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PubMed2001

Effects of estrogens in vitro and in vivo on cartilage growth in the tilapia (Oreochromis mossambicus).

To study the effects of estrogens on cartilage growth in the tilapia Oreochromis mossambicus, an epiceratobranchial cartilage radioisotope incorporation assay was employed to measure proteoglycan synthesis and prechondrocyte proliferation by incorporation of radiolabeled sulfate and thymidine, respectively. Cartilage explants were cultured with estrogens with or without recombinant bovine insulin-like growth factor-I (IGF-I). In vitro experiments using the natural teleost estrogen, 17beta-estradiol (E2), showed a trend toward inhibition of sulfate incorporation and an inhibition of thymidine incorporation at higher doses (10 micrograms/ml), but not at physiological levels. E2 also showed a trend toward inhibition of sulfate and thymidine incorporation in the presence of IGF-I. Similar results were found with other estrogenic compounds in vitro: ethinylestradiol, diethylstilbestrol (DES), genistein, and nonylphenol. Ethinylestradiol inhibited sulfate and thymidine incorporation at 1000 ng/ml in the presence of IGF-I. DES inhibited thymidine incorporation at 1000 ng/ml in untreated or IGF-I-exposed cartilage. Genistein inhibited sulfate incorporation at 100 micrograms/ml in IGF-I-exposed cartilage and inhibited thymidine uptake at 1, 10, and 100 micrograms/ml in untreated and IGF-I-exposed cartilage. Nonylphenol inhibited sulfate uptake at 100 microM in untreated and IGF-I-exposed cartilage. Nonylphenol alone at 10 and 100 microM inhibited thymidine uptake. In IGF-I-exposed cartilage nonylphenol inhibited thymidine uptake at 100 microM. Fish receiving estrogen injections (E2 or DES) in vivo at a concentration of 2 micrograms/g body weight showed increased sulfate incorporation by cartilage in vitro. Stimulation in vivo by estrogens, in contrast to the inhibition by high doses in vitro, may be a result of the influence of estrogen on pituitary growth hormone release.

Animals↗
PubMed1992

Light and electron microscopic morphology of the temporomandibular joint in growing and mature crab-eating monkeys (Macaca fascicularis): the condylar calcified cartilage.

In an attempt to show maturational alterations in the calcified cartilage, mandibular condyles of four growing and four adult male monkeys (Macaca fascicularis) were studied using light microscopy as well as transmission and scanning electron microscopy. All specimens were initially fixed by perfusion in the presence of ruthenium red. For examination of the hard tissue surfaces in the scanning electron microscope, uncalcified tissues were removed with sodium hypochlorite. In growing animals, almost the entire hard tissue surface in the joint region of the condyle was formed by calcified cartilage, while in adult animals, calcified cartilage was confined to load-bearing regions. In growing animals, the appearance of the calcified cartilage surface suggested a continuously advancing mineralizing front similar to that seen in the epiphyseal plate. Chondrocytes mostly exhibited a terminal stage of hypertrophy, and seemed to die and get lost through vascular invasion and subsequent endochondral ossification. In adult animals, most of the calcified cartilage surface appeared comparatively stable, and resembled the tidemark of articular cartilage. Chondrocytes were usually small and appeared viable. However, on the adult condyles, there were always circumscribed islands where chondrocytes and the pattern of mineralization resembled those seen in growing animals. In these regions, prominent chondroclastic activity indicated extensive articular remodelling. These observations suggest that at the end of somatic growth, condylar calcified cartilage undergoes considerable maturation from a type reminiscent of hyaline growth cartilage to a type resembling articular cartilage. Concomitantly, chondrocytes appear to change their developmental program, in that they stop enlarging and lose their commitment to death. However, they may be able to retain, or switch back to, a more immature stage, in case there is need for extensive articular remodelling.

Animals↗
PubMed1979

Bone formation in cartilage produced by transplanted epiphyseal chondrocytes.

