bluuebunny/crossref_metadata_2025_split huggingface dataset:
Extracellular matrix synthesized by clonal osteogenic cells is osteoinductive in vivo and in vitro: Role of transforming growth factor-beta1 in osteoblast cell-matrix interaction
Authors: Kirk Martin D. , Kahn Arnold J. 
Published: February 2010

Abstract
ROB-C26 (C26) is a multipotential, clonal cell line known to express several members of the TGF-β superfamily and to become more osteoblastic (e.g., express higher levels of alkaline phosphatase) upon treatment with 10−6 M retinoic acid (RA). We hypothesize that the expression of this more osteoblastic phenotype subsequent to RA exposure is the result of the treated cell's extracellular matrix (ECM) becoming a repository and active source of putative osteoinductive growth factors including, specifically, select members of the TGF-β superfamily. To test this hypothesis, we isolated the ECM from RA-treated and untreated C26 cells and assessed them for their ability to promote osteogenic differentiation in vivo and in vitro. We then explored whether the latter activities could be attributed specifically to TGF-β1. We found that the ECM of treated cells isolated by cell lysis and extensive washing induced endochondral bone formation in vivo when implanted into the thigh muscles of athymic nude mice and stimulated alkaline phosphatase (ALP) activity in vitro in freshly plated C26 cells. This latter stimulation was comparable to levels observed with direct RA treatment. This latter in vitro activity was only very partially mimicked by the ECM prepared from untreated cells and not duplicated at all by RA-treated collagen or the ECM from another RA-treated multipotential cell line. Moreover, the in vivo osteoinductive effect of the treated C26 cell ECM was not duplicated by comparable ECM prepared from untreated cells. Finally, we also found that preincubation of the ECM with specific, neutralizing antibodies to either TGF-β's 1, 2, and 3 or TGF-β1 alone substantially reduced the ability of the ECM to stimulate ALP activity. This inhibitory effect was not seen using nonspecific IgG. These data identify the C26 cell line as a valuable model system for exploring cell-matrix interaction in osteogenic differentiation, provide direct support for an autocrine role of the ECM in such differentiation, and suggest that TGF-β1 is an important ECM-based mediator in the regulation of osteoblastic development.
A rotator cuff rupture produces permanent osteoporosis in the affected extremity, but not in those with whom shoulder function has returned to normal
Authors: Kannus Pekka , Leppälä Jari , Lehto Matti , Sievänen Harri , Heinonen Ari , Järvinen Markku 
Published: February 2010

Abstract
Areal bone mineral density (BMD) and clinical status of 34 men treated surgically 9 years earlier for a rotator cuff rupture of the dominant side shoulder were determined. The BMD was measured at the lumbar spine (L2–L4) and the proximal humerus, humeral shaft, radial shaft, ulnar shaft, distal forearm, and hand of both extremities using a dual-energy X-ray absorptiometric (DXA) scanner. Thirty-four age-, height-, weight-, and profession-matched normal men (controls) were also measured. The patients' mean side-to-side BMD difference (dominant minus nondominant/nondominant × 100%) was significantly lower in the proximal humerus (patients −3.5% vs. controls +2.4%, p = 0.0002), humeral shaft (–2.6% vs. +1.6%, p = 0.0005), radial shaft (–0.4% vs. +1.9%, p = 0.0311), distal forearm (–0.2% vs. +2.4%, p = 0.0158), and hand (+2.3% vs. +4.0%, p = 0.0047). In the ulnar shaft, this difference was almost the same in the patients (–0.2%) and controls (+0.2%) (NS). Also, the lumbar spine BMD did not differ significantly between these groups (mean ± SD = 1.098 ± 0.148 g/cm2 in patients vs. 1.066 ± 0.156 g/cm2 in controls). In patients, the relative BMDs of the injured extremity did not significantly associate with the size of the rupture; time delay between the injury and the surgery; type of surgery and postoperative treatment; postoperative immobilization time; follow-up time; patient's age, muscle strength or pain assessment; and subjective assessment of shoulder function. However, they strongly associated with the objective assessment of the shoulder function: the better the observed function of the shoulder, the less bone loss caused by the injury. In proximal humerus, the side-to-side BMD difference averaged +2.0% in the patient group with “excellent” shoulder function, −3.3% in the “good” group, −5.3% in the “fair” group, and −11.5% in the “poor” group (p = 0.0012).
In conclusion, a rotator cuff rupture results in permanently reduced BMD in the injured extremity, the reduction being greatest in the proximal parts of the extremity. The observed mean decreases (6% in the proximal humerus, 4% in the humeral shaft, and 3% in the distal forearm of the injured limb) are clinically important with respect to age-related bone loss of 1% per year after the age of peak bone mass. Additional follow-up is needed to determine any increased risk of osteoporotic fractures in the injured extremity. Recovery of normal shoulder function seems to be of great importance for good bone recovery.
Several anesthetics, but not diethyl ether, cause marked elevation of serum parathyroid hormone concentration in rats
Authors: Schultz V.L. , Boass A. , Garner S.C. , Toverud S.U. 
Published: February 2010

