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Biomedical subjects

A L Boskey

Publications and source records attributed to A L Boskey.

At least 145 records · Page 8Linked to original sources
PubMed1983

Lack of lipid involvement in nonosseous tissue repair.

Calcium-acidic phospholipid-phosphate complexes (Ca-PL-PO4) have been implicated in the onset of tissue mineralization in healing fracture callus as well as in normal osteogenesis. Although these complexes are not found in nonmineralizing normal tissues, the possibility that they are more involved in healing phenomena than in actual mineralization cannot be excluded. The present study confirms that Ca-PL-PO4 complexes are only involved with osseous repair. In healing skin at 5, 8, and 11 days after wounding, Ca-PL-PO4 concentration was not significantly elevated (percentage complexed lipid P/total lipid P: 3.7, 2.4, and 3.8, respectively) relative to the value found for normal skin (2 +/- 2%), although the total lipid phosphorus content at 8 and 11 days was increased.

Animals↗
PubMed1983

Chemical, microscopic, and ultrastructural characterization of the mineral deposits in tumoral calcinosis.

The presence of hydroxyapatite has been determined based on ultrastructure, X-ray diffraction, electron diffraction, and chemical analysis, and confirmed by microprobe analysis in multiple deposits surgically excised from four unrelated patients with tumoral calcinosis. The chemical composition of each of the mineralized deposits resembled bone, rather than dermis, in mineral, uronic acid, total lipid, and complexed acidic phospholipid composition. No collagen abnormalities were detected. However, all of these deposits differed from normal bone mineral, being heavily mineralized and containing larger, more perfect hydroxyapatite crystals. Ultrastructurally, the crystals were both extracellular and within mononuclear cells in close proximity to dilated rough endoplasmic reticulum.

Adolescent↗
PubMed1982

hard tissue biochemistry: a comparison of fresh-frozen and formalin-fixed tissue samples.

Formalin fixation of hard tissues alters the levels of some, but not all, of the parameters routinely measured by bone researchers. Although mineral parameters (ash weight, particle size (beta 1/2 002) and Ca/PO4 ratio) and lipid parameters (total lipid content and composition, extractability, and Ca-acidic phospholipid phosphate content) are not affected by formalin fixation, the uronate and DNA contents are reduced in formalin-fixed bone while hydroxyproline content is elevated.

Bone and Bones↗
PubMed1982

Comparative biochemical studies of the callus matrix in immobilized and non-immobilized fractures.

Fracture healing in both non-immobilized and immobilized rat fracture callus, though different radiographically and histologically; is characterized by similar biochemical changes in the ground substance. Although the callus formed in the immobilized model is appreciably smaller than that formed when the fracture is not immobilized, the chemical composition of the organic matrix of the existing callus undergoes similar modifications regardless of fixation and histological response. Previous studies of endochondral fracture repair have demonstrated an elevation in fracture callus hexosamine content during the early stages of healing of the non-immobilized fracture. This corresponded histologically to a predominance of cartilaginous tissue in the callus matrix. In the present study, the biochemistry, histology, and roentgenographic features of stabilized and non-stabilized rat fractures are compared. Similar elevations in hexosamine are noted at two weeks in both models. These elevations are attributed to changes in proteoglycan rather than glycoprotein concentration of the tissue.

Animals↗
PubMed1982

Calcium-acidic phospholipid-phosphate complexes in diseased and normal human bone.

Ca-acidic phospholipid-PO4 complexes promote in vitro hydroxyapatite nucleation and/or growth and are believed to have similar functions in vivo. The complexed acidic phospholipid content of human bones has been studied in femoral heads obtained at surgery from patients with osteonecrosis and osteoarthritis and compared with age-matched, disease-free control bones. The content of Ca-acidic phospholipid-PO4 complexes was elevated in bones that were judged on the basis of radiographic and histological data to be actively making new bone. These data suggest that the relative concentration of Ca-acidic phospholipid-PO4 in bone may be related to the rate at which bone is being made and mineralized.

Adolescent↗
PubMed1982

Optimal conditions for Ca-acidic phospholipid-PO4 formation.

