Experimental peri-implant mucositis models vs long-standing peri-implant mucositis lesions|palmerah.implantgigi.com

Experimental studies in humans and animals have demonstrated that de novo biofilm accumulation results in an inflammatory lesion within the peri‐implant mucosa with migration of leukocytes through the barrier epithelium and the establishment of an inflammatory infiltrate with an increased proportion of T‐ and B‐cells in the connective tissue adjacent to the barrier epithelium.

Animal models

Experimental peri‐implant mucositis models have evaluated the response of the peri‐implant mucosa to both early (3 weeks) and long‐standing (90 days) periods of undisturbed biofilm accumulation. In these dog studies, comparisons were made between the response of the gingiva at teeth and the peri‐implant mucosa at implants. Clinical examinations, biofilm sampling, and biopsies were obtained at both the early and long‐standing inflammatory lesions. At 3 weeks there was abundant biofilm accumulation, and both the gingiva and the peri‐implant mucosa showed clinical signs of inflammation. Histology showed an inflammatory cell infiltrate within the connective tissue which was found in the marginal portion of the soft tissues, immediately adjacent to the barrier epithelium at implants and the junctional epithelium at teeth. In contrast, after a longer period (90 days) of undisturbed biofilm accumulation, the peri‐implant mucositis lesions contained a smaller number of fibroblasts than the gingival counterparts, and the area occupied by the inflammatory infiltrate was greater in the peri‐implant mucositis lesions than the gingivitis lesions, although it did not extend beyond the barrier epithelium.

Ericsson et al., in an experimental dog study, obtained biopsies of peri‐implant mucosa after 9 months of biofilm accumulation and showed an inflammatory infiltrate located within the marginal portion of the peri‐implant mucosa. In another experimental study in the dog model, long‐standing biofilm‐associated lesions of 5 months duration were established in the peri‐implant mucosa adjacent to three different implant systems. The findings of this study confirmed that the size and apical extension of the inflammatory infiltrate did not extend beyond the barrier epithelium for all three implant systems used.

Human studies

Experimental studies in humans have evaluated the response to 3 weeks of biofilm accumulation, corresponding to the time frame of the experimental gingivitis study by Löe et al., where reversibility of the inflammatory lesion around teeth was demonstrated after reinstitution of biofilm control after 3 weeks. There are studies reporting on human biopsies of peri‐implant tissues where long‐standing peri‐implant mucositis lesions were evaluated. Gualini et al. described the immunohistochemical features of peri‐implant mucositis lesions obtained from 10 partially edentulous subjects with implants in function between 2 and 5 years. Clinically, the degree of redness and swelling of the inflamed tissues varied; however, all sites bled on gentle probing. In all biopsies the histologic sections showed a small and well‐defined inflammatory infiltrate in the connective tissue lateral to the barrier epithelium. The lesions included 7.3% T‐cells (CD3 positive) and 4.1% B‐cells (CD19 positive). Elastase‐positive polymorphonuclear neutrophils (PMN) occured within the barrier epithelium and in the connective tissue compartment immediately lateral to the barrier epithelium. The area of the inflammatory lesions corresponded to 0.36 mm², considerably larger than the size of the lesions observed in the experimental short‐term (3 week) peri‐implant mucositis study by Zitzmann et al. and histologic samples taken mainly from clinically healthy sites. These studies confirmed the findings of Seymour et al. who also evaluated biospies of nine subjects with long‐standing peri‐implant mucositis and found an increase in size of the inflammatory lesion compared to clinically healthy sites.

Peri‐implant mucositis may be present for extensive periods of time without progression to peri‐implantitis. Conversion of the peri‐implant mucositis lesion to peri‐implantitis in humans is difficult to study in an experimental design for obvious ethical reasons. However, in a longitudinal study of patients diagnosed with peri‐implant mucositis, those with a lack of adherence to supportive peri‐implant therapy had a higher incidence of peri‐implantitis at 5 years. Hence, sites with peri‐implant mucositis should be considered at increased risk for the development of peri‐implantitis.

Experimental peri-implant mucositis models vs long-standing peri-implant mucositis lesions

Animal models

Human studies

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