Abstract
The effects of anesthetics on serum parathyroid hormone (PTH) concentrations were determined by a new homologous two-site immunoradiometric assay for rat PTH. Serum PTH concentrations (mean ± SE) from ether-anesthetized rats (14.7 ± 1.5 pg/ml, n = 22) were not significantly different from those of decapitated unanesthetized female rats (13.0 ± 1.8 pg/ml, n = 21). Serum PTH concentrations in pg/ml (n = 4–14) for other anesthetics tested were: ketamine, 12.5 ± 1.1; Na pentobarbital, 23.3 ± 2.4; methoxyflurane (inhalation), 42.2 ± 6.8; and xylazine combined with ketamine, 51.4 ± 11.3 pg/ml. The latter two concentrations were significantly (p &lt; 0.001) higher than the values for all other anesthetics and decapitation. Elevation of serum PTH induced by pentobarbital or ketamine + xylazine increased with time under anesthesia. Neither serum Ca2+ concentrations nor pH differed among any of the groups. We conclude that anesthesia induced by pentobarbital, methoxyflurane, or ketamine + xylazine in rats leads to a marked elevation of serum PTH levels that appears to be related to the duration of anesthesia and not due to any measurable fall in serum Ca2+.
Phosphate transport in immortalized cell cultures from the renal proximal tubule of normal and Hyp Mice: Evidence That the HYP gene locus product is an extrarenal factor
Authors: Dr. Nesbitt Teresa , Econs Michael J. , Byun Jong K. , Martel Josée , Tenenhouse Harriet S. , Drezner Marc K. 
Published: February 2010

Abstract
Whether renal phosphate wasting in X-linked hypophosphatemia (XLH) results from an intrinsic renal or humoral defect remains controversial. In studies of the murine homolog of XLH, harboring the Simian Virus 40 (SV40) large T antigen, we obviated the influence of renal cell heterogeneity and impressed memory by comparing Na+-phosphate cotransport in immortalized cells from the S1 segment of the proximal tubule. Cells from SV40 transgenic normal and Hyp mice exhibit characteristics of differentiated proximal tubule cells including gluconeogenesis and alkaline phosphatase activity. Surprisingly, however, we found two distinct populations of cells from the S1 proximal tubule of both normal and Hyp mice. In one, PTH treatment increases cAMP accumulation, while in the other both PTH and thyrocalcitonin enhance cAMP production. Kinetic parameters for Na+-phosphate cotransport were similar in both subpopulations of cells from normal (Km, 0.29 ± 0.03 vs. 0.39 ± 0.04 mM; Vmax, 4.6 ± 0.6 vs. 5.2 ± 0.4 nmol/mg/5 minutes) and Hyp mice (0.33 ± 0.02 vs. 0.26 ± 0.04; 6.0 ± 0.7, 4.8 ± 0.6). More importantly, phosphate transport in S1 cells of either subpopulation from Hyp mice is no different than that of normals. These data indicate that renal proximal tubule cells from Hyp mice have intrinsically normal phosphate transport and support the hypothesis that a humoral abnormality underlies renal phosphate wasting in XLH.
Effect of ovariectomy on cancellous bone in the hypophysectomized rat
Authors: Chen Meng-Meng , Dr. Yeh James K. , Aloia John F. 
Published: February 2010

