Acidosis inhibits osteoblastic and stimulates osteoclastic activity in vitro

1992 ◽  
Vol 262 (3) ◽  
pp. F442-F448 ◽  
Author(s):  
N. S. Krieger ◽  
N. E. Sessler ◽  
D. A. Bushinsky
Keyword(s):  
Alkaline Phosphatase ◽  
Metabolic Acidosis ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Collagen Synthesis ◽  
Calcium Flux ◽  
Osteoclastic Activity ◽  
Glucuronidase Activity

Metabolic acidosis induces net calcium flux (JCa) from cultured neonatal mouse calvariae through physicochemical and cell-mediated mechanisms. To determine the role of osteoblasts in acid-induced JCa, collagen synthesis and alkaline phosphatase activity were assessed in calvariae incubated in reduced pH and bicarbonate medium, a model of metabolic acidosis (Met), and compared with controls (Ctl). Collagen synthesis fell from 30.5 +/- 1.1 in Ctl to 25.1 +/- 0.4% with Met, and alkaline phosphatase decreased from 403 +/- 25 in Ctl to 298 +/- 21 nmol Pi.min-1.mg protein-1 with Met. During acidosis JCa was correlated inversely with percent collagen synthesis (r = -0.743, n = 11, P = 0.009) and with alkaline phosphatase activity (r = -0.453, n = 22, P = 0.034). To determine the role of osteoclasts in acid-induced JCa, osteoclastic beta-glucuronidase activity was determined in Ctl and Met in the absence or presence of the osteoclastic inhibitor calcitonin (CT, 3 x 10(-9) M). Met increased beta-glucuronidase (5.9 +/- 0.2) compared with Ctl (4.6 +/- 0.3 micrograms phenolphthalein released.bone-1.h-1), whereas CT inhibited beta-glucuronidase in both Ctl and Met (3.1 +/- 0.2 and 3.5 +/- 0.3, respectively). During acidosis JCa was correlated directly with beta-glucuronidase activity (r = 0.683, n = 42, P less than 0.001). Thus the cell-mediated component of JCa during acidosis in vitro appears to result from a combination of inhibited osteoblastic and stimulated osteoclastic activity.

Stimulated osteoclastic and suppressed osteoblastic activity in metabolic but not respiratory acidosis

1995 ◽  
Vol 268 (1) ◽  
pp. C80-C88 ◽  
Author(s):  
D. A. Bushinsky
Keyword(s):  
Alkaline Phosphatase ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Collagen Synthesis ◽  
Cell Function ◽  
Respiratory Acidosis ◽  
Bone Cell ◽  
Calcium Efflux ◽  
Osteoblastic Activity ◽  
Glucuronidase Activity

When bone is cultured in acidic medium produced by a reduced bicarbonate concentration ([HCO(3-)]), a model of metabolic acidosis, there is greater net calcium efflux than when the same decrement in pH is produced by an increased partial pressure of carbon dioxide (PCO2), a model of respiratory acidosis. To determine the effects of metabolic and respiratory acidosis on bone cell function we cultured neonatal mouse calvariae for 48 h under control conditions (pH approximately 7.40, PCO2 approximately 41 mmHg, [HCO(3-)] approximately 25 meq/l) or under isohydric acidic conditions simulating metabolic (pH approximately 7.09, [HCO(3-)] approximately 12) or respiratory (pH approximately 7.10, PCO2 approximately 86) acidosis and measured osteoblastic collagen synthesis and alkaline phosphatase activity and osteoclastic beta-glucuronidase activity. Collagen synthesis was inhibited by metabolic (23.2 +/- 1.3 vs. 30.3 +/- 1.0% in control) but was not altered by respiratory (32.3 +/- 0.6) acidosis. Alkaline phosphatase activity was inhibited by metabolic (402 +/- 16 vs. 471 +/- 15 nmol P.min-1.mg protein-1 in control) but not altered by respiratory (437 +/- 25) acidosis. beta-Glucuronidase activity was stimulated by metabolic (1.02 +/- 0.06 vs. 0.78 +/- 0.05 micrograms phenolphthalein released.bone-1.h-1 in control) but not altered by respiratory (0.73 +/- 0.06) acidosis. Net calcium efflux in control was increased by metabolic (783 +/- 57 vs. 20 +/- 57 nmol.bone-1.48 h-1 in control) and by respiratory (213 +/- 45) acidosis; however, calcium efflux with metabolic was greater than with respiratory acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

The inhibitory effects of vancomycin on rat bone marrow–derived mesenchymal stem cell differentiation

