image Soft Tissue Barrier at Implants

To be functionally useful, dental implants have to pierce the oral mucosa and enter the oral cavity, thus establishing a transmucosal connection between the external environment and the inner parts of the body. To avoid bacterial penetration that could jeopardize either initial healing or long-term behavior of implants, the early formation of a longstanding, effective barrier capable of biologically protecting the peri-implant structures is mandatory to prevent oral bacteria and their products from penetrating into the body.17

Establishment of this critical soft tissue barrier is the result of wound healing that establishes an effective interface between living tissues and a foreign body. The soft tissue barrier (also called biological width) has been evaluated in animals and found to have a dimension of about 3 mm in the apico-coronal direction. The interface consists of two zones, one of epithelium that covers about 2 mm of the surface and one devoted to connective tissue adhesion.

Healing Process

After installation of the transmucosal implant component, the healing of the connective tissue wound involves four distinct processes: (1) formation and (hopefully) adhesion of a fibrin clot to the implant surface, (2) adsorption of extracellular matrix proteins and subsequently of connective tissue cells to the implant surface, (3) transformation of the clot into granulation tissue, and (4) migration of epithelial cells on top of the fibrin clot/granulation tissue.8,9

Through its capacity to proliferate and to move on surfaces, the epithelium found at the border of the incision crosses over the bridge of the fibrin clot/granulation tissue that rapidly starts forming after implant/abutment installation. Upon reaching the surface of the implanted component, it moves in the corono-apical direction, giving rise to a junctional epithelium about 2 mm long.10,11 In the initial healing phases, the quality and stability of the fibrin clot adhesion to the surface of the transmucosal components probably play a role in the formation and positioning of the junctional epithelium.12

The presence of granulation tissue adhering to the surface of transmucosal implant components is considered the principal factor that stops the epithelium from moving further apically.13 The role of the connective tissue in preventing epithelium downgrowth has been clearly demonstrated in animal models.14,15 Berglundh et al.16 also speculated that the epithelium stops migrating in an apical direction because of the interaction between the soft tissue and the layer of titanium oxide. It seems that mature connective tissue interferes more effectively than granulation tissue with epithelial downgrowth.17

Once the epithelial cells have reached the implant surface, their attachment occurs directly via a basal lamina (<200 nm) and the formation of hemidesmosomes.1824 Hemidesmosomes may already be formed at 2-3 three days of healing.25

Clinical Consequences

Probing Depth

Despite comparable histological dimensions of the soft tissue compartments (junctional epithelium and connective tissue interface) at teeth and implants, it has been shown that when a probe pressure of 0.5 N is used in dogs, the probe tip penetrates on average 0.7 mm deeper at implant sites.34 The histological sections with probes in situ evidenced that around implants, the tip of the probe ended apically to the junctional epithelium, close to the bone crest, explaining why the clinical probing depth is higher. This is in accordance with the results of Gray et al.35 in baboons.

In humans, it was confirmed that 0.5-1.4 mm deeper measurements are generally found at implants.3638 These results are the consequence of the brittle adhesion of connective tissue at implant components, illustrating that at implants the probe tip ends somewhere in the connective tissue and that the significance of probing at implants and at teeth is different.

Soft Tissue Stability/Instability

Several studies have examined changes in soft tissue levels after implant placement.3640 Despite significant differences in experimental designs, a vast majority of studies conclude that a gingival recession grossly varying from 0.6-1.5 mm is unavoidable.

No significant difference could be determined between the 2-stage and the 1-stage surgical approaches41nor between one- or two-piece implants.42,43 One clinical study44 reported 1.3-mm recession from 1 month to 1 year, then an additional loss of 0.4 from 1-3 years. Another45 found 1.6 mm of mean recession at the mandible versus 0.9 mm at the maxilla. In contrast, some authors found much lower levels of recession.4649 It is important to note that these studies started measuring the soft tissue recession only 1 month,50,51 6 weeks,52 or even 3-5 months53 after mucosal piercing. This is most probably of major impact, since the clinical study of Small and Tarnow54 demonstrated that 50% of the recession is obtained after only 1 month and 90% after 3 months, with a stable level reached at 9 months. This was later confirmed in another clinical study by Kan et al.55

image Influence of Transmucosal Components on Soft Tissue Barrier Formation

Influence of Implant Design on Soft Tissue Barrier

In a one-piece implant the transmucosal component facing the soft tissues makes part of the implant. In a two-piece implant the transmucosal component dedicated at soft tissue integration is a separate part from the implant body. The interface between the transmucosal component and the implant is generally located in the neighborhood of the alveolar bone level.

