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At least 757 records · Page 42Linked to original sources
PubMed1979

Influence of magnesium depletion on matrix-induced endochondral bone formation.

The effect of magnesium deficiency on bone cell differentiation and bone formation was investigated using in vivo matrix-induced endochondral ossification as a test system. Demineralized bone matrix was implanted subcutaneously in young (35-day-old) male Long-Evans rats that had been fed a semisynthetic Mg-deficient diet (50 ppm Mg) for 7 days. Plasma Mg levels were reduced to 25-30% of control values at that time. Control rats were paired the same diet, supplemented to contain 1000 ppm Mg. The implants were harvested 7, 9, 11, 15, and 20 days after implantation and analyzed for Mg and Ca content, 45Ca incorporation, and alkaline phosphatase levels. At each stage, plaques (implants) removed from Mg-deficient rats showed retardation in cartilage and bone differentiation and matrix calcification. Magnesium content was markedly reduced when compared to the control plaques. Histological appearance of the matrix-induced plaques confirmed the retardation in bone development and mineralization suggested by the chemical indicators. Most marked was the virtual absence of bone marrow in 20-day-old plaques in Mg-depleted rats. These data show that bone cell differentiation can occur in a severely Mg-depleted environment, although the onset of mineralization and bone remodeling was delayed and bone marrow differentiation was impaired.

Alkaline Phosphatase↗
PubMed1980

A silver impregnation technique to demonstrate muscle-bone-cartilage relationships in fishes.

A modification of the Winkelmann and Schmitt (1957) technique originally designed to investigate patterns of peripheral nervous innervation is given for demonstration of developing bone growth centers and associated muscle origins and insertions in larval and small fishes. This technique offers a simpler and faster way of obtaining such ontogenetic information than the standard method of double staining with alizarin red S and Alcian blue followed by clearing with potassium hydroxide. Muscles also stain, facilitating the location of their origins and insertions.

Animals↗
PubMed1998

Immunocytochemical localization and biochemical characterization of large proteoglycans in developing rat bone.

This study used biochemical and light and electron microscopic immunohistochemical methods to localize and characterize large hyaluronate-binding proteoglycans in the developing mandible of fetal rats at embryonic day 15 (Day 15) to Day 18 using a monoclonal antibody (MAb) 5D5. This antibody is derived from bovine sclera and specifically recognizes the core protein of large proteoglycan such as versican, neurocan and brevican, but not that of aggrecan. At the light microscopic level, MAb 5D5 moderately stained the extracellular matrices among osteoblasts at the centers of ossification in Day 15 mandible specimens. Weaker staining was observed in osteoblasts, whereas Meckel's cartilage lacked staining. Ultrastructural immunocytochemistry showed the presence of immunogold particles over unmineralized matrices among osteoblasts and their intracellular organelles. In Day 16 to 18 specimens, bone nodules were recognized in LR gold sections before immunostaining, but, after immunostaining, consistently appeared devoid of mineral crystals and were seen as a demineralized structure that had an electron dense periphery within which fine filamentous and granular material were present. The appearance of these structures was created by the demineralization of thin sections on grids during immunostaining. Specific immunogold staining was clearly seen over the demineralized structures corresponding to bone nodules. The majority of immunogold particles tended to localize inside of the structures. Bone proteins were extracted from fresh, Day 18 specimens with a three-step technique: 4 M guanidine HCl (GdnCl,-extract), aqueous EDTA without GdnCl (E-extract), followed by GdnCl. Western blot analysis of SDS-polyacrylamide gel electrophoresis after chondroitinase ABC digestion, showed that G1-extract gave a 5D5 reactive band greater than 400 kDa, whereas E-extract produced two major reactive populations of small molecular size with core proteins approximately 63 and 74 kDa. These results indicate that the large proteoglycan having smaller molecular weight is preferentially localized to bone nodules and may correlate with bone matrix mineralization.

Animals↗
PubMed1981

Development of bone mineral loss in insulin-treated diabetes: a 1 1/2 years follow-up study in sixty patients.

