BMP signaling components are expressed in human fracture callus

Kloen, Peter; Paola, Michelle Di; Borens, Olivier; Richmond, Jeffrey; Perino, Giorgio; Helfet, David L.; Goumans, Marie–José

doi:10.1016/s8756-3282(03)00191-1

Cited by 127 publications

(103 citation statements)

References 38 publications

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“…An enhanced bone repair would be suggestive of an augmentation of endogenous BMP-2 since BMPs are also known to be upregulated during bone repair. [13][14][15] B2A2-K-NS resulted in marked closure of the bone defect, whereas leaving the defect untreated or treated only with carrier was ineffective in supporting full closure of the defect. The defects treated with B2A2-K-NS were at least as effective, if not better, than autograft.…”

Section: Discussionmentioning

confidence: 95%

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Augmentation of osseous phenotypes in vivo with a synthetic peptide

Lin¹,

Elliot²,

Carnes³

et al. 2006

Journal Orthopaedic Research

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ABSTRACT:The synthetic peptide B2A2-K-NS augmented the in vitro expression of osseous phenotypes when cells were stimulated with BMP-2, an osteoinductive growth factor. B2A2-K-NS significantly enhanced the effects of BMP-2-induced alkaline phosphatase activity and mineralization. In the absence of BMP-2, B2A2-K-NS did not have an effect on these endpoints. Based on these observations, in vivo studies were conducted to evaluate if B2A2-K-NS could augment osseous phenotypes in an osteoinductive environment in which BMP-2 should be present. In one study, human demineralized bone matrix (DBM) was used to generate an osteoinductive environment and the effects of B2A2-K-NS on ectopic mineralization of subcutaneous implants evaluated. In the second study, a noncritical sized defect in rabbit ulnas with inherent reparative capacity was used as the osteoinductive environment and was treated with or without B2A2-K-NS. In the DBM studies, B2A2-K-NS augmented mineralization as determined using a combination of radiographic analysis and von Kossa staining at 4 weeks postimplant. In the rabbit ulna model, B2A2-K-NS significantly increased the radiographic bone density in the defects compared to carrier-only or no-treatment controls after 6 weeks. Histological staining confirmed that B2A2-K-NS generated a pronounced bone repair response. The results are consistent with the hypothesis that B2A2-K-NS augments osseous phenotypes in an osteoinductive environment, and suggests that B2A2-K-NS may have clinical utility. ß

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Section: Discussionmentioning

confidence: 95%

“…12 BMPs and their receptors are known to be upregulated during bone repair, [13][14][15] and are widely thought to mediate bone repair.…”

Section: Discussionmentioning

confidence: 99%

Augmentation of osseous phenotypes in vivo with a synthetic peptide

Lin¹,

Elliot²,

Carnes³

et al. 2006

Journal Orthopaedic Research

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“…These include BMP-2 & 4 (Barnes et al, 1999;Deckers et al, 2002;Kloen et al, 2003), VEGF (Midy and Plouet, 1994;Deckers et al, 2000;Street et al, 2002;Ferrara et al, 2003), bFGF (Rodan et al, 1989;Montesano et al, 1986), TGF-β (Rosier et al, 1998;Bostrom and Asnis, 1998;Erlebacher et al, 1998), PDGF (Mandrachia et al, 2001;Risau et al, 1992). VEGF expression is detected on chondroblasts, chondrocytes (Pufe et al, 2001), osteoprogenitor cells and osteoblasts in the fracture callus (Tatsuyama et al, 2000) where it is highly expressed in angioblasts, osteoprogenitor and osteoblast cells during the first seven days of healing but decreases after eleven days (Uchida et al, 2003).…”

Section: Angiogenesis and Bone Fracture Repairmentioning

confidence: 99%

Osteogenesis and angiogenesis: The potential for engineering bone

Kanczler

Oreffo²

2008

eCM

870

631

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The repair of large bone defects remains a major clinical orthopaedic challenge. Bone is a highly vascularised tissue reliant on the close spatial and temporal connection between blood vessels and bone cells to maintain skeletal integrity. Angiogenesis thus plays a pivotal role in skeletal development and bone fracture repair. Current procedures to repair bone defects and to provide structural and mechanical support include the use of grafts (autologous, allogeneic) or implants (polymeric or metallic). These approaches face significant limitations due to insufficient supply, potential disease transmission, rejection, cost and the inability to integrate with the surrounding host tissue.

