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PubMed2007

Microvascular transplantation of epiphyseal plates: studies utilizing allograft donor material.

Compromised function of an epiphyseal plate caused by trauma, tumor, infection, or congenital malformation can result in significant musculoskeletal deformity. Techniques used to correct or minimize the extent of these deformities include autogenous or allogeneic cancellous bone grafts, nonvascularized cortical allografts, vascularized bone and composite tissue transfers, and distraction osteogenesis. These solutions are not ideal for children because they do not adequately address the actively growing nature of the extremity. Microvascular techniques have enabled the experimental transplantation of vascularized epiphyseal plates with high levels of postoperative viability and subsequent growth and offer a potential advantage over conventional treatments.

Animals↗
PubMed1990

Congenital rubella syndrome associated with calcific epiphyseal stippling and peroxisomal dysfunction.

An infant girl had the clinical and immunologic findings of congenital rubella syndrome but also had arthrogryposis multiplex and calcific epiphyseal stippling. Spastic quadriparesis developed, and both physical and behavioral development were slow. Increased spasticity of the legs at 5 1/2 years was related not to progressive rubella encephalomyelopathy but to spinal cord compression by abnormal cartilaginous tissue. The presence of a peroxisomal disorder was demonstrated by a greatly increased level of phytanic acid and slightly increased levels of hexacosanoate in serum and by reduced activity of peroxisomal dihydroxyacetone phosphate acyltransferase and a slightly increased ratio of cytosolic to peroxisomal catalase activity in cultured fibroblasts. A reduction in the number and size of peroxisomes was demonstrated in cultured fibroblasts, and a needle biopsy specimen of the liver also showed the peroxisomes to have a smaller diameter than usual. We recommend that any child with epiphyseal stippling be assessed for peroxisomal disease and that the potential for spinal cord compression by dysplastic bone or cartilage be recognized. The association of peroxisomal dysfunction with congenital rubella has not been described previously. The interaction between rubella virus infection and peroxisomal function may need further investigation.

Calcinosis↗
PubMed1997

Simultaneous demonstration of alkaline and acid phosphatase activity in bone, at bone-implant interfaces and at the epiphyseal growth plate in plastic-embedded undemineralized tissues.

The aim of the present study was to determine if it was possible to detect in bone, at the epiphyseal growth plate and at the bone-implant interface, the presence of alkaline and acid phosphatases using Technovit 7200 VLC resin. In the plastic-embedded specimens it was possible to observe the simultaneous presence of acid and alkaline phosphatases at the epiphyseal growth plate in the presence of intra-articular implants. The morphology of the cells positive for the phosphatases was very clear, with no apparent diffusion of the reaction product and no sputter ground staining.

Acid Phosphatase↗
PubMed1992

Changes in rat epiphyseal cartilage after treatment with dexamethasone and glycosaminoglycan-peptide complex.

In 3-month-old rats, systemic administration of glucocorticosteroids induced regressive changes in the epiphyseal plate cartilage. Dexamethasone treatment resulted in inhibition of both chondrocyte proliferation and cartilage matrix production. The inhibition of chondrocyte proliferation was determined histologically from the thickness of the epiphyseal plate, the number of cell columns and the ratio of proliferating to hypertrophied chondrocytes. The decrease in cartilage matrix production was measured autoradiographically by incorporation of radioactive 35S-sulphate. Concomitant treatment with glycosaminoglycan-peptide complex (GP-C = RUMALON) overcame the negative effect of dexamethasone. The values in the dexamethasone + GP-C group approached those of the control group and differed significantly from the group given dexamethasone alone.

Animals↗
PubMed1990

Quantifying the effect of ischemia on epiphyseal growth in an extremity replant model.

Warm ischemia (21 degrees C) of 0, 2, 4, 6, or 8 hours was produced in a modified hindlimb preparation of 35 10-week-old Lewis rats by amputation. Subsequent microvascular anastomoses of each hindlimb to a syngeneic animal was done after which fluorochrome bone labels were administered 5 minutes after operation and on day 14 after operation. Epiphyseal plate growth (that between bone labels) was analyzed histomorphometrically and statistically. Epiphyseal plate growth was found to have a linear inverse relationship to ischemia time with a correlation coefficient (r) of -0.653 and high statistical significance (p less than 0.001). Overgrowth occurred at all ischemic periods except 8 hours, and vascular pedicle patency decreased as ischemia time progressed.

