Microdamage adjacent to endosseous implants

Intense remodeling occurs in lamellar bone adjacent to osseointegrated endosseous implants. The purpose of this study was to compare microdamage accumulation subsequent to ex vivo fatigue loading of bone that surrounds an endosseous implant, (a) immediately after placement (nonadapted bone) and (b) following a 12 week healing period after placement (adapted bone). We hypothesize that there is less microdamage in the more compliant adapted bone than in the older nonadapted bone. Nonthreaded titanium plasma sprayed (TPS)-coated endosseous implants were placed into dog mid-femoral diaphyses and allowed to heal for 12 weeks. Block sections of bone, each containing one implant, were cut anteroposteriorly, resulting in an implant containing lateral cortex, and a medial cortex that was used for testing the nonadapted specimens. Control specimens (n = 14 each for adapted and nonadapted) were loaded at 0 N. Experimental specimens (n = 13, adapted; n = 14, nonadapted) were loaded at 100 N in cantilever bending for 150,000 cycles at 2 Hz, at 37 degrees C on a Bionix 858 testing machine. Specimens were bulk stained with basic fuchsin and 120-140 microm sections were obtained. Crack numerical density (Cr.Dn = Cr.N/ B.Ar, #/mm2), crack surface density (Cr.S.Dn = Tt.Cr.Le/ B.Ar, mm/mm2), and percent damage area (Dm.Ar = Cr.Ar x 100/B.Ar, mm2/mm2) were measured at x 250. Statistically significant differences (p < 0.0001) were seen for Cr.Dn, Cr.S.Dn, and Dm.Ar on the compressed cortices suggesting that adapted bone near the implant accumulated significantly less microdamage than nonadapted bone. Also, the adapted nonloaded control specimens had approximately 20-fold less damage than the respective nonadapted specimens. This study suggests that the compliant adapted bone adjacent to endosseous implants is relatively resistant to fatigue loads. The high success rates of endosseous implants may be due to the presence of a rapidly remodeling region that maintains tissue compliance and limits microdamage initiation.