Definition of osteoclast-activating factor in the Financial Dictionary - by Free online English dictionary and encyclopedia. What is osteoclast-activating factor? Meaning of osteoclast-activating factor as a finance term. What does osteoclast-activating factor mean in finance?
Patients with defective osteoclastic acidification have increased numbers of osteoclasts, with decreased resorption, but bone formation that remains unchanged. We demonstrate that osteoclast survival is increased when acidification is impaired, and that impairment of acidification results in inhibition of bone resorption without inhibition of bone formation. We investigated the role of acidification in human osteoclastic resorption and life span in vitro using inhibitors of chloride channels (NS5818/NS3696), the proton pump (bafilomycin) and cathepsin K. We found that bafilomycin and NS5818 dose dependently inhibited acidification of the osteoclastic resorption compartment and bone resorption. Inhibition of bone resorption by inhibition of acidification, but not cathepsin K inhibition, augmented osteoclast survival, which resulted in a 150 to 300% increase in osteoclasts compared to controls. We investigated the effect of inhibition of osteoclastic acidification in vivo by using the rat ...
A heavy infiltrate of foreign-body macrophages is commonly seen in the fibrous membrane which surrounds an aseptically loose cemented implant. This is in response to particles of polymethylmethacrylate (PMMA) bone cement and other biomaterials. We have previously shown that monocytes and macrophages responding to particles of bone cement are capable of differentiating into osteoclastic cells which resorb bone. To determine whether the radio-opaque additives barium sulphate (BaSO4) and zirconium dioxide (ZrO2) influence this process, particles of PMMA with and without these agents were added to mouse monocytes and cocultured with osteoblast-like cells on bone slices. Osteoclast differentiation, as shown by the presence of the osteoclast-associated enzyme tartrate-resistant acid phosphatase (TRAP) and lacunar bone resorption, was observed in all cocultures. The addition of PMMA alone to these cocultures caused no increase in TRAP expression or bone resorption relative to control cocultures. Adding PMMA
It is generally accepted that bone formation is depressed during corticosteroid treatment, but the effects of glucocorticoids on bone resorption are less well characterized. We have investigated the effects of short-term treatment with high-dose oral glucocorticoids on biochemical markers of bone turnover in 20 consecutive patients with asthma who sought help for acute respiratory obstruction in our emergency department. Serum concentrations of the carboxy-terminal cross-linked telopeptide of type 1 collagen (1CTP), reflecting bone resorption, and the carboxy-terminal propeptide of type 1 procollagen (P1CP), reflecting bone formation, were measured by radioimmunoassay. Changes of the circulating levels of the bone resorption marker 1CTP after treatment were age dependent with a significant negative correlation (r = -0.54, P = 0.01). The dependency on age remained when correcting, in a multiple linear regression analysis, for 1CTP levels at admission, weight, sex, and daily maintenance dose of ...
Do you have a protocol for osteoclast resorption on dentine slices? I have done a literature search (1966-present) and the seminal article seems to be Boyde & Jones (1984) Resorption of dentine by isolated osteoclasts in vitro. Br Dent J 156:216-220. Help! Our provencial library doesnt have this journal. Donna Montague, M.S. Research Associate Physiology/Biophysics and Orthopaedic Surgery University of Arkansas for Medical Sciences (501) 603-1239 ...
Author: Rumpler, M. et al.; Genre: Meeting Abstract; Published in Print: 2011-05-07; Title: Microcracks and osteoclast resorption activity in vitro
The three main mechanisms by which osteoporosis develops are an inadequate peak bone mass (the skeleton develops insufficient mass and strength during growth), excessive bone resorption and inadequate formation of new bone during remodeling. An interplay of these three mechanisms underlies the development of fragile bone tissue.[9] Hormonal factors strongly determine the rate of bone resorption; lack of estrogen (e.g. as a result of menopause) increases bone resorption as well as decreasing the deposition of new bone that normally takes place in weight-bearing bones. The amount of estrogen needed to suppress this process is lower than that normally needed to stimulate the uterus and breast gland. The α-form of the estrogen receptor appears to be the most important in regulating bone turnover. In addition to estrogen, calcium metabolism plays a significant role in bone turnover, and deficiency of calcium and vitamin D leads to impaired bone deposition; in addition, the parathyroid glands react ...
