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- Soluble, insoluble and geometric signals sculpt the architecture of mineralized tissues

Biomimetic biomaterial matrices can now be designed to obtain specific biological responses such that the use of biomaterials capable of initiating bone formation via osteoinduction, even in the absence of exogenously applied BMPs/OPs, is fast altering the horizons of therapeutic bone regeneration. Molecular signals of the TGF-β superfamily induce morphogenesis, and physical forces imparted by the geometric topography of the substratum dictate biological patterns and regulate the expression of osteogenic gene transcripts and their translation products initiating bone formation as a function of the structure.

The concavities of the substratum are geometric regulators of growth endowed with shape memory, recapitulating events that occur in the normal course of embryonic development and appearing to act as gates that give or withhold permission to grow and differentiate [10, 41].

Since regenerative phenomena recapitulate events that occur in the normal course of embryonic development, the multiple patterns of expression of BMPs/OPs and TGF-βs in developing tissues and organs should now be exploited to devise novel therapeutic approaches based on recapitulation of embryonic development.

Bone tissue engineering starts by erecting scaffolds of smart biomimetic matrices affecting the release of soluble molecular signals. The molecular scaffolding lies at the heart of all new tissue engineering strategies. This molecular evidence is based on a surprisingly simple and fascinating concept: morphogens exploited in embryonic development can be re-exploited for the initiation of postnatal morphogenesis and regeneration.


The work presented is derived from all at the Bone Research Unit and at the Manufacturing and Materials Technology Group, CSIR Pretoria, who contributed significantly to the understanding of the fascinating phenomenon of the geometric induction of bone formation: Jean Crooks, Thato Matsaba, Nathaniel L Ramoshebi, Louise Renton, William Ricther, June Teare, Michae Thomas, Barbara van den Heever. This work is supported by grants from the South African Medical Research Council, the University of the Witwatersrand, Johannesburg, the National Research Foundation and by ad hoc grants of the Bone Research Unit. K. Miyozono kindly donated the cDNAs for Smad-6 and Smad-7. We thank Janet Patton, Bone Research Unit, for the RT-PCR analyses and Michael Thomas and William Richter, CSIR Pretoria, for the preparation of the sintered hydroxyapatite biomatrices. 

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