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PubMed2000

Engineered bone development from a pre-osteoblast cell line on three-dimensional scaffolds.

Bone regeneration is based on the hypothesis that healthy progenitor cells, either recruited or delivered to an injured site, can ultimately regenerate lost or damaged tissue. Three-dimensional porous polymer scaffolds may enhance bone regeneration by creating and maintaining a space that facilitates progenitor cell migration, proliferation, and differentiation. As an initial step to test this possibility, osteogenic cells were cultured on scaffolds fabricated from biodegradable polymers, and bone development on these scaffolds was evaluated. Porous polymer scaffolds were fabricated from biodegradable polymers of lactide and glycolide. MC3T3-E1 cells were statically seeded onto the polymer scaffolds and cultured in vitro in the presence of ascorbic acid and beta-glycerol phosphate. The cells proliferated during the first 4 weeks in culture and formed a space-filling tissue. Collagen messenger RNA levels remained high in these cells throughout the time in culture, which is consistent with an observed increase in collagen deposition on the polymer scaffold. Mineralization of the deposited collagen was initially observed at 4 weeks and subsequently increased. The onset of mineralization corresponded to increased mRNA levels for two osteoblast-specific genes: osteocalcin and bone sialoprotein. Culture of cell/polymer constructs for 12 weeks led to formation of a three-dimensional tissue with architecture similar to that of native bone. These studies demonstrate that osteoblasts within a three-dimensional engineered tissue follow the classic differentiation pathway described for two-dimensional culture. Polymer scaffolds such as these may ultimately be used clinically to enhance bone regeneration by delivering or recruiting progenitor cells to the wound site.

3T3 Cells↗
PubMed2003

Bone development in neurofibromatosis 1.

Bony abnormalities are common findings in cases of neurofibromatosis 1. We might hypothesize that neurofibromin, the protein encoded by the neurofibromatosis 1 gene, plays important roles in bone development. Loss of function of oligodendrocyte-myelin glycoprotein gene and increased activity of ras p21 might increase the level of c-fos proto-oncogene in bones with formation of fibrous dysplasia-like tissue. Also, increased ras p21 might disturb collagen I synthesis by osteoblasts. Moreover, increased ras activity might increase the mitogenic signals to the nucleus through mitogen-activated protein kinase (MAPK) and disturb the level of the transcription factor core-binding factor alpha(1) (Cbfa1). Abnormal fibrous tissue and neurofibromas formed at the site of pseudarthrosis might represent abnormal response of periosteal fibroblasts for injury, an effect simulating the response of skin fibroblasts in neurofibromatosis 1 to injury.

Animals↗
PubMed1996

Prediction of bone mass in renal hyperparathyroidism by newly developed bone metabolic markers: evaluation of serum levels of carboxy-terminal pyridinoline cross-linked telopeptide of type I collagen and carboxy-terminal propeptide of type I procollagen.

Serum levels of the carboxy-terminal pyridinoline cross-linked telopeptide of type I collagen (ICTP) and the carboxy-terminal propeptide of type I procollagen (PICP) were measured in 95 patients with renal hyperparathyroidism who had undergone a total parathyroidectomy and autotransplantation of a small portion of the resected gland. The results were compared with the serum levels of other bone metabolic markers and bone mineral densities in the distal radius (R-BMD) and lumbar vertebrae (L-BMD), which were measured by dual energy x-ray absorptiometry and converted to the percentage of the mean value of sex- and age-matched healthy controls. The preoperative mean values of ICTP and PICP were 142.4 ng/ml and 187.8 ng/ml, respectively. Although the serum levels of PICP levels exceeded the normal range in 42.1% of the patients, those of ICTP exceeded it in all of them. The serum levels of ICTP correlated positively not only with those of tartrate-resistant acid phosphatase (TRACP), total alkaline phosphatase (ALP), and osteocalcin but also negatively with the values of %R-BMD and %L-BMD and seemed to manifest specifically the disturbance of bone metabolism. On the other hand, the serum levels of PICP correlated with those of ALP and TRACP but not with values of %BMDs. After surgery, the serum levels of ICTP decreased gradually, but those of PICP increased immediately up to peak values at 7 days and then decreased gradually after 14 days, reaching the normal range at 3 months. These changes in the bone metabolic markers seemed to reflect the change in bone metabolism that was converting from bone resorption to bone formation. The percent change in the PICP/ICTP ratio at 7 days correlated significantly with the percent change in R-BMD at 12 months, and it was suggested that postoperative bone gain might be predicted using a combination of postoperative changes in PICP and ICTP.

Absorptiometry, Photon↗
PubMed2003

The influence of alendronate on bone formation and resorption in a rat ectopic bone development model.