Calcium-acidic phospholipid-phosphate complexes (Ca-PL-PO4) cause hydroxyapatite (HA) deposition in vitro. The acidic phospholipids--phosphatidylserine (PS), phosphatidylinositol (PI), phosphatidylglycerol (PG), and diphosphatidylglycerol (DPG)--all form Ca-PL-PO4 complexes: Nonacidic phospholipids--sphingomyelin (SPL), phosphatidylcholine (PC) and phosphatidylethanolamine (PE)--do not form Ca-PL-PO4 and do not induce hydroxyapatite (HA) deposition in low ionic strength metastable calcium phosphate solution or in synthetic lymph. The extent to which each of the acidic phospholipids reacts with calcium and inorganic phosphate, and the chemical composition of the Ca-PL-PO4 complexes is a function of pH, solution composition, the nature of the phospholipid, and the method of isolation. The addition of inorganic phosphate prior to or in combination with calcium appears to be an absolute requirement for Ca-PL-PO4 formation.

Calcium↗
PubMed1981

Current concepts of the physiology and biochemistry of calcification.

The current picture of the process of biological calcifications portrays the cells within the calcifying tissues as central factors controlling the deposition of mineral crystals in the extracellular matrix. The cell responds to hormones and second messengers, and other changes in its environment, regulating the concentration of ions within the extracellular matrix and secreting macromolecules whose properties determine the ability of the matrix to be calcified. The mitochondria within the cells accumulate calcium and phosphate, releasing these ions into the matrix as calcification progresses. Extracellular matrix vesicles, derived from the cells of some, but not all, calcifying matrices, provide sites for initial mineral deposition in many tissues. Among the macromolecules secreted by the cell, collagen provides the support for the hydroxyapatite crystals; proteoglycans serve to control the extent and/or progress of mineralization. The proteoglycans, glycoproteins, enzymes and the collagen itself, along with the cells, determine the nature of the matrix, while phosphoproteins, proteolipids, and phospholipids may serve as hydroxyapatite nucleators or as surfaces upon which apatite is deposited. but it is the interaction of many or all of these factors that determines the process of biological calcification and controls the properties of the calcified matrices.

Bone and Bones↗
PubMed1980

Effect of magnesium on lipid-induced calcification: an in vitro model for bone mineralization.

The effect of Mg on hydroxyapatite proliferation induced by phosphatidyl serine, phosphatidyl inositol, and calcium-acidic phospholipid-phosphate complexes has been studied in metastable calcium phosphate solutions of constant ionic strength and variable Mg/Ca ratio. Mg inhibits formation of the Ca-acidic phospholipid phosphate complexes, probably by competing with Ca for sites on the phospholipid molecules. Once the complexed acidic phospholipids were present, Mg has no effect on the proliferation of hydroxyapatite. This is shown by the invariant first-order rate constant for the disappearance of CA during hydroxyapatite proliferation (kCa = 0.0037 h-1) in solutions with Mg/Ca weight ratios ranging 0/1 to 10/1. These studies suggest that the presence of Mg does affect in vivo calcification and that the initiation of calcification by means of a Ca-PL-PO4 complex may be dependent on the Mg/Ca ratio in the calcifying tissue.

Bone and Bones↗
PubMed1980

Relationship between proteolipids and calcium-phospholipid-phosphate complexes in Bacterionema matruchotii calcification.

Calcium-phospholipid-phosphate complexes (Ca-PL-P) were isolated from calcified and uncalcified Bacterionema matruchotii and its calcified lipid extracts. Similar complexes were absent from the noncalcifying bacterium Actinomyces naeslundii. The majority of the Ca-PL-P complexes were associated with the proteolipid acidic phospholipid component. Ca-PL-P complexes isolated from B. matruchotii and from calcified proteolipid contained phosphatidylinositol, phosphatidylinositol-4-phosphate, phosphatidylinositol-4,5-diphosphate, and phosphatidylserine. They consisted of approximately 52 mole % Ca, 32 mole % organic P, and 15 mole % Pi. During Ca-PL-P extraction from B. matruchotii or its proteolipid-containing calcified lipid extracts, the proteolipid was dissociated and the apoprotein precipitated as fluff at the aqueous-organic solvent interface, thus explaining the failure to detect protein in Ca-PL-P preparations. When the ability of Ca-PL-P complexes and lipid fractions of B. matruchotii to initiate apatite formation from metastable calcium phosphate solution was compared, the yield of hydroxyapatite decreased as follows: Ca-PL-P greater than proteolipid acidic phospholipids greater than proteolipid greater than crude phospholipid greater than total lipids greater than whole cells.

