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PubMed2002

Airborne concentrations of benzene and mineral spirits (stoddard solvent) during cleaning of a locomotive generator and traction motor.

Mineral spirits (also called Stoddard solvent), a petroleum distillate, is often used as a degreaser or an industrial cleaning agent. Although several studies measured airborne concentrations of mineral spirits in various occupational settings, none have characterized the airborne concentrations of benzene from use of mineral spirits. Recent case reports have suggested that benzene, as a contaminant in mineral spirits, might be responsible for adverse health effects. Because some claims of health effects in the railroad industry have been attributed to potential historical exposures to mineral spirits and little information is available regarding air concentrations in this type of occupational setting, a simulation study was conducted to quantitate historical exposures a railroad worker might have experienced while spraying mineral spirits on locomotive engine parts in the 1970s. To quantitate potential historical exposures, worker tasks were simulated under worst-case exposure conditions by spraying minerals spirits on a locomotive generator and traction motor. The results of both generator and traction motor cleaning events produced concentrations of mineral spirits ranging from 34 to 221 ppm and an average 1-h concentration of 121 ppm, whereas benzene concentrations associated with the spraying and drying tasks were less than the limit of detection (0.002-0.006 ppm). Results indicate that a railroad worker who cleaned a locomotive traction motor and generator with mineral spirits for 2 h each workday under worst-case exposure conditions would be exposed to an 8-h time-weighted average (based on lapel measurements) of 30.4 ppm airborne mineral spirits. On the basis of the conditions under which these concentrations were obtained, the results should be the reasonable maximum values that can be achieved in a modern-era (post-1970) workplace in the United States.

Air Pollution, Indoor↗
PubMed2002

Mechanical and chemical characteristics of mineral produced by basic fibroblast growth factor-treated bone marrow stromal cells in vitro.

It has been shown that various organ and cell cultures exhibit increased mineral formation with the addition of basic fibroblast growth factor (bFGF) and phosphate ions in the medium. However, to date there has been no attempt to relate the chemical composition of mineral formed in vitro to a measure of its mechanical properties. This information is important for understanding the in vivo mineralization process, the development of in vitro models, and the design of tissue-engineered bone substitutes. In this study we examined the reduced modulus; hardness; and mineral-to-matrix, crystallinity, carbonate-to-mineral, and calcium-to-phosphorus ratios of mineral formed by bFGF-treated rat-derived bone marrow stromal cells in vitro. The cells were treated with 1 or 3 mM beta-glycerophosphate for 3 and 4 weeks. Both mechanical parameters, reduced modulus and hardness, increased with increasing beta-glycerophosphate concentration. The only chemical measure of the mineral composition that exhibited the same dependency was the mineral-to-matrix ratio. The values of crystallinity and carbonate fraction were similar to those for intact cortical bone, but the calcium-to-phosphorus ratio was substantially lower than that of normal bone. These data indicate that the mineral formed by bFGF-treated bone cells is mechanically and chemically different from naturally formed lamellar bone tissue after 4 weeks in culture. These results can be used to improve in vitro models of mineral formation as well as enhance the design of tissue-engineered bone substitutes.

Animals↗
PubMed2003

Micronutrients and the bone mineral content of the mother, fetus and newborn.

The fluxes of the primary bone-forming minerals, calcium, phosphorus, magnesium and zinc, across the placenta and through breast milk place considerable demands on maternal mineral economy. Increases in food consumption, elevated gastrointestinal absorption, decreased mineral excretion and mobilization of tissue stores are several possible biological strategies for meeting these extra mineral requirements. This paper presents a review of the evidence on the extent to which these strategies apply in the human situation, the mechanisms by which they occur, the limitations imposed by maternal diet and vitamin D status and the possible consequences for the growth of the infant and bone health of the mother. On the strength of current evidence it appears that pregnancy and lactation are associated with physiological adaptive changes in mineral metabolism that are independent of maternal mineral supply within the range of normal dietary intakes. These processes provide the minerals necessary for fetal growth and breast milk production without requiring an increase in maternal dietary intake or compromising maternal bone health in the long term. This may not apply to pregnant women whose mineral intakes or sunlight exposure are marginal. As a vehicle for promoting optimal growth and bone mineral content of infants, supplementation of lactating women with minerals or vitamin D is unlikely to prove effective. The situation in pregnancy is less certain. Until more studies have been conducted, a precautionary case can be made for targeted supplementation of pregnant women who have very low intakes of calcium or who are at risk of vitamin D deficiency.

