Conservation of45Ca during bone growth and its loss during bone atrophy in organ culture

1976 ◽  
Vol 22 (S1) ◽  
pp. 564-567
Author(s):  
L. Klein ◽  
T. L. Chen
Keyword(s):  
Organ Culture ◽  
Bone Growth ◽  
Bone Atrophy

Fetal rat bone in organ culture: Effect of bone growth and bone atrophy on the comparative losses of45Ca and3H-tetracycline

1978 ◽  
Vol 25 (1) ◽  
pp. 255-263 ◽  
Author(s):  
Theresa L. Chen ◽  
LeRoy Klein
Keyword(s):  
Organ Culture ◽  
Bone Growth ◽  
Fetal Rat ◽  
Bone Atrophy ◽  
Rat Bone

Bone Growth in Organ Culture Modified by an Electric Field

1972 ◽  
Vol 51 (5) ◽  
pp. 1492-1499 ◽  
Author(s):  
Louis A. Norton ◽  
Ronald R. Moore
Keyword(s):  
Electric Field ◽  
Organ Culture ◽  
Bone Growth

scholarly journals PATHOGENESIS OF H-1 VIRUS INFECTION OF EMBRYONIC HAMSTER BONE IN ORGAN CULTURE

1971 ◽  
Vol 133 (3) ◽  
pp. 506-519 ◽  
Author(s):  
Alfred D. Heggie
Keyword(s):  
Virus Infection ◽  
Organ Culture ◽  
Viral Infection ◽  
Chronic Infection ◽  
Bone Growth ◽  
Direct Result ◽  
Suckling Period ◽  
Virus Inoculation ◽  
Skeletal Defects ◽  
Wet Weight

H-1 virus infection of hamsters has been shown to produce runting, microcephaly, cranial lacunae, and deformed teeth in animals inoculated during the suckling period and to cause various abnormalities, including skeletal defects, in embryos infected transplacentally. To explore the pathogenesis of these effects of viral infection on bone, the response of embryonic hamster tibiae in organ culture to inoculation with the H-1 strain of picodna virus was studied. This system made possible the direct observation of the reaction of bone to virus in a regulated environment. During a period of 7–17 days after inoculation the following observations were made: (a) H-1 virus was found to infect and replicate in bone. (b) Infected bones became more translucent, slender, and elongated than control bones. (c) Bone growth as measured by increase in wet weight was reduced in infected tibiae. (d) Infected bones showed periosteal and perichondral degeneration and diminished deposits of subperiosteal bone. It was concluded that the skeletal abnormalities which develop in embryonic and suckling hamsters after H-1 virus inoculation are the direct result of viral replication in bone, and that indirect phenomena such as those associated with chronic infection need not be postulated to explain the deformities seen in these animals.

Implant-Guided Vertical Bone Augmentation Around Extra-Short Implants for the Management of Severe Bone Atrophy

2015 ◽  
Vol 41 (5) ◽  
pp. 563-569 ◽  
Author(s):  
Eduardo Anitua ◽  
Alia Murias-Freijo ◽  
Mohammad H. Alkhraisat ◽  
Gorka Orive
Keyword(s):  
Bone Growth ◽  
Alveolar Bone ◽  
Treatment Protocol ◽  
Bone Augmentation ◽  
Adhesive Properties ◽  
Implant Surface ◽  
Invasive Approach ◽  
Short Implants ◽  
Bone Atrophy ◽  
Bone Particles

The purpose of this study is to describe the conservative treatment of severe vertical bone atrophy by combining the insertion of extra-short implants and implant-guided bone augmentation. For that, a low-speed drilling protocol was selected to facilitate the collection of bone particles and to maintain graft osteogenic properties. Extra-short implants were incompletely inserted because of the severe atrophy, and the denuded implant surface was covered by autologous bone particles held together by the adhesive properties of plasma rich in growth factors. The surgical site was then covered with resorbable fibrin membrane, and the flap was repositioned and sutured. Eight patients with a mean residual bone height of 4.19 ± 0.97 mm were treated according to the described treatment protocol. The distance between the implant shoulder and the bony crest was 1.77 ± 0.18, 2.16 ± 0.23, and 1.97 ± 0.26 mm at the mesial, central, and distal aspects, respectively. Vertical bone augmentation resulted in the coverage of 85% of exposed surface by stimulating 1.6 ± 0.5 mm of supra-alveolar bone growth. All 10 extra-short implants placed were successfully osseointegrated. After a mean of 5 ± 1.6 months, provisional screw-retained prostheses were placed. Within the limitations of this study, we conclude that the minimally invasive approach described may successfully rehabilitate extreme vertical bone atrophy in the posterior mandible.

scholarly journals Smad6/Smurf1 overexpression in cartilage delays chondrocyte hypertrophy and causes dwarfism with osteopenia

2004 ◽  
Vol 165 (3) ◽  
pp. 433-445 ◽  
Author(s):  
Mitsuru Horiki ◽  
Takeshi Imamura ◽  
Mina Okamoto ◽  
Makoto Hayashi ◽  
Junko Murai ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Transgenic Mice ◽  
Organ Culture ◽  
Bone Morphogenetic Proteins ◽  
Endochondral Ossification ◽  
Bone Growth ◽  
Regulatory Factor ◽  
Chondrocyte Proliferation ◽  
Chondrocyte Hypertrophy