Anastomosis, Surgical↗
PubMed1988

An electron microscopic and spectroscopic study of murine epiphyseal cartilage: analysis of fine structure and matrix vesicles preserved by slam freezing and freeze substitution.

Newborn mice epiphyseal growth plates were preserved by slam freezing/freeze substitution and examined by conventional electron microscopy, stereopsis, high voltage electron microscopy, and electron spectroscopic imaging (ESI). To illustrate the improved ultrastructure of this cryogenic procedure, conventional, aqueously fixed growth plates were included showing collapsed hypertrophic chondrocytes surrounded by a depleted and condensed extracellular matrix. In contrast, the cryogenically prepared epiphyses contain chondrocytes and extracellular matrix vesicles both in direct contact with proteoglycan filaments retained in an expanded state. ESI is an electron microscopic technique which enables the direct localization of atomic elements superimposed over fine structural details. This technique was used to examine the colocalization of calcium and phosphorus within matrix vesicles and within their associated extracellular environments. Matrix vesicles appeared in three distinct diameter ranges. The integrity of the matrix vesicles was examined at various stages of mineralization and also within the mineralized zone of provisional calcification.

Animals↗
PubMed2000

Exon skipping mutation in the COL9A2 gene in a family with multiple epiphyseal dysplasia.

Previous linkage analysis (Briggs, M.D., Choi, H.-C., Warman, M.L. et al., 1994. Genetic mapping of a locus for multiple epiphyseal dysplasia (EDM 2) to a region of chromosome 1 containing a type IX collagen gene. Am. J. Hum. Genet. 55, 678-684) in a large English family with multiple epiphyseal dysplasia established the EDM2 locus, a region of chromosome 1 containing the COL9A2 collagen gene. We now report that affected members of this family are heterozygous for a single base transversion (T-->G) at the sixth position of the intron 3 splice donor of COL9A2. The mutation leads to skipping of exon 3 during splicing, and results in a 36-nucleotide deletion in COL9A2 transcripts derived from the mutant allele. Skipping of exon 3 predicts an in-frame deletion of 12 amino acid residues within the COL3 domain of the alpha2(IX) chain. This is the fifth instance of an exon 3 deletion within the COL3 region of collagen IX heterotrimers causing the MED phenotype, as yet the only type IX collagen defect identified in this disorder. Electron microscopy (EM) of chondrocytes obtained from articular cartilage of one affected individual in the family demonstrated normal appearing rough endoplasmic reticulum (RER). In addition, the articular cartilage matrix did not show any gross abnormalities in the quantity or caliber of collagen fibrils.

Alleles↗
PubMed1999

c-Myc and Mxi1 immunoreactivities in the calcifying areas of the epiphyseal-plate cartilage matrix of growing rats.

We looked for the protooncogene protein, c-Myc, its dimerization partner, Max, and the repressors of its transactivation activity, Mad1 and Mxi1, in the epiphyseal-plate cartilage matrix of growing rats by immunocytochemistry in the electron microscope. c-Myc and Mxi1 immunoreactivities were found in the calcifying areas of the cartilage matrix only. There was no immunolabeling in response to anti-Max or anti-Mad1 antibodies. Mxi1 immunoreactivity was mainly in the early calcifying areas, in the calcification front and ahead of it, whereas c-Myc immunoreactivity was essentially in the incompletely calcified regions of the matrix. The two immunolabelings occurred mainly over the large type II collagen fibrils of the cartilage matrix and over the thin filaments connecting them. c-Myc and Mxi1 immunoreactivities were rarely found along the dark cristallites. There was no immunolabeling associated with the matrix vesicles, or in their immediate surroundings. The data suggest that the protooncogene proteins, c-Myc and Mxi1, could be implicated in the calcification involving type II collagen fibrils of the epiphyseal-plate cartilage. The absence of Max immunoreactivity from the calcifying cartilage matrix raises the question of whether there are other c-Myc- and Mxi1-dimerization partners.

Animals↗
PubMed2001

Mutations in the region encoding the von Willebrand factor A domain of matrilin-3 are associated with multiple epiphyseal dysplasia.

