II and type X collagen, and glycosaminoglycans (GAGs), chondroitin-4-sulfate, chondroitin-6-sulfate and keratan sulfate. Histologically and immunohistochemically, the midpalatal suture cartilage in control rats had the characteristic appearance of secondary cartilage. In the experimental groups, the center of the midpalatal suture cartilage that contained osteo-chondro progenitor cells seemed to become mature cartilage and its immuno-reaction to type II and X collagen and GAGs increased as the experiment progressed. This differentiation was dependent upon the magnitude and duration of the force applied to the midpalatal suture cartilage; i.e., cartilaginous differentiation progressed more rapidly as the applied force increased. The present results suggest that the differentiation of osteo-chondro progenitor cells into mature and hypertrophic chondrocytes in the precartilaginous cell layer is promoted by compressive force.

Animals↗
PubMed1984

Cartilage in the Atlantic hagfish, Myxine glutinosa.

Light and electron microscopic observations and biochemical analysis of the lingual cartilages from the Atlantic hagfish, Myxine glutinosa, reveal two different types of cartilage, designated types 1 and 2, respectively. The anterior and medial lingual are type 1, while the posterior lingual cartilage is type 2. Chondrocytes in type 1 cartilage are similar to those found in other vertebrate cartilages. The presence within the Golgi elements of material that resembles a component of the extracellular matrix suggests the involvement of active chondrocytes in the synthesis of the matrix. The matrix of the type 1 cartilage contains fibrils arranged to form concentric lamellae in the territorial matrix and irregularly arranged, branched fibrils in the interterritorial matrix. Biochemical analysis of the type 1 cartilage reveals that it is composed primarily of a cyanogen bromide (CNBr)-insoluble protein of unique composition that we have termed " myxinin ." Myxinin appears to be similar, but not identical, to lamprin . Type 2 cartilage bears no resemblance to any other known vertebrate cartilage. The principal cells are hypertrophied and are characterized by masses of cytoplasmic filaments. The appearance of the organelles in smaller nest cells suggests that nest cells are active in the production of some of the matrix, which consists primarily of collagen. Microfibrils and a basal lamina-like material are also present. Biochemical analysis of the type 2 cartilage reveals that the CNBr-insoluble material is different from myxinin . Comparisons of lamprey and hagfish cartilages prompt the concept that these two agnathans probably followed long-independent evolutionary histories.

Animals↗
PubMed1993

Tenascin is associated with articular cartilage development.

The roles of tenascin in cartilage development and function remain unclear. Based on the observation that tenascin is particularly abundant at the epiphyseal extremities of developing cartilaginous models of long bones in chick and mouse embryo, we tested the hypothesis that tenascin is involved in articular cartilage development. Immunofluorescence analysis revealed that tenascin was first localized in the cell condensation region of Day 4 chick embryo limb buds, where the cartilaginous models form. With further development, tenascin gene expression became indeed restricted to the articular cap of the models. Tenascin persisted in the articular cartilage of postnatal chickens but appeared to decrease with age. The protein was also abundant in embryonic and adult tracheal cartilage rings which, like articular cartilage, persist throughout postnatal life. Similar patterns of tenascin expression were seen in mouse. Using monoclonal antibodies to avian tenascin variants, we found that the bulk of articular cartilage contained the shortest tenascin variant (Tn190), whereas the largest variant (Tn230) was present in tissues associated or interacting with articular cartilage (ligaments and meniscus). The protein and its mRNA, however, were undetectable in growth plate cartilage undergoing maturation and endochondral ossification. This inverse correlation between chondrocyte maturation and tenascin production was corroborated by the finding that tenascin gene expression decreased markedly during maturation of chondrocytes in culture and during formation of a secondary ossification center within the articular cap in vivo. Thus, tenascin is intimately associated with the development of articular cartilage and other permanent cartilages whereas absence or reduced amounts of this matrix protein characterize transient cartilages which undergo maturation and are replaced by bone.

Animals↗
PubMed1992

Development of cartilage and bone tissues of the anterior part of the mandible in cichlid fish: a light and TEM study.