Monocytes are frequently found adjacent to active bone resorption surfaces in both physiological and pathological situations and may play a key role in bone resorption. There is strong circumstantial...
Mechanisms of bone invasion by squamous carcinomas of the head and neck have been investigated using fresh tumours and established tumour cell lines in an in vitro bone resorption assay with 45Ca-labelled mouse calvaria. Fresh tumours regularly resorb bone in vitro. Activity is consistently reduced by indomethacin. The tumours release E 2 prostaglandins (PGE 2) in amounts sufficient to account for ~50% of the bone resorption observed. Small amounts of non-prostaglandin (indomethacin-resistant) osteolytic factors are also produced. Control non-neoplastic tissues show a variable capacity to resorb bone in vitro; PGE 2 levels in these tissues may be related to their content of inflammatory cells. Tumour cell lines also resorb bone in vitro but, for most lines, activity is not significantly blocked by indomethacin and PGE 2 levels are generally insufficient to account for the osteolysis observed. Non-prostaglandin bone resorbing factors thus predominate. It is concluded that most squamous cancers of ...
Bone, despite its rigid nature, is not a permanent, immutable tissue. It is in fact a very dynamic and living tissue that maintains its structure via an equilibrium of opposing activities: Bone Regeneration and Bone Resorption. Both activities are constantly ongoing in living bone. This process of bone regeneration and bone resorption in equilibrium is…
Bone reabsorption is resorption of bone tissue, that is, the process by which osteoclasts break down the tissue in bones and release the minerals, resulting in a transfer of calcium from bone tissue to the blood. The osteoclasts are multi-nucleated cells that contain numerous mitochondria and lysosomes. These are the cells responsible for the resorption of bone. Osteoclasts are generally present on the outer layer of bone, just beneath the periosteum. Attachment of the osteoclast to the osteon begins the process. The osteoclast then induces an infolding of its cell membrane and secretes collagenase and other enzymes important in the resorption process. High levels of calcium, magnesium, phosphate and products of collagen will be released into the extracellular fluid as the osteoclasts tunnel into the mineralized bone. Osteoclasts are prominent in the tissue destruction found in psoriatic arthritis and rheumatology disorders. The human body is in a constant state of bone remodeling. Bone ...
To clarify what kind of process participates in bone resorption, time course of indices of bone resorption was investigated using 13-day-old embryonic chick calvaria. When calvariae were cultured...
The invention relates to a combined pharmaceutical preparation comprising parathyroid hormone and a bone resorption inhibitor, said preparation being adapted for (a) the administration of parathyroid hormone during a period of approximately 6 to 24 months; (b) after the administration of parathyroid hormone has been terminated, the administration of a bone resorption inhibitor during a period of approximately 12 to 36 months.
The invention relates to a combined pharmaceutical preparation comprising parathyroid hormone and a bone resorption inhibitor, said preparation being adapted for (a) the administration of parathyroid hormone during a period of approximately 6 to 24 months; (b) after the administration of parathyroid hormone has been terminated, the administration of a bone resorption inhibitor during a period of approximately 12 to 36 months.
Increased bone turnover may be a risk factor for fracture [Lønning 2005]. However, it is uncertain whether markers of bone resorption and markers of bone formation are both associated with fracture risk [Looker 2000]. Therefore, we will measure bone formation and bone resorption markers at baseline, year 1 and year 5. Blood specimens will be shipped to and stored in a central laboratory for future assays of bone biomarkers. For markers of bone formation, the N-terminal Propeptide of Type I Collagen (PINP) will be measured. For bone resorption markers, serum levels of cross-linked N-telopeptides of type I collagen (NTx) will be measured. Note: Subjects must fast 12-14 hours prior to blood draw ...
Osteoporosis (OP) is a common chronic skeletal disorder in aging individuals. In-spite of the progress made in this market, there is still a great demand for safer and more specific drugs for extended administration. Excessive bone resorption by osteoclasts is central to the pathogenesis of OP and other bone-related diseases. Thus, inhibition of osteoclast activity is a desired outcome in the treatment of bone and bone-related disorders. However, complete irreversible shutdown of resorption by current drugs and uncontrolled duration of activity increase the risk for hypocalcemia, atypical fractures and osteonecrosis of the jaw limiting their utilization and decreasing patients compliance to their administration.. The combined expression of M-CSF receptor c-FMS and αvβ3 integrin is unique to osteoclasts. Moreover, signaling through these receptors is essential to organize the osteoclast cytoskeleton elements and for its resorption machinery. Studies in animal models demonstrated that ...