Multiple epiphyseal dysplasia (MED) is a relatively mild and clinically variable osteochondrodysplasia, primarily characterized by delayed and irregular ossification of the epiphyses and early-onset osteoarthritis. Mutations in the genes encoding cartilage oligomeric matrix protein (COMP) and type IX collagen (COL9A2 and COL9A3) have previously been shown to cause different forms of MED (refs. 4-13). These dominant forms of MED (EDM1-3) are caused by mutations in the genes encoding structural proteins of the cartilage extracellular matrix (ECM); these proteins interact with high affinity in vitro. A recessive form of MED (EDM4) has also been reported; it is caused by a mutation in the diastrophic dysplasia sulfate transporter gene (SLC26A). A genomewide screen of family with autosomal-dominant MED not linked to the EDM1-3 genes provides significant genetic evidence for a MED locus on the short arm of chromosome 2 (2p24-p23), and a search for candidate genes identified MATN3 (ref. 18), encoding matrilin-3, within the critical region. Matrilin-3 is an oligomeric protein that is present in the cartilage ECM. We have identified two different missense mutations in the exon encoding the von Willebrand factor A (vWFA) domain of matrilin-3 in two unrelated families with MED (EDM5). These are the first mutations to be identified in any of the genes encoding the matrilin family of proteins and confirm a role for matrilin-3 in the development and homeostasis of cartilage and bone.

Adult↗
PubMed1990

Vesicles with lactate dehydrogenase and without alkaline phosphatase present in the resting zone of epiphyseal cartilage.

Matrix vesicles are membrane-invested vesicles that initiate mineralization in the extracellular matrix of calcifying tissues. The epiphyseal cartilages of young-rat rib bones were divided into the growth zone and the resting zone, followed by the isolation of matrix vesicles after collagenase treatment. Matrix vesicles with both alkaline phosphatase and lactate dehydrogenase were detected in the growth cartilage found in the epiphyseal growth plates of young rabbits [Hosokawa, Uchida, Fujiwara & Noguchi (1988) J. Biol. Chem. 263, 10045-10047], but were not detected in the resting zone. By contrast, and surprisingly, lactate dehydrogenase-containing vesicles without alkaline phosphatase were found in the resting zone, but not in the growth zone. In both the growth and resting zones, isoenzyme patterns of lactate dehydrogenase in the two different vesicles were identical with those of cytosolic lactate dehydrogenase of chondrocytes, suggesting the presence of a mechanism for specific uptake of cytosolic lactate dehydrogenase. The same results as for young-rat rib bones were obtained with the resting and growth cartilages of young-dog and monkey rib bones.

Alkaline Phosphatase↗
PubMed1999

The epiphyseal cartilage and growth of long bones in Rana catesbeiana.

The structure of the epiphyseal cartilage of the bullfrog Rana catesbeiana and its role in the growth of long bones were examined. The epiphyseal cartilage was inserted into the end of a tubular bone shaft, defining three regions: articular cartilage, lateral articular cartilage and growth cartilage. Joining the lateral cartilage to the bone was a fibrous layer of periosteum, rich in blood vessels. Osteoblasts with alkaline phosphatase activity were found on the surface of the periosteal bone, which presented a fibrous non-mineralised tip. The growth cartilage was inside the bone. The proliferative chondrocytes presented perpendicular separation of daughter cells and there was no columnar arrangement of the cells. Furthermore, chondrocyte hypertrophy was not associated with either calcification or endochondral ossification, in apparent contrast to the avian and mammalian models. Finally, there was no reinforcement system capable of directing cell volume increase into longitudinal growth. Since bone extension depends on the intramembranous ossification of the periosteum, the growth cartilage is inside and not at the end of the bone and the cells in the growth cartilage show no columnar arrangement and separate in a direction perpendicular to the long bone axis, we conclude that the growth cartilage mainly contributes to the radial expansion of the bone.

Animals↗
PubMed2005

Role of simple cold storage in preventing epiphyseal growth plate impairment after replantation surgery in immature rats.