The present paper presents ultrastructural details of chondrogenesis of Meckel's cartilage and of ossification of its associated peri- and parachondral bones in a teleost fish, the cichlid Hemichromis bimaculatus. We have distinguished four stages during chondrogenesis, each of which is characterized by specific cellular and matrix features: blastema, primordium, differentiated cartilage and cartilage surrounded by perichondral bone. The blastema is characterized by prechondroblasts and the lack of cartilage matrix; the primordium by chondroblasts and the onset of secretion of matrix of fibrillar and granular nature; differentiated cartilage is characterized by chondrocytes and larger amounts of typical hyaline cartilage matrix. Once perichondral bone is laid down, the chondrocytes show degenerative features but not true hypertrophy. Differentiation of the cartilage cells is attended with cytoplasmic changes indicative of an increasing secretory activity. There is a regional calcification of the cartilage matrix by fusion of calcospherites. Chondrogenesis of the symphyseal area is continuous with that of the rami but starts slightly later. Formation of perichondral bone at the cartilage surface is attended with the deposition of a transitional zone apparently containing a mixture of the two matrices. The role of the perichondral cells is discussed and it is proposed that they may contribute to the formation of the two matrices. The transitional zone may then result either from a diffusion process or from the simultaneous deposition of elements of the two matrices. Growth of the cartilage is argued to be largely the result of matrix secretion, except in the symphyseal area where appositional growth probably occurs until the region is completely covered by perichondral bone. This paper provides a basis for further studies on the developmental interactions between cartilage, bone and teeth during mandibular development in cichlids.

Animals↗
PubMed2003

Correlation of knee-joint cartilage morphology with muscle cross-sectional areas vs. anthropometric variables.

We tested the hypothesis that muscle cross-sectional areas (MCSAs) are more highly (and independently) correlated with cartilage morphology than are body height and weight, and that the physiological reduction of cartilage thickness with aging is associated with a proportional, age-dependent decrease in MCSAs. In 59 asymptomatic individuals (23-75 years old), morphological parameters of the knee cartilages (volume, thickness, and bone-cartilage interface area), and MCSAs were determined from magnetic resonance imaging (MRI) data. Multiple regression models were used to calculate which proportion of the variability of the normal cartilage morphology can be predicted based on independent variables. MCSAs and body height and weight showed correlation coefficients of +0.66, +0.60, and +0.25, respectively, with knee-joint cartilage volume. The correlation coefficients with cartilage thickness were +0.44, +0.35, and +0.24, respectively. Age accounted for a significant (P<0.01) reduction in cartilage thickness, but there was no proportional change of MCSAs. Approximately 76% of the variability of the knee cartilage volume could be predicted from independent variables in a multiple regression model with MCSAs contributing significant, independent information. In conclusion, we find that MCSAs are more highly correlated with cartilage morphology than are body height and weight. The significant decrease in cartilage volume and thickness with age is not associated with a proportional decrease in MCSAs.

Adult↗
PubMed2002

Cyclooxygenase 2-dependent prostaglandin E2 modulates cartilage proteoglycan degradation in human osteoarthritis explants.

OBJECTIVE: To examine cyclooxygenase-2 (COX-2) enzyme expression, its regulation by interleukin-1 beta (IL-1 beta), and the role of prostaglandin E(2) (PGE(2)) in proteoglycan degradation in human osteoarthritic (OA) cartilage. METHODS: Samples of human OA articular cartilage, meniscus, synovial membrane, and osteophytic fibrocartilage were obtained at knee arthroplasty and cultured ex vivo with or without IL-1 beta and COX inhibitors. COX expression was evaluated by immunohistochemistry and Western blot analysis. The enzymatic activity of COX was measured by conversion of arachidonic acid to PGE(2). Cartilage degradation was evaluated by measuring the accumulation of sulfated glycosaminoglycans in the medium. RESULTS: IL-1 beta induced robust expression of COX-2 and PGE(2) in OA meniscus, synovial membrane, and osteophytic fibrocartilage explants, whereas low levels were produced in OA articular cartilage. IL-1 beta also induced cartilage proteoglycan degradation in OA synovial membrane-cartilage cocultures. Increased proteoglycan degradation corresponded to the induction of COX-2 protein expression in, and PGE(2) production from, the synovial membrane. Dexamethasone, neutralizing IL-1 beta antibody, or the selective COX-2 inhibitor, SC-236, attenuated both the IL-1 beta-induced PGE(2) production and cartilage proteoglycan degradation in these cocultures. The addition of PGE(2) reversed the inhibition of proteoglycan degradation caused by SC-236. CONCLUSION: IL-1 beta-induced production of COX-2 protein and PGE(2) was low in OA articular cartilage compared with that in the other OA tissues examined. IL-1 beta-mediated degradation of cartilage proteoglycans in OA synovial membrane-cartilage cocultures was blocked by the selective COX-2 inhibitor, SC-236, and the effect of SC-236 was reversed by the addition of exogenous PGE(2). Our data suggest that induction of synovial COX-2-produced PGE(2) is one mechanism by which IL-1 beta modulates cartilage proteoglycan degradation in OA.

