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PubMed1981

Developmental appearance of the vitamin K-dependent protein of bone during calcification. Analysis of mineralizing tissues in human, calf, and rat.

Several mineralizing tissues have been analyzed for the vitamin K-dependent protein of bone (BGP) in order to establish the temporal relationship between initial mineral deposition and the appearance of BGP. These studies demonstrate that the appearance of BGP in developing bone is not dependent on birth, as had been suggested in earlier studies of rat development, but rather on the prior deposition of bone mineral. In fetal human bone, the level of BGP (grams of BGP/mol of bone PO4) rises from 5% of the adult level at 10 weeks gestational age to the adult level at 15 weeks. Thus, adult levels of BGP are reached in human bone shortly after the initial appearance of mineral and long before birth. In adolescent rats, which have overall levels of BGP in bone near the adult level, the appearance of BGP at the ends of growing bones and in bone induced by implantation of demineralized bone matrix follows mineral deposition by approximately 2 weeks. The relative absence of BGP in initially deposited bone mineral and its subsequent appearance several days later may be causally related to the maturation of bone mineral to hydroxyapatite, a structure which binds BGP. The implications of the timing of BGP appearance in mineralizing tissues to its possible function in bone are discussed.

Adult↗

PubMed1988

Proteoglycans synthesized during the cartilage to bone transition in developing chick embryos.

Osteogenesis of the long bone involves a series of cellular and molecular events culminating in the fabrication of a mineralized matrix of the long bone. These studies focus upon the chemical identity and morphology of newly synthesized proteoglycans formed during the cartilage to bone transition in embryonic chick tibia development. As early as the onset of major ossification events (day 13; Hamburger-Hamilton Stage 39), synthesis of a small, highly 4-sulfated chondroitin sulfate proteoglycan was detected in the shaft of the tibia. The characterization of the chondroitin sulfate-rich proteoglycans from cartilage, hypertrophic cartilage, bone marrow, and new bone lead to the suggestion that these molecules can be used as distinctive markers for the cellular phenotypes involved in the cartilage to bone transition.

Animals↗

PubMed1996

Altered mineral metabolism and bone mass in children during treatment for acute lymphoblastic leukemia.

Children with acute lymphoblastic leukemia (ALL) often develop bone pain, abnormal gait, and unusual fractures while in remission and receiving continuing chemotherapy. A prospective longitudinal cohort study was undertaken of bone mass and biochemical mineral status in 40 consecutive children (27 male, 13 female, aged 0.3-17.0 years) receiving therapy on the Dana-Farber Cancer Institute protocol 87-01. Radiography, lumbar spine dual-photon absorptiometry, and biochemical measurements of mineral status were performed at diagnosis and at 6-month intervals throughout 24 months of chemotherapy. Eleven patients were not completely evaluated (4 deaths and 7 off study). Radiographic evidence of osteopenia was observed in 10, 64, and 76% at diagnosis, 12 and 24 months, respectively. Fractures occurred in 39% of children during treatment. Reduction in bone mineral content (BMC), as measured by Z scores, occurred in 64% of patients and was most severe in those greater than 11 years of age at diagnosis. Reduction in BMC during the first 6 months of therapy had a positive predictive value of 64%, while an increase in BMC had a negative predictive value of 82% for subsequent fracture. By 6 months of therapy, 31/37 (84%) children were hypomagnesemic, of whom 16 (52%) were hypermagnesuric. Plasma osteocalcin was subnormal at diagnosis in 29/40 (73%) but increased to normal by 6 months of treatment. Vitamin D status was normal throughout, but plasma 1,25-dihydroxyvitamin D remained subnormal in greater than 70% of children. Urinary cross-link N-telopeptide was normal at diagnosis and became elevated in 58% of children by the end of therapy. Suppressed bone mineralization is evident at diagnosis in a minority of children with ALL. Skeletal morbidity and a reduction in bone mineral mass become more prevalent during treatment, with increased bone resorption, perhaps mainly as a consequence of corticosteroid administration.

Adolescent↗

PubMed1996

Effect of bone wax extract on the frequency of bone marrow erythrocyte micronuclei in mice.

The present study evaluated the induction of micronuclear potency of indigenously developed bone wax saline extract. The experiment was designed with 2 batches, each consisting of 8 groups with 3 male Swiss albino mice each. In each batch, the first 3 groups received Chitra's bone wax saline extract and the second 3 groups received Johnson & Johnson bone wax saline extract at 12.5, 25.0 or 50.0 ml/kg body weight ip for 2 d. The remaining 2 groups were vehicle (saline) and positive (cyclophosphamide) controls. Animals were sacrificed 24 and 36 h after the second dosing and bone marrow smears were prepared and evaluated for micronuclei. The Chitra's and Johnson & Johnson's bone wax extracts failed to induce micronuclei in bone marrow erythrocytes of mice.