Chondrocytes were isolated from rat epiphyseal cartilage, cultured in vitro, and exposed to exogenous tracers which accumulated in their lysosomes. The cells were then injected into the posterior tibial muscle of animals from the same outbred strain, where they reconstructed calcifying hyaline cartilage. The mineralization of the tissue was followed by ingrowth of blood capillaries from the host bed. Macrophage-like cells surrounding the vessels phagocytized degenerated chondrocytes and unmineralized matrix, whereas multinucleated chondroclasts removed some of the mineralized cartilage matrix. Mesenchyme-like cells accompanying the invading vessels attached to the remaining septa of calcified cartilage matrix and developed into osteoblasts depositing bone matrix on the surface of these septa. The apparent lack of inherent tracer labeling of the lysosomes in the different bone cells indicate that they were derived from the host. No signs of transformation of chondrocytes into bone cells were observed. When isolated rat epiphyseal chondrocytes were injected into the wall of the hamster cheek pouch, calcifying cartilage was reconstructed without signs of subsequent ossification. Transplantation of cartilage reconstructed in the hamster into the dorsal muscles of rats was, however, followed by formation of bone by a sequence analogous to that described above. Such an osteogenetic response was also obtained when the cartilage had been devitalized before transplantation. These experiments show that calcified cartilage, developing in or grafted into an intramuscular site, is able to induce and serve as a substrate for endochondral bone formation, similar to that occurring during normal development. They further indicate that bone induction by calcified cartilage does not require the presence of living chondrocytes.

Animals↗
PubMed1994

Temporal and spatial localization of type I and II collagens in human thyroid cartilage.

Thyroid cartilages of various ages were investigated by immunofluorescence staining for localization of the fibrillar collagen types I and II in order to understand the tissue remodeling occurring during the mineralization and ossification of thyroid cartilage. In fetal and juvenile thyroid cartilages, type I collagen was restricted to the inner and outer perichondrium, while type II collagen was localized in the matrix of hyaline cartilage. However, in advanced ages, type I collagen was also localized in the pericellular and in the interterritorial matrix of intermediate and central chondrocytes of thyroid cartilage. The matrix of peripheral chondrocytes was negative for type I collagen. This suggest that some chondrocytes in thyroid cartilage undergo a differentiation to type I collagen-producing chondrocytes. At the beginning of ossification, bone-related type I collagen was chiefly detected in the central cartilage layer, but was never deposited first from the perichondrium in the direction to the subperichondrial cartilage. This observation confirmed previous findings showing that osteogenesis mainly follows an endochondral ossification pattern. Interterritorial matrix failed to react with the type II collagen antibody in men from the beginning of the third decade, and later still in women, even after treatment with hyaluronidase. These observations indicate that major matrix changes occur faster in male than in female thyroid cartilage.

Adolescent↗
PubMed1995

Comparison of chondroitin sulphate composition of femoral head articular cartilage from patients with femoral neck fractures and osteoarthritis and controls.

The glycosaminoglycan (GAG) and uronic acid (UA) composition of human hip articular cartilage from patients with femoral neck fractures [assumed osteoporosis (OP); n = 12], from patients with osteoarthritis (OA; n = 12) and from normal controls (n = 9) was determined. Full depth tissue samples from the control and OP groups were analysed from the superior, inferior, anterior and posterior regions, while the OA tissue was from cystic (tissue growing on top of cystic bone lesions) and osteophytic regions, from normal and fibrillated resident cartilage and from regions immediately adjacent to eburnated bone. The total sulphated GAG and UA content was reduced in the inferior region of control cartilage compared to the other regions and the values of all regions of the assumed OP group. Cystic regions and OA cartilage adjacent to the bone also showed lower GAG and UA levels than the other regions. The ratios of chondroitin 6-sulphate (C6S) to chondroitin 4-sulphate (C4S) indicated a similar pattern in the different regions of controls and the patient group with femoral neck fracture (OP group). The cystic and osteophytic cartilage of the OA group exhibited lower C6S/C4S ratios than any other region. The levels of dermatan sulphate (DS) in the cartilage of all regions of the OP and control groups were very similar and low, while the tissues of the OA group contained significantly higher amounts, particularly the cartilage from osteophytes. The previously presumed compositional similarity between normal aged and osteoporotic articular hip cartilage was essentially confirmed in a comparative analysis. Significant changes in GAG and UA composition of OA cartilage from distinct regions was also recorded.