Aged↗
PubMed2002

Sites of collagenase cleavage and denaturation of type II collagen in aging and osteoarthritic articular cartilage and their relationship to the distribution of matrix metalloproteinase 1 and matrix metalloproteinase 13.

OBJECTIVE: To determine the sites of cleavage and denaturation of type II collagen (CII) by collagenase(s) in healthy and osteoarthritic (OA) human articular cartilage and their relationship to the distribution of matrix metalloproteinase 1 (MMP-1) and MMP-13. METHODS: Single (per subject) full-depth specimens from femoral condylar cartilage were isolated from articulating surfaces at autopsy from 8 subjects without arthritis and during arthroplasty from 10 patients with OA. Fixed frozen sections of cartilage were examined by immunoperoxidase localization, using antibodies to the collagenase-generated cleavage site in CII, to an intrachain epitope recognized only in denatured CII, and to MMP-1 and MMP-13 (proenzyme, activated enzyme, or enzyme/inhibitor complex). RESULTS: Staining for collagen cleavage, denaturation, and both MMPs was weak to moderate and was frequently observed in pericellular sites in cartilage from younger, nonarthritic subjects. In specimens from older subjects, this staining was often more widespread and of greater intensity. Similar staining was usually, but not always, seen for all antibodies. In OA cartilage, staining was often stronger and more intense than that in normal cartilage from older subjects, and the distribution of staining was often similar for the different antibodies. Pericellular staining in the deep zone was frequently more pronounced in arthritic cartilage and extended to territorial and sometimes interterritorial sites. In very degenerate specimens, staining was distributed throughout most of the cartilage matrix. CONCLUSION: These observations provide evidence for the presence of limited cleavage and denaturation of CII restricted to mainly pericellular and superficial sites in cartilage from younger, healthy subjects, where MMP-1 and MMP-13 are also selectively localized. Collagen degradation is more extensive and often more pronounced in cartilage from older, nonarthritic subjects. Characteristic changes in early OA are similar to those seen with aging in cartilage from older, healthy subjects, with collagen damage and collagenases concentrated closer to the articular surface. There was usually a close correspondence between the cleavage and denaturation of CII and the sites at which these collagenases were detected, suggesting that both MMPs are involved in the physiology and pathology. There was no evidence that the damage to CII is ordinarily initiated in sites other than at and near the articular surface and around chondrocytes.

Adult↗
PubMed2003

Proteoglycan degradation after injurious compression of bovine and human articular cartilage in vitro: interaction with exogenous cytokines.

