Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Osteoblastic

Pyridinium species comprise collagen cross-links that are formed during bone remodeling by osteoblasts. These cross-links are released into the serum and excreted in... [Pg.318]

Aromatase activity, and hence the capacity to synthesize estrogens, is found in a variety of tissues in the body. Gonadal sites include the ovaries in premenopausal women and the testes in men. Important extragonadal sites of aromatase activity include the placenta, chondrocytes and osteoblasts of bone, adipose tissue, muscle and brain. Aromatase plays an important... [Pg.218]

Bone metabolism comprises the processes of bone formation and bone resorption, the key actions by which skeletal mass, structure and quality are accrued and maintained throughout life. In the mature skeleton, anabolic and catabolic actions are mostly balanced due to the tight regulation of the activity of bone forming ( osteoblast) and bone resorbing ( osteoclast) cells through circulating osteotropic hormones and locally active cytokines. [Pg.277]

Osteoblasts are the primary cells responsible for bone formation. They are derived from mesenchymal (stromal) cells that first differentiate into pre-osteoblasts and then into mature, bone matrix producing osteoblasts. Inactivated or resting osteoblasts become lining cells and thus a reservoir for bone forming cells to be activated at the next remodelling cycle. Osteoblasts trapped and embedded in the mineralised matrix are called osteocyts, and are important for many properties of living bone. [Pg.278]

During bone formation, a series of sequential changes occur in cells in the osteoblast lineage, including osteoblast chemotaxis, proliferation and differentiation, which in turn is followed by formation of mineralised bone and cessation of osteoblast activity. The osteoblast changes are preceded by osteoclast apoptosis, which may be dependent on active TGF- 3 released from the resorbed bone. This is followed by chemotactic attraction of osteoblasts or their precursors to the sites of the resorption defect. Chemotactic attraction of osteoblast precursors is likely mediated by local factors produced during the resorption process. [Pg.278]

Proliferation of osteoblast precursors is an important event at the remodeling site. This is also likely to be enhanced by local osteoblast growth factors released... [Pg.278]

The final phase of the formation process is cessation of osteoblast activity. The resorption lacunae are usually repaired completely. It is not known how this level of time regulation is achieved. One possibility is that factors produced during osteoblast differentiation decrease osteoblast activity. One such factor could be TGF- 3 since active TGF- 3 decreases differentiated fimction in osteoblasts. [Pg.278]

Bone remodelling, which continues throughout adult life, is necessary for the maintenance of normal bone structure and requires that bone formation and resorption should be balanced. Bone remodelling occurs in focal or discrete packets know as bone multicellular unit (BMU). In this process, both bone formation and resorption occur at the same place so that there is no change in the shape of the bone. After a certain amount of bone is removed as a result of osteoclastic resorption and the osteoclasts have moved away from the site, a reversal phase takes place in which a cement line is laid down. Osteoblasts then synthesize matrix, which becomes mineralised. The BMU remodeling sequence normally takes about 3 months to produce a bone structure unit (Fig. 2). [Pg.279]

Inhibitors of osteoclast activity Stimulators of osteoblast activity... [Pg.280]

Statins lower plasma cholesterol levels by inhibiting HMG-CoA reductase in the mevalonate pathway (Fig. 4). Some research has shown that certain statins (but not all) stimulate BMP-2 expression in osteoblasts, increase bone formation and mimic N-BP in that they inhibit bone resorption. The use of statins in osteoporosis is presently being investigated. [Pg.282]

Fluorid ions stimulate bone formation by a direct mitogenic effect on osteoblasts mediated via protein kinase activation and other pathways. Further to these cellular effects, fluorides alter hydroxyapatite crystals in the bone matrix. In low doses, fluorides induce lamellar bone, while at higher doses abnormal woven bone with inferior quality is formed. The effect of fluorides on normal and abnormal (e.g. osteoporotic) bone therefore depends on the dose administered. [Pg.282]

PTH has a dual effect on bone cells, depending on the temporal mode of administration given intermittently, PTH stimulates osteoblast activity and leads to substantial increases in bone density. In contrast, when given (or secreted) continuously, PTH stimulates osteoclast-mediated bone resorption and suppresses osteoblast activity. Further to its direct effects on bone cells, PTH also enhances renal calcium re-absorption and phosphate clearance, as well as renal synthesis of 1,25-dihydroxy vitamin D. Both PTH and 1,25-dihydroxyvitamin D act synergistically on bone to increase serum calcium levels and are closely involved in the regulation of the calcium/phosphate balance. The anabolic effects of PTH on osteoblasts are probably both direct and indirect via growth factors such as IGF-1 and TGF 3. The multiple signal transduction... [Pg.282]

Bone Formation The building of new bone through osteoblasts. Bone formation, which is part of the bone remodelling process, includes the synthesis of organic matter (mostly collagen type 1) and subsequent mineralisation. [Pg.282]