Bone Density↗
PubMed1995

Lung cancer in radon-exposed miners and estimation of risk from indoor exposure.

BACKGROUND: Radioactive radon is an inert gas that can migrate from soils and rocks and accumulate in enclosed areas, such as homes and underground mines. Studies of miners show that exposure to radon decay products causes lung cancer. Consequently, it is of public health interest to estimate accurately the consequences of daily, low-level exposure in homes to this known carcinogen. Epidemiologic studies of residential radon exposure are burdened by an inability to estimate exposure accurately, low total exposure, and subsequent small excess risks. As a result, the studies have been inconclusive to date. Estimates of the hazard posed by residential radon have been based on analyses of data on miners, with recent estimates based on a pooling of four occupational cohort studies of miners, including 360 lung cancer deaths. PURPOSE: To more fully describe the lung cancer risk in radon-exposed miners, we pooled original data from 11 studies of radon-exposed underground miners, conducted a comprehensive analysis, and developed models for estimating radon-associated lung cancer risk. METHODS: We pooled original data from 11 cohort studies of radon-exposed underground miners, including 65,000 men and more than 2700 lung cancer deaths, and fit various relative risk (RR) regression models. RESULTS: The RR relationship for cumulative radon progeny exposure was consistently linear in the range of miner exposures, suggesting that exposures at lower levels, such as in homes, would carry some risk. The exposure-response trend for never-smokers was threefold the trend for smokers, indicating a greater RR for exposure in never-smokers. The RR from exposure diminished with time since the exposure occurred. For equal total exposure, exposures of long duration (and low rate) were more harmful than exposures of short duration (and high rate). CONCLUSIONS: In the miners, about 40% of all lung cancer deaths may be due to radon progeny exposure, 70% of lung cancer deaths in never-smokers, and 39% of lung cancer deaths in smokers. In the United States, 10% of all lung cancer deaths might be due to indoor radon exposure, 11% of lung cancer deaths in smokers, and 30% of lung cancer deaths in never-smokers. This risk model estimates that reducing radon in all homes exceeding the U. S. Environmental Protection Agency's recommended action level may reduce lung cancer deaths about 2%-4%. These estimates should be interpreted with caution, because concomitant exposures of miners to agents such as arsenic or diesel exhaust may modify the radon effect and, when considered together with other differences between homes and mines, might reduce the generalizability of findings in miners.

Adult↗
PubMed2003

Bone mineral density in children with untreated and treated celiac disease.

OBJECTIVES: Osteopenia is a common complication in adults with celiac disease. The effect of a gluten-free diet on bone mineral density is a matter of controversy. The aim of this study was to investigate bone mineral density in children with celiac disease at diagnosis and in patients treated for 1 year. METHODS: Bone mineral density and bone mineral content were measured in 34 children with untreated celiac disease at diagnosis and in 28 patients on a gluten-free diet for 1 year. The results were compared with those of 64 gender- and age-matched healthy control subjects. Serum calcium, phosphate, alkaline phosphatase, 25 -hydroxy vitamin D, and intact parathormone levels were determined in treated and untreated patients. RESULTS: The mean values of bone mineral density and bone mineral content of untreated patients with celiac were significantly lower than the control group (P = 0.006 and P = 0.005, respectively) and treated patients (P = 0.015 and P = 0.011 respectively). Treated patients had mean bone mineral density and bone mineral content values not significantly different from those of healthy control subjects. Minor hypocalcemia was detected in 17.6% of the patients with new diagnoses and 3.6% of the treated patients. Of the untreated patients, 29.4% had high intact parathormone concentrations; in untreated patients, the total was 14.3%. Untreated patients had significantly lower serum calcium and significantly higher intact parathormone levels than did treated patients. The other bone metabolism parameters were similar in the two celiac groups. CONCLUSION: Children with celiac disease are at risk for reduced bone mineral density. A strict gluten-free diet improves bone mineralization, even in 1 year. Early diagnosis and treatment of celiac disease during childhood will protect the patient from osteoporosis.