Also Known As: Bone Losses, Osteoclastic; Bone Resorptions; Loss, Osteoclastic Bone; Losses, Osteoclastic Bone; Osteoclastic Bone Losses Show All ,, ...
The tyrosine kinase inhibitor TAS-115 that blocks VEGF receptor and hepatocyte growth factor receptor MET signaling exhibits antitumor properties in xenografts of human gastric carcinoma. In this study, we have evaluated the efficacy of TAS-115 in preventing prostate cancer metastasis to the bone and bone destruction using the PC3 cell line. When PC3 cells were injected into proximal tibiae in nude mouse, severe trabecular and cortical bone destruction and subsequent tumor growths were detected. Oral administration of TAS-115 almost completely inhibited both PC3-induced bone loss and PC3 cell proliferation by suppressing osteoclastic bone resorption. In an ex vivo bone organ culture, PC3 cells induced osteoclastic bone resorption when co-cultured with calvarial bone, but TAS-115 effectively suppressed the PC3-induced bone destruction. We found that macrophage colony-stimulating factor-dependent macrophage differentiation and subsequent receptor activator of NF-κB ligand-induced osteoclast formation
Extracted from text ... SA Pharmaceutical Journal - April 2006 40 DRUG INFO Protos(r) - The first of a new class for osteoporosis: dual action bone agent Approved indication Protos(r) contains strontium ranelate and is indicated for the treatment of postmenopausal osteoporosis to reduce the risk of vertebral and peripheral fractures, including the hip. Mode of action Strontium ranelate has a unique pharmacological profile characterised by an inhibition of bone resorption and a simultaneous stimulation of bone formation. It targets the bone remodelling process by stimulating osteoblast-mediated bone formation and by inhibiting osteoclast-mediated bone resorption. The dual mode of action of strontium ranelate may ..
Osteoporosis is a common disorder which affects up to 30% women and 12% men at some point in life. This mostly age-associated disorder has becoming increasingly a major clinical and public health issue as human lifespan increases. Osteoporosis is characterized by reduced bone mass, alterations in bone micro-architecture, reduced bone strength, and elevated risk of fracture (Kanis, 1994). Although both genetic and environmental factors influence the risk of osteoporosis, it has been shown that familial traits are one of the most important clinical risk factors, suggesting the role of genetic factors. The fundamental pathogenic mechanism underlying this disorder includes, (a) failure to achieve peak bone mass during growth and development, (b) excessive bone resorption, and (c) defects in bone formation. Gene knockouts in mice have demonstrated that transcription factors Runx2 and a downstream factor Osterix (Osx) are essential for osteoblast differentiation and bone formation during development. However,
Illustration showing bone resorption; osteoclasts are breaking down bone and releasing minerals, to transfer calcium from the bone fluid into the blood. - Stock Image C024/9603
0055] Any amount of a pharmaceutical composition can be administered to a subject. The dosages will depend on many factors including the mode of administration and the age of the subject. In younger people there is extensive bone-turnover due to growing bone. Typically, the amount of a compound or agent of the present invention (e.g., 4-P-PDOT, a derivative, analog, conjugate or prodrug of 4-P-PDOT; a pharmaceutical acceptable salt thereof) contained within a single dose will be an amount that effectively prevent, delay or correct bone resorption in a subject in need thereof without inducing significant toxicity. As used herein the term "therapeutically effective amount" is meant to refer to an amount effective to achieve the desired therapeutic effect. A therapeutically effective amount is also one in which any adverse side effects of the compound are outweighed by the therapeutically beneficial effects. Typically, a compound or agent of the present invention (e.g., 4-P-PDOT, a derivative, ...
Principal Investigator:KITAZAWA Riko, Project Period (FY):1996 - 1997, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Experimental pathology
Principal Investigator:SHIBUTANI Toshiaki, Project Period (FY):1997 - 1998, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Conservative dentistry
Clodronate, Disodium Salt - CAS 88416-50-6 - Calbiochem CAS 88416-50-6 A non-amino, chloro-containing bisphosphonate that acts as a potent inhibitor of osteoclast-mediated bone resorption. - Find MSDS or SDS, a COA, data sheets and more information.