The change in bone mass during 1 1/2 years was determined in a longitudinal study of sixty adult insulin-treated diabetic out-patients. During the study period the mean bone mass decreased by 1.30 +/- 0.28 (SEM)% (P less than 0.001), to a mean value of 91.0 +/- 1.7% of normal (P less than 0.001). The rate of bone loss was significantly higher in patients with 1-6 years of diabetes (n = 29, bone loss: 1.96 +/- 0.32%/1 1/2 years) than in patients with longer duration of the disease (n = 31, bone loss: 0.61 +/- 0.44%/1 1/2 years, P less than 0.02). The endogenous insulin secretion estimated with the glucagon-stimulated serum C-peptide concentration decreased during the observation period in 58.6% of the patients with 1-6 years of diabetes compared to 16.1% among patients with 7-11 years of diabetes (P less than 0.002). The rate of bone mineral loss was almost 3 times higher in the twenty-two patients in whom endogenous insulin secretion had deteriorated (2.12 +/- 0.30%/1 1/2 years) than in the thirty-eight patients without as well as with unchanged or increased insulin secretion (0.78 +/- 0.39%/1 1/2 years, P less than 0.01). In twenty patients with an increased insulin dose during the study period the mean bone mineral loss was 2.05 +/- 0.36%/1 1/2 years compared to a mean bone mineral loss of 0.91 +/- 0.38%/1 1/2 years in the forty patients with unchanged or decreased insulin dosage (P less than 0.05). This longitudinal study further supports the hypothesis that the bone mineral loss in insulin-treated diabetic patients begins with the onset of clinical diabetes and that its development is associated with the deterioration of the beta-cell function and with the increment in insulin dosage. The rate of bone mineral loss is high during the first few years of clinical diabetes, but levels off with increasing duration of the disease.

Adult↗
PubMed1987

Developing antler, a model for endocrine regulation of bone growth. Concentration gradient of T3, T4, and alkaline phosphatase in the antler, jugular, and the saphenous veins.

Thyroxine (T4), triiodothyronine (T3), and alkaline phosphatase (AP) were assayed monthly in white-tailed deer plasma obtained from the antler (A), jugular (J), and the saphenous (S) veins during the period of antler growth and the period of mineralization. The concentrations of T3, T4, and AP in the J and S were not significantly different in any month. During the most intense antler growth period (June and July) AP levels were significantly higher and T3 significantly lower in A as compared to J and S, but no differences were found during the mineralization phase in August. T3 values from all three veins were significantly lower in the mineralization period than J and S values during the growing phase. Variations of T4 levels between A, J, and S as well as differences between months were only negligible. The data indicate that AP is produced in large quantity in the antler tissue during the growth period, but the amount is sharply reduced during the mineralization phase. T3 is utilized in the growing antler; the rate of utilization correlates with the intensity of antler growth. T4 is probably not utilized in the antler bone. Developing antler might be used as a model to study growth and mineralization processes of bony tissues.

Alkaline Phosphatase↗
PubMed2005

Crosstalk between cancer cells and bone microenvironment in bone metastasis.

Bone, as well as lung and liver, is one of the most preferential metastatic target sites for cancers including breast, prostate, and lung cancers. Although the precise molecular mechanisms underlying this preference need to be elucidated, it appears that bone microenvironments possess unique biological features that enable circulating cancer cells to home, survive and proliferate, and destroy bone. In conjunction, cancers that develop bone metastases likely have the capacity to utilize these unique bone environments for colonization and bone destruction. This crosstalk between metastatic cancer cells and bone is critical to the development and progression of bone metastases. Disruption of this interaction will allow us to design mechanism-based effective and specific therapeutic interventions for bone metastases.

Animals↗
PubMed1995

Bone composition and histological analysis of young and aged rats fed diets of varied calcium bioavailability.

