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PubMed1983

The mechanical properties of human tibial trabecular bone as a function of metaphyseal location.

Experimental determination of the elastic modulus and ultimate strength of human tibial trabecular bone as a function of metaphyseal location is presented. A 1 cm cubic matrix with planes parallel to the subchondral plate was defined on five fresh frozen cadaver tibias. Approximately 400, 7 mm X 10 mm cylindrical bone plugs were cut from the locations defined by the matrix and tested in uniaxial compressive stress at a strain rate of 0.1%S-1. Results of the study indicate that the trabecular bone properties vary as much as two orders of magnitude from one location to another. As might be predicted from Wolff's law, and noted by previous investigators, concentrations of strength arise from the medial and lateral metaphyseal cortices toward the major medial and lateral contact regions. These results may be valuable for improved analytical modeling and optimal prosthetic design.

Aged↗
PubMed1991

Mechanical properties of metaphyseal bone in the proximal femur.

We used a three-point bending test to investigate the structural behavior of 123 rectangular flat plate specimens harvested from the metaphyseal shell of the cervical and intertrochanteric regions of five fresh/frozen human proximal femora. For comparison purposes, 36 specimens of similar geometry were also fabricated from bone of the femoral diaphysis. All specimens were oriented in either the local longitudinal or transverse directions. The mean longitudinal elastic modulus was 9650 +/- 2410 (SD) MPa and demonstrated a 24% decrease from that measured for the diaphysis (12500 +/- 2140 MPa) using the same testing technique. However, the transverse elastic moduli did not differ significantly between the proximal (5470 +/- 1720 MPa) and diaphyseal (5990 +/- 1520 MPa) specimens. The globally averaged values for the ultimate tensile strengths of the metaphyseal shell were 101 +/- 26 MPa in the longitudinal and 50 +/- 12 MPa in the transverse directions. These compared with diaphyseal values of 128 +/- 16 MPa and 47 +/- 12 MPa, respectively. While these differences were largely due to the reduced density of the proximal specimens, a slight decrease in transverse anisotropy for the proximal specimens was also noted by comparing the ratio of longitudinal to transverse moduli (1.76) and tensile strength (2.02) to the diaphyseal values (2.09 and 2.71, respectively). Use of these data should lead to improved performance of analytical models for the proximal femur, and thus help focus increased attention on the structural contribution of trabecular bone to the strength and rigidity of the proximal femur.

Acrylic Resins↗
PubMed1995

Effects of on/off anabolic hPTH and remodeling inhibitors on metaphyseal bone of immobilized rat femurs. Tomographical (pQCT) description and correlation with histomorphometric changes in tibial cancellous bone.

An anabolic effect of hPTH(1-38) (s.c. doses of 200 micrograms/kg/d during 75 days) on trabecular and cortical bone mass is tomographically described in the metaphyseal region of immobilized rat femurs using pQCT technology, in agreement with previous histomorphometrical studies of the proximal tibial metaphyses. Correlations between pQCT and histomorphometrical data showed that this effect derived from a stimulation of endosteal and trabecular bone modeling that induced a transference from trabecular to cortical bone mass. Loss of effects after withdrawal, resulting from a stimulation of bone remodeling, could be total or partially prevented by subsequent s.c. injections of risedronate (5 micrograms/kg/2/wk), 17-B-estradiol (10 micrograms/kg/d) or calcitonin (10 micrograms/kg/d) given during 60 days, in this order of effectiveness. The preventive potency was proportionally related to the reduction induced in histomorphometric indices of bone resorption.

Animals↗
PubMed2005

Revision total knee arthroplasty with modular components inserted with metaphyseal cement and stems without cement.

The clinical and radiographic outcomes of 50 consecutive revision total knee arthroplasties in 47 patients, placed with metaphyseal cemented femoral and tibial components with press-fit cementless stems, were reviewed at 36-month average follow-up. Revision was performed for aseptic loosening (11/50), infection (17/50), periprosthetic fracture (8/50), component failure (6/50), instability (6/50), and malalignment (2/50). The press-fit cementless stems were 80 to 160 mm in length and tightly contacted the endosteum of the metadiaphyseal areas. Four (9%) knees were re-revised for infection, zero for aseptic loosening. The average modified Hospital for Special Surgery knee score improved from 49 to 87. One patient (2%) reported thigh pain, and 1 reported leg pain. Metaphyseal cemented revision total knee components with press-fit cementless femoral and tibial stems were not associated with significant thigh and leg pain.

Adult↗
PubMed1982

The radiological appearances of familial metaphyseal dysplasia.