2021 ◽  
pp. 1-5
Author(s):  
Kari Hanson ◽  
Carly Isder ◽  
Kristen Shogren ◽  
Anthony L. Mikula ◽  
Lichun Lu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Alkaline Phosphatase ◽  
Osteogenic Differentiation ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
High Dose ◽  
Inhibitory Effects ◽  
Alizarin Red ◽  
Osteogenic Factors

OBJECTIVE The use of intrawound vancomycin powder in spine surgery has been shown to decrease the rate of surgical site infections; however, the optimal dose is unknown. High-dose vancomycin inhibits osteoblast proliferation in vitro and may decrease the rate of solid arthrodesis. Bone marrow–derived mesenchymal stem cells (BMSCs) are multipotent cells that are a source of osteogenesis in spine fusions. The purpose of this study was to determine the effects of vancomycin on rat BMSC viability and differentiation in vitro. METHODS BMSCs were isolated from the femurs of immature female rats, cultured, and then split into two equal groups; half were treated to stimulate osteoblastic differentiation and half were not. Osteogenesis was stimulated by the addition of 50 µg/mL l-ascorbic acid, 10 mM β-glycerol phosphate, and 0.1 µM dexamethasone. Vancomycin was added to cell culture medium at concentrations of 0, 0.04, 0.4, or 4 mg/mL. Early differentiation was determined by alkaline phosphatase activity (4 days posttreatment) and late differentiation by alizarin red staining for mineralization (9 days posttreatment). Cell viability was determined at both the early and late time points by measurement of formazan colorimetric product. RESULTS Viability within the first 4 days decreased with high-dose vancomycin treatment, with cells receiving 4 mg/mL vancomycin having 40%–60% viability compared to the control. A gradual decrease in alizarin red staining and nodule formation was observed with increasing vancomycin doses. In the presence of the osteogenic factors, vancomycin did not have deleterious effects on alkaline phosphatase activity, whereas a trend toward reduced activity was seen in the absence of osteogenic factors when compared to osteogenically treated cells. CONCLUSIONS Vancomycin reduced BMSC viability and impaired late osteogenic differentiation with high-dose treatment. Therefore, the inhibitory effects of high-dose vancomycin on spinal fusion may result from both reduced BMSC viability and some impairment of osteogenic differentiation.

The influence of titanium surfaces treated by alkalis on macrophage and osteoblast-like cell adhesion and gene expression in vitro

RSC Advances ◽  
2015 ◽  
Vol 5 (99) ◽  
pp. 81378-81387 ◽  
Author(s):  
Ting Ma ◽  
Xi-Yuan Ge ◽  
Sheng-Nan Jia ◽  
Xi Jiang ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alkaline Phosphatase ◽  
Cell Adhesion ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Related Gene ◽  
Titanium Surfaces

The effect of alkali-treated titanium surfaces on inflammation-related gene expression of macrophages and alkaline phosphatase activity of osteoblast-like cells.

scholarly journals THE ROLE OF ALKALINE PHOSPHATASE IN OSTEOGENESIS

1951 ◽  
Vol 93 (5) ◽  
pp. 415-426 ◽  
Author(s):  
Robert S. Siffert
Keyword(s):  
Alkaline Phosphatase ◽  
Phosphatase Activity ◽  
Bone Matrix ◽  
Living Cells ◽  
Alkaline Solutions ◽  
Human Beings ◽  
Acid Media ◽  
Weakly Acid

The role of alkaline phosphatase in osteogenesis has been investigated by histochemical techniques with particular attention to its relationship to phosphate metabolism and matrix elaboration. The upper tibial epiphysis mainly, and other epiphyses as well of growing rabbits, and the costochondral junctions of newborn human beings were studied, as were bone grafts in growing rabbits. The findings in the newborn human beings were identical with those in the rabbits. Phosphatase activity and free phosphate localization do not universally coincide. The enzyme appears to be intimately related to preosseous cellular metabolism and to the elaboration of a bone matrix that is chemically calcifiable. It remains possible, however, that phosphatase may be in some way involved in making inorganic salts available to the calcifiable matrix. If this function does exist it is a secondary one, since the elaboration of bone matrix, which is always associated with phosphatase activity, can and does occur in the absence of calcification. Calcification may occur later, in the absence of the enzyme. There is evidence to suggest that cartilage matrix is utilized in the formation of bone matrix. Phosphatase is physiologically active only in the presence of living cells. Where it is demonstrable in the absence of living cells, as in the cartilage remnants of the metaphysis, it appears to be physiologically inactive. Since phosphatase is temporarily inactivated in weakly acid media, and readily reactivated by alkaline solutions it is possible that the enzyme might survive in a physiologically inactive state in weakly acid tissues, and yet remain capable of histochemical demonstration in vitro in an alkaline medium. Phosphatase is not related to the disappearance of chondroitin sulfate.