OBJECTIVE: The effects of varied calcium bioavailability on bone development (young animal) and bone maintenance (aged animal) were evaluated by the application of bone composition and histologic/histomorphometric techniques. METHODS: Groups of male young (3-4 weeks old) and aged (24-month-old) rats were fed nutritionally-complete but calcium-restricted (0.15%) diets in which calcium was derived from spinach or nonfat dry milk (NFDM). A 0.5% calcium casein-based diet group was included as a comparison at the National Research Council's requirement level. All animals were pair-fed to the spinach-fed group. At the end of 60 days, lumbar vertebrae, tibia and femurs were harvested for bone histomorphometric and bone composition analyses. RESULTS: Histological analysis of the fifth lumbar vertebral body of the young spinach-fed group showed retarded development and mineralization of trabecular bone. Histomorphometry revealed that the spinach-fed group seemed to respond to the lower bioavailable calcium source by reducing the mineralization of bone matrix and stimulating bone resorption with a resultant decrease in bone volume (0.027, 0.059, 0.068 mm3 in spinach, NFDM and 0.5% calcium casein-based diet groups, respectively). The aged animals, however, appeared to respond to the reduction in available dietary calcium by mobilizing skeletal reserves, with a subsequent decrease in bone volume (0.057, 0.060, 0.073 mm3 in spinach, NFDM and 0.5% calcium casein-based diet groups, respectively). CONCLUSION: This study demonstrates that a low bioavailable calcium source, spinach, suppresses calcium deposition in bones of young animals resulting in a reduction in both quality and quantity of bone. Moreover, despite the stable structure of the mature bone, a low bioavailable calcium source may also compromise the skeletal integrity of the aged animal.

Aging↗
PubMed1982

The effect of neurogenic stimulation on the development and growth of bony tissues.

In order to elucidate the mechanisms of neurogenic control of bone development and growth, the effects of traumatic and electric stimulation on the development, size, and shape of antler bone tissue were investigated. Unilateral growth of antler in a female deer was initiated after traumatic stimulation of the frontal bone. Electrical stimulation of antler nerves or antler periosteum resulted in an increase in more than 70% in antler length and over 40% in weight. Stimulation of antler nerves also resulted in abnormal shape of antlers. The role of periosteal nerves and the participation of the central nervous system in the responses to stimulation is discussed.

Aging↗
PubMed1985

Differences in permeability of microperoxidase and horseradish peroxidase into the alveolar bone of developing rats.

Microperoxidase (small m.wt tracer) and horseradish peroxidase (large m.wt tracer) were used to investigate the existence of extracellular (between blood vessels and bone cells) and intracellular transport pathways in the alveolar bone cells of five-day-old rats. HRP directly penetrated the cytoplasm and nucleus of the osteocytes and osteoblasts, but MP did not. These findings suggest that HRP at high dosages is more toxic to bone cells than is MP, since the direct penetration of HRP probably results from alteration of plasma membrane permeability. If so, MP seems to be a more suitable tracer than HRP. The findings from MP tracing suggest that a main transport pathway of bone fluid exists between the external part of the unmineralized zone, which is located in the lacunar and canalicular spaces around bone cells, and the innermost edge of the mineralized matrix, which constitutes the lacunar and canalicular walls; in addition, minor pathways as accessory routes might diverge from the main pathway to go around the bone cells.

Alveolar Process↗
PubMed2006

Influence of sex hormone disturbances on the internal structure of the mandible in newborn mice.

It has not yet been clarified how sex hormones affect craniofacial bone development immediately after birth. The purpose of this study was to examine the effects of sex hormone deficiency on craniofacial bone development immediately after birth, in terms of the internal structure of the mandible in newborn mice with orchiectomy (ORX) and ovariectomy (OVX). ORX, OVX and a sham-operation were performed on 40 five-day-old C57BL/6J mice. Eight weeks after surgery, each mandible was subjected to histomorphometric analysis of trabecular (Tr) and cortical (Ct) bone mineral density (BMD) by peripheral quantitative computed tomography (pQCT). In the experimental groups, a significant reduction in BMD was found in comparison with the control groups. In histomorphometric analysis, the number of tartrate-resistant acid phosphatase (TRAP)-positive cells in the condyle and the thickness of the condylar cartilage layer was significantly greater in the experimental mice than in the controls. Trabecular bone volume of the condyle measured on azocarmine-aniline blue (AZAN) sections was significantly less in the experimental mice than in the controls. These results indicate that mandibular growth is inhibited by sex hormone disturbances and the relevant internal structures changed. The findings show that sex hormones are one of the key determinants of mandibular growth and development immediately after birth.

Acid Phosphatase↗
PubMed1995

Lethally irradiated normal strains of mice radioprotected with SCID bone marrow develop sensitivity to low doses of staphylococcal enterotoxin B.