Aged↗
PubMed1997

Cartilage-flow phenomenon and evidence for it in perichondrial grafting.

The cartilage-flow phenomenon has been frequently described but not in connection with transplantation procedures for treatment of cartilage lesions. Consequently, we examined this particular phenomenon in an experimental sheep model originally set up to study the use of perichondrial grafts for repair of full-thickness cartilage lesions. Osteochondral lesions were made in nonweight-bearing and weight-bearing areas of knee joints in 36 sheep. The defects were filled with autologous rib perichondrial grafts and secured by either collagen sponges or fibrin glue (n = 24 animals). Defects without perichondrial grafts served as controls (n = 12 animals). Following 1 week of immobilisation of the operated leg, the plaster was removed, and animals were allowed to move freely. Animals were killed after 2, 4, 12 and 16 weeks. Grafts including rims of original surrounding cartilage and bone were removed and investigated by means of macroscopy, histology and micromorphology, including scanning electron microscopy and analysis under polarized light. Cartilage flow was observed in all specimens by 4 weeks after drilling the defects, independent of the weight-bearing condition. These flow formations exhibited a bending of the collagen fibres centrally into the defects, reduction of metachromasia, cell cluster formation and areas of reduced cell density. Time-dependent flow formations were observed related to the weight-bearing condition and whether or not the defects had been grafted. In grafted, non-weight-bearing defects further cartilage flow was stopped 8 weeks after transplantation by the growing perichondrial transplants, which had filled the defects completely. In contrast, control defects exhibited further flow formations in both areas. The same was observed in grafted defects in the weight-bearing area. In defects without complete filling as not enough spontaneously growing fibrous tissue had arisen from the bottom of the defects, two different observations were made: either the defects exhibited a fungiform mass of fibrous tissue that had overgrown the lateral flow formations, or the central mass of fibrous tissue was overgrown by the lateral flow formations. In conclusion, cartilage flow seems to be a mechanically induced phenomenon at the rims of cartilage lesions that contributes little to the reduction of size of large osteochondral defects. There was no evidence for new cartilage proliferation or production of cartilaginous matrix at the rims of the lesions.

Animals↗
PubMed1980

[Deviations of septum cartilage after unilateral separation of Mucoperichondrium in rabbits (author's transl)].

In 49 rabbits the mucoperichondrium of their nasal septa was strictly unilaterally separated according to the Cottle procedure. In addition, in some rabbits only the surface of the septal cartilage was incised and in others the cartilage was cut vertically or horizontally. Four months after the operation the following alterations of the septa were seen: The separation of the mucoperichondrium from the cartilage or superficial incision of the cartilage led to a deviation to the operated left side. If in addition parts of the cartilage septum were mobilized, thus swinging horizontally or vertically, a deviation to the other nonoperated side was seen. Similarly, if two parallel vertical stripes of cartilage were excised, the ends of the remaining cartilage plate bent and the cartilage plate itself deviated to the nonoperated side. The postoperative deviations are due to released unbalanced forces of the cartilage itself and to the disequilibrium of scar tension resulting from the unilateral separation of the mucoperichondrium. To avoid these postoperative deviations the bilateral tunneling of the mucoperichondrium is required.

Animals↗
PubMed1995

Localization of type I and II collagen during development of human first rib cartilage.

The localization of fibrillar type I and II collagen was investigated by immunofluorescence staining with specific antibodies in order to obtain a better understanding of tissue remodelling during the development of first rib cartilage. In childhood and early adolescence type I collagen was found to be restricted to the perichondrium of first rib cartilage, while type II collagen was localized in the matrix of hyaline cartilage. However, in advanced age type I collagen was also found in the territorial matrix of intermediate and central chondrocytes of first rib cartilage. The matrix of subperichondrial chondrocytes was negative for type I collagen. This suggests that some chondrocytes in first rib cartilage undergo a modulation to type I collagen-producing cells. The first bone formation was observed in rib cartilages of 20- to 25-year-old adults. Interestingly, the ossification began peripherally, adjacent to the innermost layer of the perichondrium where areas of fibrocartilage had developed. The newly formed bone matrix showed strong immunostaining for type I collagen. Fibrocartilage bordering peripherally on bone matrix revealed only a faint staining for type I collagen, but strong immunoreactivity to type II collagen. The interterritorial matrix of the central chondrocytes failed to react with the type II collagen antibody, in both men and women, from the end of the second decade. These observations indicate that major matrix changes occur at the same time in male and female first rib cartilages. Thus, our findings indicate that ossification in human first rib cartilage does not follow the same pattern as that observed in endochondral ossification of epiphyseal discs or sternal cartilage.

