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At least 361 records · Page 20Linked to original sources
PubMed1982

[Critical analysis of the diagnostic value of the first sesamoid bone of the thumb as an indicator of bone development in puberty].

Although the appearance of the first sesamoid of the thumb has been widely reported as being a good indicator of puberty, it should be noted that this finding has only been confirmed in cross-sectional studies. When trying to determine this relationship through a longitudinal study, we see that, although the correlation indices come within the limits of statistical significance, the wide range of variability in appearance reduces its practical usefulness. The sesamoid bone normally appears during puberty but neither the initial moment of this occurrence nor the exact stage of the child's development at that time can be assessed.

Adolescent↗
PubMed2003

Effects of u.v. irradiation of very young chickens on growth and bone development.

Six experiments were conducted to study the effects of exposure of young chickens to u.v. radiation. Chickens were fed a cholecalciferol (D3)-deficient diet and exposed to u.v. radiation from fluorescent lights giving total radiance (285-365 nm) at 0.15 m of 99.9 mJ/s per m(2). In Expt 1, chickens had increased body weight, bone ash and plasma Ca and decreased incidence of rickets and tibial dyschondroplasia (TD) when exposed to fluorescent light radiation 24 h per d, 24 h every 2 d, or 24 h every 3 d starting with exposure on day 1 after hatching. However, when not exposed on day 1, but on days 4, 7, 10, 13 and 16, the bone ash was reduced, and the incidence of TD and rickets was increased, compared with chickens exposed on day 1 after hatching. When chickens were exposed at 1 d of age to radiation from two lamps, each of which gave a radiance (285-365 nm) at 0.26 m of 856 mJ/s per m(2), both the length of time of radiation and location of the lamps (above or below the chicken) influenced the response as measured by body weight, bone ash, plasma Ca and incidence of rickets. When chickens that received a TD-inducing diet were exposed to 30 min u.v. radiation from below at 1 d of age they developed significantly less TD than did those not exposed when fed either 27.5 or 55.0 microg D3/kg diet.

Animals↗
PubMed1978

Sharpey fiber bone development in surgically implanted dog mandible. A scanning electron-microscopic study.

Ticonium metal implant placed surgically in the previously edentulatized adult dog mandible induced the formation of an extensive Sharpey fiber system. Sharpey's fibers extended from the peri-implant area, deep into alveolar bone. The frequency of Sharpey's fibers and the degree of their mineralization varied from scattered location and unmineralized state to heavy clustering and full mineralization. This study suggests that the formation of Sharpey's fibers and the degree of their mineralization are determined by biophysical forces of pressure received at a given site.

Alveolar Process↗
PubMed2001

Tissue specific regulation of VEGF expression during bone development requires Cbfa1/Runx2.

Vascular endothelial growth factor (VEGF) is a critical regulator of angiogenesis during development, but little is known about the factors that control its expression. We provide the first example of tissue specific loss of VEGF expression as a result of targeting a single gene, Cbfa1/Runx2. During endochondral bone formation, invasion of blood vessels into cartilage is associated with upregulation of VEGF in hypertrophic chondrocytes and increased expression of VEGF receptors in the perichondrium. This upregulation is lacking in Cbfa1 deficient mice, and cartilage angiogenesis does not occur. Finally, over-expression of Cbfa1 in fibroblasts induces an increase in their VEGF mRNA level and protein production by stimulating VEGF transcription. The results demonstrate that Cbfa1 is a necessary component of a tissue specific genetic program that regulates VEGF during endochondral bone formation.

3T3 Cells↗
PubMed2002

Expression of Runx1, -2 and -3 during tooth, palate and craniofacial bone development.

We describe the expression of three Runt-related RUNX genes (previously termed AML, Cbfa, or Pebp2alpha) Runx1 and Runx3 during the development of teeth and other craniofacial tissues and compare them to Runx2 expression reported earlier. All three genes were expressed in mesenchymal condensates. Runx1 was expressed in several cartilage primordia earlier than Runx3, and Runx2 was intense in all mesenchymal condensations of bones and teeth. Only Runx1 was expressed in epithelia, and in tooth germs transcripts were detected in outer dental epithelium. Runx1 was also intensely expressed in the midline epithelium of palatal shelves. In early tooth morphogenesis Runx3 was coexpressed with Runx2 in a thin layer of mesenchymal cells underlying dental epithelium. Unlike Runx2, Runx3 was expressed in odontoblasts. However, Runx3 mutant mice did not show obvious tooth phenotype or deviations of Runx1 and Runx2 expression patterns in the tooth.

