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PubMed1994

Desepiphysiodesis--elimination of partial premature epiphyseal closure. Experience of 17 cases.

Between 1975 and 1990, 17 growth plates have been operated on by epiphyseal bridge resection. The children were from 4 years and 10 months to 13 years and 10 months old. The etiology of partial closure was traumatic (10 times), caused by therapeutic mistakes (3 times), septic osteomyelitis (1 case), purpura fulminans (1 case), unknown (2 cases). There was always length discrepancy or deformity of bone. The regions that have been subjected to treatment were distal femur, proximal tibia, distal tibia, distal radius. Evaluation of the bone bridge was made by tomoscintigraphies and recently by MR imaging and computed tomoscintigraphy. The bone bridge size was from 2.5% to 60% of the growth plate surface; surgical technique consists of resection of bone bridge connecting epiphysis and metaphysis which is replaced by methyl metacrylate. In 16 cases simultaneous corrective osteotomy was performed. Results are poor, there were only two good results and 8 failures; seven results were medium. The failures can all be explained by mistakes in technique or indication, except one. Indications are post-traumatic narrow bridges in young children. It would be useful to know the vitality of the residual growth plate.

Adolescent↗
PubMed2000

Mutations in cartilage oligomeric matrix protein causing pseudoachondroplasia and multiple epiphyseal dysplasia affect binding of calcium and collagen I, II, and IX.

Mutations in type 3 repeats of cartilage oligomeric matrix protein (COMP) cause two skeletal dysplasias, pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED). We expressed recombinant wild-type COMP that showed structural and functional properties identical to COMP isolated from cartilage. A fragment encompassing the eight type 3 repeats binds 14 calcium ions with moderate affinity and high cooperativity and presumably forms one large disulfide-bonded folding unit. A recombinant PSACH mutant COMP in which Asp-469 was deleted (D469 Delta) and a MED mutant COMP in which Asp-361 was substituted by Tyr (D361Y) were both secreted into the cell culture medium of human cells. Circular dichroism spectroscopy revealed only small changes in the secondary structures of D469 Delta and D361Y, demonstrating that the mutations do not dramatically affect the folding and stability of COMP. However, the local conformations of the type 3 repeats were disturbed, and the number of bound calcium ions was reduced to 10 and 8, respectively. In addition to collagen I and II, collagen IX also binds to COMP with high affinity. The PSACH and MED mutations reduce the binding to collagens I, II, and IX and result in an altered zinc dependence. These interactions may contribute to the development of the patient phenotypes and may explain why MED can also be caused by mutations in collagen IX genes.

Achondroplasia↗
PubMed2002

Effects of cyclophosphamide on the femoral epiphyseal growth plate in young Sprague-Dawley rats.

The purpose of this study was to assess the effects of cyclophosphamide on cartilaginous growth and differentiation. Cyclophosphamide is a drug commonly used in the treatment of neoplastic diseases and in preparation for bone marrow transplantation. Eighteen Sprague-Dawley rats divided into control and experimental groups received 2 i.p. injections of either saline or cyclophosphamide (30 mg/kg) with a 3-day interval starting from day 10 after birth. Effects on the proximal femoral epiphyses were evaluated histomorphometrically as well as semi-quantitatively at day 31 after birth. Results showed a significant reduction in length of the cyclophosphamide-treated femora compared to the controls. This could be attributed to a significant reduction in the thickness of the growth zone. Cell differentiation throughout the growth plates was clearly disturbed, involving nesting of cells, loss of polarity, and impaired maturation as seen by areas of excessive hyalinization. Although the effects of cyclophosphamide on the growth plates were significant compared to controls, the changes were not as extensive as previous reports have indicated. This could be attributed primarily to the fact that a comparatively low dose of the drug was used in the present study. Also, a period of recovery was allowed prior to evaluation. Nevertheless, significant effects remained which should be considered when treating young children with cyclophosphamide.

Animals↗
PubMed1982

Infectious epiphysitis and valvular endocarditis in a red deer (Cervus elaphus).

