2. Types of Peri-Implant Disease and Criteria for Implant Health and Peri-Implantitis
The peri-implant disease has been divided into three separate categories by the consensus report of the 4th workgroup of the 2017 World Workshop on the classification of periodontal and peri-implant diseases and conditions (
Table 12). These are, respectively: peri-implant health, peri-implant mucositis and peri-implantitis
[221]. This division allows for clearer distinction and easier treatment planning, as peri-implantitis is not always coexistent with visible inflammation and can be easily mistaken for peri-implant mucositis. Implant success is recognized differently by different authors. Various definitions have been formulated ever since the first osseointegration cases were published by Branemark et al. Buser et al.
[232] defined implant success as lack of mobility, no noticeable radiolucency around the implant, <2 mm of crestal bone loss in the first year of functioning and no inflammatory symptoms. Furthermore, the authors highlighted the importance of the feasibility of restorations. Implant success definition was then further redefined in 2008, at the International Congress of Oral Implantologists (ICOI) Pisa Consensus Conference, as no pain or tenderness upon function, the absence of mobility, <2 mm radiographic bone loss from the initial surgery and no presence of exudate
[243]. To date, the most recent definition of peri-implantitis includes the presence of bleeding/suppuration on probing, increasing probing depth between examinations, and crestal bone loss not caused by the initial remodelling
[254][265]. The 2017 World Workshop on the classification of periodontal and peri-implant diseases and conditions formulated the following definition of peri-implantitis: “peri-implantitis is a plaque-associated pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri-implant mucosa and subsequent progressive loss of supporting bone”
[276][287]. Additionally, there are criteria for diagnosing peri-implantitis without previous radiographic and clinical implant history, which consist of a lack of bleeding/suppuration on probing, PD ≥ 6mm and bone levels ≥ 3 mm apical of the most coronal portion of the intraosseous part of the implant
[221][254][265][287][298][309][3110].
Table 12. Healthy peri-implant vs. peri-implantitis according to 2017 World Workshop on the classification of periodontal and peri-implant diseases and conditions.
3. Risk Factors Associated with Peri-Implantitis
The risk factor of peri-implantitis is dependent not only on individual host susceptibility but also on other factors with various degrees of concurrence. To what extent the risk factors will influence the appearance of peri-implantitis also depends on the frequency, intensity, and individual vulnerability to the factor (i.e., a thicker peri-implant phenotype performs better)
[3211] and the cooperation of factors acting together. The risk factors include smoking, alcohol drinking, metabolic diseases (e.g., diabetes), previously recognized periodontitis
[3312][3413][3514][3615][3716][3817], a poor level of oral hygiene, insufficiently frequent controls, an external implant–abutment connection type and inadequate screw-in torque
[3312], viral infections (HPV, HHV-4, HHV-6, HHV-7 and COVID-19)
[3817][3918][4019], genetic burdens (i.e., Papillon–Lefevre syndrome), titanium particles present after implant placement, and tissue response to prosthetic restoration
[4120][4221]. Smoking is positively correlated with peri-implant disease as it can contribute to hindering the bone blood supply and lower the cellular immunological response and MMP-8
[3211][3413][3615][4221][4322]. Alcohol drinking can also increase the risk of peri-implantitis, mainly in conjunction with smoking, highlighting the additive influence of both
[3211][3413]. There is also a statistically significant risk of peri-implantitis in obese patients because of higher C-reactive protein and MMP-8 levels in the serum and PICF
[4221][4322]. Patient compliance also plays an important role in the quick detection and effective management of implant tissues
[3413]. Patients with genetic conditions that can influence periodontal health, such as Papillon–Lefevre syndrome, are inherently more prone to peri-implantitis. In this group, despite the much higher risk, regular clinical controls either lowered or prevented peri-implantitis and its progress
[4423]. Regarding endocrine malfunctions, diabetes mellitus leads the way. Its growing significance comes from an ever-growing population of patients and new dependencies found in metabolic pathways and genetic connections. In peri-implantitis accompanying diabetes, the main reasons seem to be increased HbA1c and advanced glycemic end product (AGE) levels, which interfere with immune response, bone remodelling (promoting osteoclastogenesis), vascularization, cell apoptosis and inflammation
[3211][3514][4221][4524]. Risk factors are listed in
Figure 12.
Figure 12.
Risk factors associated with peri-implantitis.
4. Molecular Factors Contributing to Peri-Implantitis Development
Cytokines are proteins secreted by leukocytes and serve a mainly communicatory role. They influence either pro- or anti-inflammatory responses. In peri-implantitis, the balance between pro-and anti-inflammatory cytokines is disrupted in favour of pro-inflammatory. The most well-known are pro-inflammatory IL-6, IL-1 and TNFα
[4625]. The most common pro- and anti-inflammatory cytokines are listed in
Table 23 with their effects in peri-implantits in
Figure 23 and
Figure 34. The basic functions of the most common cytokines in peri-implantitis are listed in
Table 34.
Figure 23.
Pro- and anti-inflammatory cytokine effects on the oral mucosa and gingiva
.
Figure 34.
Pro- and anti-inflammatory cytokine effects on alveolar bone
.
Table 23.
Pro- and anti-inflammatory cytokines.
Table 34.
Molecular factors in peri-implantitis and their function
.