Abstract
This experiment studied the effects of hypophysectomy (HX) and ovariectomy (OV) on cancellous bone in the proximal tibia and distal 5th lumbar vertebra by dynamic histomorphometry. Forty-eight female Sprague-Dawley rats, 3 months of age, were divided into age-matched control, HX, OV, and HX + OV (HO) groups. Ten rats were sacrificed at 3 months of age as baseline controls, and the rest of the animals were sacrificed 5 weeks after the surgery. While the age-matched controls and OV rats significantly increased in body weight compared with the baseline control rats, cancellous bone volumes in the proximal tibia and distal 5th lumbar vertebra increased in the age-matched controls and decreased in the OV rats. In the HX and HO rats, body weight equaled baseline control values, and their cancellous bone volumes were decreased with a poorer trabecular architecture in both bone sites. In all HX, OV, and HO rats, uterine weight and serum estradiol were significantly decreased. OV significantly increased longitudinal bone growth and the tissue- and surface-based bone formation and bone resorption parameters in both the proximal tibia and 5th lumbar vertebra (p &lt; 0.05). HX alone or HO significantly decreased longitudinal bone growth and the tissue-based bone formation rate without significantly affecting surface-based bone formation and bone resorption parameters when compared with the age-matched controls. No significant differences were detected in any variable between the HX alone and HO rats. In this study, HX on OV rats decreased the longitudinal bone growth, cancellous bone turnover (tissuebased), and cancellous bone volume in the proximal tibia and distal 5th lumbar vertebra in young rats at 5 weeks after surgery. We suggest that the bone loss in the HO rats was due primarily to pituitary hormone deficiency and that the effect of ovarian hormone deficiency on cancellous bone is pituitary hormone dependent.
Bone structure in postmenopausal hyperparathyroid, osteoporotic, and normal women
Authors: Dr. Parisien May , Cosman Felicia , Mellish Robert W. E. , Schnitzer Michele , Nieves Jeri , Silverberg Shonni J. , Shane Elizabeth , Kimmel Donald , Recker Robert R. , Bilezikian John P. , Lindsay Robert , Dempster David W. 
Published: February 2010

Abstract
The purpose of this study was to test the hypothesis that patients with mild primary hyperparathyroidism are protected against postmenopausal (PM) loss of cancellous bone architecture. To achieve this, we compared bone structure and turnover in iliac bone biopsies from three groups: 16 women with mild primary hyperparathyroidism (PHPT; 58.2 ± 2.2 years, 11.5 ± 1.7 years PM), 17 women with untreated primary osteoporosis (OP; 65.1 ± 2.0 years, 17.2 ± 2.3 years PM), and 31 healthy women (N; 59.8 ± 1.4 years, 13.4 ± 1.5 years PM). The bone formation rate was significantly higher in PHPT than in either OP or N, and not different between OP and N. Cancellous bone volume, total strut length, and indices of connectivity (node number, node to node strut length, and node to terminus ratio) were significantly lower in OP than either PHPT or N but were the same or higher in PHPT than in N. Indices of disconnectivity were significantly lower in PHPT than in N, whereas they were the same or higher in OP than N. The data were also analyzed in subgroups matched by years PM with no changes in the results. These findings indicate that osteoporotic patients with normal bone turnover have low bone volume and micro-architectural deterioration, while patients with mild PHPT have normal bone volume and normal or greater trabecular connectivity despite higher bone turnover. These findings suggest that mild PHPT protects against the loss of cancellous bone structure that normally follows menopause.
Age and temperature related changes to the ultrastructure and composition of human bone mineral
Authors: Holden J.L. , Clement J.G. , Phakey P.P. 
Published: February 2010

Abstract
This X-ray diffraction (XRD) investigation of heat-treated human femoral bone showed that the main mineral phase of both unheated bone and bone heated to 600°C resembled that of a poorly crystalline form of hydroxy-apatite. The rod-shaped apatite crystals in unheated bone persisted in bone heated up to 400°C. Recrystallization at approximately 600°C, produced larger crystals, which either retained their original morphology or changed to tabular or equidimensional shapes. The size of the apatite crystals in unheated and heated bone specimens was dependent on both temperature and age. When heated above 600°C the crystallinity of the bone mineral increased, and the XRD pattern more closely resembled that of hydroxyapatite. Partial decomposition of the hydroxyapatite phase to calcium oxide above 1000°C, and β-tricalcium phosphate, α-tricalcium phosphate, and calcium oxide phosphate between 1200°C and 1400°C, indicated that the original apatite phase was both calcium deficient and contained carbonate. The relative peak intensities of the thermal decomposition products were related to some extent to the age of the deceased person and reflected the compositional changes that occur during bone aging. Because the thermally induced changes to the composition and ultrastructure of bone mineral were influenced by the age of the individual, this investigation proposed that the heat treatment of bone tissue may offer an alternative way of studying bone aging.
Three-dimensional nuclear magnetic resonance microimaging of trabecular bone
Authors: Chung Hsiao-Wen , Wehrli Felix W. , Williams John L. , Wehrli Suzanne L. 
Published: February 2010

