Restorative implant dentistry relies on the long-term integration of the implanted material in bone. This process is modulated by surgical factors such as the surgery plan and the prosthetic loading strategy; biological factors such as the patient’s health and the receiving bone conditions; and implant-related factors such as the base material characteristics, the surface physiochemistry, topography, final quality, and cleanliness of the manufactured implant ^[2][3].

Peri-implant bone regeneration begins with the placement of an implant and the quasi-instantaneous establishment of a new ionic balance between the surface and the receiving bed. In the quest for faster and better bone-tissue integration, implant surface designs have historically sought to imitate the structure and composition of bone tissue. Long story short: a bone-like structure at the implant surface should more easily fuse with the existing bone bed ^[3].

An alternative strategy consists in focusing on the early phases of implant-bone tissue interaction. Immediately upon implant insertion, the establishment of an ionic equilibrium at the implant-tissue interface is determined by the chemical composition of the implant surface and by the local ionic composition. The surface adsorption and exchange of proteins with the biological environment, which is a fundamental part of the process of hemostasis and inflammation, follows ^[4][5][6]. The ionic configuration of the implant surface is therefore key to the subsequent responses down the line.

For the success of the implantation, it is crucial to achieve a rapid stabilization of the implant with the surrounding tissues. The clot or provisional matrix generates this preliminary stability. It consists of a three-dimensional fibrin network that contains platelets and growth factors. A fully functional clot orchestrates the attraction, housing, development, differentiation, and function of the cells in charge of the synthesis of the mature extracellular matrix ^[1]. Fibrin is an insoluble biopolymer formed from the progressive assembly of fibrinogen subunits. Thrombin allows the ends of fibrinopeptides to be separated from the main fibrinogen unit and the new ends to react with each other and form the three-dimensional fibrin network ^[7]. Developing this scaffold intimately with the implant surface opens the possibility, among others, of improving angiogenesis, reducing inflammation, and accelerating tissue repair directly on the surface.