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“…Produkcija BMP-7, koji se u velikoj meri detektuje kod reparacije posle ekstrakcije zuba, najizraženija je u periodu između druge i 8. nedelje posle ekstrakcije, sa progresivnim padom u periodu od 12. do 24. nedelje 26,27 . To bi značilo da je ovaj faktor važan za ranu i intermedijsku fazu zarastanja kosti, tj.…”

Section: Insulin-like Growth Factor Igf-i and Igf-iiunclassified

The role of growth factors in extraction wound healing

Stojanović¹,

Tijanić²,

Jovanović³

et al. 2015

Acta stomatologica Naissi

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SažetakZarastanje rane je složeni proces koji uključuje hemostazu, inflamaciju, proliferaciju i remodelaciju tkiva. Faktori rasta su prirodni biološki posrednici koji regulišu najznačajnije ćelijske procese uključene u regeneraciju tkiva, kao što su DNA sinteza, angiogeneza, metabolička aktivnost, migracija, hemotaksa, proliferacija, diferencijacija UvodZarastanje rane je složeni proces koji uključuje hemostazu, inflamaciju, proliferaciju i remodelaciju tkiva. U procesu zarastanja rane učestvuju različiti tipovi ćelija, složena signalizaca događaja i brojni faktori rasta.Faktori rasta su prirodni biološki posrednici koji regulišu najznačajnije ćelijske procese uključene u regeneraciju tkiva, kao što su DNA sinteza, angiogeneza, metabolička aktivnost, migracija, hemotaksa, proliferacija, diferencijacija i sinteza matriksa. Faktori rasta su ćelijski specifični, što znači da svaki faktor deluje na određenu vrstu ćelija 1 . Najznačajniji faktori rasta koji učestvuju u zarastanju ekstrakcione rane i regeneraciji koštanog tkiva su: 1. trombocitni faktor rasta -PDGF; 2. transformacioni faktor rasta -TGF β superfamilija; 3. insulinu sličan faktor rasta -IGF; 4. koštani morfogenetski proteini -BMP -2, BMP -7 ; 5. vaskularni endotelijalni faktor rasta -VEGF; 6. fibroblastni faktor rasta -FGF;Polipeptidni faktori rasta ispoljavaju svoje dejstvo vezujući se za target ćelije preko svojih aktivnih krajeva "dimera" za tirozinkinazu, transmembranski receptor na površini ćelijske membrane 2 . Aktivirani T-K transmembranski receptor pokreće energetsku aktivnost ćelije podizanjem intracelularne koncentracije cirkularnog adenozin-monofosfata i dovodi do oslobađanja intracitoplazmatičnih proteina prenosioca signala. Oslobođeni od transmembranskih receptora tirozin-kinaze, proteini prenosioci signala odlaze do nukleusa, gde otključavaju specifičnu genetsku sekvencu za kontrolu ćelijske funkcije i indukciju ekspresije normalne genetske aktivnosti.Povreda tkiva praćena je inflamatornim odgovorom, aktiviranjem komplemenata i oštećenjem krvnih sudova koje uzrokuje krvaranje. Posle povrede tkiva, pokreće se kaskadni proces koagulacije krvi koji vodi u formiranje fibrinske mreže kao osnove za nakupljanje uobličenih krvnih elemenata. Na mestu povrede tkiva dolazi do adhezije i agregacije trombocita, a njihovom degranulacijom oslobađaju se mnogobrojni glikoproteini i faktori rasta kao što su faktor rasta poreklom iz trombocita (PDGF), epidermalni faktor rasta (EGF), transformišući faktor rasta beta (TGF-β), vaskularni endotelijalni faktor rasta (VEGF) i bazni fibroblastni faktor rasta (bFGF) 3,4 . Мnoštvo faktora rasta oslobođenih tokom hemostaze ima različite uloge, uključujući

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BMP signaling components are expressed in human fracture callus

Cited by 127 publications

References 38 publications

Augmentation of osseous phenotypes in vivo with a synthetic peptide

Augmentation of osseous phenotypes in vivo with a synthetic peptide

Osteogenesis and angiogenesis: The potential for engineering bone

The role of growth factors in extraction wound healing

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