scholarly journals Detection of serum bone alkaline phosphatase in 77 adolescents

2017 ◽  
Vol 1 (1) ◽  
Author(s):  
Dingping Shi ◽  
Dafang Wang ◽  
Yonggang Zheng
Keyword(s):  
Alkaline Phosphatase ◽  
Bone Growth ◽  
Bone Development ◽  
Bone Mineralization ◽  
Bone Alkaline Phosphatase ◽  
Bone Change ◽  
Growing Period ◽  
Whole Process ◽  
Second Peak ◽  
The Ideal

In the fast growing period of adolescent children, bone growth and bone mineralization are extremely active. Adulthood is the second peak of bone development, adolescent appropriate calcium intake into the ideal bone peak to achieve an important role. It is important to clear whether or not bone mineralization and to early intervene. Bone alkaline phosphatase (BALP) is the most correct indicator to reflect the whole process of bone change[2], we detected BALPon 177 cases of adolescents in 2007 to, evaluate the measuring meaning.

The influence of ‘hypophysectomy’ on bone growth and alkaline phosphatase activity in the chick embryo

Development ◽  
1973 ◽  
Vol 29 (3) ◽  
pp. 515-527
Author(s):  
D. J. McWhinnie ◽  
Robert C. Thommes
Keyword(s):  
Alkaline Phosphatase ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Bone Growth ◽  
Developmental Time ◽  
Bone Alkaline Phosphatase ◽  
Enzyme Synthesis ◽  
Skeletal Maturation ◽  
Specific Alkaline Phosphatase ◽  
Normal Increase

Wet weights, total bone alkaline phosphatase activity and specific alkaline phosphatase activity were determined on demarrowed femurs of normal, ‘hypophysectomized’ and pituitary-grafted chick embryos at selected intervals of incubation. In normal bones, all parameters noted above increased progressively through developmental time. ‘Hypophysectomy’ by means of surgical decapitation significantly retarded the normal increase of femur wet weight, total and specific alkaline phosphatase activity; in embryos bearing pituitary transplants, there was a return towards normal values. The possible role(s) of the pituitary in skeletal maturation and enzyme synthesis or activation is discussed.

scholarly journals Sorting nexin 27 couples PTHR trafficking to retromer for signal regulation in osteoblasts during bone growth

2016 ◽  
Vol 27 (8) ◽  
pp. 1367-1382 ◽  
Author(s):  
Audrey S. M. Chan ◽  
Thomas Clairfeuille ◽  
Euphemie Landao-Bassonga ◽  
Genevieve Kinna ◽  
Pei Ying Ng ◽  
...  
Keyword(s):  
Electrostatic Interactions ◽  
Bone Growth ◽  
Bone Development ◽  
Bone Mineralization ◽  
Critical Role ◽  
Receptor Internalization ◽  
Binding Motif ◽  
Endosomal Sorting ◽  
Sorting Nexin ◽  
Signal Regulation

The parathyroid hormone 1 receptor (PTHR) is central to the process of bone formation and remodeling. PTHR signaling requires receptor internalization into endosomes, which is then terminated by recycling or degradation. Here we show that sorting nexin 27 (SNX27) functions as an adaptor that couples PTHR to the retromer trafficking complex. SNX27 binds directly to the C-terminal PDZ-binding motif of PTHR, wiring it to retromer for endosomal sorting. The structure of SNX27 bound to the PTHR motif reveals a high-affinity interface involving conserved electrostatic interactions. Mechanistically, depletion of SNX27 or retromer augments intracellular PTHR signaling in endosomes. Osteoblasts genetically lacking SNX27 show similar disruptions in PTHR signaling and greatly reduced capacity for bone mineralization, contributing to profound skeletal deficits in SNX27-knockout mice. Taken together, our data support a critical role for SNX27-retromer mediated transport of PTHR in normal bone development.

scholarly journals BIOCHEMICAL INDICES OF ORAL FLUID AS MARKERS FOR THE FEATURES OF THE STRUCTURAL AND FUNCTIONAL STATE OF THE STOMATOGNATIC SYSTEM IN PERSONS WHO WERE BORN WITH MACROSOMIA

2020 ◽  
pp. 6-17
Author(s):  
O.V. Garmash
Keyword(s):  
Alkaline Phosphatase ◽  
Oral Fluid ◽  
Bone Growth ◽  
Bone Mineralization ◽  
Permanent Teeth ◽  
Anthropometric Parameters ◽  
Inflammatory Disorders ◽  
Periodontal Tissues ◽  
Younger Age ◽  
High Calcium