RICKETS, DEFICIENCY OF "ALKALINE" PHOSPHATASE ACTIVITY AND PREMATURE LOSS OF TEETH IN CHILDHOOD

PEDIATRICS ◽  
1953 ◽  
Vol 11 (4) ◽  
pp. 309-322
Author(s):  
EDNA H. SOBEL ◽  
LELAND C. CLARK ◽  
R. PHYLLIS FOX ◽  
MEINHARD ROBINOW
Keyword(s):  
Alkaline Phosphatase ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Enzyme Treatment ◽  
Deciduous Teeth ◽  
Local Factor ◽  
Plasma Alkaline Phosphatase ◽  
Serum Inorganic Phosphate ◽  
Genetically Determined

A child, studied between the ages of 1½ and 3½ years, presented an abnormally low plasma alkaline phosphatase activity (0.8-1.64 Bessey-Lowry u.), a deformed skeleton and the loss of most of her deciduous teeth. The serum Ca was normal; the serum inorganic phosphate remained at the normal relatively high levels of infancy as the child grew older Roentgenograms demonstrated deficient mineralization of the skeleton and teeth. Biopsies of the liver and the costochondral junction displayed a deficiency of tissue alkaline phosphatase activity. The architecture of the rib was consistent with rickets. There was no evidence for the presence of an inhibitor of alkaline phosphatase, such as beryllium, or for an excessive excretion of the enzyme. Treatment with purified growth hormone, ascorbic acid and thiamin chloride had no effect, while vitamin D 500 thousand u. caused little change in the enzyme activity in a 10 day period. The father had low plasma alkaline phosphatase activity and a number of similar patients are mentioned, for whom there was also evidence that the deficiency in alkaline phosphatase activity may be genetically determined. While the precise role of alkaline phosphatase activity in the metabolism of bone is not clear, the findings in this patient suggest that growing bone may require the presence of alkaline phosphatase for normal calcification, and that the skeletal disorder, which could not be distinguished from rickets, may be related to a disturbance in the local factor.

scholarly journals Endocrine Relationships of Leukocyte Alkaline Phosphatase

Blood ◽  
1965 ◽  
Vol 25 (3) ◽  
pp. 356-369 ◽  
Author(s):  
FRED ROSNER ◽  
STANLEY L. LEE
Keyword(s):  
Alkaline Phosphatase ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Mean Value ◽  
Conclusive Evidence ◽  
In Vitro Tests ◽  
Enzyme Release ◽  
Men And Women ◽  
Leukocyte Alkaline Phosphatase

Abstract Leukocyte alkaline phosphatase activity has been noted to be different in men and women. The mean leukocyte alkaline phosphatase activity for 74 normal men, aged 19 to 60 years, was 23 mg. of phosphorus per 1010 polvmorphonuclear leukocytes per hour. The corresponding mean value for 75 normal young women, age 19-48 years, was 35 (p < .001). No significant differences between boys and girls occurred until the time of puberty. After the menopause, the values for women approached the values for men. Women treated with androgens had lower leukocyte alkaline phosphatase activity than did control women. These results suggest that androgenic hormones inhibit this enzyme, and that other, as yet undefined endocrine influences, also affect its level of activity. In vitro tests with various concentrations of androgens and estrogens failed to provide conclusive evidence of direct effect on leukocytes although some degree of direct inhibition by androgens was suggested. Studies using saponin to effect enzyme release from leukocyte granules did not demonstrate whether the differences between men and women are differences of enzyme release or of content of leukocyte alkaline phosphatase.

Alkaline phosphatase activity in the plasma of children and adolescents.

1977 ◽  
Vol 23 (3) ◽  
pp. 469-472 ◽  
Author(s):  
G A Fleisher ◽  
E S Eickelberg ◽  
L R Elveback
Keyword(s):  
Alkaline Phosphatase ◽  
Public Schools ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Serum Alkaline Phosphatase ◽  
Intraclass Correlation ◽  
Serum Alkaline Phosphatase Activity ◽  
Upper Limits ◽  
Prepubertal Girls

Abstract We determined plasma (serum alkaline phosphatase activity in 854 healthy students of the Rochester, Minnesota, public schools. Prepubertal girls had somewhat greater upper limits than did boys, and there was a low trend of increasing activity in both sexes. At the beginning of adolescence increasing activities were observed, which peaked at ages 11 to 12 years in girls and at ages 13 to 14 in boys. Adult values were not reached until six to eight years later. In 180 pairs of siblings, a significant intraclass correlation was noted. A possible role of alkaline phosphatase in the regulation of protein synthesis is suggested.

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