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At least 541 records · Page 30Linked to original sources
PubMed1989

Type beta transforming growth factor regulates expression of genes encoding bone matrix proteins.

TGF beta modulates the growth and differentiation of various cell types, in part by regulating the production of extracellular matrix proteins. In rat osteoblast-like cells TGF beta stimulates the production of collagen, osteopontin and osteonectin. On the other hand, TGF beta inhibits the production of osteocalcin, one of the most abundant non-collagenous bone matrix proteins, which is only expressed in osteoblasts. Inhibition of osteocalcin expression by TGF beta in the rat osteoblastic osteosarcoma, ROS 17/2.8 cells, occurs at least in part through transcriptional control.

Animals↗
PubMed1995

Bone matrix deposition of T1, a homologue of interleukin 1 receptors.

The mouse T1 glycoprotein is a secreted molecule of the immunoglobulin superfamily with significant homology to interleukin 1 receptors. It is expressed during bone development, and the extracellular diffusible gene product is found associated with newly formed bone but not cartilage matrix. During osteogenic differentiation of mandibular condyles of newborn mice in vitro, T1 gene expression is induced shortly after cultivation and is observed throughout the differentiation process. The temporal expression pattern of the gene is an mandibular condyles indicates that T1 expression is an early marker of osteogenic differentiation. This view is substantiated by the analysis of T1 gene regulation in continuous osteogenic cell lines. Both in differentiating osteoblast-like KM-1K cells derived from mandibular condyles and in MC3T3 cells, T1 gene activity is preferentially associated with early differentiation stages. In mandibular condyles, the secreted extracellular T1 protein is deposited into newly formed osteoid but not into cartilage matrix. This novel bone matrix protein may locally modulate the availability of its ligand.

Animals↗
PubMed1982

Bone matrix and mineral abnormalities in postmenopausal osteoporosis.

Iliac crest biopsies from 56 postmenopausal osteoporotic females with spontaneous compression fractures and decreased total body Ca were compared to similar tissue from 48 normal controls. Biopsies were analyzed for bone density, Na, Ca, Mg, P, Co3, and hydroxyproline (OH-P). From the results OH-P/matrix, % mineral, and the ion content of the mineral were calculated. osteoporotic subjects showed decreased bone density, % mineral in bone, and OH-P in the bone matrix. Within the mineral, CO3 and Ca/P were decreased, while Na and Mg were increased. Statistical analysis showed that matrix OH-P and % mineral varied independently, and therefore the patients were separated into 4 subgroups: Group Ia: decreased matrix OH-P with normal % mineral (n = 9), Group Ib: decreased matrix OH-P with decreased % mineral (n = 5), Group IIa: normal matrix OH-P with normal % mineral (n = 33), Group IIb: normal matrix OH-P with decreased % mineral (n = 9). Decreased % mineral was associated with decreased bone density and an increase in Na and Mg in the mineral, which suggests skeletal Ca deficiency. Decreased matrix OH-P was associated with decreased bone density and, in the low % mineral group, with decreased mineral CO3 and Ca/P, suggesting a mineral of decreased mean crystal size. When both abnormalities coexisted (Group Ib), the greatest reduction in total body Ca was seen. Patients with normal matrix and normal % mineral (Group IIa) still had decreased bone density. The results suggest that in a large, clinically homogeneous population of postmenopausal osteoporotic women, 4 subgroups can be identified by differences in chemical composition of iliac crest biopsies.

Adult↗
PubMed1993

Incomplete coverage of mammalian bone matrix by lining cells.

A functional "membrane" is thought to exist that separates the general extracellular fluid from the bone extracellular fluid. Many investigators have concluded that bone lining cells form this barrier. It is posited that alterations in this barrier may lead to the recruitment of osteoclasts and contribute to the control of extracellular calcium homeostasis. The present ultrastructural studies, however, demonstrated that significant portions of the resting bone are in contact with the general extracellular fluid. In certain regions of the cochlea, up to 88% of the bone surface is in contact with extracellular fluid. These anatomic observations require a critical reevaluation of current theories of the physiologic roles of bone lining cells in osteoclast recruitment and calcium homeostasis.

Animals↗
PubMedDate not supplied

Influence of fluvastatin on bone formation induced by demineralized bone matrix in mice.

In the last decade, statins became widely used drugs in hypercholesterolemia treatment. Several studies have demonstrated that statins may also be successfully administered in the treatment of osteoporosis. There are, however, no reports regarding the effect of statins on heterotopic ossification (HO). In this paper, we examined the influence of fluvastatin on heterotopically induced bone formation in mice. HO was induced by implantation of rat-derived demineralized bone matrix (DBM) into intramuscular pockets in CFW mice. Mice in the experimental groups received fluvastatin at 3.6 mg/kg per day for 25 consecutive days whilst mice in the control group received placebo. Twenty five days after DBM implantation blood samples were collected to measure total serum cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C) and alkaline phosphatase (AP) activity. Mass of mineral deposited in the induced ossicle was established after hydrolysis of soft tissues surrounding the induced ossicles. In fluvastatin-treated mice, the mass of mineral deposited in heterotopically induced ossicles and AP serum concentration were significantly increased while TG and TC concentrations were decreased, when compared to mice receiving placebo. These results show that administration of statins, in some instances, may affect heterotopic ossification and that during hypocholesterolemic treatment of patients with predisposition to HO, following hip arthroplasty, such treatment may increase risk of HO.

Alkaline Phosphatase↗
PubMed1998

Gene expression of noncollagenous bone matrix proteins in the limb joints and intervertebral disks of the twy mouse.