Comparative studies were performed in dogs to determine the influence of implant design on soft tissue integration. Abrahamsson et al.62 demonstrated that the dimensions of the junctional epithelium and of the connective tissue are similar on one-piece implants and on two-piece implants. In addition, their position relative to the bone crest was also comparable, with the soft tissue integration located on the smooth implant’s neck on one-piece implants and at the abutment level on two-piece implants. Using the same experimental conditions, but after 6 months of undisturbed plaque accumulation, it was shown63 that the extent of the plaque-related inflammatory infiltrate was comparable around one- and two-piece implants.

Using experimental implants with either a one-piece or a two-piece design, Hermann et al.64 showed significantly higher apical migration of the soft tissues and marginal bone resorption with two-piece implants, suggesting a role for the subgingival position of the abutment/implant interface (so-called microgap) on tissue remodeling. It must be noted that all two-piece implants in this experiment were clinically and histologically surrounded by an intense inflammatory process. This is in strong opposition with several animal studies6576 in which a soft tissue integration occurred at the abutment level.

In another experiment by the same group, it was demonstrated that the size of the microgap between implants and abutments has little influence on marginal bone remodeling, whereas micromovements of the abutments induce a significant bone loss, independent of the microgap’s size. This strongly suggests that the mechanical disruption of the soft tissue interface is of importance.

An inflammatory cell infiltrate has been demonstrated at two-piece implants, in the close vicinity of the abutment/implant interface.77 This infiltrate does not impair the formation of effective soft tissue integration and seems to be present at implant systems with an external implant/abutment connection as well as at systems with an internal morse taper connection, but not at one-piece implants.77

In some experiments using commercially available implants, the infiltrate proved to be very limited in size (<0.5 mm) and was not linked to a higher bone loss as compared to one-piece implants, whereas Broggini et al.78 linked the 0.5-mm inflammatory infiltrate seen in their samples with experimental implants to a higher bone loss than at one-piece implants.

It has been shown that the seal provided by a locking taper connection at the implant/abutment interface effectively impairs bacterial leakage. But it has not been clearly shown that the bacterial contamination of the internal components of some two-piece implant systems79 is responsible for the inflammatory cell infiltrate seen at the abutment/implant interface.

An intentional or unintentional disconnection of abutments is possible at two-piece implants. Based on results by Hermann et al., an unintentional abutment loosening will lead to a disruption of the soft tissue integration and to increased bone remodeling.64

It also has been shown that repeated intentional abutment disconnection and reconnection after alcoholic disinfection induce an apical repositioning of the soft tissues and marginal bone resorption80; a single shift of a healing abutment and replacement by a final abutment proved to induce no marginal bone remodeling.81

Influence of Transmucosal Component Design on the Soft Tissue Barrier

Several studies have examined changes in soft tissue levels after implant placement.82,83 Despite significant differences in experimental designs, a vast majority of studies conclude that a gingival recession grossly varying from 0.6-1.5 mm is unavoidable. All these studies used transmucosal components with divergent designs.

In contrast, favorable results have been described with slightly concave abutments. By using abutments that have a diameter narrower than their two-piece implants, Cooper et al. showed a mean vertical gain of 0.34 mm of soft tissue.

More recently, Rompen et al. showed that with concave, gingivally converging abutment components the frequency and magnitude of recessions can be dramatically reduced. In contrast with existing data from the literature showing that a 0.5-1.5-mm recession must be expected on a majority of implants, 87% of their cases showed facial soft tissue stability or gain, while recessions (13% of the sites) were never greater than 0.5 mm. These results remained stable from the time of placement of the definitive restoration to 12, 18, and 24 months, suggesting that using inwardly narrowed transmucosal profiles for implant components allows for more predictable soft tissue stability in aesthetic areas than divergent profiles.

The hypothesis is that the positive soft tissue behavior with the particular transmucosal design evaluated in the present study is linked to a combination of three primary factors. First, the circumferential macrogroove creates a void chamber in which a blood clot forms and that provides space for soft tissue regeneration. The result is a nonsurgical, localized thickening of the soft tissues. Second, the highly curved profile allows increased soft tissue-to-implant interface length, facilitating a biological seal of 3 mm despite a shorter crown-to-implant distance. Third, after maturation of the soft tissues, a ring-like seal (Figure 11-1) is created that could stabilize the connective tissue adhesion and functionally mimic the effect of Sharpey’s fibers at teeth (Figure 11-2).

Jan 7, 2015 | Posted by in Implantology | Comments Off on 11: PERI-IMPLANT SOFT TISSUES
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