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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↗
PubMed1986

A longitudinal study of carpal bone development in Perthes' disease: its significance for both radiologic standstill and bilateral disease.

This paper reports a longitudinal study of carpal bone development in 125 children (98 boys, 27 girls) attending a clinic for Perthes' disease. The age at appearance of ossification in each carpal bone was estimated by studying consecutive radiographs obtained at six-months intervals. The results were compared with the findings for normal children published by Stuart et al. Three radiologic groups of carpal bone maturation are defined: not delayed (capitate and hamate); markedly delayed (triquetral and lunate); and slightly delayed (scaphoid, trapezium, and trapezoid). Overall, the bone age delay is severely abnormal at three to five years of chronologic age and indicates the time in development when general abnormalities occur. The mean age at diagnosis (and standard deviation) for 34 boys with skeletal standstill was 4.49 +/- 1.07 years, compared with 7.28 +/- 2.40 years for 51 boys without such standstill; the mean age at appearance of carpal bones was not significantly different between these two groups, suggesting an equally profound delay of carpal maturation in the group of later-diagnosed boys. Boys with bilateral hip disease show a significant delay in age at ossification of the trapezoid compared with boys who have unilateral disease. The immaturity of bone age may be present during a latent period and be of etiologic significance in the onset of the hip disease, but at present the evidence links it only with bilateral disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Carpal Bones↗
PubMed1990

Long-term effects of tissue expansion on cranial and skeletal bone development in neonatal miniature swine: clinical findings and histomorphometric correlates.

Progressive tissue expansion induces significant gross, histologic, and bony changes in skulls and long bones of neonatal miniature swine. These bony changes consist of erosion underlying tissue expanders, with bony lipping and bone deposition at the periphery of the expander. Cranial suture lines underneath expanders appear effaced and convoluted. Serial CT scans reveal decreased bone thickness and volume (p less than 0.02) but identical bone density (p = 0.60) beneath expanders. Increased bone volume and thickness occur at the periphery of expanders (p less than 0.02). Bone density (CT number) is unaffected by tissue expansion in both cranial and long bones. These findings have histomorphometric correlates: Osteoclastic bone resorption occurs underneath expanders with periosteal reaction at the periphery of expanders. Cranial sutures are similarly affected, but no cranial synostosis results. No changes to the inner table of the skull or stigmata of increased intracranial pressure were observed either in CT scans or in behavioral changes in long-term animals. The pathophysiology of bony changes is a remodeling effect, not one of simple pressure deformation. Increased bone resorption and complete inhibition of bone formation occur until the pressure is removed. Cranial bone is significantly more affected than long bone. After removal of the expanders, reparative bone remodeling begins within 5 days and nearly complete healing of the cranial defects occurs within 2 months (p less than 0.02). No plagiocephaly results despite early coronal suture changes. On the basis of this study, we conclude that tissue expansion causes significant but reversible effects, readily monitored by high-resolution CT scans, on neonatal and infant cranial and long bones.

Animals↗
PubMed1992

Comparison of the effects of cassava (Manihot esculenta Crantz) organic cyanide and inorganic cyanide on muscle and bone development in a Nigerian breed of dog.

Effects of cassava (Manihot esculenta Crantz)-borne organic cyanide and inorganic cyanide in the form of sodium cyanide on bone and muscle development were investigated in eighteen dogs of Nigerian breed. After 16 weeks of stabilization in the laboratory from the time of purchase when the dogs were fed on the same diet, they were randomly assigned to three experimental groups of six dogs each. The control group was fed on rice while the other two groups were fed on either cassava (gari) or rice plus cyanide. The three diets were made isoenergetic and isonitrogenous by varying the quantity of meat incorporated into them. The results obtained after 14 weeks of feeding the respective diets indicated that there was retardation of muscle development in the gari-fed dogs. This may have resulted from gluconeogenesis from muscle protein associated with suppression of production of insulin by the pancreas in this group. The results indicated also that the effects of inorganic dietary cyanides on muscle development were different. Both forms of dietary cyanides, however, had no adverse effect on bone development.

Animals↗
PubMed1992

Vascularization and endochondral bone development: changes in plasminogen activator activity.

