Effect of Collagen Cross-Link Deficiency on Incorporation of Grafted Bone.

Bone matrix collagen, is one of the major contributors to bone quality. No studies have examined how bone quality affects the results of bone transplantation. Collagen cross-links (CCL) are the key factor in collagen properties. The purpose was to investigate the influences of CCL for both grafted bone and recipient site bone on the success of bone augmentation. Four-week-old male Wister rats (n = 54) were divided into control and test groups. Control and test groups equally sub-divided into donors and recipients. An additional six rats were used to characterize bone at day zero. Test groups received 0.2% beta-aminoproperionitrile (BAPN) for 4 weeks as CCL inhibitor. Animals were further divided into donor and recipient groups. The transplanted bone chips integrated with host bone by 25% more in CCL-deficient animals compared to control. However, no difference in cortical thickness among all conditions. CCL-deficient transplanted bone did not show any extra signs of osteocyte apoptosis, while sclerostin expression was comparable to that in control. The host periosteum of CCL-deficient animals showed higher cellular activity, as well as higher bone quantity and osteoclast activity. Collagen cross-links deficiency in host bone might accelerate the incorporation of grafted bone. effect. Incorporation of the bone grafts appears to depend mainly on host condition rather than graft condition.

Proliferation of preosteoblasts on TiO2 nanotubes is FAK/RhoA related.

Topographies promote surface-dependent behaviors which may positively influence peri-implant bone healing. In this study the topological effects of TiO2 nanotubes (TNTs) on aspects of preosteoblast behavior was investigated. Specifically, we hypothesize that TNTs can influence cell proliferation of preosteoblasts through cell adhesion and related modulation of FAK and RhoA. By culturing MC3T3-E1 cells on TNTs with different diameters (40nm and 150nm diameters), topography-dependent modulation in cell morphology and cell growth were observed. The average spreading area of the cell on Flat Ti, 40nm TNTs and 150nm TNTs were respectively 2176.05 µm2, 1510.44 µm2 and 800.72 µm2. Proliferation increased among cells cultured on the 150nm TNTs (28.6%) compared with on Flat Ti (17.06%). The expression of FAK was 86.2% down regulated superimposition of TNTs topography. RhoA expression only slightly decreased (45.9%). Increasing TNT diameter enhanced initial adherent cell growth, which was relevant to the increased RhoA-to-FAK ratio in the cell. Increased TNT diameter was associated with higher ratio and greater proliferation in the first 24 hours. These findings not only support our hypothesis, but suggest that RhoA might be critically involved in TNTs mediated cell proliferation. Future investigation using functional gain and loss of RhoA may further reveal its mechanism.