Biochemical markers of bone turnover reflect bone formation or bone resorption. These markers (both formation and resorption) may be elevated in high-bone-turnover states (eg, early postmenopausal ost... more
Type 2 diabetes mellitus (T2DM) is the most common type of diabetes mellitus. It accounts for more than 90% of diabetic patients and usually develops after 35-40 years of age. T2DM is characterized by hyperglycemia and redundant fatty acid secretion due to insulin resistance and decreased insulin sensitivity (Schwartz, 2016). Diabetic osteoporosis is a major complication of T2DM that originates mainly from alterations in the bone microenvironment (Zhang et al., 2016), thus leading to subsequent bone loss, mineral density reduction and fractures (Schwartz, 2016).. High glucose (HG) and free fatty acids (FFA) reportedly inhibit osteogenic differentiation (You et al., 2014) and induce apoptosis of osteoblasts (Feng et al., 2011). Bone metabolic homeostasis relies on the balance between osteoblast-induced bone formation and osteoclast-induced bone resorption (Raisz, 2005). Diabetic osteoporosis primarily results from the disequilibrium between osteoblast and osteoclast, as osteoblast activity is ...
The pattern of changes in serum PTH, combined with the pattern of elevation in biochemical markers of bone remodeling (increases in bone formation markers followed by increases in bone resorption markers), suggests a pathway through which daily PTH injection may temporarily uncouple bone ...
Questions and answers about tooth root bone resorption Teeth gums roots and bone can resorb for a number of reasons or causes Learn how the diagnosis process starts what can be done to stop cure or prevent it suggested treatments More dental questions, dentist practices, Learn new fix treat repair replace options.
Buy fosamax generic - paypal. Active alendronate ingredient - non-hormonal specific inhibitor of an osteoclastic bone resorption, suppresses osteoclasts
Introduction: Inflammation is a critical hallmark of autoimmune arthritis (AA) and cancer. We have previously shown that the site of chronic inflammation linked to AA creates a milieu that attracts tumor cells to home and grow in the inflamed bones and lungs which are frequent sites of breast cancer metastasis. We have identified IL-17, a critical pro-inflammatory cytokine involved in osteoclastic bone resorption in AA as the underlying mechanism for increased metastasis. In addition, high levels of cyclooxygenase 2 (COX-2) is linked to both AA and breast cancer metastasis. We report that blocking the IL-17 and COX-2 pathways simultaneously significantly reduces the development of breast cancer associated metastasis in a spontaneous model of AA.. Methods: 4T1 mammary gland tumors were generated in mice genetically prone to develop AA (designated SKG mice). When tumors reached , 0.2 gms, anti-IL17 antibody treatment was injected intraperitoneally once a week for three weeks. Celecoxib, a specific ...
1 The collection of new therapeutic entities first launched in 2003 originated from the following sources (a) CIPSLINE, Prous database (b) Iddb, Current Drugs database (c) IMS R& D Focus (d) Adis Business Intelligence R& D Insight (e) Pharmaprojects. 2 A. I. Graul, Drug News Perspect., 2004, 17, 43. 3 C. Boyer-Joubert, E. Lorthiois and F. Moreau, Ann. Rep. Med. Chem., 2003, 38, 347. 4 P. Bernardelli, B. Gaudilliere and F. Vergne, Ann. Rep. Med. Chem., 2002, 37, 257. 5 B. Gaudilliere, P..... ...
Nedwin, G E.; Mohler, M A.; and Luben, R A., "Cloning of the coding sequences of a human lymphokine, osteoclast-activating factor. Abstr." (1982). Subject Strain Bibliography 1982. 3923 ...