OBJECTIVE: Traumatic joint injury leads to an increased risk of osteoarthritis (OA), but the progression to OA is not well understood. We undertook this study to measure aspects of proteoglycan (PG) degradation after in vitro injurious mechanical compression, including up-regulation of enzymatic degradative expression and cytokine-stimulated degradation. METHODS: Articular cartilage tissue explants were obtained from newborn bovine femoropatellar groove and from adult normal human donor knee and ankle tissue. Following injurious compression of the cartilage, matrix metalloproteinase 3 (MMP-3) and MMP-13 messenger RNA (mRNA) expression levels were measured by Northern analysis, and PG loss to the medium after cartilage injury was measured in the presence and absence of added exogenous cytokine (interleukin-1alpha [IL-1alpha] or tumor necrosis factor alpha [TNFalpha]). RESULTS: During the first 24 hours after injury in bovine cartilage, MMP-3 mRNA levels increased 10-fold over the levels in control cartilage (n = 3 experiments), whereas MMP-13 mRNA levels were unchanged. PG loss was significantly increased after injury, but only by 2% of the total PG content and only for the first 3 days following injury. However, compared with injury alone or cytokine treatment alone, treatment of injured tissue with either 1 ng/ml IL-1alpha or 100 ng/ml TNFalpha caused marked increases in PG loss (35% and 54%, respectively, of the total cartilage PG content). These interactions between cytokine treatment and injury were statistically significant. In human knee cartilage, the interaction was also significant for both IL-1alpha and TNFalpha, although the magnitude of increase in PG loss was lower than that in bovine cartilage. In contrast, in human ankle cartilage, there was no significant interaction between injury and IL-1alpha. CONCLUSION: The cytokines IL-1alpha and TNFalpha can cause a synergistic loss of PG from mechanically injured bovine and human cartilage. By attempting to incorporate interactions with other joint tissues that may be sources of cytokines, in vitro models of mechanical cartilage injury may explain aspects of the interactions between mechanical forces and degradative pathways which lead to OA progression.

Adult↗
PubMed1983

Relationship between matrix proteoglycan content and the effects of salicylate and indomethacin on articular cartilage.

When 160 microgram/ml sodium salicylate was added to the culture medium, glycosaminoglycan synthesis in slices of normal articular cartilage from habitually loaded areas of canine femoral condyles was diminished by 24% (P less than 0.01). Although glycosaminoglycan synthesis in cartilage from habitually unloaded regions of the same joints was similar to that in cartilage from loaded sites, the mean uronic acid content of the former was about 25% less, and salicylate suppressed glycosaminoglycan synthesis in unloaded cartilage to a much greater extent (42% of control) than it did in loaded cartilage (P less than 0.01). Furthermore, 1.5 micrograms/ml indomethacin, which had no effect on cartilage from loaded regions, suppressed glycosaminoglycan synthesis in cartilage from unloaded regions by 31%. However, if cartilage from loaded regions was treated with testicular hyaluronidase, indomethacin inhibited glycosaminoglycan synthesis, and inhibition of glycosaminoglycan metabolism by salicylate in hyaluronidase-treated cartilage was greater than in untreated cartilage. The data suggest that the effects of nonsteroidal antiinflammatory drugs on glycosaminoglycan metabolism in articular cartilage are dependent on proteoglycan content of the extracellular matrix.

Animals↗
PubMed1997

Collagenase-3 (matrix metalloprotease 13) is preferentially localized in the deep layer of human arthritic cartilage in situ: in vitro mimicking effect by transforming growth factor beta.

OBJECTIVE: To examine, by immunohistochemistry, the localization and distribution of human collagenase-3 in normal, osteoarthritis (OA), and rheumatoid arthritis (RA) cartilage, and to investigate the effects of interleukin-1beta (IL-1beta) and transforming growth factor beta (TGFbeta) on the synthesis and distribution of collagenase-3. METHODS: Human cartilage specimens were obtained from tibial plateaus. In the first series of experiments, the OA specimens were excised from fibrillated and nonfibrillated areas of cartilage, and RA specimens were excised from lesional areas, including the cartilage-pannus junction when present. In the second series, full strips of cartilage were processed for culture in the presence or absence of IL-1beta (100 units/ml) or TGFbeta (150 ng/ml). Each specimen was processed for immunohistochemical analysis using a collagenase-3 monoclonal antibody. RESULTS: The number of cells that stained for collagenase-3 in normal cartilage was very low (approximately 3%). In OA cartilage, the percentage increased dramatically, and no difference was found between fibrillated and nonfibrillated areas. A statistically significant increase in the percentage of cells staining for collagenase-3 was found in the deep layer compared with the superficial layer. This finding was noted in both the fibrillated areas (mean +/- SEM 58.4 +/- 1.6% and 40.1 +/- 3.9%, respectively; P < 0.007) and the nonfibrillated areas (55.4 +/- 3.2% and 43.2 +/- 2.7%; P < 0.01). Similarly, RA cartilage showed a statistically significant (P < 0.001) increase in the level of chondrocytes staining positive for collagenase-3 in the deep layers (46.4 +/- 4.1%) compared with the superficial layers (26.2 +/- 3.4%). In these RA specimens, the numbers of positively staining chondrocytes were similar both close to and at a distance from the pannus junction. Both IL-1beta and TGFbeta increased the number of chondrocytes producing collagenase-3. Interestingly, in normal specimens, TGFbeta had a predominant effect in the deep layers, while IL-1beta had a greater effect on the superficial layers. CONCLUSION: This study demonstrates that, in situ, the increase in the level of chondrocytes synthesizing collagenase-3 in arthritic cartilage is predominant in the deep layers. The results further indicate that TGFbeta can up-regulate the level of this enzyme and, in normal cartilage in vitro, can cause a mimicking of the in situ distribution observed in arthritic cartilage.

