Modification of xenogenic bone substitute materials – effects on the early healing cascade in vitro

Initial platelet activation with subsequent cytokine release at the defect site plays a crucial role in tissue integration. The aim of this study was to evaluate the influence of topographic and biomimetic collagen modifications of a xenogenic bone substitute material ( BSM ) on in vitro platelet activation and cytokine release. Material and Methods Three types of xenogenic BSM were used. Two BSM with different levels of granularity (large granule BSM [ XBSM /L], small granule BSM [ XBSM /S]) and a BSM with collagen ( XBSM /C). All three samples were incubated with platelet concentrate of four healthy volunteers at room temperature for 15 min. For all groups, highly thrombogenic collagen type 1 served as a reference and an additional preparation with platelet concentrate only (without XBSM ) served as control. Platelet count and cytokine release of VEGF , PDGF , TGF ‐β, and IGF into the supernatant were measured. Results C ompared with the control group, XBSM /C showed an increase in platelets consumption (mean 41,000 ± 26,000/ml vs. 471,000 ± 38,000/ml), cytokine release of VEGF (mean 46.8 ± 7.2 pg/ml vs. 18.8 ± 2.7 pg/ml), and PDGF (mean 18,350 ± 795 pg/ml vs. 2726 ± 410 pg/ml) but not IGF (194,728 ± 51,608 pg/ml vs. 1,333,911 ± 35,314 pg/ml). There was also an increase in cytokine release of TGF ‐ß in XBSM /C compared with XBSM /S (77,188 ± 27,413 pg/ml vs. 38,648 ± 13,191 pg/ml), but no such difference when compared with XBSM /L (77,188 ± 27,413 pg/ml vs. 53,309 ± 29,430 pg/ml). XBSM /L showed higher platelets consumption (301,000 ± 45,000 vs. 415,000 ± 98,000) and a higher cytokine release of PDGF (3511 ± 247 pg/ml vs. 3165 ± 78 pg/ml) compared with XBSM /S. There was no distinct difference in the levels of VEGF , TGF ‐ß, and IGF between XBSM /L and XBSM /S. Conclusions Topographic as well as biomimetic modifications of the xenogenic BSM showed an increased platelet activation and cytokine release in vitro . This effect on the intrinsic healing cascade could result in comparable enhanced soft‐ and hard‐tissue regeneration in vivo .