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Alteration of clot architecture using bone substitute biomaterials (beta-tricalcium phosphate) significantly delays the early bone healing process.

Abstract
When a bone substitute biomaterial is implanted into the body, the material's surface comes into contact with circulating blood, which results in the formation of a peri-implant hematoma or blood clot. Although hematoma formation is vital for the early bone healing process, knowledge concerning the biomaterial-induced structural properties of blood clots is limited. Here, we report that implantation of beta-tricalcium phosphate (β-TCP) in a bone defect healing model in rats resulted in significantly delayed early bone healing compared to empty controls (natural healing). In vitro studies showed that β-TCP had a profound effect on the overall structure of hematomas, as was observed by fibrin turbidity, scanning electron microscopy (SEM), compaction assays, and fibrinolysis. Under the influence of β-TCP, clot formation had a significantly shortened lag time and there was enhanced lateral fibrin aggregation during the clot polymerization, which resulted in clots composed of thinner fibers. Furthermore, fibrin clots that formed around β-TCP exhibited reduced compaction and increased resistance to fibrinolysis. Together, these results provide a plausible mechanism for how implanted bone-substitute materials may impact the structural properties of the hematoma, thereby altering the early bone healing processes, such as cell infiltration, growth factor release and angiogenesis.
AuthorsXin Wang , Yan Luo , Yan Yang , Baoyu Zheng , Fuhua Yan , Fei Wei , Thor E Friis , Ross W Crawford , Yin Xiao
JournalJournal of materials chemistry. B (J Mater Chem B) Vol. 6 Issue 48 Pg. 8204-8213 (Dec 28 2018) ISSN: 2050-7518 [Electronic] England
PMID32254940 (Publication Type: Journal Article)

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