Aged↗
PubMed1993

Insulin-like growth factor binding protein-4 inhibits both basal and IGF-mediated chick pelvic cartilage growth in vitro.

This laboratory has purified a unique insulin-like growth factor binding protein (IGFBP-4) that was previously demonstrated to be inhibitory to bone cell proliferation. In this study, the hypothesis that IGFBP-4 is inhibitory to insulin-like growth factor (IGF) actions on cartilage was tested using the pelvic cartilages of 10-day-old chick embryos as an in vitro model system. Pelvic leaflets were incubated in serum-free medium for 18 h with effectors (BSA, IGF-I, IGF-II, IGFBP-4, or a combination of IGF and IGFBP-4). After the first 8 h, 1.5 microCi [3H]thymidine per well was added. Cartilage growth was assayed by TCA-insoluble [3H]thymidine incorporation into DNA. Additional experiments were conducted under similar conditions to assess the actions of the effectors on cartilage dry weight over a 72 h time period. In separate experiments, serum-free medium conditioned by chick pelvic cartilages for 72 h was assayed for IGF-II by radioreceptorassay, IGF-I by radioimmunoassay, and IGFBP by western ligand analysis. Exogenous IGF addition increased [3H]thymidine incorporation and dry weight of cartilages compared to controls. IGFBP-4 decreased both parameters in basal cartilage growth and also inhibited IGF-mediated cartilage growth. Pelvic cartilages secreted in vitro both IGF-I and IGF-II and a 32-34 kD IGFBP. In conclusion, the IGFs are stimulatory to cartilage growth in vitro and embryonic chick cartilage in vitro produces both IGF-I and II as well as an IGFBP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Biochemistry and antigenicity of osteoarthritic and rheumatoid cartilage.

The purpose of this study was to test whether cartilage serves as the source or repository of antigenic components active in the stimulation of inflammation in rheumatoid arthritis through an analysis of peripheral blood lymphocyte proliferation. Articular cartilage samples were obtained from patients with osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis undergoing joint replacement surgery. Each sample was homogenized and characterized biochemically with respect to the content of proteoglycan, collagen, and immunoglobulin. Proteoglycan content of rheumatoid cartilage was reduced by 71% when compared to osteoarthritic cartilage; the proteoglycan content of ankylosing spondylitis cartilage was reduced by 40% when compared to osteoarthritic cartilage. Immunoglobulins were detectable in all cartilage samples when analyzed by ELISA or end-plate titration. Lymphocyte proliferation, quantified by uptake of 3H-thymidine, was unaltered by addition of cartilage fragments, low (saline) and high salt extracts (2.0 M CaCl2), or cartilage residues. Both autologous and heterologous lymphocytes were tested against the cartilage samples with no difference in reactivity. Purified bovine articular proteoglycans and Type II collagen were also inactive. Although tetanus toxoid and phytohemagglutinin were effective stimulants of proliferation, lymphocytes from arthritis patients were suppressed relative to those of normal individuals. Analysis of arthritic articular cartilage by these techniques failed to demonstrate the presence of antigen(s) stimulating proliferation of peripheral blood lymphocytes.

Adult↗
PubMed1986

Fibronectin and water content of articular cartilage explants after partial depletion of proteoglycans.

