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Chmielewski, M.; Pilloni, A. Molecular, Cellular and Genetic Aspects of Peri-Implantitis. Encyclopedia. Available online: (accessed on 05 December 2023).
Chmielewski M, Pilloni A. Molecular, Cellular and Genetic Aspects of Peri-Implantitis. Encyclopedia. Available at: Accessed December 05, 2023.
Chmielewski, Marek, Andrea Pilloni. "Molecular, Cellular and Genetic Aspects of Peri-Implantitis" Encyclopedia, (accessed December 05, 2023).
Chmielewski, M., & Pilloni, A.(2023, July 20). Molecular, Cellular and Genetic Aspects of Peri-Implantitis. In Encyclopedia.
Chmielewski, Marek and Andrea Pilloni. "Molecular, Cellular and Genetic Aspects of Peri-Implantitis." Encyclopedia. Web. 20 July, 2023.
Molecular, Cellular and Genetic Aspects of Peri-Implantitis

Peri-implantitis is a multi-factorial disease with an inflammatory background that occurs in both soft and hard tissues surrounding implants. A wide array of cells stands behind peri-implantitis, as well as cytokines and their genetic variations that take part in the process. Recently, growing interest in this topic has led to the introduction of specific new diagnostic tools to enable a better understanding of patients’ responses to treatment and, in turn, to even enable prediction of the risk of developing peri-implant disease.

inflammation peri-implantitis cellular response molecular factors genetic polymorphism cytokines

1. Introduction

The wide spread of prosthetic restorations based on dental implants enables optimal oral rehabilitation of totally and partially edentulous patients, expanding the available treatment possibilities. Currently, the most common implant materials are pure titanium, Ti-6Al-4V alloy and zirconia. Additional modifications of the implant surface, for example, acid etching and sandblasting or coating, enhance the osseointegration process, extend the bone–implant contact area and reduce the risk of implant failure [1]. The prevalence of dental implants in the global population is estimated to reach up to 23% by the year 2026 [2]. The growing number of patients translates to a higher number of potential peri-implant complications. One of these is peri-implantitis. It is defined as a progressive, irreversible disease affecting both hard (alveolar bone) and soft tissues (supracrestal tissues and mucosa) surrounding dental implants. The amount of keratinized mucosa, the supracrestal tissue height and the peri-implant bone thickness can all affect peri-implantitis occurrence [3]. Additionally, in peri-implantitis, there can be bone loss, hindered implant osseointegration and pathological pocket formation [4]. It is commonly associated with bacterial challenge inducing the inflammatory process in surrounding soft tissues and loss of bone support. Like periodontitis, the main bacteria responsible for the development of peri-implantits belong to Socransky’s red complex. These are Porphyromonas gingivalis, Tannarella forsythia and Treponema denticola [5], however the range of suspected bacteria involved in the development of peri-implant pockets is broader. Often found microbes in the peri-implant pockets are often not specific, but commonly present, like Campylobacter, Gemella, Bacteroides, Actinomyces, Peptostreptococcus, Streptococcus, Candida, Treponema, E. corrodes and P. nigrescens [6]. While the microbial flora in peri-implantitis is relatively well known, much less information is available regarding the cellular and molecular responses. In medicine, cytokines are widely used as diagnostic and prognostic tools [7]. They are used to monitor the status of patients undergoing treatment for asthma, cancer, AIDS, heart disease, degenerative diseases and rheumatoid arthritis, to name only a few of them [7][8][9][10][11]. In dentistry, the use of cytokines is uncommon, only recently becoming more widespread [12]. The fields of dentistry that utilize them are periodontics and implantology. An increase in implant surgeries and implant-supported restorations has led to a higher incidence of peri-implant disease occurrence in the population. The most-investigated biomarkers in periodontal and peri-implant tissues are IL-1β, VEGF, MMP-8, TIMP-2 and OPG, as they alter soft and hard tissue cellular metabolism and seem to have different mean local concentrations during bacterial infections [13][14][15][16][17]. Peri-implant cervical fluid (PICF) is used as a site-specific and easy-to-obtain fluid. PICF is similar to gingival cervical fluid exerted from the gingival sulcus and contains cells, bacteria, cytokines and active mediators [18]. To collect PICF, sterile paper strips are placed within the sulcus or peri-implant crevice and held for 30 s to properly soak up the fluid [19]. It is important that the paper strips do not become contaminated with blood or pus. The strips are then placed in tubes containing buffered saline and phenylmethylsulfonyl fluoride and centrifuged [19][20]. PICF is further used to conduct ELISA tests for proteins and PCR for DNA and RNA or to perform oral-based point-of-care (PoC) tests [21]. Currently, the ELISA test is the most widely used.

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 1). These are, respectively: peri-implant health, peri-implant mucositis and peri-implantitis [22]. 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. [23] 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 [24]. 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 [25][26]. 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” [27][28]. 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 [22][25][26][28][29][30][31].
Table 1. 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) [32] and the cooperation of factors acting together. The risk factors include smoking, alcohol drinking, metabolic diseases (e.g., diabetes), previously recognized periodontitis [33][34][35][36][37][38], a poor level of oral hygiene, insufficiently frequent controls, an external implant–abutment connection type and inadequate screw-in torque [33], viral infections (HPV, HHV-4, HHV-6, HHV-7 and COVID-19) [38][39][40], genetic burdens (i.e., Papillon–Lefevre syndrome), titanium particles present after implant placement, and tissue response to prosthetic restoration [41][42]. 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 [32][34][36][42][43]. Alcohol drinking can also increase the risk of peri-implantitis, mainly in conjunction with smoking, highlighting the additive influence of both [32][34]. 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 [42][43]. Patient compliance also plays an important role in the quick detection and effective management of implant tissues [34]. 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 [44]. 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 [32][35][42][45]. Risk factors are listed in Figure 1.
Figure 1. 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 [46]. The most common pro- and anti-inflammatory cytokines are listed in Table 2 with their effects in peri-implantits in Figure 2 and Figure 3. The basic functions of the most common cytokines in peri-implantitis are listed in Table 3.
Figure 2. Pro- and anti-inflammatory cytokine effects on the oral mucosa and gingiva [47][48][49][50][51][52][53][54].
Figure 3. Pro- and anti-inflammatory cytokine effects on alveolar bone [47][48][49][50][51][52][53][54].
Table 2. Pro- and anti-inflammatory cytokines.
Table 3. Molecular factors in peri-implantitis and their function [47][48][49][50][51][52][53][54].


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