scholarly journals Intramembranous bone formation after callus distraction is augmented by increasing axial compressive strain

PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0195466 ◽  
Author(s):  
Julian Schuelke ◽  
Nicholaus Meyers ◽  
Sandra Reitmaier ◽  
Svenja Klose ◽  
Anita Ignatius ◽  
...  
2009 ◽  
Vol 8 (11) ◽  
pp. 1377-1387 ◽  
Author(s):  
Kang Ting ◽  
Lee Ann Petropulos ◽  
Masaru Iwatsuki ◽  
Ichiro Nishimura

2008 ◽  
Vol 366 (2) ◽  
pp. 450-456 ◽  
Author(s):  
Harumi Kawaki ◽  
Satoshi Kubota ◽  
Akiko Suzuki ◽  
Tomohiro Yamada ◽  
Tatsushi Matsumura ◽  
...  

1990 ◽  
Vol 110 (6) ◽  
pp. 2195-2207 ◽  
Author(s):  
M E Joyce ◽  
A B Roberts ◽  
M B Sporn ◽  
M E Bolander

We have investigated the ability of exogenous transforming growth factor-beta (TGF-beta) to induce osteogenesis and chondrogenesis, critical events in both bone formation and fracture healing. Daily injections of TGF-beta 1 or 2 into the subperiosteal region of newborn rat femurs resulted in localized intramembranous bone formation and chondrogenesis. After cessation of the injections, endochondral ossification occurred, resulting in replacement of cartilage with bone. Gene expression of type II collagen and immunolocalization of types I and II collagen were detected within the TGF-beta-induced cartilage and bone. Moreover, injection of TGF-beta 2 stimulated synthesis of TGF-beta 1 in chondrocytes and osteoblasts within the newly induced bone and cartilage, suggesting positive autoregulation of TGF-beta. TGF-beta 2 was more active in vivo than TGF-beta 1, stimulating formation of a mass that was on the average 375% larger at a comparable dose (p less than 0.001). With either TGF-beta isoform, the dose of the growth factor determined which type of tissue formed, so that the ratio of cartilage formation to intramembranous bone formation decreased as the dose was lowered. For TGF-beta 1, reducing the daily dose from 200 to 20 ng decreased the cartilage/intramembranous bone formation ratio from 3.57 to zero (p less than 0.001). With TGF-beta 2, the same dose change decreased the ratio from 3.71 to 0.28 (p less than 0.001). These data demonstrate that mesenchymal precursor cells in the periosteum are stimulated by TGF-beta to proliferate and differentiate, as occurs in embryologic bone formation and early fracture healing.


PEDIATRICS ◽  
1971 ◽  
Vol 48 (6) ◽  
pp. 883-895
Author(s):  
N. T. Griscom ◽  
J. N. Craig ◽  
E. B. D. Neuhauser

Three very small premature infants developed systemic bone disease, discovered in their third month of life. Roentgenograms showed epiphyseal separations, extensive subperiosteal new bone, metaphyseal cupping, rib fractures, porosis, and enlarged costochondral junctions. The babies were hypoproteinemic and anemic. One was severely neutropenic, the others moderately so. In two infants, the abnormalities slowly disappeared. The most severely affected infant died of an apparently unrelated congenital malformation. Examination of the bones post-mortem confirmed porosis, fractures, epiphyseal shippages, and periosteal new bone. There was failure of normal enchondral bone growth, which was much more severely affected than intramembranous bone formation. We believe the cause of this illness to be metabolic and probably nutritional. It is unlike any of the better known deficiency syndromes. There are similarities to the syndrome reported in copper deficiency depletion. Whatever the cause, the illness may be fairly common among small premature infants.


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