The aim of this study was to test the hypothesis that fibronectin in cartilage of osteoarthritic joints accumulates in increased quantities in response to a reduction in proteoglycan content in the matrix. We determined fibronectin content in an ELISA system, uptake of plasma 125I-fibronectin from the medium, and glycosaminoglycan content by a dye method. The proteoglycan content of canine articular cartilage was reduced by co-incubation of the cartilage with canine synovium, partially purified catabolin, or retinoic acid. Data suggested that proteoglycan loss alone was not sufficient to result in the increased fibronectin accumulation that has been reported in the deteriorating articular cartilage of osteoarthritic joints. Cartilage that lost as much as 75% of its proteoglycan content did not have increased fibronectin content and did not take up more fibronectin from the external medium. A related goal of this study was to evaluate the percentage of water in proteoglycan-depleted but disease-free cartilage, as the percentage of water is known to be elevated in osteoarthritic cartilage. Data indicated that the percentage of water in the depleted cartilage increased in proportion to the decrease in proteoglycan content, but the total amount of water in the cartilage did not increase; water content appeared to be unchanged. Under the conditions used, the proteoglycan content was reduced and the percentage of water was elevated, but fibronectin content was not increased. Thus, the cartilage incubated in vitro did not mimic osteoarthritic cartilage.

Animals↗
PubMed2005

Free electron laser ablation of articular and fibro-cartilage at 2.79, 2.9, 6.1, and 6.45 microm: mass removal studies.

BACKGROUND AND OBJECTIVE: The wavelength and tissue-composition dependence of cartilage ablation was examined using selected mid-infrared laser wavelengths. STUDY DESIGN/MATERIALS AND METHODS: The mass removal produced by pulsed laser ablation of articular and fibro-cartilage (meniscus) were measured. The wavelengths examined were 2.79, 2.9, 6.1, and 6.45 microm and provided by a free electron laser (FEL) emitting 4 microsecond macropulses consisting of 1-2 picoseconds duration micropulses delivered at 350 picosecond intervals. The measurement of tissue mass removal was conducted using a microbalance during laser ablation. RESULTS: These studies demonstrated that for articular cartilage the highest mass removal was achieved at lambda = 6.1 microm followed by, in order, lambda = 2.79, 2.9, and 6.45 microm. In comparison, the maximum mass removal for fibro-cartilage was achieved using lambda = 6.1 microm radiation with no statistically significant differences in mass removal provided by the other wavelengths. In evaluation of the comparative influence of each wavelength on tissue type, there was no difference in ablation efficiency between articular and fibro-cartilage at lambda = 6.1 microm. However, the ablation efficiency of articular cartilage was higher than that of fibro-cartilage at both lambda = 2.79 and 2.9 microm. By contrast, lambda = 6.45 microm radiation ablated fibro-cartilage more efficiently than articular cartilage at radiant exposures greater than 12 J/cm2. CONCLUSIONS: The mass removal of articular and fibro-cartilage produced by FEL ablation at selected mid-IR wavelengths was measured as a function of incident radiant exposure. The ablation efficiency was found to depend on both wavelength and tissue type. The 6.1 microm wavelength was found to provide the highest ablation efficiency for both articular and fibro-cartilage.

Animals↗
PubMed2006

Mid-IR laser ablation of articular and fibro-cartilage: a wavelength dependence study of thermal injury and crater morphology.

