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inflammation, bleeding on probing (BOP) and/or suppuration, increased PDs and/or recession of the mucosal margin, in addition to radiographic bone loss compared with previous examinations (Berglundh et al., 2018). The primary etiological factor for peri- implantitis onset and progression is the accumulation of a peri- implant plaque biofilm. Important risk factors/indicators have been identified, including a history of severe periodontitis, poor plaque control and no regular supportive peri-implant care (SPIC) following implant therapy. Less conclusive evidence was found for smoking and diabetes, or local factors such as the presence of submucosal cement following prosthetic restoration of the implant, or position- ing of implants limiting access to oral hygiene (OH) and mainte- nance. Other factors such as the absence of peri-implant keratinized mucosa (PIKM), occlusal overload, presence of titanium particles within peri-implant tissues, bone compression necrosis, overheating, micromotion or biocorrosion have been proposed as risk factors for peri-implant diseases onset and/or progression, but further research is required to clarify their true roles (Schwarz et al., 2018). Peri-implant diseases, especially peri-implantitis, represent a growing public health problem due to their high prevalence and the associated consequences (implant and implant-supported prosthesis loss), including dental care costs, which are substantial.
peri-implantitis develop, as it is believed that peri-implant mucositis always precedes peri-implantitis (Berglundh et al., 2018; Heitz-May- field & Salvi, 2018). The primary aetiological agent for peri-implantitis is also the accu- mulation of the peri-implant biofilm, with human observational studies demonstrating a higher risk of incident peri-implantitis in patients with poor biofilm control and/or non-adherence to maintenance care, and based on intervention studies using anti-infective approaches (Berglundh et al., 2018). Peri-implantitis lesions are larger than those associated with peri- implant mucositis or with periodontitis and are characterized by greater number of neutrophils and larger proportions of B cells when compared with peri-implant mucositis. Consistent with periodontitis lesions, plasma cells and lymphocytes predominate within the immune-inflammatory infiltrate (Schwarz et al., 2018). However, these characteristic histological features have not been associated with spe- cific bacteria (Sahrmann et al., 2020) or proinflammatory cytokine pro- files (Berglundh et al., 2018).
1.1.3 | Prevalence
During the XI European Workshop in Periodontology (2014), entitled ‘ Effective Prevention of Periodontal and Peri-implant Diseases ’ , a sys- tematic review (SR) was specifically commissioned to address the prevalence of peri-implant diseases. Eleven studies were selected and the meta-analyses demonstrated a patient-level prevalence estimate of 43% (95% confidence interval — CI [32; 54]) for peri-implant mucosi- tis and 22% (95% CI [14; 30]) for peri-implantitis (Derks & Tomasi, 2015). Another SR, comprising 47 studies, reported a preva- lence of 46.83% (95% CI [38.30; 55.36]) for peri-implant mucositis and of 19.83% (95% CI [15.38; 24.27]) for peri-implantitis (Lee et al., 2017).
1.1.2 | Pathophysiology
To better understand the pathophysiology of peri-implant diseases, knowledge of the pathophysiology of periodontal diseases has been extensively used, and findings on peri-implant mucositis have been lik- ened to those of biofilm-induced gingivitis. The same applies to peri- implantitis and periodontitis. However, when compared with periodontal tissues, peri-implant tissues lack cementum and periodontal ligament; thus, there are only two peri-implant tissue layers, alveolar bone and peri-implant mucosa. Additional differences are found in the peri-implant mucosa: the peri-implant epithelial attachment is usually longer; the con- nective tissue exhibits no fibres inserting into the supra-crestal area; and vascularization is lower. Peri-implant biofilms are considered to be the primary aetiological factor for peri-implant mucositis, based on strong evidence derived from animal and human studies (Berglundh et al., 2018). Such biofilms form on the hard, non-shedding surfaces of the implant and implant- supported restorations, similar to the formation of dental plaque biofilms on teeth (Bermejo et al., 2019; Sanchez et al., 2014). Histologically, peri-implant mucositis is similar to gingivitis: a well-defined inflammatory lesion, adjacent to the junctional/pocket epithelium, richly infiltrated by vascular structures, plasma cells and lymphocytes, but not extending apically to the junctional/pocket epithelium, or into the supra-crestal area (Berglundh et al., 2018; Heitz-Mayfield & Salvi, 2018). Evidence exists to support the contention that peri-implant mucositis is treatable, and can be successfully managed by careful control of the peri-implant biofilm. However, if allowed to persist,
1.1.4 | Consequences of failure to treat peri- implant diseases
As described above, peri-implant mucositis can be treated and resolved, but if left untreated, can progress to peri-implantitis; peri- implant mucositis is widely believed to precede peri-implantitis. Peri- implantitis can be initiated rapidly following prosthetic restoration and loading of the fixture during function, and if no treatment is provided, it is likely to progress in a non-linear accelerating pattern (Berglundh et al., 2018), and at a faster rate than is typically seen in periodontitis lesions (Schwarz et al., 2018). Progression of peri-implantitis will most likely lead to the loss of the affected implant and the implant-supported prosthesis. Limited information is available on the impact of peri-implant dis- eases on the quality of life. One study concluded that neither peri- implantitis nor surgical treatment of the same had any impact on Oral Health Related Quality of Life (Rustand et al., 2022), while another study assessing morbidity after non-surgical and surgical treatment of
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