BACKGROUND: Most bone grafting techniques that include bone marrow, alloplastic materials, and extracellular bone matrix produce new bone mass, filling bone defects unpredictably. In most cases, the new bone undergoes resorption due to low local strains, resulting in significant bone loss. Recently, it was shown that alendronate and other bisphosphonates reduce bone loss when administered systemically or locally. The aim of this study was to investigate whether alendronate is effective on bone formation or bone resorption. METHODS: A total of 64 rats were divided into 2 main groups. In all the rats, fresh bone marrow removed from DA young rats was placed into demineralized rat femur cylinders (DBMC) and implanted into subcutaneous sites of host DA rats, to form new bone. Group A served as an alendronate treatment group, and group B served as a non-treated control. Group A received 100 microl of 1.5 mg/ml alendronate solution at 1, 2, and 3 weeks (group A1) and at 3, 4, and 5 weeks (group A2). At designated times, the rats were sacrificed, and the implanted DBMC was dissected out of the thorax and processed for histological and microradiography image analysis. RESULTS: Alendronate given at 1, 2, and 3 weeks (during the bone formation phase) did not increase the amount of bone or the visual bone density in comparison to the time-matched control, after 4 and 8 weeks. When alendronate was injected at 3, 4, and 5 weeks, the bone mass increased by 70% and by 166% after 6 and 10 weeks, respectively, in comparison to the untreated control. The visual bone density in group A2 was maintained at the level of 140 +/- 15 at 6 weeks and 152 +/- 15 at 10 weeks. The matched, non-treated control group B2 was significantly lower, 106 +/- 20 and 108 +/- 15, respectively. The histological sections showed that alendronate treatment at 3, 4, and 5 weeks maintained the normal appearance of the ossicle at 6 and 10 weeks in comparison to the osteopenic bone appearance in the matched controls. CONCLUSIONS: This study suggests that alendronate is effective in inhibiting bone loss, but ineffective during the bone formation phase. We suggest, therefore, that alendronate should be administered in procedures where bone resorption is expected.

Alendronate↗
PubMed1991

The effects of 1,25-dihydroxycholecalciferol on performance and bone development in the turkey poult.

The effect was studied of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] at various levels of vitamin D3, with adequate or inadequate dietary calcium, on performance and bone development in turkey poults. Two experiments were conducted. Experiment 1 lasted 16 days and was a 4 x 2 factorial arrangement using a low calcium diet (.7%), with dietary levels of vitamin D3 of 450, 900, 1,800, and 3,600 ICU/kg of diet and with or without 10 micrograms of dietary 1,25-(OH)2D3. Experiment 2 lasted 14 wk and was a 2 x 2 x 2 factorial arrangement with vitamin D3 levels of 900 or 2,700 ICU/kg of diet, calcium levels at 58 or 100% of the National Research Council requirement (which varies with age), and with or without 10 micrograms/kg of dietary 1,25-(OH)2D3. In Experiment 1, increasing levels of vitamin D3 and 1,25-(OH)2D3 supplementation significantly increased bone ash. Pairwise contrasts at specific vitamin D3 levels indicated that this effect of 1,25-(OH)2D3 was greater at lower levels of vitamin D3. In Experiment 2, the 2,700-ICU level of vitamin D3 decreased the incidence of rickets at 3 wk and partially ameliorated a calcium deficiency, as indicated by an increase in growth at the 2,700-ICU level of vitamin D3 in calcium-deficient diets from 8 to 14 wk. Vitamin D3 by calcium interactions on rickets at 14 wk of age and bone ash at 3 and 14 wk were similar and indicated also that vitamin D3 partially ameliorated a calcium deficiency. In general, the addition to the diet of 1,25-(OH)2D3 increased bone ash and decreased the incidence of rickets in diets deficient in calcium but high in vitamin D3. There is very little evidence in the present study that indicates that 1,25-(OH)2D3 has any effect on tibial dyschondroplasia.

Animals↗
PubMed1991

Induced bone development in transplants of fresh human pseudomalignant heterotopic ossification tissue in athymic nude mice.

Biopsy specimens of mature trabecular bone from tumors of two typical cases of pseudomalignant heterotopic ossification (PHO; myositis ossificans circumscripta) were transplanted into athymic nude mice. Specimens of normal metaphyseal bone in adjacent areas were also transplanted in the contralateral hindquarter muscles for controls. By seven days, control bone transplants were necrotic and enveloped in granulation tissues whereas PHO transplants were surrounded by proliferating connective tissue derived from the host-bed muscle tissues. In the intervals from 14 and 21 days, the PHO transplants showed vascular and hypertrophied connective-tissue proliferation with appositional deposits of new bone. The microscopic features of the new bone suggested that it was of mouse host-bed origin because the new bone from Case 1, a female, showed nuclei without sex chromatin. The quantities of new bone were measured by correlated histomorphometric and computer image analysis of microradiographs. Little or no cartilage development was noted at any stage. The normal control trabecular bone tissue was slowly resorbed by macrophages and mononuclear phagocytes; multinucleated giant cells were few and relatively small. Except in one questionably small area of one transplant, nontumorous undemineralized normal human bone failed to induce bone formation within the 28-day period of observation. The quantity of new bone formed in athymic mice in response to implants of PHO, estimated from equivalent quantities of bone developed from implants of lyophilized matrix-free bone morphogenetic protein (BMP) was about 1 microgram/g of wet PHO tumor weight. Although circumstantial evidence implicates BMP in the pathogenesis of heterotopic ossification, more research should be directed toward regional and systemic factors inhibiting bone development in normal and abnormal conditions, including malignant bone tumors.