Animals↗

PubMed1994

Lethal skeletal dysplasia from targeted disruption of the parathyroid hormone-related peptide gene.

The parathyroid hormone-related peptide (PTHrP) gene was disrupted in murine embryonic stem cells by homologous recombination, and the null allele was introduced into the mouse germ line. Mice homozygous for the PTHrP null mutation died postnatally, probably from asphyxia, and exhibited widespread abnormalities of endochondral bone development. Histological examination revealed a diminution of chondrocyte proliferation, associated with premature maturation of chondrocytes and accelerated bone formation. Analysis of earlier developmental stages revealed that disturbance in cartilage growth preceded abnormal endochondral bone formation. There were no morphological abnormalities apparent in other tissues. These results provide direct evidence implicating PTHrP in normal skeletal development and serve to emphasize its potential involvement in human osteochondrodysplasias.

Animals↗

PubMed2004

Bone morphogenetic protein-2 stimulates angiogenesis in developing tumors.

Bone Morphogenetic Protein-2 (BMP-2) is highly overexpressed in the majority of patient-derived lung carcinomas. However, a mechanism revealing its role in cancer has not been established. Here we report that BMP-2 enhances the neovascularization of developing tumors. Recombinant BMP-2 stimulated blood vessel formation in tumors formed from A549 cells injected s.c. into thymic nude mice. Recombinant BMP-2 also enhanced angiogenesis in Matrigel plugs containing A549 cells in nude mice. The BMP-2 antagonist noggin abrogated BMP-2-induced angiogenic response. Furthermore, antisense transfection of BMP-2 cDNA resulted in a decrease in blood vessel formation in the Matrigel assays. BMP-2 induced tube formation in both human aortic endothelial cells (HAEC) and umbilical vein endothelial cells. BMP-2 also stimulated proliferation of HAEC. The ability of BMP-2 to activate endothelial cells was further demonstrated by its ability to phosphorylate Smad 1/5/8 and ERK-1/2 and to increase expression of Id1. This study reveals that BMP-2 enhanced the angiogenic response in developing tumors. Furthermore, these data suggest that BMP-2 stimulation of angiogenesis may involve the activation of endothelial cells.

Active Transport, Cell Nucleus↗

PubMed1990

Exposure of the pregnant rat to warfarin and vitamin K1: an animal model of intraventricular hemorrhage in the fetus.

Pregnant Sprague-Dawley rats were given daily oral doses of sodium warfarin (100 mg/kg) and concurrent intramuscular injections of vitamin K1 (10 mg/kg). This dosing regimen did not have any apparent deleterious effect on the dams and did not affect the fetuses when administered from day 1 to day 12 of pregnancy. However, similar treatment from day 9 to 20 caused hemorrhage in the fetuses examined on day 21 of gestation. There were no hemorrhages in the control fetuses from dams receiving vitamin K1 only. The lowest effective dose of warfarin, in conjunction with daily doses of vitamin K1, was 3 mg/kg. This dose caused hemorrhage in 28% of fetuses; the incidence of affected fetuses was not further increased by doses of warfarin up to 100 mg/kg. Hemorrhages affected the fetal brain, face, eyes, and ear and occasionally the limbs. Brain hemorrhages were frequently intraventricular and caused various degrees of hydrocephaly. Bony defects were not a feature of prenatal exposure to warfarin. These results show that prenatal exposure of the rat to warfarin and vitamin K duplicates the hemorrhagic abnormalities and pathology associated with prenatal exposure to warfarin in the human. It did not induce bony or facial defects probably because the vitamin K-dependent components of bone development occur postnatally in the rat. This model should allow detailed determination of the role of vitamin K-dependent proteins in development.

Animals↗

PubMed1999

Expression of TGFbeta3 RNA during chick embryogenesis: a possible important role in cardiovascular development.

We examined the temporal and spatial expression pattern of transforming growth factor (TGF)-beta3 RNA during chick embryogenesis from stage 6 to stage 33 (Hamburger and Hamilton scale) by using in situ hybridization. During cardiogenesis, TGFbeta3 mRNA was first expressed in the premyocardium at stage 8 and thereafter it was localized in endocardial cushion tissue and the ventricular myocardium until the end of embryogenesis. During the formation of the major arteries, mRNA for TGFbeta3 was found in smooth muscle progenitor cells, but not in endothelium. In addition, TGFbeta3 mRNA was detectable in various mesoderm-derived tissues, such as the notochord, myotome, pleura, peritoneum, mesenchymal cells in the limb, and developing bone. These results suggest that TGFbeta3 plays an important role in the development of the cardiovascular system and of other mesodermal derivatives during chicken embryogenesis.