Absorptiometry, Photon↗
PubMed2005

Unique coexpression in osteoblasts of broadly expressed genes accounts for the spatial restriction of ECM mineralization to bone.

Extracellular matrix (ECM) mineralization is a physiological process in bone and a pathological one in soft tissues. The mechanisms determining the spatial restriction of ECM mineralization to bone physiologically are poorly understood. Here we show that a normal extracellular phosphate concentration is required for bone mineralization, while lowering this concentration prevents mineralization of any ECM. However, simply raising extracellular phosphate concentration is not sufficient to induce pathological mineralization, this is because of the presence in all ECMs of pyrophosphate, an inhibitor of mineralization. ECM mineralization occurs only in bone because of the exclusive coexpression in osteoblasts of Type I collagen and Tnap, an enzyme that cleaves pyrophosphate. This dual requirement explains why Tnap ectopic expression in cells producing fibrillar collagen is sufficient to induce pathological mineralization. This study reveals that coexpression in osteoblasts of otherwise broadly expressed genes is necessary and sufficient to induce bone mineralization and provides evidence that pathological mineralization can be prevented by modulating extracellular phosphate concentration.

Alkaline Phosphatase↗
PubMed1980

Lignocellulose mineralization by arctic lake sediments in response to nutrient manipulation.

Mineralization of specifically labeled C-cellulose- and C-lignin-labeled lignocelluloses by Toolik Lake, Alaska, sediments was examined in response to manipulation of various environmental factors. Mineralization was measured by quantifying the amount of labeled CO(2) released from the specifically labeled substrates. Nitrogen (NH(4)NO(3)) and, to a greater degree, phosphorus (PO(4)) additions enhanced the mineralization of white pine (Pinus strobus) cellulose during the summer of 1978. Nitrogen and phosphorus together had no cumulative effect. During the summer of 1979, nitrogen or phosphorus alone had only a slight stimulatory effect on the mineralization of a sedge (Carex aquatilis) cellulose; however, together, they had a dramatic effect. This variable response of mineralization to nutrient addition between 1978 and 1979 was probably attributable to year-to-year variation in nutrient availability within the lake. Cellobiose addition and oxygen depletion inhibited the amount of pine cellulose mineralized. Whereas addition of nitrogen to oxygen-depleted treatments had limited effect, addition of phosphorus resulted in mineralizations equal to or greater than that of the controls. Nitrogen had no effect on mineralization of pine or Carex lignins. Phosphorus, however, inhibited mineralization of both lignins. With Carex lignin, the phosphorus inhibition occurred at a concentration as low as 0.1 muM. The antagonistic role of phosphorus in cellulose and lignin mineralizations may be of significance in understanding the increased proportion of lignin relative to cellulose in decomposing litter.

Journal Article↗
PubMed1996

Accelerated Mineralization of Pentachlorophenol in Soil upon Inoculation with Mycobacterium chlorophenolicum PCP1 and Sphingomonas chlorophenolica RA2.