Adult↗
PubMed1989

Cellular and molecular events during embryonic bone development.

The cellular events underlying the processes of bone maintenance, remodeling, and repair have their basis in the embryonic production of bone. Although it has been suggested that the cartilaginous model which resides in the center of developing limbs provides the scaffolding for new bone formation, our detailed morphological and histochemical studies indicate otherwise. In particular, there exists a layer of four to six cells, referred to as Stacked Cells, which surrounds a prechondrogenic core of undifferentiated cells in the limb. These Stacked Cells give rise to the lineage of osteogenic cells responsible for the formation of all structural bone. This bone is fabricated outside of the cartilage core, and the core is not replaced by bone, but rather, is replaced by marrow and vascular elements. Several generalizations arise from analysis of the cellular and molecular events of embryonic osteogenesis, and they are as follows: 1) osteogenesis and chondrogenesis are independent events which are programmed early in development, 2) bone formation is a vascular driven phenomenon which is characterized by the directional nature of osteoid secretion, and 3) the fundamental events of bone formation are consistent in chick, rat, and human long bones.

Animals↗
PubMed2001

Modeling of cross-sectional bone size, mass and geometry at the proximal radius: a study of normal bone development using peripheral quantitative computed tomography.

It is becoming increasingly accepted that bone size is an important determinant of bone mass. Studies on the development of bone size may therefore promote a better understanding of the basis of diseases which are due to low bone mass. Here, we characterize the temporal changes in cross-sectional bone size, geometry and mass at the radial diaphysis in healthy subjects from 6 to 40 years of age (n = 469; 273 females). Peripheral quantitative computed tomography was used to measure total and cortical cross-sectional area, bone mineral content (BMC) and volumetric bone mineral density (BMD) at the site of the forearm whose distance from the ulnar styloid process corresponded to 65% of forearm length. Over the age range of the study, total cross-sectional area increased by 39 mm2 (50%) in females and by 85 mm2 (116%) in males. Cortical area increased to a similar extent in both sexes. Between 6-7 years and adulthood, BMC increased by 52 mg/mm (111%) in females and by 73 mg/mm (140%) in males and was significantly higher in males after the age of 15 years. Volumetric BMD increased by 246 mg/cm3 (48%) in females but by only 132 mg/cm3 (23%) in males and was significantly higher in women than in men. In summary, these data show that BMC in men is higher than in women, because periosteal modeling continues longer in boys than in girls. Volumetric BMD is higher in women, partly because the size of the marrow cavity does not increase in girls as it does in boys.

Adolescent↗
PubMed2003

Progression of calvarial bone development requires Foxc1 regulation of Msx2 and Alx4.

Calvarial bones form by direct ossification of mesenchyme. This requires condensation of mesenchymal cells which then proliferate and differentiate into osteoblasts. Congenital hydrocephalus (ch) mutant mice lack the forkhead/winged helix transcription factor Foxc1. In ch mutant mice, calvarial bones remain rudimentary at the sites of initial osteogenic condensations. In this study, we have localized the ossification defect in ch mutants to the calvarial mesenchyme, which lacks the expression of transcription factors Msx2 and Alx4. This lack of expression is associated with a reduction in the proliferation of osteoprogenitor cells. We have previously shown that BMP induces Msx2 in calvarial mesenchyme (Development 125, 1241-1251, 1998). Here, we show that BMP also induces Alx4 in this tissue. We also show that BMP-induced expression of Msx2 and Alx4 requires Foxc1. We therefore suggest that Foxc1 regulates BMP-mediated osteoprogenitor proliferation and that this regulation is required for the progression of osteogenesis beyond the initial condensations in calvarial bone development.

Animals↗
PubMed1981

Changes in intracellular enzymes of collagen biosynthesis during matrix-induced cartilage and bone development.

The activities of five intracellular enzymes of collagen biosynthesis were determined during cartilage and bone formation induced in rats by demineralized bone matrix. The five enzymes, prolyl 4-hydroxylase, prolyl 3-hydroxylase, lysyl hydroxylase, hydroxylysyl galactosyltransferase and galactosyl-hydroxylysyl glucosyltransferase, exhibited broadly parallel profiles; the activities rising steeply from day one to reach their highest values on day nine and decreasing gradually thereafter. The maximal enzyme activity correlated with the period of chondrogenesis and hypertrophic cartilage characterized by the synthesis of cartilage-specific type II collagen. Prolyl 4-hydroxylase was also studied in respect of its tissue distribution and cellular location using indirect immunofluorescence. The enzyme was mainly located in the mesenchymal cells on day three, in the chondrocytes and hypertrophic chondrocytes on days seven to nine, and in the osteoblasts on day eleven and thereafter.

Animals↗