The purpose of this study was to investigate the effect of ischemia time on longitudinal bone growth after replantation, and to evaluate the usefulness of simple cold storage of an amputated limb in preventing epiphyseal growth-plate impairment. A hind-limb replantation model was produced with 5-week-old rats after various ischemia times. With more than 6 hr of warm ischemia, growth disturbance was observed, and extensive necrosis was histologically apparent in the central region of the growth plate of the proximal tibia, even at 1 week postoperatively. Destruction of the growth plate was complete at 4 weeks after surgery. By simple cold storage of the amputated limb, growth disturbance was not observed, even following ischemia for 9 hr, and no abnormal findings were observed histologically. Segmental necrosis and destruction of the growth plate observed histologically suggested the possibility of indirect impairment of the epipyseal chondrocytes due to disturbance of the epiphyseal arterial system, attributable to ischemia. The study confirmed experimentally that cold storage of the amputated part may prevent longitudinal bone-growth disturbance after extension of ischemia time.

Amputation, Traumatic↗
PubMed2000

A mutation in the alpha 3 chain of type IX collagen causes autosomal dominant multiple epiphyseal dysplasia with mild myopathy.

Multiple epiphyseal dysplasia (MED) is a degenerative cartilage condition shown in some cases to be caused by mutations in genes encoding cartilage oligomeric matrix protein or type IX collagen. We studied a family with autosomal dominant MED affecting predominantly the knee joints and a mild proximal myopathy. Genetic linkage to the COL9A3 locus on chromosome 20q13.3 was established with a peak log(10) odds ratio for linkage score of 3.87 for markers D20S93 and D20S164. Reverse transcription-PCR performed on the muscle biopsy revealed aberrant mRNA lacking exon 3, which predicted a protein lacking 12 amino acids from the COL3 domain of alpha3(IX) collagen. Direct sequencing of genomic DNA confirmed the presence of a splice acceptor mutation in intron 2 of the COL9A3 gene (intervening sequence 2, G-A, -1) only in affected family members. By electron microscopy, chondrocytes from epiphyseal cartilage exhibited dilated rough endoplasmic reticulum containing linear lamellae of alternating electron-dense and electron-lucent material, reflecting abnormal processing of mutant protein. Type IX collagen chains appeared normal in size and quantity but showed defective cross-linking by Western blotting. The novel phenotype of MED and mild myopathy is likely caused by a dominant-negative effect of the exon 3-skipping mutation in the COL9A3 gene. Patients with MED and a waddling gait but minimal radiographic hip involvement should be evaluated for a primary myopathy and a mutation in type IX collagen.

Cartilage↗
PubMed1998

Matrilin-3 forms disulfide-linked oligomers with matrilin-1 in bovine epiphyseal cartilage.

A comparison of noncollagenous matrix proteins from different types of bovine cartilage by SDS-polyacrylamide gel electrophoresis showed a prominent 240-kDa component in extracts of epiphyseal but not tracheal tissue. On amino-terminal sequence analysis, it gave two sequences. One matched the NH2 terminus of cartilage matrix protein (CMP) as reported for tracheal cartilage. The other did not match any known protein sequence. Further analysis of the 240-kDa protein after reduction of disulfides resolved two bands on SDS-polyacrylamide gel electrophoresis. Isolation and sequence analysis of tryptic peptides confirmed that one was bovine CMP and the other a CMP homolog. A data base search identified the latter as matrilin-3, a molecule recently predicted from human and mouse cDNA sequences (Wagener, R., Kobbe, B., and Paulsson, M. (1997) FEBS Lett. 413, 129-134). Matrilin-3 and CMP (matrilin-1) were prominent in equimolar amounts in fetal bovine epiphyseal cartilage and absent from adult articular cartilage. Adult tracheal cartilage contained almost exclusively CMP. Although the mechanism of polymeric assembly is unknown, the matrilin-3 chain appears to function in the matrix linked to matrilin-1 in the form of disulfide-bonded heteromeric molecules. The results indicate a molecular stoichiometry of (matrilin-1)2(matrilin-3)2.

Amino Acid Sequence↗
PubMed2001

Immunocytochemical demonstration of glucose transporters in epiphyseal growth plate chondrocytes of young rats in correlation with autoradiographic distribution of 2-deoxyglucose in chondrocytes of mice.

