Healthy peri‐implant mucosa is characterized by the presence of an oral epithelium extending into a non‐keratinized barrier epithelium with basal lamina and hemidesmosomes facing the implant or abutment surface. In the connective tissue adjacent to the epithelial barrier, inflammatory cell infiltrates representing the host's defense against the bacterial challenge are present. In healthy peri‐implant mucosal conditions, the barrier epithelium and the presence of scattered inflammatory cells constitute the soft tissue seal separating the peri‐implant attachment from the oral cavity.

Peri‐implant mucositis develops from healthy peri‐implant mucosa following accumulation of bacterial biofilms around osseointegrated dental implants. A cause‐and‐effect relationship between experimental accumulation of bacterial biofilms around titanium dental implants and the development of an inflammatory response (i.e., experimental peri‐implant mucositis) has been demonstrated in humans.

In an early study by Pontoriero et al., twenty partially edentulous patients received dental implants following successful completion of periodontal therapy. After 6 months of supervised oral hygiene, the peri‐implant mucosa was characterized by the absence of obvious signs of clinical inflammation. Following this period, the patients were asked to abolish oral hygiene practices for 3 weeks. At the end of this period, optimal biofilm control was reinstituted. At all examinations the following clinical parameters were assessed around the implants: plaque index (PI), gingival index (GI), sulcus bleeding index (SBI), probing depths (PD), and marginal recession (REC). The 3‐week period of abolished oral hygiene practices revealed the development of visible signs of mucosal inflammation, such as swelling, redness, and bleeding. This cause‐and‐effect relationship between the accumulation of bacterial biofilms and the development of peri‐implant mucositis is consistent with the results obtained in the experimental gingivitis model by Löe et al. In another study by Zitzmann et al. involving 12 partially edentulous patients the inflammatory. The inflammatory response to the experimental bacterial challenge was characterized by the enumeration of the proportions of T‐ and B‐cells in peri‐implant tissues. Biopsies harvested around implants in a clinically healthy situation and after 21 days of experimental biofilm accumulation indicated that the connective tissue surrounding the implants displayed an increased volume of T‐ and B‐lymphocytes as a consequence of abolished oral hygiene practices. It was also noted that the size of the inflammatory cell infiltrate and the number of several immune cell populations was not significantly different when comparing biopsies from gingiva at teeth and biopsies from peri‐implant mucosa.

Outcomes of a comparative study in humans by Salvi et al. indicated that 3 weeks of experimental biofilm accumulation resulted in a higher proportion of bleeding sites in the peri‐implant mucosa when compared with that in the gingiva. In that study, the PI at tooth sites was significantly elevated when compared with that at implant sites after 3 weeks of abolished oral hygiene. However, the increase of the GI at tooth sites was significantly lower compared with that at implant sites, indicating that a comparable bacterial challenge yielded a more severe inflammatory response at implant sites.

A recent study, by Meyer et al., compared clinical and biologic responses during experimental gingivitis and peri‐implant mucositis in subjects aged ≥70 years. Although less biofilm accumulation was observed at implant sites, the peri‐implant mucosa yielded a higher proportion of bleeding sites compared with that observed in the gingiva, thus confirming the results by Salvi et al. obtained in a younger patient sample.