Mineralization of pentachlorophenol (PCP) was studied in nonsterile soil from a PCP-contaminated site upon inoculation with two PCP-degrading bacterial strains. At spiked [(sup14)C]PCP concentrations of 30 and 100 mg/kg, the effects of organism type, different inoculation techniques, including structural amendment with sawdust and cell attachment to polyurethane (PU), as well as the effect of different inoculum sizes of 10(sup4) to 10(sup8) cells per g (dry weight) of soil were compared with PCP mineralization by indigenous bacteria. Gas chromatographic analysis was used to monitor PCP disappearance and to check mass balances. The survival and activity of the released bacteria were examined by immunofluorescence microscopy and respiking experiments. Noninoculated soil completely mineralized 30 mg of PCP per kg within 7 months but showed no or only low degradation activity at 100 mg/kg in the same period. Structural amendment with PU or sawdust initiated slow mineralization after half a year. Soil inoculation with Sphingomonas chlorophenolica RA2 shortened the mineralization time drastically to 1 month at 30 mg of PCP per kg using 10(sup8) cells per g, with approximately 80% of the added radioactivity being converted to CO(inf2). The inoculated cells disappeared rapidly, with a count of 2 x 10(sup6) cells per g after 2.3 months and nondetectability after 7 months. At 100 mg/kg, mineralization was slower because of PCP toxicity but approached completion within 7.5 months. The inhibition could be overcome by addition of sawdust (1 g/kg of soil), resulting in a mineralization rate of 3 to 4 mg/kg(middot)d. PU had the opposite effect. Lower inoculum densities resulted in prolonged lag phases and lower rates, although mineralization was still enhanced over the background level. At 30 mg of PCP per kg, inoculation with Mycobacterium chlorophenolicum PCP1 increased mineralization slightly over the indigenous bacterial activity, regardless of inoculum size, but only when the organisms were attached to PU. At 100 mg of PCP per kg, only 27% were mineralized within 7.5 months. After 7 months, the original strain PCP1 inoculum of 10(sup8) cells per g was recovered at 5 x 10(sup6) to 3 x 10(sup7) cells per g, depending on the PCP concentration, but independent of PU amendment. Amendment with sawdust had no effect on the performance of this organism. Possible reasons for the poor performance of this strain include its sensitivity to PCP and its preference for slightly acidic soil conditions.

Journal Article↗
PubMed2005

Role of the progressive ankylosis gene (ank) in cartilage mineralization.

Mineralization of growth plate cartilage is a critical event during endochondral bone formation, which allows replacement of cartilage by bone. Ankylosis protein (Ank), which transports intracellular inorganic pyrophosphate (PP(i)) to the extracellular milieu, is expressed by hypertrophic and, especially highly, by terminally differentiated mineralizing growth plate chondrocytes. Blocking Ank transport activity or ank expression in terminally differentiated mineralizing growth plate chondrocytes led to increases of intra- and extracellular PP(i) concentrations, decreases of alkaline phosphatase (APase) expression and activity, and inhibition of mineralization, whereas treatment of these cells with the APase inhibitor levamisole led to an increase of extracellular PP(i) concentration and inhibition of mineralization. Ank-overexpressing hypertrophic nonmineralizing growth plate chondrocytes showed decreased intra- and extracellular PP(i) levels; increased mineralization-related gene expression of APase, type I collagen, and osteocalcin; increased APase activity; and mineralization. Treatment of Ank-expressing growth plate chondrocytes with a phosphate transport blocker (phosphonoformic acid [PFA]) inhibited uptake of inorganic phosphate (P(i)) and gene expression of the type III Na(+)/P(i) cotransporters Pit-1 and Pit-2. Furthermore, PFA or levamisole treatment of Ank-overexpressing hypertrophic chondrocytes inhibited APase expression and activity and subsequent mineralization. In conclusion, increased Ank activity results in elevated intracellular PP(i) transport to the extracellular milieu, initial hydrolysis of PP(i) to P(i), P(i)-mediated upregulation of APase gene expression and activity, further hydrolysis and removal of the mineralization inhibitor PP(i), and subsequent mineralization.

Alkaline Phosphatase↗
PubMed1994

Bone mineral content and density in healthy subjects and in osteogenesis imperfecta.