Abstract
The conventional approach to measuring structural parameters in trabecular bone rests on stereology from optical images, derived from sections of embedded bone. In order to provide data that are statistically representative of a sufficiently large volume, multiple sections need to be analyzed in each of the three orthogonal planes. In this work, an alternative technique is presented which is based on three-dimensional (3D) volumetric proton nuclear magnetic resonance (NMR) microimaging. The method presented provides images from 9 × 9 × 4 mm3 volumes of defatted bone specimens in 15–20 minutes scan time at isotropic resolution corresponding to (78 μm)3 voxel size. Surface-rendered images of bovine and human trabecular bone are shown and an algorithm was developed and implemented for determining the orientation and magnitude of the principal axes of the mean intercept length tensor.
Osteoblasts are regulated by the cellular adhesion through ICAM-1 and VCAM-1
Authors: Dr. Tanaka Yoshiya , Morimoto Isao , Nakano Yoichiro , Okada Yosuke , Hirota Seiichi , Nomura Shintaro , Nakamura Toshitaka , Eto Sumiya 
Published: February 2010

Abstract
The two major processes of bone metabolism—bone formation and resorption—are regulated by cellular interactions. Osteoblasts and osteoclasts play a significant role in bone metabolism, which is known to be regulated by local soluble factors and systemic hormones. Although bone is a heterogeneous tissue comprised of osteogenic and hematopoietic cells, cellular adhesion of osteoblasts and its regulation remains to be understood. We first demonstrate that cellular adhesion by which osteoblasts communicate with opposing cells in bone milieu is involved in the osteoblast activation: (a) purified human osteoblasts obtained from osteoarthritis patients expressed particular adhesion molecules, ICAM-1, VCAM-1, and LFA-3; (b) the osteoblasts adhered to T cells which were used as representative adhesive partners, since T cells possess all the receptors to these adhesion molecules; (c) mRNA transcription and secretion of IL-1β and IL-6 were induced in the osteoblasts by the cellular adhesion to T cells and they were reduced by interrupting the adhesion; (d) cross-linking of ICAM-1 and VCAM-1 on the osteoblasts induced IL-6 secretion from the osteoblasts. These results indicate that osteoblasts adhere to opposing cells through particular adhesion molecules on their surface and that the adhesion molecules on the osteoblasts not only function as glue with opposing partners but transduce activation signals that facilitate the production of bone-resorbing cytokines. We propose that cellular adhesion of osteoblasts as well as soluble factors is significant for the regulation of bone metabolism.
Short-term effect of testosterone treatment on reduced bone density in boys with constitutional delay of puberty
Authors: Bertelloni Silvano , Baroncelli Giampiero I. , Battini Roberta , Perri Giuseppe , Saggese Giuseppe 
Published: February 2010

Abstract
We studied bone mineral content (BMC), bone mineral density (BMD), cortical thickness/total width (CT/TW) ratio and cortical area/total area (CA/TA) ratio in boys with constitutional delay of puberty and the effect of short-term testosterone treatment on bone mass. Seventeen boys (age 13.1-15.8 years) who met the family history and the clinical criteria of constitutional delay of puberty were selected and enrolled in the study. All subjects were eating a diet assuring an adequate intake of calories and calcium. A subset of 8 boys (group A) was treated with testosterone depot (100 mg/month x 6 months) while 9 boys (group B) were not. At inclusion, BMC and BMD were reduced in the patients according to their chronological age (BMC -4.04 ± 1.34 standard deviation scores [SDS]; BMD -2.95 ± 0.56 SDS), statural age (BMC -1.75 ± 0.79 SDS; BMD -1.69 ± 0.78 SDS), and bone age (BMC -1.80 ± 0.65 SDS; BMD -1.86 ± 0.68 SDS). No significant differences between the groups were found (group A: BMC 0.480 ± 0.57 g/cm, BMD 0.488 ± 0.037 g/cm2, CT/TW ratio 0.43 ± 0.4, CA/TA ratio 0.68 ± 0.04; group B: BMC 0.476 ± 0.060, p = NS vs. group A; BMD 0.491 ± 0.036 g/cm2, p = NS vs. group A, CT/TW ratio 0.42 ± 0.05, p = NS vs. group A; CA/TA ratio 0.67 ± 0.06, p = NS vs. group A). At 12 months of follow-up, BMC, BMD, CT/TW ratio, and CA/TA ratio significantly increased in group A (BMC 0.70 ± 0.13 g/cm, δ +41.1 ± 28.8%, p &lt; 0.003 vs. 0 month; BMD 0.617 ± 0.082 g/cm2, δ + 26.2 ± 13.6%, p &lt; 0.005 vs. 0 month; CT/TW ratio 0.52 ± 0.05, δ +20.59 ± 10.65%, p &lt; 0.001 vs. 0 month; CA/TA ratio 0.77 ± 0.05, δ +13.60 ± 6.65%, p &lt; 0.004 vs 0 month), but not in group B (BMC: 0.48 ± 0.05 g/cm; δ +5.1 ± 7.8%, p = NS vs. 0 month; BMD: 0.492 ± 0.037 g/cm2; δ + 0.54 ± 8.7%, p = NS vs. 0 month; CT/TW ratio 0.44 ± 0.04, δ +4.04 ± 6.75%, p = NS vs. 0 month; CA/TA ratio 0.68 ± 0.05, δ +2.39 ± 5.90%, p = NS vs. 0 month). We conclude that boys with constitutional delay of puberty have reduced BMC and BMD. The delay in statural and bone ages did not totally account for the decreased bone mass. Testosterone treatment for 6 months significantly increased BMC, BMD, CT/TW ratio, and CA/TA ratio in these patients, but definitive conclusions on the efficacy of the treatment in improving adult bone mass can be drawn only when our patients reach early adulthood.
Effect of menopause on femoral and vertebral bone loss
Authors: Pouilles J.M. , Tremollieres F. , Dr. Ribot Claude 
Published: February 2010