Adolescent↗
PubMed1996

Localization of collagens and alkaline phosphatase activity during mineralization and ossification of human first rib cartilage.

The localization of type X collagen and alkaline phosphatase activity was examined in order to gain a better understanding of tissue remodelling during development of human first rib cartilage. First rib cartilages from children and adolescents showed no staining for type X collagen and alkaline phosphatase activity. After onset of mineralization in the late second decade, a peripheral ossification process preceded by mineralized fibrocartilage could be distinguished from a more central one preceded by mineralized hyaline cartilage. No immunostaining for type X collagen was found in either type of cartilage. However, strong staining for alkaline phosphatase activity was detected around chondrocyte-like cells within fibrocartilage adjacent to the peripheral mineralization front, while a weaker staining pattern was observed around chondrocytes of hyaline cartilage near the central mineralization front. In addition, the territorial matrix of some chondrocytes within the hyaline cartilage revealed staining for type I collagen, suggesting that these cells undergo a dedifferentiation process, which leads to a switch from type II to type I collagen synthesis. The study provides evidence that mineralization of the hyaline cartilage areas in human first rib cartilage occurs in the absence of type X collagen synthesis but in the presence of alkaline phosphatase. Thus, mineralization of first rib cartilage seems to follow a different pattern from endochondral ossification in epiphyseal discs.

Adolescent↗
PubMed2001

1H and 13C HR-MAS NMR investigations on native and enzymatically digested bovine nasal cartilage.

Rheumatic diseases are accompanied by a progressive destruction of the cartilage layer of the joints. Despite the frequency of the disease, degradation mechanisms are not yet understood and methods for early diagnosis are not available. Although some information on pathogenesis could be obtained from the analysis of degradation products of cartilage supernatants, the most direct information on degradation processes would come from the native cartilage as such. We have used 1H as well as 13C HR-MAS (high resolution magic angle spinning) NMR spectroscopy to obtain suitable line-widths of NMR resonances of native cartilage. 1D and 2D NMR spectra of native cartilage were compared with those of enzymatically-treated (collagenase and papain) samples. In the 1H NMR spectra of native cartilage, resonances of polysaccharides, lipids and a few amino acids of collagen were detectable, whereas the 13C NMR spectra primarily indicated the presence of chondroitin sulfate. Treatment with papain resulted only in small changes in the 1H NMR spectrum, whereas a clear diminution of all resonances was detectable in the 13C NMR spectra. On the other hand, treatment with collagenase caused the formation of peptides with an amino acid composition typical for collagen (glycine, proline, hydroxyproline and lysine). It is concluded that the HR-MAS NMR spectra of cartilage may be of significance for the investigation of cartilage degradation since they allow the fast evaluation of cartilage composition and only very small amounts of sample are required.

Animals↗
PubMed2004

Hyaluronan enhances cartilage repair through low grade tissue remodeling involving cytokines and matrix metalloproteinases.

OBJECTIVE AND DESIGN: To determine whether the ability of high molecular weight hyaluronan (HA) to reverse cartilage damage caused by specific catabolic mediators of cartilage damage, fibronectin fragments (Fn-fs), occurs through a low grade of enhanced catabolic events such as enhanced matrix metalloproteinase (MMP) expression or cytokine activities. MATERIAL: HA from 6.8-kDa to 2 million daltons was studied. TREATMENT: The ability of HA to enhance matrix metalloproteinase-3 (MMP-3) epitopes and cartilage proteoglycan (PG) degradation neoepitopes was tested in bovine cartilage, as well as the ability of recombinant human interleukin-1 receptor antagonist protein (rhIRAP) to reverse PG depletion in cartilage first exposed to Fn-f. RESULTS: All HA forms enhanced MMP-3 epitopes and PG degradation in normal undamaged cartilage and in the case of HA800, the degradation was not sufficient to decrease steady state levels of cartilage PG. When HA800 was added to Fn-f damaged cartilage, restoration of PG occurred, but this was blocked by rhIRAP. CONCLUSIONS: These results collectively suggest that some of the repair activity of HA800 is through proteolytic activity which is not sufficient to decrease matrix PG content, but is nonetheless elevated above levels in cartilage not treated with HA800.

