|
Sign In to gain access to subscriptions and/or personal tools.
|
Molecular Analysis of Healing at a Bone-Implant Interface
C. Colnot1,
D.M. Romero1,
S. Huang1,
J. Rahman1,
J.A. Currey2,
A. Nanci3,
J.B. Brunski2,* and
J.A. Helms4
1 Department of Orthopaedic Surgery, University of California, San Francisco, CA 94110-1342, USA;
2 Department of Biomedical Engineering, Jonsson Engineering Center, Rensselaer Polytechnic Institute, Troy, NY 12180-3590, USA;
3 Faculty of Dentistry, Université de Montréal, Canada; and
4 Department of Plastic and Reconstructive Surgery, Stanford University, 257 Campus Drive, Room GK207, Stanford, CA 94305, USA
View larger version (166K):
[in this window]
[in a new window]
|
Figure 1. Establishing the time-course and type of healing in the implant bed. A 1.0-mm drill hole was created in the proximal tibiae; samples were then collected at d5, d7, and d28, and stained with Trichrome (TC) and tartrate-resistant acid phosphatase (TRAP). (A–B) At d5, there is no evidence of new bone formation. The injury site is filled with densely packed fibroblasts, (B) while bone debris from the drilling process is engulfed by TRAP-positive osteoclasts. (C–D) By d7, new bone is first detected and undergoes rapid remodeling. (E–F) By d28, woven bone has been replaced by cortical bone fused with the old cortex. Scale bar = 100 microns. (See color version of this Fig. in the online APPENDIX.)
|
|
View larger version (132K):
[in this window]
[in a new window]
|
Figure 2. Molecular analyses of healing in the implant bed. Localization of mRNA for collagen type I (Col 1), Osteocalcin (Oc), and Osteopontin (Op) by in situ hybridization on sections adjacent to those shown in Fig. 1 . (A–C) By d3, low expression levels for Col 1 are found in the marrow cavity (arrow), while Oc and Op are not expressed. (D–F) By d5, Col 1 is up-regulated in and around the defect within the marrow cavity. Oc mRNA is still not detected. Op-expressing cells are localized near the cortical defect (asterisk). (G–I) By d7, strong expression of all three markers is detected in the defect and in the marrow space underlying the defect. Scale bar = 200 microns. (See color version of this Fig. in the online APPENDIX.)
|
|
View larger version (72K):
[in this window]
[in a new window]
|
Figure 3. Healing at the bone-implant interface. Schematic representations of Ti-6Al-4V alloy and BioPin implants, and photomicrographs of these implants after placement (below). At post-surgical d5, longitudinal sections through (A) the Ti-6Al-4V implant and the (B,C) BioPin implant show evidence (by Trichrome staining) of new bone formation (arrowheads). (D–F) Bone formation around the implants was increased at d7. (G–I) Bone encasing the implants underwent remodeling until only a thin shell remained in the bone marrow cavity. A schematic drawing representing a direct interface and a minimal gap interface around an implant. Areas in the black box and the red box are illustrated on the tissue sections stained with Safranin-O Fast green (SO/FG) (J–M) and Trichrome (TC) (N–O). (J) On d3, the direct bone-implant interface was not populated by cells, whereas in (K), the gap interface was filled with a fibrous hematoma (bracket). (L) By d28, new bone was juxtaposed to the implant (arrowheads indicate stained nuclei of new osteoblasts), while in the gap (M), a new bone interface has been created by the mineralization of the fibrous matrix (bracket), and stained nuclei distinguish new osteoblasts from old osteocytes. Scale bar in A and corresponding magnifications = 0.5 mm; C and other high-magnification images = 50 microns. (See color version of this Fig. in the online APPENDIX.)
|
|
View larger version (147K):
[in this window]
[in a new window]
|
Figure 4. The presence of an implant accelerated osteoblast differentiation. Cellular and molecular analyses at the Ti-6Al-4V (A–C) and 303 SS (D–F) implant surfaces. (A) At post-surgical d5, Trichrome staining indicates the initiation of endosteal bone formation (arrowhead). (B) AP staining corresponds to the areas of new mineralization (arrow), (C) which are undergoing extensive osteoclastic remodeling. (D–F) In situ hybridization on d3 indicates that cells surrounding the implant up-regulate Runx2 and Op; these cells are osteo- rather than chondroprogenitors, because of the absence of Col II expression. Scale bar = 200 microns. (See color version of this Fig. in the online APPENDIX.)
|
|
Journal of Dental Research, Vol. 86, No. 9,
862-867 (2007)
DOI: 10.1177/154405910708600911
 CiteULike  Complore  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter What's this?
|
|
