Interpenetrating polymer networks (IPNs) of poly(acrylamide-co-ethylene glycol/acrylic acid) (p(AAm-co-EG/AAc)) functionalized with an -Arg-Gly-Aspcontaining 15 amino acid peptide (-RGD-) derived from rat bone sialoprotein, were grafted to titanium implants in an effort to modulate osteoblast behavior both in vitro and in vivo. Surface characterization data were consistent with the presence of the IPN on titanium, and -RGD- density measurements established a range that spanned three orders of magnitude (0.01-20 pmol/cm2). In vitro biological characterization of the modified implants in the primary rat calvarial osteoblast model resulted in the identification of a critical ligand density for maximal support of the osteoblast phenotype (0.01 < Γ_crit < 0.1 pmol/cm²). The observed effects were attributed to specific interactions with the -RGDpeptide, as -RGE- negative controls failed to produce similar results. Efforts to extend this modulation to in vivo biological performance using the rat femoral ablation model were less successful. Bone formation on implants coated with the -RGD- modified IPN was similar to controls, and decreased as a function of implantation time. Bone-implant contact on -RGD- modified IPNs was enhanced relative to hydroxyapatite tricalcium phosphate (HATCP) coated implants, but similar to all other groups. Only HATCP coated implants supported significant (> 1 MPa) integration strength, despite exhibiting lower overall bone-implant contact, an indication that bone ingrowth was the primary mode of implant fixation. While no evidence was found to support the hypothesis that -RGD- modified IPN coated implants significantly impacted in vivo biological performance, results suggest that the study may have been limited by its failure to provide sufficient opportunity for bone ingrowth on the IPN coated implants (i.e., surface roughness). Future experiments will be designed to address the limitations of the current study in an effort to either conclusively achieve success or accurately determine the mechanism of failure.