scholarly journals Delayed short-course treatment with teriparatide (PTH1-34) improves femoral allograft healing by enhancing intramembranous bone formation at the graft-host junction

2011 ◽  
Vol 27 (1) ◽  
pp. 26-37 ◽  
Author(s):  
Masahiko Takahata ◽  
Edward M Schwarz ◽  
Tony Chen ◽  
Regis J O'Keefe ◽  
Hani A Awad
Keyword(s):  
Bone Formation ◽  
Intramembranous Bone ◽  
Short Course ◽  
Intramembranous Bone Formation

Altered cartilage phenotype expressed during intramembranous bone formation

2009 ◽  
Vol 8 (11) ◽  
pp. 1377-1387 ◽  
Author(s):  
Kang Ting ◽  
Lee Ann Petropulos ◽  
Masaru Iwatsuki ◽  
Ichiro Nishimura
Keyword(s):  
Bone Formation ◽  
Intramembranous Bone ◽  
Intramembranous Bone Formation

scholarly journals Functional requirement of CCN2 for intramembranous bone formation in embryonic mice

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

scholarly journals Transforming growth factor-beta and the initiation of chondrogenesis and osteogenesis in the rat femur.

1990 ◽  
Vol 110 (6) ◽  
pp. 2195-2207 ◽  
Author(s):  
M E Joyce ◽  
A B Roberts ◽  
M B Sporn ◽  
M E Bolander
Keyword(s):  
Growth Factor ◽  
Bone Formation ◽  
Fracture Healing ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tgf Beta ◽  
Intramembranous Bone ◽  
Growth Factor Beta ◽  
Beta 2 ◽  
Intramembranous Bone Formation

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.

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 ◽  
...  
Keyword(s):  
Bone Formation ◽  
Compressive Strain ◽  
Callus Distraction ◽  
Intramembranous Bone ◽  
Intramembranous Bone Formation

SYSTEMIC BONE DISEASE DEVELOPING IN SMALL PREMATURE INFANTS

PEDIATRICS ◽  
1971 ◽  
Vol 48 (6) ◽  
pp. 883-895
Author(s):  
N. T. Griscom ◽  
J. N. Craig ◽  
E. B. D. Neuhauser
Keyword(s):  
Bone Formation ◽  
Congenital Malformation ◽  
Premature Infants ◽  
Bone Disease ◽  
Bone Growth ◽  
Copper Deficiency ◽  
Post Mortem ◽  
Intramembranous Bone ◽  
Intramembranous Bone Formation ◽  
Affected Infant

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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