Peri-implant mucositis.

Objectives: This narrative review was prepared for the 2017 World Workshop of the American Academy of Periodontology and European Federation of Periodontology to address key questions related to the clinical condition of peri-implant mucositis, including: 1) the definition of peri-implant mucositis, 2) conversion of peri-implant health to the biofilm-induced peri-implant mucositis lesion, 3) reversibility of peri-implant mucositis, 4) the long-standing peri-implant mucositis lesion, 5) similarities and differences between peri-implant mucositis at implants and gingivitis at teeth, and 6) risk indicators/factors for peri-implant mucositis.

Methods: A literature search of MEDLINE (PubMed) and The Cochrane Library up to and including July 31, 2016, was carried out using the search strategy (peri-implant[All Fields] AND ("mucositis"[MeSH Terms] OR "mucositis"[All Fields])) OR (periimplant[All Fields] AND mucosits[All Fields]). Prospective, retrospective, and cross-sectional studies and review papers that focused on risk factors/indicators for peri-implant mucositis as well as experimental peri-implant mucositis studies in animals and humans were included.

Findings: Peri-implant mucositis is an inflammatory lesion of the soft tissues surrounding an endosseous implant in the absence of loss of supporting bone or continuing marginal bone loss. A cause-and-effect relationship between experimental accumulation of bacterial biofilms around titanium dental implants and the development of an inflammatory response has been demonstrated. The experimental peri-implant mucositis lesion is characterized by an inflammatory cell infiltrate present within the connective tissue lateral to the barrier epithelium. In long-standing peri-implant mucositis, the inflammatory cell infiltrate is larger in size than in the early (3-week) experimental peri-implant mucositis lesion. Biofilm-induced peri-implant mucositis is reversible at the host biomarker level once biofilm control is reinstituted. Reversal of the clinical signs of inflammation may take longer than 3 weeks. Factors identified as risk indicators for peri-implant mucositis include biofilm accumulation, smoking, and radiation. Further evidence is required for potential risk factors, including diabetes, lack of keratinized mucosa, and presence of excess luting cement.

Conclusions: Peri-implant mucositis is caused by biofilm accumulation which disrupts the host-microbe homeostasis at the implant-mucosa interface, resulting in an inflammatory lesion. Peri-implant mucositis is a reversible condition at the host biomarker level. Therefore, the clinical implication is that optimal biofilm removal is a prerequisite for the prevention and management of peri-implant mucositis. An understanding of peri-implant mucositis is important because it is considered a precursor for peri-implantitis.