A 10-month-old male red deer (Cervus elaphus) was presented with severe lameness and enlargement of the fetlock areas of both front and one hind legs. Radiographs demonstrated an epiphysitis and osteomyelitis of the distal metacarpal and metatarsal bones. Post mortem revealed pus containing Corynebacterium pyogenes and Staphylococcus aureus in the lesions, and an accompanying valvular endocarditis of the right atrioventricular valve.

Journal Article↗
PubMed2006

Review of the effects of anti-angiogenic compounds on the epiphyseal growth plate.

The formation of new blood vessels from a pre-existing vascular bed, termed "angiogenesis," is of critical importance for the growth and development of the animal since it is required for the growth of the skeleton during endochondral ossification, development and cycling of the corpus luteum and uterus, and for the repair of tissues during wound healing. "Vasculogenesis," the de novo formation of blood vessels is also important for the proper function and development of the vascular system in the embryo. New blood vessel formation is a prominent feature and permissive factor in the relentless progression of many human diseases, one of the most important examples of which is neoplasia. It is for this reason that angiogenesis is considered to be one of the hallmarks of cancer. The development of new classes of drugs that inhibit the growth and proper functioning of new blood vessels in vivo is likely to provide significant therapeutic benefit in the treatment of cancer, as well as other conditions where angiogenesis is a strong driver to the disease process. During the preclinical safety testing of these drugs, it is becoming increasingly clear that their in vivo efficacy is reflected in the profile of "expected toxicity" (resulting from pharmacology) observed in laboratory animals, so much so, that this profile of "desired" toxicity may act as a signature for their anti-angiogenic effect. In this article we review the major mechanisms controlling angiogenesis and its role during endochondral ossification. We also review the effects of perturbation of endochondral ossification through four mechanisms-inhibition of vascular endothelial growth factor (VEGF), pp60 c-Src kinase and matrix metalloproteinases as well as disruption of the blood supply with vascular targeting agents. Inhibition through each of these mechanisms appears to have broadly similar effects on the epiphyseal growth plate characterised by thickening due to the retention of hypertrophic chondrocytes resulting from the inhibition of angiogenesis. In contrast, in the metaphysis there are differing effects reflecting the specific role of these targets at this site.

Angiogenesis Inhibitors↗
PubMed1983

An effect of parathyroid hormone on the epiphyseal plate and osteoblasts: studies towards a cytochemical bioassay.

There are reports of an apparent dissociation between the responses of kidney and bone to parathyroid hormone (PTH): certain fragments or analogues have been shown to have differential activity in these two tissues. Consequently, cytochemical bioassay techniques have been applied to the development of an assay for PTH using the epiphyseal plate of the rat metatarsal as the target organ. Glucose 6-phosphate dehydrogenase activity in the zone of hypertrophic cartilage is stimulated in a log-linear fashion with increasing concentrations of parathyroid hormone over the range 0.001 - 1.0 pg/ml. A parallel response was found in the osteoblasts of the metaphysis. Measurements of a normal and a hyperparathyroid plasma sample showed good parallelism to the standard graph and good discrimination. Addition of a PTH - specific antibody inhibited both the effect of the standard preparation of the hormone, and the response induced by dilutions of a normal plasma.

Animals↗
PubMedDate not supplied

Review: clinical variability and genetic heterogeneity in multiple epiphyseal dysplasia.

This review reports on multiple epiphyseal dysplasia (MED), first described clinically in the early part of the 20th century. Over 50 years later, we are now beginning to unravel the mystery behind the genetic mutations involved in triggering the changes in cartilage observed in this condition. In the past decade considerable progress has been made in identifying the underlying genetic defect in some forms of MED. Understanding the precise effect that these molecular changes have on the integrity of the cartilage extracellular matrix will lead the way in identifying the complex disease pathophysiology that defines MED. In addition, a greater understanding of the role and interactions of specific cartilage molecules may reveal the basis of more widespread cartilage disorders such as osteoarthritis.

Animals↗
PubMed1998

Diverse mutations in the gene for cartilage oligomeric matrix protein in the pseudoachondroplasia-multiple epiphyseal dysplasia disease spectrum.

Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are autosomal dominant osteochondrodysplasias that result in mild to severe short-limb dwarfism and early-onset osteoarthrosis. PSACH and some forms of MED result from mutations in the gene for cartilage oligomeric matrix protein (COMP; OMIM 600310 [http://www3.ncbi.nlm. nih.gov:80/htbin-post/Omim/dispmim?600310]). We report the identification of COMP mutations in an additional 14 families with PSACH or MED phenotypes. Mutations predicted to result in single-amino acid deletions or substitutions, all in the region of the COMP gene encoding the calmodulin-like repeat elements, were identified in patients with moderate to severe PSACH. We also identified within this domain a missense mutation that produced MED Fairbank. In two families, one with mild PSACH and the second with a form of MED, we identified different substitutions for a residue in the carboxyl-terminal globular region of COMP. Both the clinical presentations of these two families and the identification of COMP-gene mutations provide evidence of phenotypic overlap between PSACH and MED. These data also reveal a role for the carboxyl-terminal domain in the structure and/or function of COMP.

Achondroplasia↗
PubMed1999

COL9A3: A third locus for multiple epiphyseal dysplasia.

Multiple epiphyseal dysplasia (MED), an autosomal dominant osteochondrodysplasia, is a clinically and genetically heterogeneous disorder characterized by mild short stature and early-onset osteoarthritis. The phenotypic spectrum includes the mild Ribbing type, the more severe Fairbank type, and some unclassified forms. Linkage studies have identified two loci for MED. One of these, EDM1, is on chromosome 19, in a region that contains the cartilage oligomeric matrix protein (COMP) gene. Mutations have been identified in this gene in patients with the Ribbing type, the Fairbank type, and unclassified forms of MED. The second locus, EDM2, maps to chromosome 1, in a region spanning COL9A2. Recently, a splice-site mutation was found in COL9A2, causing skipping of exon 3 in one family with MED. Because of the exclusion of the EDM1 and EDM2 loci in some families, the existence of a third locus has been postulated. We report here one family with MED, evaluated clinically and radiologically and tested for linkage with candidate genes, including COMP, COL9A1, COL9A2, and COL9A3. No linkage was found with COMP, COL9A1, or COL9A2, but an inheritance pattern consistent with linkage was observed with COL9A3. Mutation analysis of COL9A3 identified an A-->T transversion in the acceptor splice site of intron 2 in affected family members. The mutation led to skipping of exon 3 and an in-frame deletion of 12 amino acid residues in the COL3 domain of the alpha3(IX) chain and thus appeared to be similar to that reported for COL9A2. This is the first disease-causing mutation identified in COL9A3. Our results also show that COL9A3, located on chromosome 20, is a third locus for MED.

Adolescent↗
PubMed2001

A mutation in COL9A1 causes multiple epiphyseal dysplasia: further evidence for locus heterogeneity.

Multiple epiphyseal dysplasia (MED) is an autosomal dominantly inherited chondrodysplasia. It is clinically highly heterogeneous, partially because of its complex genetic background. Mutations in four genes, COL9A2, COL9A3, COMP, and MATR3, all coding for cartilage extracellular matrix components (i.e., the alpha2 and alpha 3 chains of collagen IX, cartilage oligomeric matrix protein, and matrilin-3), have been identified in this disease so far, but no mutations have yet been reported in the third collagen IX gene, COL9A1, which codes for the alpha1(IX) chain. MED with apparently recessive inheritance has been reported in some families. A homozygous R279W mutation was recently found in the diastrophic dysplasia sulfate transporter gene, DTDST, in a patient with MED who had a club foot and double-layered patella. The series consisted of 41 probands with MED, 16 of whom were familial and on 4 of whom linkage analyses were performed. Recombination was observed between COL9A1, COL9A2, COL9A3, and COMP and the MED phenotype in two of the families, and between COL9A2, COL9A3, and COMP and the phenotype in the other two families. Screening of COL9A1 for mutations in the two probands from the families in which this gene was not involved in the recombinations failed to identify any disease-causing mutations. The remaining 37 probands were screened for mutations in all three collagen IX genes and in the COMP gene. The probands with talipes deformities or multipartite patella were also screened for the R279W mutation in DTDST. The analysis resulted in identification of three mutations in COMP and one in COL9A1, but none in the other two collagen IX genes. Two of the probands with a multipartite patella had the homozygous DTDST mutation. The results show that mutations in COL9A1 can cause MED, but they also suggest that mutations in COL9A1, COL9A2, COL9A3, COMP, and DTDST are not the major causes of MED and that there exists at least one additional locus.