The twy (tiptoe walking Yoshimura) mouse is an autosomal recessive mutant manifesting multiple osteochondral lesions characterized by pathologic calcium deposition. To elucidate the pathophysiology of the limb joint lesions and the intervertebral disk lesions of the twy mouse, we assessed the mRNA expression of noncollagenous bone matrix proteins such as osteocalcin, osteonectin, osteopontin, and matrix Gla protein (MGP) by in situ hybridization, but only expression of MGP was observed in association with the pathologic calcium deposits in twy mice. Mild degeneration and abnormal growth of the cartilage in contact with the joint capsule was observed at 5 weeks in the articular cartilage of the ankle joint of the twy mouse, and MGP gene expression was observed at the same time. Simultaneous growth of synovial membrane cells and relatively undifferentiated articular cartilage cells in the knee joint, and of cartilage-like cells near the insertion of the cruciate ligament was observed in the twy mouse, and MGP gene expression was found to be present at the same time. Hypertrophy of abnormally proliferated chondrocyte-like cells, which are different from fibrocartilaginous cells of the annulus fibrosus, was observed in the intervertebral disks of the twy mouse at 3 weeks of age, and MGP gene expression was noted at the same time. These findings suggest that abnormal expression of MGP plays a major role in the pathologic calcification of the twy mouse.

Animals↗
PubMed1987

Bridging large defects in bone by demineralized bone matrix in the form of a powder. A radiographic, histological, and radioisotope-uptake study in rats.

Demineralized bone powder was used as an osteoinductive substance to bridge very large defects (more than 50 per cent of the total length of the bone) in one radius of each of thirty-three rats. An identical defect was produced in the contralateral radius of each animal for use as a control. The defect on the control side was left unbridged or was bridged by large chips of autologous bone or an autologous inlay graft. All rats showed formation of new bone throughout the length of the radial defect only on the side in which the demineralized bone powder had been implanted. The control side, in which an autologous graft in the form of chips or inlay had been implanted, showed resorption of the graft. The maximum rate of formation of bone occurred fifteen to twenty-one days after implantation of the demineralized bone powder. At thirty-five days, the experimental defect was fully bridged, forming solid bone, in 71 per cent of the rats, and the remaining 29 per cent showed bridging of 95.8 per cent of the length of the defect, with union on one side. Analysis of the sequential radiographs, technetium-99m scans, and histological findings showed that the formation of bone and bridging of the defect were superior on the side in which the demineralized bone powder had been implanted compared with the side in which pieces of autologous bone or an autologous inlay graft had been used.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Search for an endogenous collagenase in chicken endochondral bone matrix vesicles.

While isolating matrix vesicles from avian endochondral bone, collagenase activity was discovered unexpectedly. The question was raised whether this collagenase activity was endogenous or if it was due to the bacterial collagenase used to release the matrix vesicles from bone. In related experiments done, collagen partially degraded by collagenase mineralized better than undegraded collagen. This study would then attempt to show if an endogenous collagenase is found, whether it facilitates collagen mineralization by allowing better access for matrix vesicles by the "nicking" of collagen. From this two-month study evidence was found that an endogenous collagenase as well as a gelatinase was present on matrix vesicles. SDS gel electrophoresis and zymography were used to determine the presence of collagenases in purified matrix vesicle fractions. Western blots with antibodies to bacterial collagenase, matrix metallo-proteinases 13 (MMP-13), an endogenous collagenase, and MMP-2, an endogenous gelatinase, were also done to determine the presence of an endogenous collagenase. Another facet was added to this study to determine if contamination by exogenous collagenase during matrix vesicle isolation could be removed. From the final Western blots done, it was verified that even after exhaustive washings of the column and centrifugation, purified matrix vesicles contained contaminating bacterial collagenase. Due to the research completed, the matrix vesicle isolation protocol was changed from using bacterial collagenase to a trypsin isolation method to prevent any exogenous collagenase contamination.

Achilles Tendon↗
PubMed1986

Induction of chondrogenesis in muscle, skin, bone marrow, and periodontal ligament by demineralized dentin and bone matrix in vivo and in vitro.

Induction of chondrogenesis in vivo by rolls of demineralized dentin implanted in muscle, subcutaneous connective tissue of skin, medullary cavity of femur, and periodontal ligament of rat was investigated. Specimens were examined at various times up to 21 days after implantation, using light microscopy and morphometric analysis. Induction of cartilage occurred most quickly in muscle, followed by subcutaneous connective tissue of skin and medullary cavity of femur, and most slowly in periodontal ligament. Significantly more cartilage was found in muscle than in subcutaneous connective tissue of skin and medullary cavity of femur at the times examined, and least of all in periodontal ligament. Outgrowth of cells from rat muscle, dermis and subcutaneous tissue, bone marrow and periodontal ligament cultured in vitro on demineralized bone matrix for up to 35 days produced similar results.

Animals↗
PubMed1999

Gaucher's disease with valve calcification: possible role of Gaucher cells, bone matrix proteins and integrins.

Gaucher's disease, an autosomal recessive storage disease, leads to deposition of glucocerebrosides in various organs, especially those of the reticuloendothelial system. The heart is not thought to be frequently involved and studies of patients with cardiac involvement have concentrated on myocardial involvement. Despite careful prior investigation Gaucher cells have never been detected in the valves of these patients. Pathological findings of a patient with Gaucher's disease, type IIIc, with prominent cardiac valvular involvement are reported and, for the first time, the presence of Gaucher cells in the valve tissue is documented. There is evidence that the pathogenesis of the valvular injury may be by way of a cell-mediated mechanism involving bone matrix proteins and integrins.

Adolescent↗