Читать книгу Bone and Soft Tissue Augmentation in Implantology - Группа авторов - Страница 25

The postulated osteoinductive effect attributed to autografts is questionable. By definition, the unlimited osteoinductive effect of autografts can only be proven by ectopic bone formation outside the skeletal system, and not only in or on the bone. Osteoinductive refers to demineralized bone but also dentin matrix, both of which can trigger new bone formation after implantation, e.g. in the muscle of a rat.⁶³ This demineralized bone matrix ultimately leads to the isolation and molecular characterization of bone morphogenetic proteins (BMPs). It is not widely known that the isolation of BMPs requires 5 to 20 kg of bone to obtain sufficient protein for purification testing, including in vitro osteogenic differentiation and in vivo osteoinductive bone formation.^8,83,133 However, there is no evidence for ectopic bone regeneration after transplantation of bone chips in a muscle; in fact, it is the opposite – that the bone chips are resorbed without the induction of new bone by host-derived induced osteoblasts.¹³

Fig 1-12 New bone formation on the surface of transplanted bone chips. In the SBB technique, after 3 months, healing areas of nascent bone formation are detectable. The structure of future bone formation can already be anticipated. Even though the origin of the bone is not defined, it seems that bone formation originates from the transplanted osteogenic cells.

When implanted into the muscle pouches of beagle dogs, bone grafts resorbed quickly, while alloplasts and a synthetic biphasic calcium phosphate showed minor signs of ectopic bone formation.⁸⁷ Also, in Wistar rats, autologous bone chips from a corticocancellous bone block grafted in a muscle were entirely resorbed after 6 weeks.⁸⁸ If native bone chips were actually unlimitedly osteoinductive, it would mean that, were bone chips to enter the soft tissue, new bone would be formed there. This side effect of ectopic bone formation in soft tissue would be clinically undesirable. However, there is evidence that, at least during bone remodeling, osteoclasts release TGF-βb1 from the bone matrix, which recruits mesenchymal progenitors to the remodeling sites.³² It was recently confirmed that TGF-β1 released by acid lysis of bone is a major regulator of gene expression in mesenchymal cells in vitro.¹¹⁷ Moreover, acid bone lysates delayed bone formation in a rat calvaria defect model.¹¹⁶ Since the accumulation of these results makes a major involvement of BMPs in graft consolidation unlikely, and proposes that TGF-β1 supports the immigration of progenitor cells, the idea of the osteoinductive properties of autografts needs to revisited, and has to be limited only to the support of bone formation in direct contact with bone tissue.