Animals↗
PubMed2006

Utility of delayed gadolinium-enhanced MRI (dGEMRIC) for qualitative evaluation of articular cartilage of patellofemoral joint.

Delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) was used for the measurement of relative proteoglycan depletion of articular cartilage in the patellofemoral (PF) joint following a proprietary protocol, which was compared with the X-ray images, proton density weighted MR images (PDWI) and arthroscopic findings. The study examined 30 knees. The ages ranged from 16 to 74 (average 40.3) years. The Gd-DTPA(2-)containing contrast medium was used in a single dose. The subjects were made to exercise the knee joint for 10 min; and MR images were taken 2 h after intravenous injection of contrast medium. T1-calculated images were produced and the region of interest (ROI) was set as follows. (1) ROI1: entire articular cartilage in a slice through the center of the patella. (2) ROI2: low signal region in T1-calculated images, which were set in a blind fashion by two observers. (3) ROI3: articular cartilage on one side that includes ROI2 where low signal region were detected (medial or lateral). ROI3 was set to examine the contrast of ROI2 with surrounding articular cartilage. The average T1 values of ROI1 was 393.5+/-33.6 ms for radiographic grade 0 and 361.3+/-11.1 ms for grade I, which showed a significant difference (P=0.036). The T1 value of ROI2 was 351.6+/-28.2 ms for grade I, 361.9+/-38.3 ms for grade II, 362.1+/-67.7 ms for grade III, and 297.8+/-54.1 ms for grade IV according to arthroscopic Outerbridge classification. All cases, that demonstrated decrease of T1 values on dGEMRIC (ROI2), showed abnormal arthroscopic or direct viewing findings. The ratio (ROI3/ROI2) in cases of only slight damage classified as Outerbridge grade I (6 cases) was an average of 1.04+/-0.02 and was 1.0 or greater in all cases, thereby indicating well-defined contrast with the surrounding cartilage. The diagnosis of damage in articular cartilage was possible in all 16 cases with radiographic K-L grade I on dGEMRIC, while the intensity changes were not found in 10 of 16 cases on PDWI. The dGEMRIC with a single-dose would be useful on a diagnosis of the area demonstrating early relative proteoglycan depletion in the articular cartilage of the PF joint prior to any discernible changes in the subchondral bone on X-ray images and exceeds to plain MR images for examining deterioration of articular cartilage.

Adolescent↗
PubMed1996

Retinoic acid stimulates pyrophosphate elaboration by cartilage and chondrocytes.

Abnormal metabolism of extracellular inorganic pyrophosphate (PPi) by articular cartilage contributes to calcium pyrophosphate dihydrate (CPPD) crystal formation and the resultant arthritis known as CPPD deposition disease. The factors causing excess PPi elaboration in affected cartilage remain poorly defined. Retinoic acid (RA), a naturally occurring vitamin A metabolite, promotes cartilage degeneration and mineralization, two correlates of CPPD crystal deposition. RA was examined as a potential modifier of cartilage PPi elaboration. All-trans RA (200-1000 nM) increased PPi levels in culture medium of normal porcine cartilage and chondrocytes 2-3-fold over control values at 96 hours of incubation (P < 0.01). IGF1 and anti-EGF antibody diminished the effects of RA on PPi elaboration. RA modestly increased activity of the PPi-generating ectoenzyme NTPPPH in culture medium (P < 0.01). As some RA effects are mediated through increased activity of TGFbeta, a known PPi stimulant, we examined the effect of anti-TGFbeta antibody on RA-induced PPi elaboration. PPi levels in medium were reduced from 30 +/- 7 microM in cartilage cultures with 500 nM RA to 14 +/- 4 microM PPi in cartilage cultures with RA and anti-TGFbeta. Anti-TGFbeta antibody, however, had no significant effect on RA-induced PPi elaboration in chondrocyte cultures. Thus, RA, along with TGFbeta and ascorbate, can now be included in the list of known PPi stimulants. All three of these factors promote mineralization in growth plate cartilage. These data support a central role for TGFbeta in CPPD disease, and provide further evidence linking processes of normal and pathologic calcification in cartilage.