Affiliation:埼玉医大,医学部,助教授, Research Field:Orthopaedic surgery,Hematology, Keywords:OCIF,ODF,巨核球,転写制御,破骨細胞分化因子,骨吸収,bone resorption,活性型ビタミンD_3,proplatelet_formation,胞体突起形成(prpplatelet formation, PPF), # of Research Projects:2, # of Research Products:3
Regulation of RANKL (receptor activator of nuclear factor κB ligand)-induced osteoclast differentiation is of current interest in the development of antiresorptive agents. Osteoclasts are multinucleated cells that play a crucial role in bone resorption. In this study, we investigated the effects of N-methylpyrrolidone (NMP) on the regulation of RANKL-induced osteoclastogenesis. NMP inhibited RANKL-induced tartrate-resistant acid phosphatase activity and the formation of tartrate-resistant acid phosphatase-positive multinucleated cells. The RANKL-induced expression of NFATc1 (nuclear factor of activated T cells, cytoplasmic 1) and c-Fos, which are key transcription factors for osteoclastogenesis, was also reduced by treatment with NMP. Furthermore, NMP induced disruption of the actin rings and decreased the mRNAs of cathepsin K and MMP-9 (matrix metalloproteinase-9), both involved in bone resorption. Taken together, these results suggest that NMP inhibits osteoclast differentiation and ...
Bone is composed of a living protein framework upon which mineral crystals are placed. As bone breaks down, bits of this living protein framework appear in the urine. Tests of bone breakdown, called bone resorption tests, measure the amount of one specific bone protein in the urine (or in the blood) and thus gauge the current rate of bone breakdown. Urinary markers of bone breakdown (known as markers of bone resorption) are simple urine tests that can help determine if you are currently losing bone or not. Such bone breakdown testing can also indicate if your bone-building program is effective at reducing and normalizing the bone breakdown process.. As bone is broken down certain bone protein by-products are excreted in the urine. Measurement of the amount of these bone breakdown by-products can determine the rate of bone breakdown. A high rate of bone breakdown is strongly suggestive of current, ongoing bone loss and a greater risk for osteoporotic fracture. A low rate of bone resorption would ...
|i|Background.|/i| Sublesional osteoporosis (SLOP) is characterized by excessive bone resorption at the hip and knee region after spinal cord injury (SCI), resu...
New research in animals triggered by a combination of serendipity and counterintuitive thinking could point the way to treating fractures caused by rapid bone loss in people, including patients with metastatic cancers.. A series of studies at the University of North Carolina School of Medicine found that steroid drugs, known for inducing bone loss with prolonged use, actually help suppress a molecule thats key to the rapid bone loss process. A report of the new findings appears online Feb. 5, 2013 in the journal PLOS ONE.. Osteoporosis or the loss of bone mass is a major public health problem in the Western world and commonly results in hip and spine fractures. "But rib fractures are the most common and yet most unreported osteoporotic fractures and also occur in many cancers such as breast cancer, malignant melanoma, and myelomas, that metastasize and spread to the ribs," says Arjun Deb, MD, assistant professor in the departments of Medicine and Cell Biology and Physiology at UNC.. "While ...
Material and methods/results The authors used organ cultured neonatal mouse calvarial bones and isolated periosteal osteoblasts which express TLRs to study the role of TLR2 in bone resorption. LPS from the perio-pathogenic bacterium Porphyromonas gingivalis (Pg; which is a weak agonist for TLR4 but a strong for TLR2 because of the contaminating lipoprotein), enhanced number of osteoclasts, 45Ca release and bone matrix degradation (CTX) by a process inhibited by osteoprotegerin and zolendronic acid. LPS Pg enhanced the expression of osteoclastic genes (c-Fos, trap, oscar and cathepsin K) and reduced the expression of osteoblastic genes (osteocalcin, runx2, alp and procollagen α1). The effects were associated with increased mRNA and protein expression of RANKL, whereas OPG mRNA and protein were unaffected. Similar to LPS Pg, Pam2CSK4 (synthetic ligand for TLR2/TLR6), Pam3CSK4 (ligand for TLR1/TLR2), HKLM (a heat killed preparation of Listeria monocytogenes, a TLR2 agonist) and FSL1 (a synthetic ...
Fingerprint Dive into the research topics of Growth hormone protects against ovariectomy-induced bone loss in states of low circulating Insulin-like Growth Factor (IGF-1). Together they form a unique fingerprint. ...
