Endogenous protein adsorption and functional presentation at bone-regenerative biointerfaces

Bone-regenerative materials rapidly acquire proteins from blood, marrow fluid, and the surrounding tissue. The resulting interface depends on protein quantity, identity, orientation, conformation, and exchange, rather than total adsorption alone. This narrative critical review examines selected mechanisms through which these features influence receptor recognition and responses relevant to bone repair. We use the descriptive term interfacial protein state and propose a joint reporting profile for comparisons made under matched exposure and sampling conditions. Primary evidence is distinguished by protein source, experimental setting, causal perturbation, and limits of interpretation. The strongest mechanistic examples concern fibronectin presentation and integrin signaling, selected fibrinogen-dependent inflammatory pathways, and material-assisted presentation of exogenous growth factors. Quantitative examples of surface density, accessibility, dissociation, and retained BMP-2 dose are reported with their experimental conditions. Autologous platelet-rich plasma and platelet-rich fibrin are considered as clinically relevant precoatings whose preparation and release behavior require separate characterization. Competition between host cells and bacteria for the conditioned interface is also addressed. Hemostatic-inflammatory, angiogenic-matrix-forming, and mineralization-remodeling processes are presented as overlapping biological contexts, not as a validated schedule for programming protein exchange. Evidence from purified coatings and dispersed nanoparticles is not treated as proof of endogenous recruitment or clinical bone healing. Predicting outcomes across materials, guiding patient-specific implant selection, and replacing growth-factor delivery through endogenous capture remain unvalidated. The proposed measurements organize causal tests and identify evidence gaps; they do not define a universal protein-state score or an established clinical design rule.