Animals↗
PubMed2003

Mandibular coronoid process in parathyroid hormone-related protein-deficient mice shows ectopic cartilage formation accompanied by abnormal bone modeling.

Parathyroid hormone-related protein (PTHrP) null mutant mice were analyzed to investigate an additional role for PTHrP in cell differentiation. We found ectopic cartilage formation in the mandibular coronoid process in newborn mice. While many previous studies involving PTHrP gene knockout mouse have shown that the cartilage in various regions becomes smaller, this is the first report showing an "increase" of cartilage volume. Investigations of mandibular growth using normal mice indicated that coronoid secondary cartilage never formed from E 15 to d 4, but small amount of cartilage temporally formed at d 7, and this also applies to PTHrP-wild type mice. Therefore, PTHrP deficiency consequently advanced the secondary cartilage formation, which is a novel role of PTHrP in chondrocyte differentiation. In situ hybridization of matrix proteins showed that this coronoid cartilage had characteristics of the lower hypertrophic cell zone usually present at the site of endochondral bone formation and/or "chondroid bone" occasionally found in distraction osteogenesis. In addition, the coronoid process in the PTHrP-deficient mouse also showed abnormal expansion of bone marrow and an increase in the number of multinucleated osteoclasts, an indication of abnormal bone modeling. These results indicate that PTHrP is involved in bone modeling as well as in chondrocyte differentiation. In situ hybridization of matrix protein mRNAs in the abnormal mandibular condylar cartilage revealed that this cartilage was proportionally smaller, supporting previous immunohistochemical results.

Animals↗
PubMed2000

Distinct non-collagen based cartilages comprising the endoskeleton of the Atlantic hagfish, Myxine glutinosa.

Previous evidence from our laboratories showed that collagen is not the major matrix protein of the cartilaginous endoskeleton of the lamprey (Petromyzon marinus). Here we have characterized the cartilage matrix proteins of the only other extant agnathan, the hagfish (Myxine glutinosa). Using morphological, immunochemical and biochemical methods, we show that the structural proteins of the cartilaginous endoskeleton of the hagfish are also non-collagenous in nature. Although these hagfish cartilage proteins share properties both with each other and with lamprey cartilage proteins, including resistance to solubilization with cyanogen bromide and an usual amino acid composition rich in glycine and non-polar amino acids, it is clear that at least two and probably more hagfish cartilage proteins can be distinguished, with distinct distributions in different cartilage structures. Furthermore, in spite of their similarities, matrix proteins from hagfish cartilage are not identical to the proteins we have previously characterized in lamprey cartilage. These results suggest the existence of a larger family of similar but not identical proteins that form the major structural elements of cartilage tissues of agnathans. These data also support our previous conclusion that type II collagen became the predominant structural protein of cartilage only after the divergence of the agnathans from the ancestral line of the vertebrates.

Amino Acids↗
PubMed1998

Quantitative relationships of normal cartilage volumes of the human knee joint--assessment by magnetic resonance imaging.