Animals↗

PubMed1985

Further studies of degenerative hip disease; antitrochanteric degeneration in turkeys and broiler type chickens.

Postmortem examination revealed antitrochanteric degeneration in turkeys (8 male, 2 female) and broiler type chickens (5 male, 1 female). Antitrochanteric degeneration was detected in birds aged 20 weeks or older but histological examination identified lesions in others with grossly normal antitrochanters. Normal and abnormal antitrochanteric development was studied in male, skeletally immature, turkeys and broilers. Differential subchondral bone growth occurred, with relatively delayed ilial bone development. As a result, hyaline cartilage was retained dorsally and persisted even in adult birds. Retained hyaline, and in younger birds growth plate, cartilage was prone to osteochondrosis. When cartilage flap formation involved fissures traversing retained hyaline cartilage, the term osteochondrosis dissecans was appropriate. In other cases of antitrochanteric degeneration, changes typical of osteoarthrosis were present with, in some instances, no evidence of pre-existing osteochondrosis. Certain sites of antitrochanteric cartilage may be susceptible to fatigue failure in these cases.

Animals↗

PubMed2005

Distribution patterns of the anti-angiogenic protein ADAMTS-1 during rat development.

A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS-1) belongs to the large ADAM family of proteins. ADAMTS-1 contains a metalloproteinase domain, a disintegrin domain and three thrombospondin-like repeats but unlike ADAMs lacks a transmembrane domain. For the elucidation of the biological functions of ADAMTS-1, we raised new antibodies against ADAMTS-1. We show an accumulation of ADAMTS-1 protein at the basal lamina of rat embryonal epithelia of intestines, nasal cavity, choroid plexus, skin and in intracellular storage vesicles of epithelial cells. ADAMTS-1 protein seems to play a role in the development of the neuronal system, adipose tissue, muscle, heart, liver and adrenal glands. At the time of birth its presence is reduced in most organs. However, in the developing bone as well as in the skin, labelling increased towards late embryonal development. Immunoblots revealed a strong presence of a 62 kDa ADAMTS-1 fragment in kidneys, adrenal glands, lungs, intestines and heart. ADAMTS-1 was also present in the corresponding adult rat organs, but in more restricted distribution patterns. It was typically found in principal cells of collecting ducts, of the renal medulla, in ependymal cells of the ventricles and in some neurons. The results were confirmed by real-time PCR. The specific distribution pattern of ADAMTS-1 in a variety of organs during embryogenesis suggests a role of the molecule in tissue remodelling, vasculogenesis and angiogenesis.

ADAM Proteins↗

PubMed2005

[Craniofacial fibrous dysplasia: a case report].

Fibrous dysplasia is classified among benign bone tumors. It is a bone development anomaly characterized by hamartoma proliferation of fibrous tissue within the medullary bone, with secondary bony metaplasia, producing immature, newly formed and weakly calcified bone, without maturation of the osteoblast. It can be monostotic or polyostotic. The craniofacial localization occurs in 10%-25% of cases in monostotic forms and in 50% of cases in polyostotic forms. Fibrous dysplasia essentially affects children and young adults, with no sex preference. Its diagnosis is not always straightforward because the functional symptomology is often absent or not specific. Medical imagery is necessary and in difficult cases a bone biopsy. The major complication of the illness remains sarcomatous degeneration. Only symptomatic forms are treated. We report an observation of craniofacial fibrous dysplasia affecting a child and discovery of proptosis, with no other ocular or general functional signs.

Child↗

PubMed2001

Control of osteoclastogenesis and bone resorption by members of the TNF family of receptors and ligands.