Two hundred sixty eight people in the Kharkiv and surrounding Provinces' population have been examined: one hundred sixty eight persons were born with macrosomia, and fifty persons were born with weight and height parameters that correspond to the norm. The macrosomic-at-birth persons were divided into groups, with allowance for the features of their intrauterine development. The levels of total calcium, inorganic phosphorus, and alkaline phosphatase activity were determined in an unstimulated oral fluid. In the macrosomic-at-birth persons, who did not show the symptoms of overweight at the time of birth (Subgroups 1 and 2), the high levels of calcium, phosphorus, and alkaline phosphatase have been revealed in the oral fluid over younger age periods, which may be a consequence of intrauterine hyperthyroidism. The high calcium levels may also be due to the exposure to the elevated concentrations of growth hormone, which stimulated bone growth, and which shifted the peak of jaw growth to a younger age. This is an explanation for the high prevalence of dentoalveolar abnormalities in children. In such individuals, a significant increase in the activity of alkaline phosphatase and in the levels of phosphorus and calcium in the oral fluid is observed to occur with age, which is associated with the formation of dystrophic and inflammatory disorders of periodontal tissues with a predominance of the inflammatory component (periodontitis). In the 4–11-year-old macrosomic-at-birth persons born with the signs of overweight (Subgroups 3 and 4), a decrease in the activity of alkaline phosphatase and in the levels of phosphorus and calcium in the oral fluid has been revealed, which provides evidence for a low level of bone mineralization in such individuals, obviously due to an intrauterine decrease in thyroid activity. This explains the formation of a higher percentage of dentoalveolar abnormalities and agrees well with the information about the high intensity of deciduous and permanent teeth caries. In such individuals, the level of calcium in the oral fluid significantly increased in older age periods, which is consistent with information on the formation of dystrophic and inflammatory disorders of periodontal tissues in most of these individuals with a predominance of dystrophic component (periodontosis). Due to the modulation of the activity of the corresponding enzymes, an increase in the level of calcium is associated with hypercortisolemia and with the effect of cortisol on bone remodeling processes, and it is a consequence of the progression of metabolic inflammation. Conclusions. Changes in the indices of phosphorus-calcium metabolism and in the activity of alkaline phosphatase in the oral fluid can be used as markers for the development of disorders of the stomatognathic system, for various variants of the course of dystrophic-inflammatory diseases of periodontal tissues, and for caries in individuals who were born with macrosomia, taking into account their various anthropometric parameters at birth.

scholarly journals Bone Alkaline Phosphatase and Tartrate-Resistant Acid Phosphatase: Potential Co-regulators of Bone Mineralization

2017 ◽  
Vol 101 (1) ◽  
pp. 92-101 ◽  
Author(s):  
Cecilia Halling Linder ◽  
Barbro Ek-Rylander ◽  
Michael Krumpel ◽  
Maria Norgård ◽  
Sonoko Narisawa ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Acid Phosphatase ◽  
Bone Mineralization ◽  
Bone Alkaline Phosphatase ◽  
Tartrate Resistant Acid Phosphatase

Taurine, Bone Growth and Bone Development

2008 ◽  
Vol 4 (2) ◽  
pp. 135-144 ◽  
Author(s):  
Sung-Jin Kim ◽  
Hyeon Lee ◽  
Ramesh Gupta
Keyword(s):  
Bone Growth ◽  
Bone Development

P1237TISSUE-NONSPECIFIC ALKALINE PHOSPHATASE, A CULPRIT DURING ARTERIAL MEDIA CALCIFICATION BUT INDISPENSABLE DURING PHYSIOLOGICAL BONE FORMATION/-MINERALIZATION IN RATS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Britt Opdebeeck ◽  
José Millan Luis ◽  
Anthony Pinkerton ◽  
Anja Verhulst ◽  
Patrick D'Haese ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Bone Formation ◽  
Vascular Calcification ◽  
Rat Model ◽  
Bone Mineralization ◽  
Calcium Content ◽  
Marker Genes ◽  
Peripheral Arteries ◽  
Calcium Phosphorus ◽  
Chondrogenic Marker