BACKGROUND AND OBJECTIVE: The aim of this study was to evaluate areas of collateral thermal injury and crater morphology for evidence of wavelength-dependent effects on the ablation of articular cartilage and fibro-cartilage (meniscus) using selected mid-IR wavelengths produced by a free electron laser. STUDY DESIGN/MATERIALS AND METHODS: Two types of cartilage, articular cartilage and fibro-cartilage were used in the study. The wavelengths (lambda) evaluated were 2.79, 2.9, 6.1, and 6.45 microm generated by a free electron laser (FEL) using a 4 microseconds macropulse configuration. The zone of thermal injury and crater morphology produced by laser ablation were examined by light microscopy following standard histologic processing. RESULTS: The zone of thermal injury and crater morphology created in cartilage by the FEL at selected mid-IR wavelengths were examined as a function of incident radiant exposure. Ablation using lambda = 6.1 microm provided the largest crater size for both articular and fibro-cartilage at all radiant exposures. For the zones of collateral thermal injury in articular cartilage, lambda = 6.1 microm produced the least thermal injury at the radiant exposure of 7.6 J/cm2. When the radiant exposure is increased to 20.4 J/cm2, both lambda = 6.1 and 6.45 microm produced less thermal injury than the ablation using lambda = 2.79 and 2.9 microm. The greatest amount of collateral thermal injury was produced by lambda = 2.79 microm for both tissue types. CONCLUSIONS: The results demonstrate that crater depth and collateral thermal injury produced in articular cartilage and fibro-cartilage are wavelength-dependent with 6.1 microm providing the largest craters at all radiant exposures. The least amount of thermal injury was created in articular cartilage using lambda = 6.1 microm at the radiant exposure of 7.6 J/cm2. Both 6.1 and 6.45 microm wavelengths demonstrated similar amount of thermal injury at 20 J/cm2 that was less than lambda = 2.79 and 2.9 microm at similar fluences. These observations are explained based on the absorption by water and protein in the tissue types studied. It is further observed that the use of crater dimensions may not provide a reliable estimate for the amount of tissue removal provided by an ablation procedure.

Animals↗
PubMed2005

MRI-based technique for determining nonuniform deformations throughout the volume of articular cartilage explants.

Articular cartilage is critical to the normal function of diarthrodial joints. Despite the importance of the tissue and the prevalence of cartilage degeneration (e.g., osteoarthritis), the technology required to noninvasively describe nonuniform deformations throughout the volume of the tissue has not been available until recently. The objectives of the work reported in this paper were to 1) describe a noninvasive technique (termed the cartilage deformation by tag registration (CDTR) technique) to determine nonuniform deformations in articular cartilage explants with the use of specialized MRI tagging and image processing methods, 2) evaluate the strain error of the CDTR technique using a custom MRI-compatible phantom material, and 3) demonstrate the applicability of the CDTR technique to articular cartilage by determining 3D strain fields throughout the volume of a bovine articular cartilage explant. A custom MRI pulse sequence was designed to tag and image articular cartilage explants at 7 Tesla in undeformed and deformed states during the application of multiple load cycles. The custom pulse sequence incorporated the "delays alternating with nutations for tailored excitation" (DANTE) pulse sequence to apply tags. This was followed by a "fast spin echo" (FSE) pulse sequence to create images of the tags. The error analysis using the phantom material indicated that deformations can be determined with an error, defined as the strain precision, better than 0.83% strain. When this technique was applied to a single articular cartilage explant loaded in unconfined compression, hetereogeneous deformations throughout the volume of the tissue were evident. This technique potentially can be applied to determine normal cartilage deformations, analyze degenerated cartilage, and evaluate cartilage surgical repair and treatment methodologies. In addition, this technique may be applied to other soft tissues that can be appropriately imaged by MR.

Animals↗
PubMed2000

Sodium visibility and quantitation in intact bovine articular cartilage using high field (23)Na MRI and MRS.

Noninvasive methods of detecting cartilage degeneration can have an impact on identifying the early stages of osteoarthritis. Accurate measurement of sodium concentrations within the cartilage matrix provides a means for analyzing tissue integrity. Here a method is described for quantitating sodium concentration and visibility in cartilage, with general applications to all tissue types. The sodium concentration in bovine patellar cartilage plugs was determined by three different methods: NMR spectroscopy of whole cartilage plugs, NMR spectroscopy of liquefied cartilage in concentrated HCl, and inductively coupled plasma emission spectroscopy. Whole bovine patellae were imaged with relaxation normalized calibration phantoms to ascertain sodium concentrations inside the articular cartilage. Sodium concentrations in intact articular cartilage were found to range from approximately 200 mM on the edges to approximately 390 mM in the center, with an average of approximately 320 mM in five separate bovine patellae studied. In essence, we have created sodium distribution maps of the cartilage, showing for the first time, spatial variations of sodium concentration in intact cartilage. This average concentration measurement correlates very well with the values obtained from the spectroscopic methods. Furthermore, sodium was found to be 100% NMR visible in cartilage plugs. Applications of this method in diagnosing and monitoring treatment of osteoarthritis are discussed.

Animals↗