Skeletal mass is maintained by a balance between cells which resorb bone (osteoclasts) and cells which form bone (osteoblasts). Bone development and growth is an on-going, life-long process. Bone is formed during embryonic life, grows rapidly through childhood, and peaks around 20 years of age (formation exceeds resorption). For humans the skeleton then enters a long period, approximately 40 years, when bone mass remains relatively stable. Skeletal turnover continues but the net effect of resorption and formation on bone mass is zero. For women this ends when they enter menopause and similar bone loss occurs for men, but later in life. These opposite functions are coupled, resorption precedes formation, and osteoblasts, or their precursors, stromal cells, regulate osteoclast formation and activity. Until recently, the molecular nature of this regulation, was poorly understood. However, recent observations have identified members of the TNF family of ligands and receptors as critical regulators of osteoclastogenesis. Osteoprotegerin (OPG) a decoy receptor was first identified. Its ligand, receptor activator of nuclear factor-kappaB ligand (RANKL), was quickly found, and shown to be expressed on stromal cells and osteoblasts. Its cognate receptor, RANK, was found to be expressed in high levels on osteoclast precursors. The interaction between RANKL and RANK was shown to be required for osteoclast formation. These observations have provided a molecular understanding of the coupling between osteoclastic bone resorption and osteoblastic bone formation. Moreover, they provide a framework on which to base a clear understanding of normal (e.g. postmenopausal osteoporosis and age associated bone loss) and pathologic skeletal changes (e.g. osteopetrosis, glucocorticoid-induced osteoporosis, periodontal disease, bone metastases, Paget's disease, hyperparathyroidism, and rheumatoid arthritis).

Animals↗

PubMed2000

Immunolocalization of matrix metalloproteinases and their inhibitors in clinical specimens of bone metastasis from breast carcinoma.

Matrix metalloproteinases (MMPs) are essential in several stages of the metastatic process, and in normal bone development and remodeling. We explored whether the interaction between tumor cells and bone leads to changes in MMP and tissue inhibitor of MMP (TIMP) expression thus affecting osteolysis in metastatic bone disease. Using immunohistochemistry we have investigated the MMP/TIMP expression in tumor cells, fibroblasts, osteoblasts and osteoclasts. Thirty one specimens of bone metastasis from breast carcinoma were stained for MMP-1, -2, -9, MT1-MMP and TIMP-1, and -2 and compared with staining in normal breast tissue, primary breast carcinoma and normal bone. Specimens came from patients in three clinical scenarios: from open biopsies without or with pathological fracture, or bone marrow biopsies containing tumor from patients with pancytopenia but without clinical evidence of osteolysis. By bone histomorphometry the latter group showed a heavy tumor load not different from the open biopsy groups but displayed little active bone resorption and low numbers of osteoclasts. Cell type-specific MMP/TIMP expression was observed and the staining patterns were comparable between the three groups of patients. Though no major differences in the MMP/TIMP staining of tumor cells and fibroblasts were observed between bone metastasis and primary tumor, we showed that tumor cells do express MMPs capable of degrading bone matrix collagen. The number and activity of osteoclasts and osteoblasts was increased dramatically in bone metastases, their MMP/TIMP profiles, however, were not different from normal bone, suggesting that the mechanism of bone degradation by osteoclasts is not different from normal bone remodelling.

Bone Neoplasms↗

PubMed2001

The serum level of the amino-terminal propeptide of type I procollagen is a sensitive marker for prostate cancer metastasis to bone.

OBJECTIVE: To assess the level of a bone-formation marker, the amino-terminal propeptide of type I procollagen (PINP), for its utility in indicating bone metastasis in patients with prostate cancer. PATIENTS AND METHODS: Several bone formation markers, i.e. PINP, the carboxy-terminal propeptide of type I procollagen (PICP), bone-specific alkaline phosphatase (BALP), and bone Gla protein (BGP), a bone resorption marker (pyridinoline cross-linked carboxy-terminal telopeptide, ICTP), and prostate specific antigen (PSA) were measured in 40 patients without and 25 patients with bone metastasis. No patient had undergone previous treatment, except for six who developed bone metastasis while undergoing hormone therapy. RESULTS: All markers except BGP were significantly higher in patients with bone metastasis than in those without. The levels of PINP correlated best with the extent of disease, although the levels of PSA, BALP and ICTP also correlated well. While PINP had the largest area under the receiver-operator characteristic curve, PSA, BALP and ICTP also produced useful curves. CONCLUSION: The bone formation marker PINP seems to be useful for discriminating patients with and without bone metastasis. PINP may help in the early and accurate diagnosis of bone metastasis in such patients.

Aged↗

PubMed2001

Prefabricated bone graft induced from grafted periosteum for the repair of jaw defects: an experimental study in rabbits.