Changes in plasminogen activator activity were studied during the sequential developmental stages of matrix-induced cartilage, bone, and bone marrow development. The morphological transitions were correlated with biochemical parameters. Morphologic evidence of vascularization of calcified hypertrophic cartilage was accompanied by a concomitant rise in plasminogen activator activity. Thereafter, a steady decline during mineralization and deposition of new bone was observed. Maximal plasminogen activator activity occurs at approximately the same time as peak activity of alkaline and acid phosphatase. These results imply a role for plasminogen activator during angiogenesis, vascular invasion, and attendant bone differentiation.

Animals↗
PubMed1992

[Effect of vitamin D over-dosage on the tooth and bone development of rabbits].

The paper investigated the changes of rabbit's tooth and jaw tissues by vitamin-D poisoning experiment. The results showed the dentin, periodontium, jaw bone and long bone of rabbit were all changed. X-ray showed subperiosteum absorbation and periosteum reaction. The mineral content of the rabbit's epiphysis and long bone diaphysis in experiment group were lower than that of control group. The histopathological findings were irregular hyperplasia of dentin, arrange disturbance of periodontal fibers, absorbation of the alveolar bone and mal-ossification of long bones. The above changes were more significant during 30-45 days of rabbit poisoning, after 60 days of poisoning the above signs were gradually released.

Animals↗
PubMed1975

Abnormal bone development and lameness associated with secondary copper deficiency in young cattle.

Lameness in a group of 5- to 12-month-old calves was found to be clinically, radiographically, and pathologically associated with abnormal bone development of the distal growth plates of the metacarpus and metatarsus. Copper concentrations in serum and liver were low. Serum calcium, phosphorus, and alkaline phosphatase values were normal. In pasture forage samples, sulfate, zinc, and molybdenum concentrations were high, whereas copper, calcium, and phosphorus concentrations were normal. Red blood cell (RBC) counts and hemoglobin values were within normal limits. Radiographic findings included a widened zone of cartilage and lipping of the medial and lateral areas of the physeal plate. Histologic findings included focal widenings of the growth plate consisting of tongues of uncalcified cartilage.

Animal Feed↗
PubMed1987

The Mr 24,000 phosphoprotein from developing bone is the NH2-terminal propeptide of the alpha 1 chain of type I collagen.

Using nondegradative isolation procedures, we have purified and characterized the Mr 24,000 phosphoprotein from developing bovine and human bone where it constitutes 5% of the noncollagenous protein in the mineral compartment. This hydroxyproline-containing protein could not be cleaved by cyanogen bromide. The purified, intact product spontaneously formed a complex consistent with a collagen-like trimer that remained a trimer even in sodium dodecyl sulfate-polyacrylamide gels. The ability to form the complex was lost upon treatment with bacterial collagenase, a treatment that resulted in an NH2-terminally blocked fragment of Mr 17,000. After deblocking, the NH2-terminus of the intact, Mr 24,000 bovine product was shown to have virtually the same amino acid sequence (residues 1-24 with asparagine rather than aspartic acid at position 20 as reported earlier by Horlein et al. (Horlein, D., Fietzek, P. P., Wachter, E., Lapiere, C. M., and Kuhn, K. (1979) Eur. J. Biochem. 90, 31-38) as the amino-terminal segment of dermatosparatic calf skin alpha 1 type I procollagen. Furthermore, pulse-chase studies showed a precursor-product relationship between procollagen and the Mr 24,000 protein. Anti-serum made against the bovine bone protein bound to bands on electrotransfers that were consistent with the positions of both alpha 1(I) procollagen and the procollagen chain missing its COOH-terminal extension peptide (pN-alpha 1(I), as well as the original Mr 24,000 product in extracts of bone, skin, tendon, cornea, and other type I collagen-containing tissues. Fetal calf serum contained an average of 106 micrograms/ml of the Mr 24,000 protein as determined by quantitative enzyme-linked immunosorbent assay. The only serine residue in the bovine bone protein was phosphorylated. It is unknown whether the corresponding collagen NH2-terminal pro-peptides in other tissues and serum are similarly phosphorylated.

Animals↗