Pharmacological Action:. Raloxifene : Raloxifene binds to estrogen receptors, resulting in differential expression of multiple estrogen-regulated genes in different tissues. Raloxifene produces estrogen-like effects on bone, reducing resorption of bone and increasing bone mineral density in postmenopausal women, thus slowing the rate of bone loss. The maintenance of bone mass by raloxifene and estrogens is, in part, through the regulation of the gene-encoding transforming growth factor-β3 (TGF-β3), which is a bone matrix protein with antiosteoclastic properties. Raloxifene activates TGF-β3 through pathways that are estrogen receptor-mediated but involve DNA sequences distinct from the estrogen response element. The drug also binds to the estrogen receptor and acts as an estrogen agonist in preosteoclastic cells, which results in the inhibtion of their proliferative capacity. This inhibition is thought to contribute to the drugs effect on bone resorption. Other mechanisms include the ...
The underlying mechanism in all cases of osteoporosis is an imbalance between bone resorption and bone formation. Either bone resorption is excessive, or bone formation is diminished. Bone matrix is manufactured by the osteoblast cells, whereas bone resorption is accomplished by osteoclast cells. Trabecular bone is the sponge-like bone in the center of long bones and vertabrae. Cortical bone is the hard outer shell of bones. Because osteoblasts and osteoclasts inhabit the surface of bones, trabecular bone is more active, more subject to bone turnover, to remodeling. Long before any overt fractures occur, the small spicules of trabecular bone break and are reformed in the process known as remodeling. Bone will grow and change shape in response to physical stress. The bony prominences and attachments in runners are different in shape and size than those in weightlifters. It is an accumulation of fractures in trabecular bone that are incompletely repaired that leads to the manifestation of ...
Pathological bone resorption by osteoclasts is primarily treated with bisphosphonates. Because the administration of bisphosphonates is associated with a risk for multiple adverse symptoms, a precise understanding of the mechanisms underlying osteoclastogenesis is required to develop drugs with minimal side-effects. Osteoclastogenesis depends on receptor activator of nuclear factor kappa B (RANK) signaling mediated by TRAF6. We previously identified a highly conserved domain in the cytoplasmic tail of RANK (HCR), which did not share any significant homology with other proteins and was essential for osteoclastogenesis. HCR acts as a platform for the formation of Gab2- and Vav3-containing signal complexes, and ectopic expression of the HCR peptide inhibits osteoclastogenesis. Here, we uncover the mechanisms of HCR peptide-mediated inhibition of osteoclastogenesis. Expression of either the amino- or carboxyl-terminal half of the HCR peptide (N- or C-peptide) independently inhibited RANK signaling ...
The reciprocal interaction between cancer cells and the tissue-specific stroma is critical for primary and metastatic tumor growth progression. Prostate cancer cells colonize preferentially bone (osteotropism), where they alter the physiological balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption, and elicit prevalently an osteoblastic response (osteoinduction). The molecular cues provided by osteoblasts for the survival and growth of bone metastatic prostate cancer cells are largely unknown. We exploited the sufficient divergence between human and mouse RNA sequences together with redefinition of highly species-specific gene arrays by computer-aided and experimental exclusion of cross-hybridizing oligonucleotide probes. This strategy allowed the dissection of the stroma (mouse) from the cancer cell (human) transcriptome in bone metastasis xenograft models of human osteoinductive prostate cancer cells (VCaP and C4-2B). As a result, we generated the ...
p38 mitogen-activated protein kinase (MAPK), which is constitutively activated in human myeloma, has been implicated in bone destruction by this cancer, but the processes it recruits are obscure. In this study, we show that p38 activity in myeloma inhibits osteoblast differentiation and bone formation, but also enhances osteoclast maturation and bone resorption. p38 regulated the expression and secretion of the Wnt pathway antagonist DKK-1 and the monocyte chemoattractant MCP-1. Attenuating p38, DKK-1, or MCP-1 were each sufficient to reduce bone lesions in vivo. Although it is well known that DKK-1 inhibits osteoblast differentiation, we found that together with MCP-1, it could also promote osteoclast differentiation and bone resorption. The latter effects were mediated by enhancing expression of RANK in osteoclast progenitor cells and by upregulating secretion of its ligand RANKL from stromal cells and mature osteoblasts. In summary, our study defined the mechanisms by which p38 signaling in ...