The epiphyseal growth plate, where chondrocytes proliferate and differentiate, is the major site for longitudinal bone growth, matrix synthesis and mineralization. Glucose is an important energy source for the metabolism and growth of chondrocytes. The family of facilitative glucose transporters (GLUTs) mediates glucose transport across the plasma membrane in mammalian cells. We used immunocytochemical methods with anti-GLUT antibodies to investigate the localization of GLUTs in chondrocytes of the epiphyseal growth plate in 3 age groups of rats (3, 7, and 28 days after birth). Intense immunoreactivity of GLUT isoforms 1-5 was detected in chondrocytes of 3-day and 7-day old rats, and all GLUTs were localized in the maturation zone of the hypertrophic zone. On postnatal day 28, chondrocytes in the maturation zone showed intense GLUT1, 4 and 5 immunoreactivity, and weak GLUT2 and 3 immunoreactivity. In addition to chondrocytes in the maturation zone, those in the degenerative zone and in the zone of provisional calcification showed strong GLUT4 and 5 immunoreactivity. Autoradiography of bone sections from 4-week old mice injected with 14C-2-deoxyglucose showed high silver grain density within matrix tissue in the reserve and proliferative zones but not around chondrocytes. However, in the hypertrophic zone, silver grain density was high in matrix and chondrocytes. These data indicate that chondrocytes in the hypertrophic zones use glucose as energy source. High levels of GLUT4 expression imply that glucose use in chondrocytes is regulated by insulin. Expression of GLUT5 in chondrocytes suggests that fructose is also used as an energy source.

Aging↗
PubMed1989

Comparative studies of type X collagen expression in normal and rachitic chicken epiphyseal cartilage.

The levels of type X collagen in mineralizing normal chicken epiphyses and nonmineralizing rachitic chicken tibial epiphyses were measured and compared. Qualitative immunoperoxidase studies with anti-chick type X collagen monoclonal antibodies on sections from normal and rachitic cartilage demonstrated that the type X collagen levels in rachitic growth plates are reduced. Northern hybridization of mRNA and biosynthetic studies have confirmed that type X collagen synthesis in rickets is also decreased. In hypocalcemic rickets, the level of type X collagen mRNA is reduced by 80% whereas the level of type X collagen mRNA is only reduced by 50% in normocalcemic rickets. These observations provide additional evidence that type X collagen is involved in the process of cartilage mineralization and also suggest that the partial recovery of type X collagen synthesis in normocalcemic rickets may be related to the elevated plasma concentration of calcium. Calcium concentration may therefore play an important role in the control of type X collagen synthesis.

Animals↗
PubMedDate not supplied

Remodeling of Salter-Harris type II epiphyseal plate injury of the distal radius.

The authors studied the relation between residual angulation at the time of healing and final orientation of the distal radius as well as the clinical outcome in patients after Salter-Harris type II epiphyseal plate injury of the distal radius. Eighty-five patients were reviewed with a median follow-up of 8.5 years. Anteroposterior and lateral radiographs were taken at follow-up. The mobility of both wrists and forearms was examined, together with grip strength. Pain with activities and sports was evaluated. At follow-up, 73 patients (86%) were anatomically normal on radiographs; the remaining 12 patients had an incomplete remodeling of the volar and/or radial inclination of the distal radius. Premature closure of the growth plate in the distal radius or ulna did not occur in any of these children. Complete remodeling was seen in children aged up to 10 years in all but one patient. Remodeling after Salter-Harris type II epiphyseal plate injury occurs in all age groups, but the potential is greater in children up to 10 years of age. The incomplete remodeling does not seem to have any substantial long-term negative effect on mobility of the wrist and grip strength.

Adolescent↗
PubMedDate not supplied

Three epiphyseal fractures (distal radius and ulna and proximal radius) and a diaphyseal ulnar fracture in a seven-year-old child's forearm.

SUMMARY: The authors report a rare case of fracture separations at both ends of the radius combined with an epiphyseal and diaphyseal fracture of the ipsilateral ulna. A seven-year-old girl fell one story and sustained a closed injury of her forearm. A closed reduction was unsuccessful, and an open reduction was performed with three of the four fractures being secured with Kirschner wires. These wires were removed one month later, and range-of-motion exercises were started. Thirty months after surgery, both forearms were equal in length, although the proximal radial epiphyseal line appeared partially closed. Joint motions, including forearm rotation, were normal. Radiologically, the ulnar diaphysis and the radial neck were posteriorly convex 20 degrees and 18 degrees, respectively.

Child↗