Adolescent↗
PubMed2003

Homozygous mutations in IHH cause acrocapitofemoral dysplasia, an autosomal recessive disorder with cone-shaped epiphyses in hands and hips.

Acrocapitofemoral dysplasia is a recently delineated autosomal recessive skeletal dysplasia, characterized clinically by short stature with short limbs and radiographically by cone-shaped epiphyses, mainly in hands and hips. Genomewide homozygosity mapping in two consanguineous families linked the locus to 2q35-q36 with a maximum two-point LOD score of 8.02 at marker D2S2248. Two recombination events defined the minimal critical region between markers D2S2248 and D2S2151 (3.74 cM). Using a candidate-gene approach, we identified two missense mutations in the amino-terminal signaling domain of the gene encoding Indian hedgehog (IHH). Both affected individuals of family 1 are homozygous for a 137C-->T transition (P46L), and the three patients in family 2 are homozygous for a 569T-->C transition (V190A). The two mutant amino acids are strongly conserved and predicted to be located outside the region where brachydactyly type A-1 mutations are clustered.

Animals↗
PubMed1992

The use of avian epiphyseal chondrocytes for in vitro studies of skeletal metabolism.

Chondrocytes from the postembryonic avian epiphyseal growth plate are easily obtained and can be successfully cultured for a considerable length of time. Under the proper culture conditions, the chondrocytes will become confluent and achieve a hypertrophic morphology followed by mineralization of the extracellular matrix. Although this can be accomplished with a serum-free medium, the process is accelerated in the presence of serum. Minimal growth factor requirements for the serum-free medium include fibroblast growth factor and insulin-like growth factor. Transforming growth factor-beta and parathyroid hormone are also mitogenic for chondrocytes. Chondrocytes may have more critical requirements for amino acids because further supplementation of a conventional medium such as Dulbecco's modified Eagle's medium results in improved performance of the cultured cells. Ascorbic acid in the medium is very important for matrix vesicle production and mineralization of cartilage nodules.

Animals↗
PubMed2002

Short-term zinc deficiency inhibits chondrocyte proliferation and induces cell apoptosis in the epiphyseal growth plate of young chickens.

The purpose of this study was to investigate the effect of zinc deficiency on chondrocyte proliferation, differentiation and apoptosis in the epiphyseal growth plate of juvenile chickens. Newly hatched broiler chickens were fed either a low zinc (10 mg/kg diet) or a zinc-adequate (68 mg/kg diet) soy protein-based purified diet. Cell proliferation in the growth plate was evaluated with bromodeoxyuridine (BrdU) labeling. Apoptosis was assessed using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method. Chondrocyte differentiation was evaluated with immunostaining of osteonectin as a marker of maturation. As early as d 3 of feeding, zinc deficiency significantly inhibited chondrocyte proliferation, promoted cell differentiation and induced cell apoptosis in the growth plate. These effects were manifested primarily in areas remote from the blood supply. Immunostaining for local growth factors such as insulin-like growth factor-1 (IGF-1), parathyroid hormone-related protein (PTHrP) and fibroblast growth factor-2 (FGF-2) did not reveal any differences between growth plates of zinc-deficient and zinc-adequate chickens after 3 d of feeding. By d 7, severe growth plate lesions characterized by reduced cellularity and abnormally shaped cells were formed in areas remote from blood vessels. Immunoreactive IGF-1, PTHrP and FGF-2 were all greatly reduced in the lesion. However, the growth rate and food intake of zinc-deficient chickens were not different from those of the controls during the 7-d experiment. Therefore, a direct effect of zinc deficiency on proliferation, differentiation, and apoptosis of growth plate chondrocytes was indicated.

Animals↗
PubMed1979

Multiple epiphyseal dysplasia: a family study.

Three generations of a single family exhibited evidence of multiple epiphyseal dysplasia. The distribution of involvement was entirely consistent with an autosomal dominant mode of inheritance. The family was characterized by premature osteoarthrosis of the hips developing in adolescence or early adulthood. In most patients there were no obvious signs of an underlying anomaly and the diagnosis was not recognized for a long time. Eventual diagnosis of the disorder allowed easy genetic counselling.