Abstract
The aim of this study was to investigate the effect of menopause on bone loss in the proximal femur and the lumbar spine. The rates of change in bone mineral density (BMD) were measured longitudinally by dual X-ray absorptiometry (DXA) at the femoral neck (FN), Ward's triangle (WT), and trochanter (TR) together with the lumbar spine in 81 healthy postmenopausal women (45-65 years of age) who had passed a natural menopause, 6 months to 12 years before. A significant correlation between the rate of change and interval since menopause was evidenced. The best fit of the data was a binomial function of interval since menopause at the spine, FN, and WT and a simple linear regression at TR level. At each skeletal site, the rate of bone loss (mean ± SD) was significantly different (p &lt; 0.05) and twice as high in women who were between 6 months and 2 years postmenopausal at enrollment (FN, -1.82 ± 1.1.%; WT, -2.43 ± 1.7%; TR, -1.12 ± 1.7%) than in those who were beyond 5 years of menopause (FN, -0.48 ± 0.8%; WT, -0.68 ± 2.1%; TR, 0.41 ± 1.2%). A poor correlation (r = 0.39 - 0.42, p &lt; 0.001) was found between the rate of vertebral and that of femoral postmenopausal bone loss. This study demonstrates that menopause is associated with a rapid and transient bone loss in BMD of the proximal femur, which declines with time after 3 years. These data suggest that therapy should be initiated as early as possible after menopause to prevent bone loss.
Defect in formation of functional matrix vesicles by growth plate chondrocytes in avian tibial dyschondroplasia: Evidence of defective tissue vascularization
Authors: Nie Daotai , Genge Brian R. , Wu Licia N.Y. , Prof. Wuthier Roy E. 
Published: February 2010

AbstractAvian tibial dyschondroplasia (ATD), a disease characterized by an almost total lack of mineralization in affected areas of growth plate cartilage, may involve defective matrix vesicle (MV) mineralization. To explore the biochemical defect in ATD, both normal and diseased tissue were analyzed for the amount of isolatable MVs, their chemical composition, and their ability to induce mineral formation. We found significantly fewer MVs in ATD tissue, and in contrast to normal MVs, which rapidly mineralized when incubated in synthetic cartilage lymph, those isolated from ATD lesions induced only limited mineralization even after prolonged incubation. Analysis by detergent extraction revealed a nearly dysfunctional nucleational core in ATD MVs. Thus, in ATD tissue, there is a defect in the formation of MVs, and those that form are nearly inactive. There were also alterations in the lipid-dependent Ca2+-binding proteins (annexins) in ATD MVs. There were lower levels of annexins II and VI in endogenously produced collagenase-released matrix vesicles (CRMVs), but not in matrix vesicle–enriched microsomes (MVEMs) produced by tissue homogenization. These findings indicate that there is insufficient Ca2+ in ATD cells to enable incorporation of the annexins into MVs. Finally, there was evidence of phospholipid breakdown in ATD MVs, as well as in ATD tissue generally. This indicated that the ATD lesions were becoming necrotic. Taken together, these findings indicate that there is a defect in tissue vascularization such that the supply of mineral ions and nutrients to ATD cartilage is inadequate to support normal MV formation and subsequent mineralization.