Familial metaphyseal dysplasia (FMD) is a rare genetical conditional characterised by symmetrical metaphyseal splaying of the tubular bones. The diagnosis of FMD was made in four patients from two families in Japan; abnormal modelling defects were observed in the flat bones as well as tubular bones in some of the patients. In addition, quantitative measurement of the mineral content of the bone was carried out and was found to be one-quarter of the normal value.

Adult↗
PubMed2000

The use of interlocked 'customised' blade plates in the treatment of metaphyseal fractures in patients with poor bone stock.

Balanced and stable fixation in metaphyseal fractures and nonunion can be difficult because of osteoporosis, disuse osteopenia, comminution, joint proximity or malignant infiltration. Five patients with nonunion and four with comminuted or pathological acute fractures of metaphyseal areas of the tibia or humerus were treated with a 'customized' interlocked blade plate. The plates are standard AO dynamic compression plates of a suitable length that are bent to an acute angle in an industrial vice and 'interlocked'. The nine patients with a mean age of 62.2 years (range 30-91) were followed up for a mean of 7.2 months. At follow-up all fractures had healed with a single complication of subacromial impingement in a patient with a proximal humeral fracture.

Adult↗
PubMed1997

Intracranial calcifications, epilepsy, and optic atrophy associated with metaphyseal dysplasia: a case report.

A 15-year-old boy presenting with epilepsy, optic atrophy and intracranial calcifications was diagnosed as having metaphyseal dysplasia by bone X-ray examinations. The patient had no laboratory data suggesting other metabolic or endocrinologic disorders. In addition, CT scans showed unique intracranial calcifications of the corpus callosum and periventricular and subcortical white matter, which were distinct from those of previously reported disorders. This case may represent a unique subset or a new type of metaphyseal dysplasia associated with intracranial calcifications and central nervous system symptoms.

Adolescent↗
PubMed1997

Metaphyseal fibrous defect (nonossifying fibroma) in the mandible. A case report.

A 7-year-old boy presented in whom a metaphyseal fibrous defect was diagnosed. The lesion was enucleated under local anesthesia. The postoperative course was uneventful and there have been no signs of recurrence as of 14 months after operation. Although rare, metaphyseal fibrous defect should be included in the differential diagnosis of tumors arising in the jaws.

Bone Diseases, Developmental↗
PubMed1991

Ultrastructural immunolocalization of osteopontin in metaphyseal and cortical bone.

The ultrastructural localization of osteopontin in bone was determined especially focussing on the relationship to bone forming cells, i.e. osteoblasts and osteocytes. Thus, rat metaphyseal and cortical bone was fixed in a mixture of low concentration glutar- and paraformaldehyde and embedded at low temperature in Lowicryl K11M. Polyclonal antibodies raised against rat osteopontin fusion protein were incubated on ultrathin sections and protein G coated with 5-nm colloidal gold was used for detection. The results demonstrate most intensive labeling in the mineralization front of newly formed bone; whereas lower concentration of label was found in the osteoid both in metaphyseal and cortical bone. The concentration of marker was substantially higher in newly formed bone near osteoblasts compared to bone constituting the osteocyte lacuna. Intracellularly the prevailing localization of label was to large Golgi vesicles in osteoblasts. Only focally local accumulation of marker was seen at the cell/osteoid surface. The observations suggest a function of osteopontin also in the mineral turnover of newly formed bone.

Animals↗
PubMed2002

Regulation of bone volume is different in the metaphyses of the femur and vertebra of C3H/HeJ and C57BL/6J mice.

The C3H/HeJ (C3H) mice exhibited a greater bone formation rate (BFR) and a greater mineral apposition rate (MAR) in the cortical bone of the midshafts of the femur and tibia than did C57BL/6J (B6) mice. This study sought to determine if these strain-related differences would also be observed in cancellous bone. Metaphyses of the femur and lumbar vertebra (L5-6) from C3H and B6 mice, 6 and 12 weeks of age, were analyzed by histomorphometry. Similar to cortical bone, the bone volume in the femoral metaphysis of C3H mice was greater (by 54% and 65%, respectively) than that of B6 mice at both 6 and 12 weeks of age. Higher BFR and mineral apposition rate (MAR) contributed to the higher bone volume in the C3H mice compared with the B6 mice. In contrast, bone volume (by 59% and 13%, respectively, p < 0.001) and trabecular number (by 55% and 35%, respectively, p < 0.001) in the vertebrae were lower in the C3H mice than in B6 mice at 6 and 12 weeks of age. At 6 weeks of age, MAR was higher (by 43%, p = 0.004) in C3H mice, but because of a low trabecular number, the BFR (by 37%, p = 0.026) and tetracycline-labeled bone surface (by 52%, p < 0.001) per tissue were lower in the vertebrae of C3H mice than B6 mice. The low bone volume in vertebrae of C3H mice was probably not due to a higher bone resorption, because the osteoclast number (by 55%, p < 0.001) and eroded surface (by 61%, p <0.001) per tissue area in the C3H mice were also lower in B6 mice. At 12 weeks, the trabecular thickness had increased (by 36%, p < 0.001) in the C3H mice and the difference in bone volume between strains was less than that at 6 weeks. These contrasting and apparently opposing strain-related differences in trabecular bone parameters between femur and vertebra in these two mouse strains suggest that the genetic regulation of bone volume in the metaphyses of different skeletal sites is different between C3H and B6 mice.

