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Endosseous implant anchorage is critically dependent on mechanostructural determinants of peri‐implant bone trabeculae

Low bone mass is highly prevalent among patients receiving endosseous implants. In turn, the implantation prognosis in low‐density skeletal sites is poor. However, little is known about the mechanostructural determinants of implant anchorage. Using metabolic manipulations that lead to low bone densi...

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Bibliographic Details
Published in:Journal of bone and mineral research 2010-03, Vol.25 (3), p.575-583
Main Authors: Gabet, Yankel, Kohavi, David, Voide, Romain, Mueller, Thomas L, Müller, Ralph, Bab, Itai
Format: Article
Language:English
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Summary:Low bone mass is highly prevalent among patients receiving endosseous implants. In turn, the implantation prognosis in low‐density skeletal sites is poor. However, little is known about the mechanostructural determinants of implant anchorage. Using metabolic manipulations that lead to low bone density and to its rescue, we show here that anchorage is critically dependent on the peri‐implant bone (PIB). Titanium implants were inserted horizontally into the proximal tibial metaphysis of adult rats 6 weeks after orchiectomy (ORX) or sham ORX. Systemic intermittent administration of human parathyroid hormone (1–34) [iahPTH(1–34)] or vehicle commenced immediately thereafter for 6 weeks. The bone‐implant apparatus was then subjected to image‐guided failure assessment, which assesses biomechanical properties and microstructural deformation concomitantly. Anchorage failure occurred mainly in PIB trabeculae, 0.5 to 1.0 mm away from the implant. Mechanically, the anchorage performed poorly in ORX‐induced low‐density bone, attributable mainly to decreased trabecular number. iahPTH(1–34) rescued the PIB density and implant mechanical function by augmenting trabecular thickness (Tb.Th). However, implant biomechanical properties in low‐density bone were relatively insensitive to implant surface treatment that affected only the osseointegration (%bone‐implant contact). These results support a model wherein anchorage failure involves buckling of the weakest trabecular struts followed by sequential failure of the stronger trabeculae. Treatment with iahPTH(1–34) induced thicker struts, which were able to delay and even prevent failure of individual elements, thus implicating trabecular thickness as a prime target for enhancing implant anchorage by systemic bone anabolic therapy. © 2010 American Society for Bone and Mineral Research.
ISSN:0884-0431
1523-4681
DOI:10.1359/jbmr.090808