Lumbar spine bone mineral density in a cross sectional study of healthy subjects increased by 0.012 and 0.016 g/cm2/year in boys and girls respectively between 5 and 11 years of age. These rates increased five-fold in girls and threefold in boys between the ages of 11 and 13 years as a result of the bone mineral content increasing more rapidly than the coronal area at this age. By the age of 11 years the girls had 66% of the coronal area, 61% of the bone mineral density, and 41% of the bone mineral content of subjects aged 18-23 years. The ratio (lumbar spine bone mineral content/body weight) was constant in boys aged 6-13 years, but there were significant variations in girls. Femoral neck bone mineral density in both sexes changed little between 6 and 11 years and at 11 years was 69% of the adult values. Subjects with osteogenesis imperfecta had a low bone mineral density and bone mineral content for their age and weight. The z score of bone mineral density at the femoral neck was significantly lower than at the lumbar spine. In patients with recurrent fractures a low bone mineral density may help in identifying those with osteogenesis imperfecta and assist in their subsequent management.

Absorptiometry, Photon↗
PubMed2000

Lung function prediction equations derived from healthy South African gold miners.

OBJECTIVES: To estimate lung function prediction equations and to identify appropriate normal reference values for the population of about 250 000 of South African gold miners. METHODS: Data from a lung function screening programme conducted at a large South African gold mine from 1994 to 1998 were used to estimate the lung function prediction equations. The most reliable period of lung function testing was identified in a previous study of a temporal pattern in reliability, and lung function tests from this period were used. Miners with a history of pulmonary tuberculosis or with radiological abnormalities were excluded from the study. The prediction equations were estimated cross sectionally on 15 772 black and 2752 white miners, and published reference equations that fitted most closely the observed data were identified. RESULTS: The estimated prediction equations for forced vital capacity (FVC) are as follows: for black men, FVC (l)=- 2.901-0.025xage+4.655xheight; and for white men, FVC(l)=-4.407-0.036xage+ 5.940xheight. For forced expiratory volume in one second (FEV(1)) these equations are: for black men, FEV(1)(l)=-1.654- 0.30xage+3.665xheight; and for white men, FEV(1)(l)= -2.341- 0.038xage+4.314xheight. Units are years for age and metres for height. Knudson's and the European Community of Coal and Steel (ECCS) reference values provided the closest fit to the data on lung function of white miners, but the lower limits of normal from the ECCS equations were the closest to the observed one sided lower 95% confidence intervals (95% CIs). For black miners, reference equations that fitted best were derived by Louw et al on asymptomatic black South African men unexposed to occupational dust. There were significant differences between the two groups of miners in the estimated height adjusted mean lung function values for a 40 year old 1.7 m tall man (220 ml (5.2%) for FVC and 110 ml (3.2%) for FEV(1)); white men had higher FVC and FEV(1), but lower FEV(1)/FVC ratio. The ECCS reference values scaled by a conversion factor of 0. 93 for the FVC and 0.95 for the FEV(1) provided close fits to the data for black miners, but the rate of decline with age was higher than that in the observed data. None of the linear equations provided a good fit for the 20-29 and more than 55 years old age categories. CONCLUSION: The ECCS and Knudson equations provided the best fit to the data for white miners, whereas the equations by Louw et al estimated on asymptomatic black South African bank workers provided the best fit to the data for black miners. The ECCS reference values scaled by a factor of 0.93 for FVC and by 0.95 for FEV(1) provided close fits, but the rate of decline with age was higher than that in the data for black miners.

Adult↗
PubMed1992

Changes in glycosaminoglycan binding to collagen during desmoid mineralization as revealed by different electron-microscopic staining techniques.