Abstract Background and Aims Vascular media calcification is frequently seen in elderly and patients with chronic kidney disease (CKD), diabetes and osteoporosis. Pyrophosphate is a well-known calcification inhibitor that binds to nascent hydroxyapatite crystals and prevents further incorporation of inorganic phosphate into these crystals. However, the enzyme tissue-nonspecific alkaline phosphatase (TNAP), which is highly expressed in calcified arteries, degrades extracellular pyrophosphate into phosphate ions, by which pyrophosphate loses its ability to block vascular calcification. Here, we aimed to evaluate whether a TNAP inhibitor is able to prevent the development of arterial calcification in a rat model of warfarin-induced vascular calcification. Method To induce vascular calcification, rats received a diet containing 0.30% warfarin and 0.15% vitamin K1 throughout the entire study and were subjected to the following daily treatments: (i) vehicle (n=10) or (ii) 10 mg/kg/day TNAP-inhibitor (n=10) administered via an intraperitoneal catheter from start of the study until sacrifice at week 7. Calcium, phosphorus and parathyroid hormone (PTH) levels were determined in serum samples as these are important determinants of vascular calcification. As TNAP is also expressed in the liver, serum alanine aminotransferase (ALT) and aspartate (AST) levels were analyzed. At sacrifice, vascular calcification was evaluated by measurement of the total calcium content in the arteries and quantification of the area % calcification on Von Kossa stained sections of the aorta. The mRNA expression of osteo/chondrogenic marker genes (runx2, TNAP, SOX9, collagen 1 and collagen 2) was analyzed in the aorta by qPCR to verify whether vascular smooth muscle cells underwent reprogramming towards bone-like cells. Bone histomorphometry was performed on the left tibia to measure static and dynamic bone parameters as TNAP also regulates physiological bone mineralization. Results No differences in serum calcium, phosphorus and PTH levels was observed between both study groups. Warfarin exposure resulted in distinct calcification in the aorta and peripheral arteries. Daily dosing with the TNAP inhibitor (10 mg/kg/day) for 7 weeks significantly reduced vascular calcification as indicated by a significant decrease in calcium content in the aorta (vehicle 3.84±0.64 mg calcium/g wet tissue vs TNAP inhibitor 0.70±0.23 mg calcium/g wet tissue) and peripheral arteries and a distinct reduction in area % calcification on Von Kossa stained aortic sections as compared to vehicle condition. The inhibitory effects of SBI-425 on vascular calcification were without altering serum liver markers ALT and AST levels. Furthermore, TNAP-inhibitor SBI-425 did not modulate the mRNA expression of osteo/chondrogenic marker genes runx2, TNAP, SOX9, collagen 1 and 2. Dosing with SBI-425 resulted in decreased bone formation rate and mineral apposition rate, and increased osteoid maturation time and this without significant changes in osteoclast- and eroded perimeter. Conclusion Dosing with TNAP inhibitor SBI-425 significantly reduced the calcification in the aorta and peripheral arteries of a rat model of warfarin-induced vascular calcification and this without affecting liver function. However, suppression of TNAP activity should be limited in order to maintain adequate physiological bone mineralization.

scholarly journals New insights into vitamin D regulation: is there a role for alkaline phosphatase?

2021 ◽  
Author(s):  
G. Bellastella ◽  
L. Scappaticcio ◽  
M. Longo ◽  
R. Carotenuto ◽  
C. Carbone ◽  
...  
Keyword(s):  
Vitamin D ◽  
Alkaline Phosphatase ◽  
Liver Function ◽  
Significant Negative Correlation ◽  
Liver Function Tests ◽  
Bone Alkaline Phosphatase ◽  
Gamma Glutamyl Transpeptidase ◽  
Function Tests ◽  
Group 2 ◽  
Group 1