Adolescent↗
PubMedDate not supplied

Chondrocyte-to-osteocyte transformation in grafts of perichondrium-free epiphyseal cartilage.

When perichondrium-free pieces of embryonic quail epiphyseal cartilage are incubated on the chorioallantoic membranes of chick embryos, 2 developmental changes are observed. First, most grafts develop a periosteum in which the osteoblasts and osteocytes are of donor, i.e., chondrocytic origin. No such periosteum is observed around explants of demineralized, inductive bone matrix. Second, the matrix surrounding some chondrocytes within the original graft became more bone-like with respect to staining pattern, birefringence and collagen morphology. We conclude that, under some conditions, the avian chondrocyte may in situ or subsequent to release from the cartilage lacuna synthesize a bone-like matrix and, in this sense, be thought to have undergone a "transformation" into an osteocytic or osteoblastic type of cell.

Allantois↗
PubMedDate not supplied

"Functional retroversion" of the femoral head in Legg-Calvé-Perthes disease and epiphyseal dysplasia: analysis of head-neck deformity and its effect on limb position using three-dimensional computed tomography.

We studied femoral head and neck deformity in Legg-Calvé-Perthes disease (LCPD) and epiphyseal dysplasia using three-dimensional computed tomography (3DCT) in 17 patients (22 hips). The deformed femoral head can be divided into two portions: (i) the portion that protrudes anterolaterally and inferiorly (false head), often blocking internal rotation (lower margin is radiographic "sagging rope" sign) and (ii) the posteromedial superior portion (true head), representing the original articulating femoral head. This remodeled segment is retroverted in relation to the anterolateral segment resulting in "functional retroversion," which causes an externally rotated gait. This position also produces "functional coxa vara" measured by the relationship with the greater trochanter. These studies contradict previous reports of increased anteversion in LCPD and explain the paradox of supposed increased anteversion on radiograph in a child who walks with the limb externally rotated.

Adolescent↗
PubMedDate not supplied

Surgical correction of "functional retroversion" and "functional coxa vara" in late Legg-Calvé-Perthes disease and epiphyseal dysplasia: correction of deformity defined by new imaging modalities.

We studied six patients with severe femoral head deformity treated surgically by valgus-flexion-internal-rotation femoral osteotomy plus simultaneous acetabuloplasty based on the concept of "functional retroversion" and "functional coxa vara" of the deformed femoral head in late severe Legg-Calvé-Perthes disease and epiphyseal dysplasia. The combined procedure achieves the following: (i) corrects the "functional coxa vara" and hinge abduction (valgus osteotomy); (ii) establishes a more normal articulation between the posteromedial portion of the true femoral head and the acetabulum, while moving the anterolateral protruding portion of the femoral head away from the anterolateral acetabular margin (valgus-flexion osteotomy); (iii) corrects external-rotation deformity of the distal limb (internal-rotation osteotomy); (iv) improves joint congruity and anterolateral femoral-head coverage in hips with associated acetabular dysplasia (acetabuloplasty).

Adolescent↗
PubMedDate not supplied

Epiphyseal stapling and recombinant human growth hormone for correction of genu valgum in children with chronic renal insufficiency.

Genu valgum (GV) and growth retardation are known complications of chronic renal insufficiency (CRI) in children. Physeal stapling is the preferred method for GV correction, provided epiphyseal growth continues after stapling. Growth retardation in these children thus renders this mode of therapy unreliable. The only alternative is corrective osteotomy with the associated risks, such as non-union of bone and recurrence. The authors sought to determine if recombinant human growth hormone (rhGH) administered after stapling can bring about continued physeal growth needed for correction. The medical records of five patients with CRI, GV, and growth retardation who had physeal stapling performed and received rhGH were reviewed. Resolution of GV and improvement in linear height was achieved in four patients within 2 years. The authors conclude that children with CRI, growth retardation, and moderate GV benefit from the simultaneous use of rhGH and knee stapling for correction of GV, thus avoiding osteotomies.

Adolescent↗