PURPOSE: The purpose of the study was to determine whether a prefabricated graft of new bone induced from periosteum grafted into muscle was an effective material for the repair of jaw defects. MATERIAL AND METHODS: Artificial mandibular jaw defects in young Japanese rabbits were covered either with free grafted periosteum (n = 5) or a prefabricated graft of newly formed bone induced from periosteum, which was first grafted into the floor of the mouth, and placed as a revascularized muscle-pedicled bone flap (n = 5). Bone formation in jaw defects was examined radiographically and histologically 28 days after grafting into defects. RESULTS: Bone formation was confirmed radiographically and histologically in both groups. However, the free grafted periosteum formed thin bone and fibrous tissue existed between the new and the original bone. In contrast, more active bone formation was observed with the prefabricated graft. This grafted new bone developed further and fused to the mandible. Blood vessels surrounding the new bone were observed histologically. CONCLUSION: These experimental findings suggested that prefabricated bone grafts induced from periosteum grafts are potentially useful for correction of jaw defects.

Animals↗

PubMed1997

[Computerized tomography of the epiphyseal union of the medial clavicle: an auxiliary method of age determination during adolescence and the 3d decade of life?].

PURPOSE: To establish a reference population for the stages of epiphyseal union of the medical clavicle determined by CT. MATERIAL AND METHODS: Retrospectively, the thoracic CTs of patients under 30 years of age were reevaluated. Basic conditions were the lack of a bone development disorder and a sufficient assessment of the medial clavicle in a bone window setting. The stages of epiphyseal union were categorized as follows: Stage 1 refers to nonunion without ossification of the epiphysis, Stage 2 to nonunion with a separate and ossified epiphysis, Stage 3 to partial, and Stage 4 to complete union. RESULTS: Up to now, 279 individuals could be included in the study. Stage 1 was observed till age 16, Stage 2 occurred from ages 13 through 22, Stage 3 was found from ages 16 through 26. Stage 4 was first noted at age 22, and in 100% of the sample at age 27. CONCLUSIONS: CT is well suitable to determine the stages of epiphyseal union of the medial clavicle. It may become a generally accepted method of age identification during adolescence and the 3rd decade of life. The presented data serve as a reference population at least for white Europeans.

Adolescent↗

PubMedDate not supplied

Fine needle aspiration cytology of fibrous dysplasia: a case report.

BACKGROUND: Fibrous dysplasia (FD) is a benign disorder of bone consisting of intramedullary proliferation of fibrous tissue and irregularly distributed, poorly developed bone. Although tumorlike in appearance, FD is probably a condition resulting from failure of maturation from woven to lamellar bone. The histology of FD has been well characterized since Lichtenstein first reported it, in 1938; however, the cytologic appearance has been described only rarely. To our knowledge, this is the first case report of fine needle aspiration (FNA) cytomorphology of FD. CASE: A 30-year-old female with breast carcinoma, diagnosed a month earlier, underwent computed tomography-guided FNA of a rib lesion radiologically thought to represent FD, although metastatic cancer could not be excluded. The smears contained blood, occasional osteoclastic multinucleated giant cells and frequent C-shaped fibrillary structures with dark central areas and lighter peripheries, representing woven bone. The cytologic/radiologic impression of FD was confirmed histologically. CONCLUSION: FNA cytodiagnosis of FD is possible in the setting of consistent clinical and radiologic findings.

Adult↗

PubMed1996

A longitudinal evaluation of bone mineral density in adult men with histories of delayed puberty.

We have previously demonstrated that men with histories of constitutionally delayed puberty have significantly lower spinal and radial bone mineral density than normal men. Because these men were in their mid-twenties, it is possible that bone density was decreased because bone development was still incomplete. In addition, there is no information on the bone density of the proximal femur, the most important clinical site for osteoporotic fractures, in men with histories of delayed puberty. To address these issues, we performed repeat measurements of radial and spinal bone mineral density 2 yr after the initial evaluations in 18 men with histories of delayed puberty. Bone mineral density of the femoral neck was also measured at the time of follow-up evaluations. The mean radial bone mineral density at the time of the repeat evaluations was similar to the mean value from the initial evaluations (0.74 +/- 0.08 vs. 0.74 +/- 0.07 g/em2) and the mean change was 0.00 +/- 0.04 g/cm2. Similarly, the mean spinal bone mineral density at the time of the repeat evaluations was similar to the mean value from the initial evaluations (1.02 +/- 0.10 vs. 1.01 +/- 0.10 g/cm2) and the mean change was -0.01 +/- 0.04 g/cm2. Bone mineral density of the femoral neck was significantly lower in the men with histories of delayed puberty than in normal men (0.88 +/- 0.11 vs. 0.98 +/- 0.14 g/cm2 P < 0.02). These data indicate that bone accretion is complete by the mid-twenties in men with histories of constitutionally delayed puberty and that their bone mineral density does not improve with time. In addition, these men have decreased bone density of the femoral neck, which might increase their risk for hip fractures when they are older.

Adult↗