BLOG

1.1.1 Definition

Peri-implant diseases are inflammatory conditions that affect the peri-implant tissues and are induced by peri-implant biofilms. There are two distinct conditions: peri-implant mucositis and peri-implantitis.

Peri-implant mucositis is ‘an inflammatory lesion of the peri-implant mucosa, in the absence of continuing marginal bone loss’ (Heitz-Mayfield & Salvi, 2018). It is characterized clinically by bleeding on gentle probing. Other clinical signs of inflammation may be present, such as erythema, swelling and/or suppuration, and an increase in probing depth (PD) is frequently observed in the presence of peri-implant mucositis due to oedema or a decrease in probing resistance (Berglundh et al., 2018). Peri-implant mucositis is primarily caused by a disruption of host–microbial homeostasis at the implant–mucosa interface and is a reversible condition when assessed indirectly at the host biomarker level (Heitz-Mayfield & Salvi, 2018). Additional factors associated with the onset and progression of peri-implant mucositis include biofilm accumulation, smoking and radiation therapy (Berglundh et al., 2018).

Peri-implantitis has been defined as a ‘peri-implant biofilm-associated pathological condition, occurring in tissues around dental implants, and characterized by inflammation in the peri-implant mucosa and subsequent progressive loss of supporting bone’ (Berglundh et al., 2018). Clinically, peri-implantitis sites exhibit 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 positioning of implants limiting access to oral hygiene (OH) and maintenance. 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.

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 likened 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 connective 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, peri-implantitis develop, as it is believed that peri-implant mucositis always precedes peri-implantitis (Berglundh et al., 2018; Heitz-Mayfield & Salvi, 2018).

The primary aetiological agent for peri-implantitis is also the accumulation 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 specific bacteria (Sahrmann et al., 2020) or proinflammatory cytokine profiles (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 systematic 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 mucositis and 22% (95% CI [14; 30]) for peri-implantitis (Derks & Tomasi, 2015). Another SR, comprising 47 studies, reported a prevalence 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).

1.1.4 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 diseases 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 peri-implantitis concluded that pain levels were low to moderate and most pronounced in the first 2 days (Norum et al., 2019).

1.1.5 Financial aspects

According to a market analysis report (Grand View Research, 2022), the global market size of dental implants is estimated at US $4.6 billion in 2022 and is expected to grow at an annual rate of around 10%, up to 2030. The increase is based upon the demand for treatment with dental implants by the population and on the widening range of clinicians providing implant therapy. It is also associated with the growing need for longer term supportive care to avoid/control biological and mechanical complications, including managing complications with implant-supported restorations and maintaining peri-implant tissue health (Alani et al., 2014). There is increasing awareness of the need to plan long-term supportive care programmes during the treatment planning phase, and of the financial, biological and legal consequences of not doing so. For example, patients may be able to cover the initial cost of dental implants and their associated restorations at the time of implant placement, when they are employed and earning a living, but the long-term cost of supportive care may not be explained clearly to patients and may impact when they are no longer economically active (Alani et al., 2014). A Swedish study of 514 subjects recently calculated such costs (Karlsson et al., 2022), including the costs of preventive measures and of procedures to treat implant complications, over a period of 8.2 years. The mean cost ranged from €878 (single-tooth restoration) to €1210 (full-arch restoration), the larger proportion of the cost being for prevention (€741), while implant loss was the most expensive complication (€1508), followed by peri-implantitis (€1244).

A cost-effectiveness analysis was undertaken to assess preventive, non-surgical and surgical interventions (Schwendicke et al., 2015), with the model assuming that each implant was followed for 20 years. The annual provision of SPIC was dichotomized and the risk profile of patients was also considered, with implant loss and cost as primary outcomes. For management of peri-implantitis, 11 approaches (non-surgical and surgical instrumentation alone or with adjuncts) were compared. The authors concluded that, within the limitations of their study methodology, not providing annual SPIC increased the risk of peri-implant diseases. Conversely, providing SPIC could prevent or delay the onset of disease and was cost-effective, especially in high-risk groups.

Cost-effectiveness has also been evaluated for non-surgical treatment approaches of peri-implantitis (Listl et al., 2015). Change in PD was the primary outcome when comparing eight interventions. Instrumentation alone, use of an air-polishing device, or combining instrumentation with local antiseptics/antibiotics provided better value for money than Er:YAG laser, a specific ultrasonic device (Vector®), photodynamic therapy (PDT) or instrumentation combined with chlorhexidine.

Of relevance is the cost comparison of SPIC with that of the supportive care of teeth. This was assessed in a private practice in Norway (Fardal & Grytten, 2013) in 43 patients with 847 teeth and 119 implants. The mean number of ‘disease-free years’ was 8.66 for implants, 9.08 for neighbouring teeth, and 9.93 for teeth on the contra-lateral side of the mouth, with no statistically significant differences. However, due to the high prevalence of peri-implantitis, the extra cost of maintaining implants was five times higher than for teeth.

Finally, financial considerations should include the economic impact of edentulism. While not yet clearly established, at least two factors may support its importance: firstly, the need for rehabilitation and the associated costs; secondly, and in case of lack of rehabilitation, the negative consequences for quality of life, nutrition, systemic health and well-being. In addition, it is also widely contended that individual- and community-level social inequalities strongly impact on levels of edentulism (Ito et al., 2015).