Mineralization at collagen fibrils is regulated by glycosaminoglycans (GAG). Alterations in proteoglycan composition during mineralization as well as inhibition of mineralization by GAGs are well documented. Collagen-GAG interactions during desmoid osteogenesis in fetal rat calvariae were investigated ultrastructurally by means of different fixation techniques. Mineralization was restricted to the collagen of the osteoid at the ectocranial side. Beyond the osteoid, one layer containing degenerated cells was found, followed by sheets of healthy osteoblasts with nonmineralized collagen fibrils. These fibrils were ordered in bundles, but were irregularly arranged in the mineralized osteoid. After fixation in glutaraldehyde-ruthenium red (GA-RR), small RR-positive granules were periodically attached to the fibrils of the nonmineralized collagen. These granules were absent at collagen in the mineralized osteoid. Periodically bound granules (periodicity of 62 nm) could clearly be demonstrated along collagen fibrils by pretreatment with the positively charged protamine sulfate and subsequent fixation in GA-RR in the nonmineralized collagen. In the mineralized osteoid, however, these granules were present, but periodic binding was missing. Heparin pretreatment followed by fixation in GA-RR revealed periodically bound fine strands between collagen fibrils running parallel in the nonmineralized collagen; these threads were absent in the mineralizing osteoid. Restriction of mineralization to osteoid at the mineralization border may be reflected by the observed changes in GAG binding to collagen fibrils within the osteoid of developing fetal calvariae in contrast to binding to collagen in nonmineralized areas.

Animals↗
PubMed2000

Changes in bronchoalveolar lavage indices associated with radiographic classification in coal miners.

Previous studies on symptomatic coal miners have shown that alveolar macrophages, recovered by bronchoalveolar lavage (BAL), release excessive amounts of reactive oxygen species (ROS) and inflammatory cytokines. It has been proposed that these secretions may mediate cell injury and initiate the disease process. We hypothesized that acellular bronchoalveolar lavage fluid (BALF) indices in coal miners chronically exposed to coal dust may reflect the status of important homeostatic modulations in the lung that lead to the development of coal workers' pneumoconiosis (CWP). To test this hypothesis, we measured inflammatory status, oxidant burden, antioxidant defenses, cytokines, growth factors, fibronectin, and alpha(1)-antitrypsin (alpha(1)-AT) in the BALF of healthy never-smoker control subjects, never-smoker underground coal miners with negative radiographs (ILO 0/0-1/0), and two miners with moderate changes in the chest radiographs (ILO 2/2). Interestingly, indices of injury and inflammation increased with the progression of disease in coal miners. Antioxidant enzymes, such as catalase, glutathione peroxidase, and superoxide dismutase, showed a 19-fold, 22-fold, and 6-fold increase above control, respectively, in coal miners with category 2/2 CWP. Significant increases in the secretion of IL-1, IL-6, TNF-alpha, TGF-beta, fibronectin, and alpha(1)-AT also were evident in coal miners with disease. This up-regulation of antioxidant defenses and cytokines was not evident in coal miners in the absence of clinically evident radiographic disease. In addition, the concentration of lipid peroxidation by products in the BALF of coal miners without evidence of radiographic disease showed a moderate 3-fold increase, whereas, in coal miners with category 2/2 CWP it showed a 59-fold increase compared to control subjects. These results are in good agreement with our hypothesis that development of CWP and its progression may be correlated with an oxidative stress and up-regulation of cytokines and mediators of growth.

Adult↗
PubMed2001

Matrix gamma-carboxyglutamic acid protein is a key regulator of PTH-mediated inhibition of mineralization in MC3T3-E1 osteoblast-like cells.

