Primary stability derives mainly from mechanical involvement with the cortical bone and the lack of mobility in the bone bed at the insertion of the implant and depends on the quantity and quality of the bone, the surgical technique, and the design of the implant. The titles were captured in the database PubMed, Scielo, and relevant Brazilian magazines to identify the primary stability, after the insertion of the implant in the region indicated in the protocol. Tapered implants showed greater primary stability compared to cylindrical implants, when placed under bone density conditions. The geometry of the implant is an important factor in the degree of primary stability. Based on this, large threads are desirable in cases of poor bone quality. The insertion torque values are very important for the clinical determination of the levels of primary stability and the absence of micro movements whenever an immediate load is applied. The implant, used as if it were the last cutter, when correctly inserted, penetrates with pressure in the bone store if its diameter is larger than that of the cutter perforation. The implant design plays an influential role in achieving its primary stability.

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The osseointegration is the stable and functional union between the bone and a titanium surface. A new bone can be found on the surface of the implant about 1 week after its installation; the bone remodeling begins between 6 and 12 weeks and continues throughout life. After the implant insertion, depending on the energy of the surface, the plasma fluid immediately adheres, in close contact with the surface, promoting the adsorption of proteins and inducing the indirect interaction of the cells with the material. Macrophages are cells found in the tissues and originated from bone marrow monocytes. The M1 macrophages orchestrate the phagocytic phase in the inflammatory region and also produce inflammatory cytokines involved with the chronic inflammation and the cleaning of the wound and damaged tissues from bacteria. On the other hand, alternative-activated macrophages (M2) are activated by IL-10, the immune complex. Its main function consists on regulating negatively the inflammation through the secretion of the immunosuppressant IL-10. The M2 macrophages present involvement with the immunosuppression, besides having a low capacity for presenting antigens and high production of cytokines; these can be further divided into M2a, M2b, and M2c, based on the gene expression profile.

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