Abstract Purpose The diagnosis of vitamin D deficiency is based on the determination of total plasma 25-hydroxyvitamin D (25-OHD) concentrations, but the regulation of vitamin D 25-hydroxylation is not a major consideration and very little information is available on this activity. To check what factors could interfere with the activity of vitamin D-25-hydroxylase and thus alter the 25-OHD concentrations, we looked for potential correlations between 25-OHD and results of liver function tests in healthy adults. Methods This single-centre study was retrospective and consisted of evaluating the correlations between 25-OHD and the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), alkaline phosphatase (ALP), and bone alkaline phosphatase (BALP) in 349 healthy subjects aged from 18 to 65 years. In particular, in Group 1 (n = 119), we looked for correlations between 25OHD and all liver function tests and in Group 2 (n = 230) the correlation between 25OHD and BALP. Results In Group 1, we found no correlation between 25OHD and AST (r =  − 0.03; p = 0.8), ALT (r =  − 0.02; p = 0.91), GGT (r =  − 0.08; p = 0.68), direct bilirubin (r =  − 0.02; p = 0.89), indirect bilirubin (r =  − 0.24; p = 0.21), and total bilirubin (r =  − 0.24; p = 0.21) but one between 25OHD and ALP (r =  − 0.2; p = 0.007); in Group 2, we found a significant negative correlation between 25-OHD and BALP (r =  − 0.2; p = 0.0008). Conclusions The correlations that we found suggest that ALP and BALP might be involved in the regulation of vitamin D-25-hydroxylase activity, but further studies are mandatory to confirm our assumptions.

scholarly journals PP2A in LepR+ mesenchymal stem cells contributes to embryonic and postnatal endochondral ossification through Runx2 dephosphorylation

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Yu-Ting Yen ◽  
May Chien ◽  
Pei-Yi Wu ◽  
Shih-Chieh Hung
Keyword(s):  
Stem Cells ◽  
Alkaline Phosphatase ◽  
Mesenchymal Stem Cells ◽  
Bone Density ◽  
Endochondral Ossification ◽  
Bone Growth ◽  
Leptin Receptor ◽  
Trabecular Bone Density ◽  
Mature Adipocyte ◽  
Ossification Centers

AbstractIt has not been well studied which cells and related mechanisms contribute to endochondral ossification. Here, we fate mapped the leptin receptor-expressing (LepR+) mesenchymal stem cells (MSCs) in different embryonic and adult extremities using Lepr-cre; tdTomato mice and investigated the underling mechanism using Lepr-cre; Ppp2r1afl/fl mice. Tomato+ cells appear in the primary and secondary ossification centers and express the hypertrophic markers. Ppp2r1a deletion in LepR+ MSCs reduces the expression of Runx2, Osterix, alkaline phosphatase, collagen X, and MMP13, but increases that of the mature adipocyte marker perilipin, thereby reducing trabecular bone density and enhancing fat content. Mechanistically, PP2A dephosphorylates Runx2 and BRD4, thereby playing a major role in positively and negatively regulating osteogenesis and adipogenesis, respectively. Our data identify LepR+ MSC as the cell origin of endochondral ossification during embryonic and postnatal bone growth and suggest that PP2A is a therapeutic target in the treatment of dysregulated bone formation.

scholarly journals Hypophosphatasia: A Unique Disorder of Bone Mineralization

2021 ◽  
Vol 22 (9) ◽  
pp. 4303
Author(s):  
Juan Miguel Villa-Suárez ◽  
Cristina García-Fontana ◽  
Francisco Andújar-Vera ◽  
Sheila González-Salvatierra ◽  
Tomás de Haro-Muñoz ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Genetic Disease ◽  
Therapeutic Strategy ◽  
Pediatric Patients ◽  
Bone Mineralization ◽  
Clinical Manifestations ◽  
Allelic Heterogeneity ◽  
Specific Enzyme ◽  
Inorganic Pyrophosphate ◽  
Enzyme Replacement

Hypophosphatasia (HPP) is a rare genetic disease characterized by a decrease in the activity of tissue non-specific alkaline phosphatase (TNSALP). TNSALP is encoded by the ALPL gene, which is abundantly expressed in the skeleton, liver, kidney, and developing teeth. HPP exhibits high clinical variability largely due to the high allelic heterogeneity of the ALPL gene. HPP is characterized by multisystemic complications, although the most common clinical manifestations are those that occur in the skeleton, muscles, and teeth. These complications are mainly due to the accumulation of inorganic pyrophosphate (PPi) and pyridoxal-5′-phosphate (PLP). It has been observed that the prevalence of mild forms of the disease is more than 40 times the prevalence of severe forms. Patients with HPP present at least one mutation in the ALPL gene. However, it is known that there are other causes that lead to decreased alkaline phosphatase (ALP) levels without mutations in the ALPL gene. Although the phenotype can be correlated with the genotype in HPP, the prediction of the phenotype from the genotype cannot be made with complete certainty. The availability of a specific enzyme replacement therapy for HPP undoubtedly represents an advance in therapeutic strategy, especially in severe forms of the disease in pediatric patients.

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