It has been shown by studies conducted from the early 1990s to the early 2000s with external hex design that the mucosal barrier surrounding dental implants is formed by a crevicular oral epithelium ranging in mean 1.5–2 mm (but it may reach up to 4 mm) and a connective tissue barrier in mean ranging 1–2 mm [6–8]. Moreover, the oral epithelium presents an extension with a thin junctional epithelium facing the implant surface and extending about 1.64–2.35 mm from the mucosal margin (Fig. 6.1, 6.2, and 6.3) [6–8]. In general terms, the length from the marginal portion of the peri-implant mucosa to the first bone-to-implant contact has been found to be approximately 3 mm [6–8].

In addition, it was demonstrated that a 2 mm height saucer-shaped crestal bone resorption occurs (a phenomenon called as “saucerization”) when submerged, 2-piece implants are used based on the location of the microgap, whereas for non-submerged, 1-piece implants, none or minimal loss may occur (Fig. 6.4) [9, 10]. It is also important to note for the 2-piece implants that such a bone change only occurs after the period of osseointegration/healing (submerged healing phase), within the first month following the placement of abutments [10]. The specific mechanisms linked to this crestal bone remodeling in 2-piece implants are not completely known [5], but these have been related in some animal model studies to microbial colonization of the microgap, micro-movements of the abutment, or an interruption of the blood supply when implants and abutments are placed transmucosally [10–12].

Around dental implants, BW determines the minimum dimensions to ensure junctional epithelium and connective tissue to attain an ideal seal and to provide protection from mechanical and external biological agents [13]. Also, an external agent invading the BW would induce a response from the epithelium that migrates beyond this agent trying to isolate it [2, 3, 13]. The resulting bone resorption produces a reestablishment of the BW dimension.

In humans, recent data showed that the biologic width around one- and two-piece retrieved implants is formed by (1) a crevicular epithelium composed of 4–6 layers of parakeratinized epithelial cells; (2) a junctional epithelium formed by 5–10 layers of epithelial cells, where the middle and apical portion of the JE consisted of 3–5 cells layers; and (3) a connective tissue (at the abutment area) containing few blood vessels (only from the supraperiosteal plexus), dense collagen fibers, and reduced number of fibroblasts (when compared to the lamina propria of the gingiva) oriented parallel to the longitudinal axis of the abutment [14]. Regarding to the dimensions of the biologic width around these implants, the following can be expected (Fig. 6.5):

In addition, the biologic width formation and maturation around dental implants take place between 6 and 8 weeks of wound healing, and the connective tissue of the implant mucosa is similar in composition (cells, fiber orientation, and vascularization) to a scar tissue [16].