Pathogenesis

Although the term mucositis is used to describe soft tissue inflammation, there is disagreement in the literature whether histologically the soft tissue around a dental implant more closely resembles mucosa or gingiva. Nevertheless, the obvious pathogenic comparison of peri-implant mucositis is to gingivitis, where only the surrounding soft tissue shows inflammation and the alveolar crestal bone is intact. Predictably, like gingivitis, peri-implant mucositis is reversible.

Peri-implantitis mirrors the pathogenesis of periodontitis.  Exposed titanium surfaces accumulate glycoproteins forming a salivary pellicle and as bacteria move onto a surface, the dynamic process of biofilm formation begins.  Implant-associated biofilm resembles that of chronic periodontitis, i.e., mixed, non-specific microbes, dominated by gram-negative anaerobes.9-11  A notable difference between the two conditions is the association of S. aureus with peri-implantitis.12,13

In peri-implantitis, as in periodontitis, the biofilm triggers an inflammatory response. Blood vessels adjacent to the gingivae/mucosal tissue enlarge and become permeable, allowing the migration of neutrophils (PMNs) into the pocket space around the implant. As inflammation progresses, collagen around the blood vessels is lost and lymphocytes, which subsequently transform into plasma cells and macrophages accumulate in the area.

Fibroblast- and PMN-derived collagenases catalyze collagen loss apical to the pocket epithelium. The underlying connective tissue exhibits increasing lymphocytic infiltrates. Pocket formation is enhanced in the peri-implant space characterized by “pot-hole”-like defects (Figure 1), creating an environment that favors microbial proliferation. The products of these pathogens further challenge host immune defenses and degenerative changes progress apically into the underlying connective tissue.

Figure 1.
Image: Pocket formation in the peri-implant space characterized by a “pot-hole”-like defect.
Pocket formation in the peri-implant space characterized by a “pot-hole”-like defect.

At this point, the analogy between periodontitis and peri-implantitis briefly diverges.  Inflammatory activity around implants is more pronounced than that observed around natural teeth and the tissues are more susceptible to the spread of plaque-associated infection into alveolar bone.14,15  When cases of peri-implantitis were systematically compared to cases of periodontitis, the results revealed that tissue destruction is more severe in association with peri-implantitis.16,17

One explanation for the apparent greater severity and increased rate of progression of tissue destruction is the structural differences between periodontal and peri-implant tissues. Unlike natural teeth, dental implants do not have cementum or Sharpey’s fibers, they are not bounded by periodontal ligament, and, consequently, there is direct contact between bone and implant surface. It is axiomatic that infection can progress without impediments from soft to hard tissue.

Ultimately, as the inflammatory process reaches the crest of alveolar bone, both in peri-implantitis and periodontitis, osteoclastic bone resorption begins (Figures 2 & 3). The inflammatory cells release cytokines such as interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Bone destruction occurs though osteoclastic action which is triggered by cytokines and other inflammatory mediators, including IL-1β and PGE2.

Figure 2.
Image: At low magnification, the start of osteoclastic action around teeth affected with periodontitis.
At low magnification, the start of osteoclastic action around teeth affected with periodontitis.
Figure 3.
Image: At high magnification, note connective tissue inflammatory infiltrate, which is common to inflammation around natural teeth and dental implants.
At high magnification, note connective tissue inflammatory infiltrate, which is common to inflammation around natural teeth and dental implants.