Fluoride stimulates bone formation by protein kinase activation mediated effects on osteoblasts. Fluorides have been used in the treatment of osteoporosis, but their anti-fracture effect is not undisputed. [Pg.508]

An osteoblast is the cell forming new bone. Osteoblasts are derived from stromal bone marrow stem cells. [Pg.918]

One of the cell types involved in bone metabolism. In concert with osteoblasts, their cellular counterpart, these cells maintain bone hemostasis and constant... [Pg.918]

A cell embedded within the mineralised matrix of bone. Osteocytes are derived from former osteoblasts and are responsible for intra-skeletal sensing and signalling. [Pg.918]

Osteoporosis is a common condition, in which bone density is decreased as a consequence of an imbalance between bone formation (osteoblast) and bone loss (osteoclast). This leads to fragile bones, which are at an increased risk for fractures. The term porosis means spongy, which describes the large holes seen in these bones. [Pg.918]

Systemic regulators of osteoblast, osteocyte and osteoclast functions, and therefore of bone metabolism. The major bone-seeking hormones are parathyroid hormone (PIH), 1,25-dihydroxy vitamin D3 (calcitriol) and the various ex hormones. [Pg.918]

OGR1 (GPR68) 14q31 cAMP t (Gs) pH sensor of osteoblasts, osteoclasts, smooth muscle cells... [Pg.1036]

P2Y2 Immune cells, epithelial and endothelial cells, kidney tubules, osteoblasts UTP= ATP, UTPyS, INS 37217, INS 365 Suramin > RB2, AR-C126313 Gq/Gn and possibly Gj PLC-p activation... [Pg.1050]

OTRs are mainly expressed in myoepithelial cells of the galactiferus channels and the myometrium. The OTRs in vascular endothelial cells, renal epithelial cells (macula densa, proximal tubule) and cardiomyocytes induce the production of NO (vasodilation), natriuresis and release of ANP, respectively. The endometrium, ovary, amnion, testis, epididymis, prostate and thymus also express the OTR supporting a paracrine role of this peptide. Osteoblasts, osteoclasts, pancreatic islets cells, adipocytes, and several types of cancer cells also express OTRs. More over, expression of the OTR... [Pg.1276]

Vitamin K carboxylase is a transmembraneous protein in the lipid bilayer of the endoplasmatic reticulum (ER). It is highly glycosilated and its C-terminal is on the luminal side of the membrane. Besides its function as carboxylase it takes part as an epoxidase in the vitamin K cycle (Fig. 1). For the binding of the y-carboxylase the vitamin K-dependent proteins have highly conserved special recognition sites. Most vitamin K-dependent proteins are carboxy-lated in the liver and in osteoblasts, but also other tissues might be involved, e.g., muscles. [Pg.1298]

Human osteoblast-like MG63 cells were cultured on the macroporous chitosan scaffolds reinforced with hydroxyapatite or calcium phosphate invert glass were fabricated using a thermally induced phase separation technique. [Pg.171]


See other pages where Osteoblastic is mentioned: [Pg.222]    [Pg.224]    [Pg.243]    [Pg.185]    [Pg.125]    [Pg.121]    [Pg.307]    [Pg.112]    [Pg.277]    [Pg.277]    [Pg.277]    [Pg.277]    [Pg.278]    [Pg.278]    [Pg.280]    [Pg.282]    [Pg.303]    [Pg.849]    [Pg.918]    [Pg.918]    [Pg.1036]    [Pg.1051]    [Pg.1052]    [Pg.1129]    [Pg.1498]    [Pg.197]   
See also in sourсe #XX -- [ Pg.367 , Pg.368 ]




SEARCH



Bone biology osteoblasts

Collagen from osteoblasts

Culture human osteoblasts

Effect on osteoblasts

Human fetal osteoblast cell

Human osteoblast cell

Intracellular osteoblastic cell

Lacunae, osteoclasts/osteoblasts

Mineralization osteoblast transport

Ossification Osteoblast

Osteoblast apoptosis

Osteoblast cell culture

Osteoblast cells

Osteoblast cells proliferation

Osteoblast markers

Osteoblast modulators

Osteoblast-like cell adhesion

Osteoblastic differentiation markers

Osteoblasts

Osteoblasts

Osteoblasts adhesion

Osteoblasts alkaline phosphatase

Osteoblasts attachment

Osteoblasts biomaterials

Osteoblasts bone remodeling

Osteoblasts bone-forming cells

Osteoblasts integrin expression

Osteoblasts lycopene effect

Osteoblasts nanoceramics enhancing

Osteoblasts proliferation

Osteoblasts protein-mediated cell adhesion

Osteoclast/osteoblast balanced functions

Osteoclasts and osteoblasts

Oxidative stress osteoblasts

SaOS-2 cell line osteoblastic cells

Scaffolds osteoblasts-cultured

Scurvy Osteoblasts

Transcription factor osteoblast-specific

Vitamin D (cont osteoblasts

© 2024 chempedia.info