The objective of this study was to assess the normal range of cartilage volumes in the knee joints of healthy adults, the ratio between the patellar, femoral, and tibial cartilages, and the correlation of the volumes with age, body weight, height, body mass index (obesity), patellar bone size, and the diameter of the tibial head. We examined the knee joints of nine healthy volunteers and eleven normal post-mortem specimens with an age range of 24 to 82 years. The cartilage volumes of the patella, femur, medial tibia and the lateral tibia were quantified, using a fat-suppressed FLASH-3D sequence (resolution 2x0.31x0.31 mm3) and digital postprocessing, involving three-dimensional reconstruction. The mean total volume of the knee joint cartilage was 23,245 mm3, the relative standard deviation (CV%) 19%, and the range 16,341 to 33,988 mm3. In the patella, femur and tibia, the CV% amounted to between 22 and 25%. These joint surfaces occupied a relatively variable proportion of the total knee joint volume, the percentage of the patella being 11 to 22%, that of the femur 54 to 69%, that of the medial tibia 7 to 12%, and that of lateral tibia 11 to 16%. The volumes of the lateral tibia were systematically higher than those of the medial tibia (P<0.001). There was no significant correlation of the knee joint cartilage volume with age (r=+0.05), body weight (r=+0.38), height (r=+0.39) or body mass index (r=+0.29), but a relatively high correlation with the diameter of the tibial head (r=+0.78, P<0.001). After normalising the volumes to this diameter, the CV% of the total knee joint cartilage volume was reduced to 13%, its variation being 12 to 21% in the patella, femur and tibia. MRI is available for measuring cartilage volume during growth, functional adaptation, and tissue loss in degenerative joint disease. The study shows that a wide variation of cartilage volumes exists in the knee joints of normal adults. To reduce the variability between individuals, the cartilage volumes may be normalised to the head of the tibial diameter.

Adult↗
PubMed2004

Involvement of ATP, increase of intracellular calcium and the early expression of c-fos in the repair of rat fetal articular cartilage.

To compare the potential of adult and fetal animals to repair articular cartilage, we investigated the early process after creating superficial defects in the femoral knee cartilage in rat models. In fetuses at 19 days of gestation, both chondrocytes and the extracellular matrix responded notably by 48 h after artificial injury. Staining patterns with safranin O revealed that, by 1 h after injury, some components of the extracellular matrix around the wound were modified, and the change spread from the limited region to the entire knee cartilage within 24 h. The chondrocytes in the area surrounding the wound transiently expressed increased level of c-fos from 1 h to 6 h. The wound remained 1 day after birth, i.e., 72 h after injury, but was completely repaired 10 days after birth. In contrast, neither visible responses nor transient c-fos expression was observed in 12-week-old adult articular cartilage 48 h after injury. We also examined the relationships between the intracellular Ca2+ concentration ([Ca2+]i) and the induction of c-fos expression in the cartilage. Applications of ATP or Ca2+ ionophore A23187, both of which increase [Ca2+]i, induced immediate expression of c-fos in primary cultured chondrocytes: 1 microM ATP elicited an increase of [Ca2+]i in chondrocytes in fetal cartilage slices, but 1 mM was required in adult cartilage slices. Our findings show the presence of a signaling pathway that is apparently active in the repair of fetal but not adult articular cartilage and that involves the intercellular transfer of ATP, increase of [Ca2+]i, and expression of c-fos in cartilage.

Adenosine Triphosphate↗
PubMed2005

In vitro cartilage formation of composites of synovium-derived mesenchymal stem cells with collagen gel.

Graft implantation is one of the more popular procedures for repairing cartilage defects; however, sacrifices of the donor site have been an issue. Mesenchymal stem cells (MSCs) are a fascinating source for regenerative medicine because they can be harvested in a less invasive manner and are easily isolated and expanded, with multi-potentiality including chondrogenesis. MSCs can be isolated from various adult mesenchymal tissues including synovium. Here, we attempted to form cartilage from the composites of synovium-derived MSCs with collagen gel in vitro. After 21 days of culture, the composites had increased their cartilage matrix, as demonstrated by toluidine blue staining and immunohistochemistry for type II collagen. The composites consisting of 5 x 10(7) and 10(8) cells/ml in gel were richer in proteoglycans than those consisting of lower cell densities. After 1 day, MSCs/gel composites contracted and the diameter decreased by 30%; however, they were stable thereafter. Round cells with short processes producing collagen fibrils showing a similar morphology to that of chondrocytes were seen in the composites by transmission electron microscopy. During composite culture, chondroitin sulfate and mRNA expression for cartilage-related genes increased, demonstrating cartilage maturation. Using an optimized method, we obtained cartilage discs with a diameter of 7 mm and a thickness of 500 microm. Our procedure should thus make it possible to produce a large cartilage matrix in vitro. The tissue engineering of autologous cartilage from the composites of synovium-derived MSCs with collagen gel in vitro for transplantation may be a future alternative to graft implantation for patients with cartilage defects.

Adult↗