Actinomycetaceae↗
PubMed1979

Effect of diphosphonates on hydroxyapatite formation induced by calcium-phospholipid-phosphate complexes.

The diphosphonates disodium ethane-1-hydroxy-1, 1-diphosphonate (EHDP) and disodium dichloromethylene diphosphonate (Cl2MDP) prevent hydroxyapatite (HA) formation in metastable calcium phosphate solutions, induced by calcium-phospholipid-phosphate complexes and by the acidic phospholipids phosphatidyl serine and phosphatidyl inositol. The diphosphonates appear to act not only as HA crystal poisons but also as surfactants which probably change the nature of the lipid micelle and the charge and conformational properties of the lipid molecules. The surfactants sodium dodecyl sulfate (SDS) and Non-Idet P-40 (NP-40), like the diphosphonates, prevent HA formation by the acidic phospholipids and complexed lipids, but do not act as HA surface poisons. The lipid surfactant lyso-phosphatidyl serine did not induce HA formation from solution. The relevance of the ability of the diphosphonates to act as lipid surfactants to the in vivo use of these agents is discussed.

Calcium↗
PubMed1979

The crystal chemistry of submandibular and parotid salivary gland stones.

The mineral composition of 38 human salivary gland stones was described qualitatively on the basis of X-ray diffraction and chemical analysis. In 32 submandibular stones, hydroxyapatite was the most frequently observed phase with a magnesium-substituted whitlockite co-phase (octacalcium phosphate was rarely present). In six parotid gland stones, apatite, magnesium substituted whitlockite and octacalcium phosphate were noted to be the major crystalline phases. Brushite was rarely found in either submandibular or parotid stones. This is the first report of octacalcium phosphate in salivary gland stones. All stones had ash weights ranging from 75--80%, but their Ca/P ratios could not be used to predict the crystalline phases present. Whitlockite was observed more frequently in the central regions of the submandibular stones than in the outer crusts. Possible explanations for the presence of each of these phases are discussed.

Calcium Phosphates↗
PubMed1977

The role of synthetic and bone extracted Ca-phospholipid-PO4 complexes in hydroxyapatite formation.

The calcium-phospholipid-phosphate (Ca-PL-PO4) complex isolated from young bone has been shown to initiate hydroxyapatite formation from a metastable calcium phosphate solution. The action of the complex was compared to that of the acidic phospholipids: phosphatidyl serine, phosphatidyl inositol and phosphatidic acid. These phospholipids first remove calcium, and a small amount of phosphate from the metastable solution forming a material similar to the complex isolated from bone, and then form hydroxyapatite. The rate of hydroxyapatite proliferation, once phosphatidyl serine and phosphatidyl inositol are converted to Ca-PL-PO4 complexes, is the same as the rate observed for comparable weights of the complex isolated from bone. It is suggested that the complex isolated from bone was formed in a manner similar to the complexes in our in vitro experiments. Finally, our evidence supports the possibility that a similar complex is responsible for the initial mineralization in matrix vesicles.

Bone Development↗
PubMed1976

Extraction of a calcium-phospholipid-phosphate complex from bone.

A calcium-phospholipid-phosphate complex with a constant 1:1 calcium to total phosphate molar ratio is shown to exist in rabbit and calf bone. This complex, which may be involved in the transport and deposition of bone mineral, appears to constitute a significantly greater proportion of the lipids of younger bone than of more mature bone. The comples was isolated by a modified Folch extraction employing ultrasonic disruption of cellular material. Evidence is presented to show that the complex is a natural constituent of bone rather than one created artifactually during extraction.

Age Factors↗