As part of its overall function as a major regulator of calcium homeostasis, PTH stimulates bone resorption and inhibits osteoblast-mediated biomineralization. To determine the basis for the inhibitory actions of this hormone, we compared the time course of PTH-dependent inhibition of mineralization in MC3T3-E1 osteoblast-like cells with changes in mRNA levels for several extracellular matrix proteins previously associated either with induction or inhibition of mineralization. Mineralizing activity was rapidly lost in PTH-treated cells ( approximately 30% inhibition after 3 h, 50% inhibition at 6 h). Of the proteins examined, changes in matrix gamma-carboxyglutamic acid protein were best correlated with PTH-dependent inhibition of mineralization. Matrix gamma-carboxyglutamic acid protein mRNA was rapidly induced 3 h after PTH treatment, with a 6- to 8-fold induction seen after 6 h. Local in vivo injection of PTH over the calvaria of mice also induced a 2-fold increase in matrix gamma-carboxyglutamic acid protein mRNA. Warfarin, an inhibitor of matrix gamma-carboxyglutamic acid protein gamma-carboxylation, reversed the effects of PTH on mineralization in MC3T3-E1 cells, whereas vitamin K enhanced PTH activity, as would be expected if a gamma-carboxyglutamic acid-containing protein were required for PTH activity. Levels of the other mRNAs examined were not well correlated with the observed changes in mineralization. Osteopontin, an in vitro inhibitor of mineralization, was induced approximately 4-fold 12 h after PTH addition. Bone sialoprotein mRNA, which encodes an extracellular matrix component most frequently associated with mineral induction, was inhibited by 50% after 12 h of PTH treatment. Osteocalcin mRNA, encoding the other known gamma-carboxyglutamic acid protein in bone, was also inhibited by PTH, but, again, with a significantly slower time course than was seen for mineral inhibition. Taken together, these results show that the rapid inhibition of osteoblast mineralization induced by in vitro PTH treatment is at least in part explained by induction of matrix gamma-carboxyglutamic acid protein.

1-Carboxyglutamic Acid↗
PubMed2003

Relationship of leptin to bone mineralization in children and adolescents.

Serum leptin concentrations and bone mass are concordant in several respects. Obesity is associated with increased serum leptin concentrations and bone mineral, whereas undernutrition reduces serum leptin concentrations and bone mineral. Furthermore, both bone mineral and serum leptin concentrations increase at the initiation of puberty. However, there is a lack of empirical evidence of an independent association of serum leptin concentrations and bone mineral in youth. Thus, we used hierarchical regression to determine whether serum leptin concentrations were related to bone mineral in boys (n = 28) and girls (n = 31). Bone mineral content, density, and apparent density of the total body and body regions were measured by dual-energy x-ray absorptiometry and statistically adjusted for chronological age, fat mass, bone-free fat-free mass, and serum IGF-I and estradiol concentrations. Sequential addition of serum log((10)) leptin concentrations to the block of body size variables and the block of hormone variables did not increase R(2) for any of the total or regional bone mineral content, bone mineral density, and bone mineral apparent density variables. We conclude that serum leptin concentrations do not add to the prediction of bone mineral in youth after accounting for age, fat mass, bone-free fat-free mass, and serum IGF-I and estradiol concentrations.

Adipose Tissue↗
PubMed1991

Clinical and anthropometric correlates of bone mineral acquisition in healthy adolescent girls.

We studied the acquisition of bone mineral in 45 healthy prepubertal and pubertal girls and related changes in bone mass to age, body mass, pubertal status, calcium intake, and exercise. A subgroup of 12 girls was followed longitudinally. Bone mineral content (BMC) of the lumbar spine, whole body, and femoral neck was measured by dual energy x-ray absorptiometry and that at the midradius by single photon absorptiometry. For comparison, spine and whole body mineral contents were also measured by dual photon absorptiometry. Bone mass was expressed in conventional terms of BMC and area density (BMD). However, we show that BMD fails to account for differences in bone thickness. Since bone size increases during adolescence, we present a new expression, bone mineral apparent density (BMAD), which is BMC normalized to a derived bone reference volume. This term minimizes the effect of bone geometry and allows comparisons of mineral status among bones of similar shape but different size. BMC increased with age at all sites. These increases were most rapid in the early teens and plateaued after 16 yr of age. When bone mineral values at all sites were regressed against age, height, weight, or pubertal stage, consistent relationships emerged, in which BMC was most strongly correlated, BMD was correlated to an intermediate degree, and BMAD correlated only modestly or without significance. Dietary calcium and exercise level did not correlate significantly with bone mass. From these relationships, we attribute 50% of the pubertal increase in spine mineral and 99% of the change in whole body mineral to bone expansion rather than to an increase in bone mineral per unit volume. In multiple regressions, pubertal stage most consistently predicted mineral status. This study emphasizes the importance of pubertal development and body size as determinants of bone acquisition in girls. BMAD may prove to be particularly useful in studies of bone acquisition during periods of rapid skeletal growth.

