Pathophysiological implication of Autotaxin on osteoclast function

2016 ◽  
Author(s):  
Sacha Flammier ◽  
Tristan Gicquel ◽  
Francois Duboeuf ◽  
Olivier Peyruchaud ◽  
Fabienne Coury ◽  
...  
Keyword(s):  
Osteoclast Function

Paget’s disease: clinical update

2011 ◽  
Vol 152 (33) ◽  
pp. 1337-1346
Author(s):  
Judit Donáth ◽  
Gyula Poór
Keyword(s):  
Alkaline Phosphatase ◽  
Serum Alkaline Phosphatase ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Etiologic Role ◽  
Osteoblast Activity ◽  
Chronic Disorder ◽  
Abnormal Increase ◽  
Osteoclast Function ◽  
High Level

Paget’s disease is a chronic disorder of bone remodeling, characterized by an abnormal increase of osteoclast and, hence, osteoblast activity. The imbalance of bone turnover results in the formation of unhealthy and fragile bone. It also leads to impairment of adjacent joints and to a risk of various complications. Current research focuses on the elucidation of the etiologic role viral infection and predisposing genetic factors. Paget’s disease is commonly discovered by chance; its suspicion is raised either by high level of alkaline phosphatase or by the X-ray of the pathological bone. Bisphosphonates have proven to be effective in controlling disease activity because they inhibit osteoclast function. Their use is recommended when bone-derived serum alkaline phosphatase is high and/or when disease localizations are highly suspected for the development of complications. Orv. Hetil., 2011, 152, 1337–1346.

scholarly journals Absence of Dap12 and the αvβ3 integrin causes severe osteopetrosis

2014 ◽  
Vol 208 (1) ◽  
pp. 125-136 ◽  
Author(s):  
Wei Zou ◽  
Steven L. Teitelbaum
Keyword(s):  
Bone Mass ◽  
Αvβ3 Integrin ◽  
Skeletal Phenotype ◽  
Osteoclast Function ◽  
Deficient Mice

In vitro, ligand occupancy of αvβ3 integrin induces phosphorylation of Dap12, which is essential for osteoclast function. Like mice deleted of only αvβ3, Dap12−/− mice exhibited a slight increase in bone mass, but Dap12−/− mice, lacking another ITAM protein, FcRγ, were severely osteopetrotic. The mechanism by which FcRγ compensates for Dap12 deficiency is unknown. We find that co-deletion of FcRγ did not exacerbate the skeletal phenotype of β3−/− mice. In contrast, β3/Dap12 double-deficient (DAP/β3−/−) mice (but not β1/Dap12 double-deficient mice) were profoundly osteopetrotic, reflecting severe osteoclast dysfunction relative to those lacking αvβ3 or Dap12 alone. Activation of OSCAR, the FcRγ co-receptor, rescued Dap12−/− but not DAP/β3−/−osteoclasts. Thus, the absence of αvβ3 precluded compensation for Dap12 deficiency by FcRγ. In keeping with this, Syk phosphorylation did not occur in OSCAR-activated DAP/β3−/− osteoclasts. Thus, FcRγ requires the osteoclast αvβ3 integrin to normalize the Dap12-deficient skeleton.

A new mutation in the KINDLIN-3 gene ablates integrin-dependent leukocyte, platelet, and osteoclast function in a patient with leukocyte adhesion deficiency-III

2015 ◽  
Vol 62 (9) ◽  
pp. 1677-1679 ◽  
Author(s):  
Roman Crazzolara ◽  
Kathrin Maurer ◽  
Harald Schulze ◽  
Barbara Zieger ◽  
Jozef Zustin ◽  
...  
Keyword(s):  
Leukocyte Adhesion ◽  
Leukocyte Adhesion Deficiency ◽  
New Mutation ◽  
Osteoclast Function

Osteoclast Function

2008 ◽  
pp. 193-209 ◽  
Author(s):  
H. Kalervo Väänänen ◽  
Haibo Zhao
Keyword(s):  
Osteoclast Function

scholarly journals Plasminogen/plasmin modulates bone metabolism by regulating the osteoblast and osteoclast function.

2014 ◽  
Vol 289 (22) ◽  
pp. 15154-15154 ◽  
Author(s):  
Yosuke Kanno ◽  
Akira Ishisaki ◽  
Eri Kawashita ◽  
Naoyuki Chosa ◽  
Keiichi Nakajima ◽  
...  
Keyword(s):  
Bone Metabolism ◽  
Osteoclast Function

scholarly journals Long Term Cyclic Pamidronate Reduces Bone Growth by Inhibiting Osteoclast Mediated Cartilage-to-Bone Turnover in the Mouse

2008 ◽  
Vol 2 (1) ◽  
pp. 121-125 ◽  
Author(s):  
K.D Evans ◽  
L.E Sheppard ◽  
D.I Grossman ◽  
S.H Rao ◽  
R.B Martin ◽  
...  
Keyword(s):  
Bone Turnover ◽  
Growth Plate ◽  
Bone Growth ◽  
Cathepsin K ◽  
Chondrocyte Apoptosis ◽  
Cell Numbers ◽  
Hypertrophic Chondrocyte ◽  
Osteoclast Function ◽  
And Function

Bisphosphonates, used to treat diseases exhibiting increased osteoclast activity, reduce longitudinal bone growth through an as yet undefined mechanism. Pamidronate, an aminobisphosphonate, was given weekly to mice at 0, 1.25, or 2.50 mg/kg/wk beginning at 4 weeks of age. At 12 weeks of age, humeral length, growth plate area, regional chondrocyte cell numbers, chondrocyte apoptosis, TRAP stained osteoclast number, and osteoclast function assessed by cathepsin K immunohistochemistry were quantified. Humeral length was decreased in pamidronate treated mice compared to vehicle control mice, and correlated with greater growth plate areas reflecting greater proliferative and hypertrophic chondrocyte cell numbers with fewer hypertrophic cells undergoing apoptosis. Pamidronate treatment increased TRAP stained osteoclast numbers yet decreased cathepsin K indicating that pamidronate repressed osteoclast maturation and function. The data suggest that long term cyclic pamidronate treatment impairs bone growth by inhibition of osteoclast maturation thereby reducing cartilage-to-bone turnover within the growth plate.

Analysis of Osteoclast Function in Mouse Calvarial Cultures

2003 ◽  
pp. 169-182
Author(s):  
Michael J. Marshall ◽  
Marit N. Rowlands
Keyword(s):  
Osteoclast Function
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