Animals↗
PubMed2002

Gender differences in expression of androgen receptor in tibial growth plate and metaphyseal bone of the rat.

In this study, we investigate the expression of the androgen receptor (AR) in the tibial growth plate and metaphyseal bone of male and female rats at the mRNA and protein level. Using in situ hybridization and immunohistochemistry, AR mRNA and protein were demonstrated in proliferating and early hypertrophic chondrocytes in the growth plate of 1-, 4-, and 7-week-old male and female rats. Immunostaining for AR was observed both in the nucleus and the cytoplasm. After sexual maturation at 12 and 16 weeks of age, AR expression decreased in both genders and was confined to a small rim of prehypertrophic chondrocytes. In female rats of 40 weeks of age, this expression pattern was still visible. In most age groups there was a tendency toward an increased AR mRNA expression in male vs. female rats except in the 7-week-old animals. At the protein level, sexually maturing 7-week-old male rats demonstrated a higher staining intensity compared to their female counterparts. At this stage, AR staining in the males was mainly confined to the nucleus, whereas in females staining was predominantly found in the cytoplasm. In the tibial metaphysis, AR mRNA was detected in lining cells, osteoblasts, osteocytes, and osteoclasts at all stages of development. At the protein level, a similar expression pattern was observed, except for an absence of immunostaining in the lining cells. The staining was both nuclear and cytoplasmic. In most age groups, mRNA and protein signals were higher in males compared with females. We have demonstrated the presence of AR mRNA and protein in the tibial growth plate and the underlying metaphyseal bone during development of the rat. In male rats, the presence of higher messenger and protein staining intensities, as well as preferential nuclear staining during sexual maturation, suggests that direct actions of androgens in chondrocytes and in bone forming cells may be involved in establishing the gender differences in the skeleton.

Animals↗
PubMed1980

[Effect of the metaphyseal involvement in Perthes' disease and its importance for the definitive development of the head of the femur].

The article describes the effect of the metaphysical involvement in Perthes' disease on the definitive development of the head of the femur. The classification according to Eyring et al. was used as evaluation criterion. Assessment of the results was affected according to the final deformities seen in the head of the femur, as well as according to the epiphyseal quotient and the quotient of the femoral head/neck, and the degree of shortening of the leg. It was found that the severe types of metaphyseal involvement in Perthes' disease have an extremely unfavourable prognosis.

Child↗
PubMed1981

[Fibrous metaphyseal defect (fibrous cortical defect, non-ossifying fibroma) (author's transl)].

Fibrous cortical defect and non-ossifying fibromas can be classified together as fibrous metaphyseal defects (FMD) since they have the same pathological substrate, with a tendency to the same localisation around the knee, and occurring at the same age. They have a tendency to spontaneous healing, are clinically silent and are usually discovered accidentally during radiological examination. A radiological survey of 5.674 metaphyseal regions in the upper and lower extremities of 2.065 unselected patients aged one to 20 years revealed an incidence of 1.8%; exclusive examination of the distal femur showed an incidence of 2.7%. 96% of all lesions were in the lower extremities and only 4% in the upper. The marked discrepancy in the incidence rate between American and German publications is discussed.

Adolescent↗
PubMed1999

Folding and assembly of type X collagen mutants that cause metaphyseal chondrodysplasia-type schmid. Evidence for co-assembly of the mutant and wild-type chains and binding to molecular chaperones.

Schmid metaphyseal chondrodysplasia results from mutations within the COOH-terminal globular domain (NC1) of type X collagen, a short chain collagen expressed in the hypertrophic region of the growth plate cartilage. Previous in vitro studies have proposed that mutations prevent the association of the NC1 domain of constituent chains of the trimer based upon a lack of formation of a trimeric structure that is resistant to dissociation with sodium dodecyl sulfate. To examine the effect of mutations on folding and assembly within a cellular context, bovine type X cDNAs containing analogous disease causing mutations Y598D, N617K, W651R, and wild-type were expressed in semi-permeabilized cells. We assessed trimerization of the mutant chains by their ability to form a collagen triple helix. Using this approach, we demonstrate that although there is an apparent lower efficiency of association of the mutant NC1 domains, they can drive the formation of correctly aligned triple helices with the same thermal stability as the wild-type collagen. When epitope-tagged mutant and wild-type collagen were co-expressed, heterotrimers could be detected by sequential immunoprecipitation. Both wild-type and mutant type X chains were found in association with the molecular chaperones protein disulfide isomerase and Hsp 47. The implications of these findings on the likely mechanism of Schmid metaphyseal chondrodysplasia will be discussed.