Normal strains of mice are rendered sensitive to small amounts (3-10 micrograms) of staphylococcal enterotoxin B (SEB) by transplanting bone marrow cells of SCID donor mice to lethally irradiated recipients. Four to 12 weeks post-transplantation, SEB induces 56-100% lethality. Transplantation of normal mouse bone marrow cells, either alone or with the SCID mouse selected bone marrow cells, does not confer SEB sensitivity. These data imply that either irradiation ablates certain cell population(s), that confer resistance to SEB in normal mice (populations that are absent in the SCID donor mice) or that the donor cells selectively repopulate recipients with SEB-sensitive cells. This model will help elucidate the cells, cytokines and the SEB peptide fragments responsible for SEB toxicity and will be useful in identifying promising vaccine candidates and in developing preventive medicines to protect against this potent toxin.

Animals↗
PubMed2000

Bone metastasis model with multiorgan dissemination of human small-cell lung cancer (SBC-5) cells in natural killer cell-depleted SCID mice.

Lung cancer is commonly associated with multiorgan metastasis, and bone is a frequent metastatic site for lung cancer. Nevertheless, no bone metastasis model of lung cancer with multiorgan dissemination is available, which could provide opportunity to study the molecular pathogenesis. We examined the abilities of eight human lung cancer cell lines injected intravenously into natural killer (NK) cell-depleted SCID mice to generate metastatic nodules in bone and multiple organs, and explored the correlation of the parathyroid hormone-related protein (PTHrP) with the bone metastasis. Although all the small-cell carcinoma cell lines (SBC-5, SBC-3, SBC-3/ADM, H69, H69/VP) formed metastatic nodules in multiple organs (liver, kidney, and lymph nodes), only SBC-5 cells reproducibly developed bone metastases. Squamous cell carcinoma (RERF-LC-AI) cells metastasized mainly into the liver and kidneys, whereas adenocarcinoma (PC-14, A549) mainly produced colonies in the lungs. As assessed by X-ray photography, the osteolytic bone metastases produced by SBC-5 cells were detected as early as on day 28, and all recipient mice developed bone metastasis by day 35. The expression of PTHrP in eight cell lines was directly correlated with the formation of bone metastasis. No correlation was observed between the formation of bone metastasis and the expression of other metastasis-related cytokines (IL-1, IL-6, IL-8, IL-10, IL-11, TNF-alpha, VEGF, M-CSF). Consistent with the formation of bone metastasis by SBC-5 cells, the levels of PTHrP and calcium in the mouse serum were increased in a time-dependent manner, suggesting that PTHrP produced by human lung cancer may play a crucial role in the formation of bone metastasis and hypercalcemia. These findings indicate that a bone metastasis model of SBC-5 cells may be useful for clarifying the molecular aspects of the metastatic processes in different organ microenvironments and the development of therapeutic modalities for lung cancer patients with bone metastases.

Animals↗
PubMed1986

Influence of level of feeding and nutrient content of the concentrate on growth and development of yearling horses.

Three experiments using 63 Thoroughbred and Quarter Horse yearlings were conducted to evaluate the influence of level of feeding, and protein and calculated energy content of pelleted concentrates on growth and bone development. Animals were housed in drylot paddocks and individually fed concentrates twice daily. Coastal bermudagrass (Cynodon dyctylon) hay was group-fed. Yearlings offered a corn-based concentrate (3.56 Mcal digestible energy [DE]/kg) consumed levels of dry matter similar to yearlings fed a mixed-grain concentrate (3.32 Mcal DE/kg but consumed slightly more digestible energy. No differences in growth or bone development were detected. Yearlings fed restricted levels of concentrate that provided approximate National Research Council (NRC) recommendations for protein and DE had lower weight and girth gains (P less than .05) than those provided ad libitum concentrate intake during two 1.5-h daily feeding periods. Restricting concentrate intake had no effect on skeletal growth (P less than .05) but resulted in numerically lower values for bone radiographic density. Protein addition to a diet restricted to approximate NRC energy intake recommendations had no effect on weight gain, body measurements or bone mineral deposition (P greater than .05) and growth and development was less than that resulting from higher intakes of a lower protein concentrate.

Aging↗
PubMed1986

Pneumatization of the articular eminence of the temporal bone: prevalence, development, and surgical treatment.

Routine panoramic radiographs of 784 patients were evaluated retrospectively for the presence of pneumatization of the articular eminence of the temporal bone (PAT). The radiographs of eight patients showed signs of PAT. These eight patients ranged in age from 32 to 69 years, and four patients had bilateral involvement of the temporal bone. The use of tomography is recommended before surgical procedures involving the eminence to determine the extent of the pneumatization.