Animals↗
PubMed1999

Infectious stunting syndrome associated with disturbances of mineral metabolism and bone development in broiler chickens.

On a broiler farm with a rearing capacity of about 200,000 chickens, a disease characterised by growth retardation, variability in chick size, 'leg weakness', diarrhoea and increased mortality at 3 weeks of age occurred repeatedly, in several successive broiler flocks. Gross and histopathological findings were dominated by widening of the hypertrophic and ossification layers of the physes of long bones as well as by thickening, unevenness and defective calcification of the cartilage trabeculae. In the parathyroid gland, vacuolar degeneration of the cytoplasm of glandular epithelial cells, connective tissue proliferation and, here and there, cyst formation were seen. Additional findings included severe cerebellar oedema and neuronal degeneration. The pancreatic, myocardial and intestinal changes typical of infectious stunting syndrome (ISS) occurred only in a mild form. Four-week-old chickens exhibiting 'leg weakness' had significantly lower blood inorganic phosphate concentration and tibial ash content as compared to healthy chickens. The disease was successfully transmitted by oral administration of small intestinal homogenate from affected chickens. In a second experiment, however, the disease could not be transmitted with intestinal homogenate sterilized by irradiation. Large doses of vitamin D3 reduced the rate of growth retardation and defective calcification of bones. The digestive enzyme activities of the pancreas and small intestinal mucosa of 'infected' chickens were decreased as is typical of ISS.

Animals↗
PubMed1979

Abnormal canine bone development associated with hypergravity exposure.

Chronic centrifugation of 85- to 92-day-old Beagles at 2.0 X g and 2.6 X g for 26 weeks during the time of active skeletal growth caused skeletal abnormalities in the radius and the ulna of ten of 11 dogs. The pattern of change mimicked that found in naturally occurring and experimentally induced premature distal ulnar physeal closure or delayed growth at this physis. Minimal changes in bone density were detected by sensitive photon absorptiometric techniques. Skeletal abnormalities also were found in five of the six cage-control dogs, although the run-control dogs were radiographically normal.

Animals↗
PubMed1991

Effect of calcium on skeletal development, bone loss, and risk of fractures.

In assessing the role of calcium, it must be stressed that calcium is not the cause of bone health but simply a necessary condition for it. It is mechanical usage that is of primary importance for bone. In just the same way iron is essential for hemoglobin synthesis and protein is essential for muscle mass, but neither is sufficient by itself. What, then, ought we to expect from a high calcium intake? Can we prevent estrogen-withdrawal bone loss? No. Calcium is not a substitute for estrogen, anymore than it is a substitute for exercise. Will calcium slow the remodeling loss that occurs with aging? Yes, to some extent; as calcium slows remodeling, it will inevitably slow remodeling-related loss. But most importantly, a high calcium intake will prevent calcium-deficiency bone loss. The only question, therefore, is the extent to which calcium deficiency loss may contribute significantly to bone fragility in various populations. The bone loss and fracture data reviewed briefly here indicate that an important portion of the osteoporotic fracture burden is calcium-related. What that portion is will be a function of the fraction of the population with inadequate intakes in any given country. Better than half of all adult American women have calcium intakes less than 500 mg/day, whereas only a small fraction of Dutch or Danish women, for example, would be under that level. Hence, a population-wide program to increase calcium intake in the United States would be likely to yield a greater benefit than in either the Netherlands or Denmark. That does not mean, of course, that there could not be substantial benefit to individuals with low intakes in all countries. Calcium intakes of greater than or equal to 1,500 mg are both safe and natural. While not all bone loss and low trauma fractures are due to low calcium intake, some almost certainly are. Adaptation to low intakes does occur, but it is seldom sufficient to compensate for the low intake. We cannot easily distinguish those who need more calcium from those who need less, and for that reason it makes good sense to ensure an adequate calcium intake for the entire adult population. What should that intake be? During adolescence, 1,500 mg will come close to ensuring the achievement of genetically programmed levels of peak bone mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone and Bones↗