Animals↗
PubMed2000

Aberrant signal peptide cleavage of collagen X in Schmid metaphyseal chondrodysplasia. Implications for the molecular basis of the disease.

Schmid metaphyseal chondrodysplasia results from mutations in the collagen X (COL10A1) gene. With the exception of two cases, the known mutations are clustered in the C-terminal nonhelical (NC1) domain of the collagen X. In vitro and cell culture studies have shown that the NC1 mutations result in impaired collagen X trimer assembly and secretion. In the two other cases, missense mutations that alter Gly(18) at the -1 position of the putative signal peptide cleavage site were identified (Ikegawa, S., Nakamura, K., Nagano, A., Haga, N., and Nakamura, Y. (1997) Hum. Mutat. 9, 131-135). To study their impact on collagen X biosynthesis using in vitro cell-free translation in the presence of microsomes, and cell transfection assays, these two mutations were created in COL10A1 by site-directed mutagenesis. The data suggest that translocation of the mutant pre-alpha1(X) chains into the microsomes is not affected, but cleavage of the signal peptide is inhibited, and the mutant chains remain anchored to the membrane of microsomes. Cell-free translation and transfection studies in cells showed that the mutant chains associate into trimers but cannot form a triple helix. The combined effect of both the lack of signal peptide cleavage and helical configuration is impaired secretion. Thus, despite the different nature of the NC1 and signal peptide mutations in collagen X, both result in impaired collagen X secretion, probably followed by intracellular retention and degradation of mutant chains, and causing the Schmid metaphyseal chondrodysplasia phenotype.

Animals↗
PubMed1957

Some aspects of the metabolism of sulfate-S35 and calcium-45 in the metaphyses of immature rats: influence of beta-estradiol benzoate.

Weanling rats were given 2 mg. of 17-beta-estradiol benzoate at weekly intervals for 4 weeks. Twenty-four hours after each intraperitoneal injection of the estrogen 100 microc. of S(35)-sulfate or 11 microc. of Ca(45) was similarly injected. The animals were sacrificed 24 hours after the last dose of isotopes. An effect of estradiol benzoate on calcium metabolism was deduced from the observation that the concentration of calcium in some tissues of the treated rats was higher than the concentration in the tissues of untreated rats. Alkaline extracts of the distal metaphyses of femurs from the estradiol-treated and from control rats, given S(35)-sulfate, were shown by chromatography on an anion exchange resin to contain from 9 to 22 per cent of the S(35) as inorganic sulfate. From similar bone samples, 6 to 21 per cent of the S(35) was removed by decalcification with sodium versenate. Most of the remaining S(35) was associated with uronic acid and hexosamine; on paper chromatograms and paper electrophoretograms S(35) was shown to be part of material which migrated and was metachromatic in the same way as purified chondroitin sulfate. Autoradiograms of the proximal ends of tibiae from the animals given estradiol benzoate showed that both the S(35) and Ca(45) were deposited in the metaphyses in strata. The arrangement of the strata of S(35), however, was different from the arrangement of the strata of Ca(45). This difference in arrangement is interpreted as indicating that most of the S(35) in the metaphysis was derived from the chondroitin sulfate of the cartilage plate which the metaphysis had replaced.

Animals↗
PubMed1994

Additional mutations of type X collagen confirm COL10A1 as the Schmid metaphyseal chondrodysplasia locus.

Type X collagen is a short chain collagen expressed in hypertrophic chondrocytes during bone growth. A 13bp deletion has been shown to segregate with Schmid metaphyseal chondrodysplasia, an autosomal dominant disorder of the osseous skeleton, in a large Mormon kindred. To increase our understanding of the role type X collagen plays in development we have used SSCP analysis to identify three additional mutations in patients with Schmid metaphyseal chondrodysplasia. Two are frameshift mutations (1856delC and 1992delCT) and one is a missense mutation (C591R). Of interest, the apparently unaffected mother of the patient with the missense mutation is a somatic mosaic for the mutant allele. All three mutations are in the carboxy-terminal non-collagenous domain suggesting that the effect of these mutations is to impair the mutant polypeptide's ability to participate in chain association and trimer formation.

Alleles↗