TY - JOUR. T1 - Cytokine regulation and the signaling mechanism of osteoclast inhibitory peptide-1 (OIP-1/hSca) to inhibit osteoclast formation. AU - Koide, Masanori. AU - Maeda, Hidefumi. AU - Roccisana, Jennifer L.. AU - Kawanabe, Noriaki. AU - Reddy, Sakamuri V.. PY - 2003/3/1. Y1 - 2003/3/1. N2 - The osteoclast (OCL) is the primary bone resorbing cell. OCL formation and activity is regulated by local factors produced in the bone microenvironment. We recently identified OCL inhibitory peptide-1 (OIP-1/ hSca) as a novel inhibitor of OCL formation and bone resorption that is produced by OCLs. OIP-1 is a glycosylphosphatidyl-inositol (GPI)-linked membrane protein (16 kDa) related to the mouse Ly-6 family of hematopoietic proteins. OIP-1 mRNA is expressed in human OCL precursors, granulocyte-macrophage colony-forming unit (GM-CFU), bone marrow cells, and osteoblast cells. We used cycle-dependent reverse transcriptase-polymerase chain reaction (RT-PCR) analysis, which further demonstrated that ...
Background: Hypothyroidism is associated with dysfunction of the bone turnover with reduced osteoblastic bone formation and osteoclastic bone resorption. Mesenchymal stem cells (MSCs) secrete various factors and cytokines that may stimulate bone regeneration.  The aim of this study was to determine the effects of MSCs-conditioned medium (CM) in hypothyroidism male ...
To determine whether 1,25-dihydroxyvitamin D (1,25(OH)2 D) can exert an anti-osteoporosis role through anti-aging mechanisms, we analyzed the bone phenotype of mice with 1,25(OH)2 D deficiency due to deletion of the enzyme, 25-hydroxyvitamin D 1α-hydroxylase, while on a rescue diet. 1,25(OH)2 D deficiency accelerated age-related bone loss by activating the p16/p19 senescence signaling pathway, inhibiting osteoblastic bone formation, and stimulating osteoclastic bone resorption, osteocyte senescence, and senescence-associated secretory phenotype (SASP). Supplementation of exogenous 1,25(OH)2 D3 corrected the osteoporotic phenotype caused by 1,25(OH)2 D deficiency or natural aging by inhibiting the p16/p19 pathway. The proliferation, osteogenic differentiation, and ectopic bone formation of bone marrow mesenchymal stem cells derived from mice with genetically induced deficiency of the vitamin D receptor (VDR) were significantly reduced by mechanisms including increased oxidative stress, DNA ...
Periodontitis is a common disease that is characterized by resorption of the alveolar bone and mediated by commensal bacteria that trigger host immune responses and bone destruction through unidentified mechanisms. We report that Nod1, an innate intracellular host receptor for bacterial peptidoglycan-related molecules, is critical for commensal-induced periodontitis in a mouse model. Mice lacking Nod1 exhibit reduced bone resorption as well as impaired recruitment of neutrophils to gingival tissues and osteoclasts to the alveolar bone, which mediate tissue and bone destruction. Further analysis showed that accumulation of a Nod1-stimulating commensal bacterium, NI1060, at gingival sites was sufficient to induce neutrophil recruitment and bone resorption. Genomic sequencing revealed that NI1060 is a mouse-specific bacterium that is related to bacteria associated with the development of aggressive periodontitis in humans. These findings provide insight into commensal-host interactions contributing ...
They display a characteristic ruffled border where proteases and acid are secreted, allowing for bone resorption and formation of resorption pits in the bone surface [25]. Osteoclast morphology varies between mammals and teleosts (bony fishes), and also between different groups of teleosts [20]. In the skeleton of young zebrafish for example, osteoclast activity is carried out by both mononucleated and multinucleated cells [26]. In fact, there is an ontogenetic progression from mono- towards multinucleated osteoclasts. In juvenile zebrafish, bone resorbing cells in the developing lower jaw are. at first mononucleated. In thin skeletal tissues such as the neural arch, mononucleated cells are even predominant in adults [26]. In rainbow trout, scale resorption Selleck BIBF1120 PD0325901 is predominantly carried out by mononucleated osteoclasts [27]. Although in mammals these mononucleated cells are often just regarded as osteoclast precursors, in fish mononucleated osteoclasts are active bone ...