Adult↗
PubMed2005

Selective Runx2-II deficiency leads to low-turnover osteopenia in adult mice.

Runx2 transcribes Runx2-II and Runx2-I isoforms with distinct N-termini. Deletion of both isoforms results in complete arrest of bone development, whereas selective loss of Runx2-II is sufficient to form a grossly intact skeleton with impaired endochondral bone development. To elucidate the role of Runx2-II in osteoblast function in adult mice, we examined heterozygous Runx2-II (Runx2-II(+/-)) and homozygous Runx2-II (Runx2-II(-/-))-deficient mice, which, respectively, lack one or both copies of Runx2-II but intact Runx2-I expression. Compared to wild-type mice, 6-week-old Runx2-II(+/-) had reduced trabecular bone volume (BV/TV%), cortical thickness (Ct.Th), and bone mineral density (BMD), decreased osteoblastic and osteoclastic markers, lower bone formation rates, impaired osteoblast maturation of BMSCs in vitro, and significant reductions in mechanical properties. Homozygous Runx2-II(-/-) mice had a more severe reduction in BMD, BV/TV%, and Ct.Th, and greater suppression of osteoblastic and osteoclastic markers than Runx2-II(+/-) mice. Non-selective Runx2(+/-) mice, which have an equivalent reduction in Runx2 expression due to the lack one copy of Runx2-I and II, however, had an intermediate reduction in BMD. Thus, selective Runx2-II mutation causes diminished osteoblastic function in an adult mouse leading to low-turnover osteopenia and suggest that Runx2-I and II have distinct functions imparted by their different N-termini.

Animals↗
PubMed1990

Malignant fibrous histiocytoma developing in bone 44 years after shrapnel trauma.

Tumors induced by foreign bodies are uncommon in humans, but they are a relatively common occurrence in some experimental animals. The development of sarcoma in association with metallic foreign bodies has rarely been reported. The development of a malignant fibrous histiocytoma in a 65-year-old man 44 years after shrapnel fragments lodged in his left arm is described. The literature regarding metallic foreign body-induced cancer in humans is reviewed.

Aged↗
PubMed2003

Serum osteoprotegerin is a major determinant of bone density development and prevalent vertebral fracture status following cardiac transplantation.

Osteoprotegerin (OPG) is an antiresorptive cytokine and a key regulator of osteoclastogenesis and activity. Since OPG is downregulated by glucocorticoids and cyclosporine A in vitro we examined whether immunosuppressive therapy would play a role in the development of transplantation osteoporosis. We enrolled 57 cardiac transplant recipients (median time since transplantation, 3.2 years (1.1-11.5 years)) in this cross-sectional study. Standardized spinal X-rays as well as hip bone density measurements were performed in all patients. Serum OPG was determined using a commercially available ELISA. Vertebral fractures were present in 56% of the patients. Bone densities of all femoral neck subregions were correlated to serum OPG concentrations (r values between 0.40 and 0.48, all P < 0.005). Multiple regression analysis revealed OPG levels to be independently correlated to femoral neck Z scores (r = 0.49, P = 0.002). After adjustment for age, BMI, neck Z score, renal function, and months since transplantation, serum OPG was the only significant predictor of prevalent vertebral fractures (P = 0.001). In a separate 6-month prospective study of 14 heart transplant recipients receiving calcium and vitamin D serum OPG levels fell by 41% (P = 0.0004) after 3 months and 47% (P = 0.0001) after 6 months following cardiac transplantation. Bone loss at the lumbar spine and femoral neck after 6 months was correlated to the decrease in serum OPG at 6 months (r = 0.82, P < 0.0001, and r = 0.60, P = 0.02, respectively) as well as 3 months after cardiac transplantation (r = 0.65, P = 0.01, and r = 0.69, P = 0.006, respectively). Serum OPG alone accounted for 67% of the variance of lumbar spine bone density changes over the first 6 months posttransplantation. We conclude that serum OPG levels decline consistently in all patients following initiation of immunosuppressive therapy and are independently correlated with changes in bone density. We hypothesize that OPG plays a major role in the development of transplantation osteoporosis.

Aged↗