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Osteoclast markers

Andersson G, Lindunger A, Ek-Rylander B (1989) Isolation and characterization of skeletal acid ATPase-a new osteoclast marker Connect Tissue Res 20 151-158... [Pg.166]

In bone, three proteins have been described which are vitamin K-dependent, osteocalcin (bone Gla protein), matrix Gla protein (MGP), and protein S. Osteocalcin is synthetized by osteoclasts, regulated by the active form of vitamin D, calcitriol. Its capacity to bind calcium needs a vitamin K-dependent y-carboxylation of three glutamic acid residues. The calcium binding capacity of osteocalcin indicates a possible role in bone mineralization, but its exact function is still unclear. However, it is widely used as a serum marker for bone mineralization. Protein S, mainly a coagulant, is also vitamin-K dependent and synthesized in the liver. Children with... [Pg.1299]

Osteoclast differentiation Raw264, bone marrow macrophages, hematopoetic stem cells Rankl Comparison of response markers across models to identify common mechanisms [23]... [Pg.420]

The most important organic components of bone are collagens (mainly type 1 see p.344) and proteoglycans (see p. 346). These form the extracellular matrix into which the apatite crystals are deposited (biomineralization). Various proteins are involved in this not yet fully understood process of bone formation, including collagens and phosphatases. Alkaline phosphatase is found in osteoblasts and add phosphatase in osteoclasts. Both of these enzymes serve as marker enzymes for bone cells. [Pg.340]

Markers of bone formation produced by osteoblasts Markers of bone resorption produced by osteoclasts Products of collagen type I degradation... [Pg.274]

Critical differences of two subsequent measurements for serum analytes produced by the osteoblasts and osteoclasts are recorded in Table 6. Variability of the serum markers produced by the osteoblasts and osteoclasts is significantly—about two times—lower than the variability of urinary, and probably also serum markers, of the degradation of collagen type I. See Table 5. [Pg.284]

Clinical PK/PD Calcitonin has a well-established mechanism of action published literature supports that salmon calcitonin, mediated through calcitonin receptors located on osteoclasts, inhibits bone resorption, thereby increasing bone mineral density. Since serum beta-CTx (C-telopeptides of type 1 collagen, corrected for creatinine) is a recognized marker of bone resorption, the effect of administered salmon calcitonin on serum beta-CTx is considered to be an adequate surrogate for pharmacodynamic comparisons. [Pg.52]

Osteoclasts are multinucleated cells found on the endosteal surface of bone, in Haversian systems and periosteal surfaces. PTH activates osteoclasts (indirectly via osteoblasts that possess PTH receptors). Calcitonin is a potent inhibitor of osteoclast activity. Local cytokine factors, including interleukin-1 (IL-1), tumour-necrosis factor (TNF), TGF- 0 and interferon-y (INF-y), are important regulators. Osteoclast resorption of bone releases collagen peptides, pyridinoline cross-links and calcium from the bone matrix, through the action of lysosomal enzymes (collagenases and cathepsins). The collagen breakdown products in serum and urine (e.g. hydroxyproline) can be used as biochemical markers. [Pg.186]

The only nonbone condition in which elevated activities of TR-ACP are found in serum is Gaucher s disease of spleen, a lysosomal storage disorder. Its source in this disease is the abnormal macrophages in spleen and other tissues, which overexpress this normal macrophage constituent. The hairy cells of hairy-ceU leukemia (leukemic reticuloendotheliosis) also express the osteoclast-type AGP, providing a useful histological marker. However, in this condition, the isoenzyme does not enter the plasma in increased amounts. [Pg.625]

Therapy is directed at decreasing osteoclastic bone resorption. Bisphosphonates (alendronate, risedronate, pamidronate, and etidronate) and calcitonin are effective in decreasing bone pain, serum ALP, and markers of bone resorption. Patients may occasionally need surgery for skeletal deformity that limits mobility or for arthritic changes, fractures, or nerve compression. [Pg.1934]

Bone specific acid phosphatase A lysosomal enzyme of osteoclasts Urine Markers All of these are collagen breakdown products... [Pg.889]

S-100 and vimentin. However, some cells of the sarcomatous component also retain keratin in some cases. " Spindle cell carcinomas may also have osteoclast-like giant cells, in which case the osteoclast-like giant cells express histiocytic differentiation markers. ... [Pg.572]

Osteopontin (formerly known as bone sialoprotein I) binds tightly to hydroxyapatite in bone and thus forms an integral part of the mineralised matrix. It has been postulated to be a ligand for the vitronectin receptor, and this suggests a possible role of osteopontin in osteoclast attachment and function (Merry et al., 1993). Hence, it functions as a potent marker of ossification and consequently its expression serves to quantify the degree of mineralisation of bone tissue in contact with bioceramic materials including coatings. [Pg.407]

Paget s disease (Table 35.6) is characterized by excessive bone resorption, followed by replacement of the normally mineralized bone with soft, poorly mineralized tissue (20). It has been determined that the osteoclasts have an abnormal structure, are hyperactive, and are present at elevated levels (20). Patients afflicted with this painful condition often suffer from multiple compression fractures. Administration of calcitonin and oral calcium and phosphate supplements had been the treatment of choice until the bisphosphonate risedronate was approved by the U.S. Food and Drug Administration (FDA). Daily administration of risedronate results in a decreased rate of bone turnover and a decrease in the levels of serum alkaline phosphatase and urinary hydroxyproline, two biochemical markers of bone turnover (4,20). A significant advantage to treatment with the bisphosphonates is long-term suppression of the disease (20). Calcium supplementation, which often is necessary in these patients, must be dosed separately from risedronate, because calcium- and aluminum- or... [Pg.1411]

Strontium ranelate is an orally active agent that can be classified as both an antiresorptive agent and a bone-forming agent (42,43). It is able not only to stimulate replication of preosteoblastic cells to promote bone formation but also is able to decrease osteoclastic activity to prevent bone resorption. Biochemical markers for bone formation (e g., bone-specific alkaline phosphatase), which normally decrease in the presence of antiresorptive therapy, are elevated in the presence of strontium ranelate (44). Lumbar spine BMD increased 11.4% in patients treated with this new agent. [Pg.1424]


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Osteoclasts

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