Biochemical experiments have shown that Smad6 and Smad ubiquitin regulatory factor 1 (Smurf1) block the signal transduction of bone morphogenetic proteins (BMPs). However, their in vivo functions are largely unknown. Here, we generated transgenic mice overexpressing Smad6 in chondrocytes. Smad6 transgenic mice showed postnatal dwarfism with osteopenia and inhibition of Smad1/5/8 phosphorylation in chondrocytes. Endochondral ossification during development in these mice was associated with almost normal chondrocyte proliferation, significantly delayed chondrocyte hypertrophy, and thin trabecular bone. The reduced population of hypertrophic chondrocytes after birth seemed to be related to impaired bone growth and formation. Organ culture of cartilage rudiments showed that chondrocyte hypertrophy induced by BMP2 was inhibited in cartilage prepared from Smad6 transgenic mice. We then generated transgenic mice overexpressing Smurf1 in chondrocytes. Abnormalities were undetectable in Smurf1 transgenic mice. Mating Smad6 and Smurf1 transgenic mice produced double-transgenic pups with more delayed endochondral ossification than Smad6 transgenic mice. These results provided evidence that Smurf1 supports Smad6 function in vivo.

Bone growth in organ culture: Effects of phosphate and other nutrients on bone and cartilage

1974 ◽  
Vol 14 (1) ◽  
pp. 31-48 ◽  
Author(s):  
Patricia J. Bingham ◽  
Lawrence G. Raisz
Keyword(s):  
Organ Culture ◽  
Bone Growth ◽  
Culture Effects ◽  
And Cartilage

An Electrode Designed for Altering Bone Growth in Organ Culture

1972 ◽  
Vol 51 (5) ◽  
pp. 1503-1503 ◽  
Author(s):  
Louis A. Norton ◽  
Dwight E. Kramer
Keyword(s):  
Organ Culture ◽  
Bone Growth

Fluoride: Its Effects on Two Parameters of Bone Growth in Organ Culture

Science ◽  
1964 ◽  
Vol 145 (3635) ◽  
pp. 932-934 ◽  
Author(s):  
W. R. Proffit ◽  
J. L. Ackerman
Keyword(s):  
Organ Culture ◽  
Bone Growth ◽  
Two Parameters

Freeze-etch observations on the tight junctions of sertoli cells grown in organ culture with FSH

1978 ◽  
Vol 36 (2) ◽  
pp. 340-341
Author(s):  
Rita Meyer ◽  
Zoltan Posalaky ◽  
Dennis Mcginley
Keyword(s):  
Organ Culture ◽  
Tight Junctions ◽  
Sertoli Cell ◽  
Germ Cells ◽  
Sertoli Cells ◽  
Barrier Function ◽  
Cell Junction ◽  
Intramembranous Particles ◽  
Junctional Complexes ◽  
Oriented Parallel

The Sertoli cell tight junctional complexes have been shown to be the most important structural counterpart of the physiological blood-testis barrier. In freeze etch replicas they consist of extensive rows of intramembranous particles which are not only oriented parallel to one another, but to the myoid layer as well. Thus the occluding complex has both an internal and an overall orientation. However, this overall orientation to the myoid layer does not seem to be necessary to its barrier function. The 20 day old rat has extensive parallel tight junctions which are not oriented with respect to the myoid layer, and yet they are inpenetrable by lanthanum. The mechanism(s) for the control of Sertoli cell junction development and orientation has not been established, although such factors as the presence or absence of germ cells, and/or hormones, especially FSH have been implicated.

Distraction Osteogenesis in the Treatment of Craniofacial Anomalies: Applications and Outcomes

2020 ◽  
Vol 5 (6) ◽  
pp. 1469-1481 ◽  
Author(s):  
Joseph A. Napoli ◽  
Carrie E. Zimmerman ◽  
Linda D. Vallino
Keyword(s):  
Distraction Osteogenesis ◽  
Bone Growth ◽  
Upper Airway ◽  
Craniofacial Anomalies ◽  
Craniofacial Skeleton ◽  
Facial Skeleton ◽  
Psychosocial Impairment ◽  
And Function ◽  
Correct Structure

Purpose Craniofacial anomalies (CFA) often result in growth abnormalities of the facial skeleton adversely affecting function and appearance. The functional problems caused by the structural anomalies include upper airway obstruction, speech abnormalities, feeding difficulty, hearing deficits, dental/occlusal defects, and cognitive and psychosocial impairment. Managing disorders of the craniofacial skeleton has been improved by the technique known as distraction osteogenesis (DO). In DO, new bone growth is stimulated allowing bones to be lengthened without need for bone graft. The purpose of this clinical focus article is to describe the technique and clinical applications and outcomes of DO in CFA. Conclusion Distraction can be applied to various regions of the craniofacial skeleton to correct structure and function. The benefits of this procedure include improved airway, feeding, occlusion, speech, and appearance, resulting in a better quality of life for patients with CFA.

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