Absorptiometry, Photon↗
PubMed1997

A collagenous cementum-derived attachment protein is a marker for progenitors of the mineralized tissue-forming cell lineage of the periodontal ligament.

The periodontal ligament (PDL) is a fibrous and cellular connective tissue that mediates tooth attachment to bone, and it comprises fibroblastic and mineralized tissue-forming (MTF) progenitors. The MTF progenitors are believed to give rise to the cementoblastic and osteoblastic lineages. Cementum attachment protein (CAP) is a collagenous cementum-derived protein which binds strongly to osteoblasts, moderately to PDL cells, and weakly to gingival fibroblasts. The aim of the present study was to determine the relationship between the capacity of PDL progenitors to bind CAP and their potential to express alkaline phosphatase (ALP) and form mineralized-like tissue in culture. Cloned human PDL progenitor populations obtained from nine human donors were assayed for their constitutive capacity to bind CAP and express ALP, and for the dexamethasone-induced potential to form mineralized-like tissue in culture in the presence of ascorbic acid and beta-glycerophosphate. Forty percent of the progenitor clones produced mineralized-like tissue. Two patterns of mineralization were observed: a spread and flat pattern similar to that produced by human bone cells in culture and a nodular ridge-like type resembling that formed by human cementoma-derived cells. A direct correlation was found between the percentage of ALP positive cells in each progenitor clone and the amount of mineralized-like tissue formed (r = 0.565). Similar correlations were found between the number of ALP positive cells and the binding capacity of each clone (r = 0.392) and between the CAP binding capacity and mineralized-like tissue formation (r = 0.584). Multiple regression analysis indicated that the constitutive capacity of a clone to bind CAP and express ALP is directly correlated to its dexamethasone-induced potential to form mineralized tissue (r = 0.675). These results indicate that CAP binding and ALP expression can serve as markers for the identification of MTF progenitors in the heterogeneous cultured population of the human periodontal ligament. These data show for the first time that binding capacity to extracellular components of mineralized tissues can be a marker for mineralized tissue-forming progenitors.

Alkaline Phosphatase↗
PubMed2002

Mineralization of developing mouse calvaria as revealed by Raman microspectroscopy.

Raman microspectroscopy is a nondestructive vibrational spectroscopic technique that permits the study of organic and mineral species at micron resolution, offers the ability to work with hydrated and dehydrated specimens in vivo or in vitro, and requires minimal specimen preparation. We used Raman microspectroscopy to determine the composition of the mineral environments present in mouse calvaria, the flat bones that comprise the top of the skull. We have acquired Raman transects (lines of point spectra) from mouse calvaria during a developmental time course ranging from embryonic day 13.5 (E13.5; 6 days before birth) to 6 months of age. Exploratory factor analysis (FA) reveals the presence of a variety of apatitic mineral environments throughout the tissue series. The earliest mineral is observed in the fetal day 15.5 (F15.5) mice and is identified as a carbonated apatite. The presence of a heterogeneous mineralized tissue in the postnatal specimens suggests that ionic incorporation and crystal perfection in the lattice yary as the mouse develops. This variation is indicative of the presence of both recently deposited mineral and more matured remodeled mineral. Band area ratios reveal that the mineral/matrix ratio initially increases, reaches a plateau, and then increases again. The carbonate/phosphate band area ratio remains constant from F18.5 to postnatal day 3 (PN3) and then increases with age. Insights into the chemical species, the degree of mineralization, and the multiple mineral environments that are present in normal calvarial tissue will enable us to better understand both normal and abnormal mineralization processes.

Animals↗