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Peri‐Implant Diseases
Edgard El Chaar1 and Cecilia White2
1Department of Periodontics, University of Pennsylvania, Dental Medicine, Philadelphia, PA, USA
2Private practice, Princeton, NJ, USA
Introduction
The prevalence of inflammatory diseases of bacterial origin around dental implants has been very well reported in literature making it an essential component of clinical implant care (Lang and Berglundh 2011; Sanz and Chapple 2012; Shibli et al. 2008; Lindhe et al. 2008). Two clinical conditions are described: peri‐implant mucositis and peri‐implantitis, defined as the inflammation in the mucosa surrounding an implant without signs of loss of supporting bone (Lindhe et al. 2008; Zitzmann and Berglundh 2008).
Peri‐implantitis: Inflammatory disease of the soft tissues surrounding an implant, accompanied by bone loss that exceeds normal physiologic remodeling (Zitzmann and Berglundh 2008; Sanz and Chapple 2012). It is accepted that mucositis precedes peri‐implantitis (Jepsen et al. 2015) and if left untreated, peri‐implant mucositis can lead to peri‐implantitis (Jepsen et al. 2015; Costa et al. 2012).
The world workshop between the AAP and EFP in 2017 (Schwarz et al. 2018) concluded the following parameters related to peri‐implantitis:
- Peri‐implantitis is a pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri‐implant connective tissue and progressive loss of supporting bone.
- The histopathologic and clinical conditions leading to the conversion from peri‐implant mucositis to peri‐implantitis are not completely understood.
- The onset of peri‐implantitis may occur early during follow‐up and the disease progresses in a non‐linear and accelerating pattern.
- Peri‐implantitis sites exhibit clinical signs of inflammation and increased probing depths compared with baseline measurements.
- At the histologic level, compared with periodontitis sites, peri‐implantitis sites often have larger inflammatory lesions.
- Surgical entry at peri‐implantitis sites often reveals a circumferential pattern of bone loss.
- There is strong evidence that there is an increased risk of developing peri‐implantitis in patients who have a history of chronic periodontitis, poor plaque control skills, and no regular maintenance care after implant therapy. Data identifying “smoking” and “diabetes” as potential risk factors/indicators for peri‐implantitis are inconclusive.
- There is some limited evidence linking peri‐implantitis to other factors such as: post‐restorative presence of submucosal cement, lack of peri‐implant keratinized mucosa, and positioning of implants that make it difficult to perform oral hygiene and maintenance.
- Evidence suggests that progressive crestal bone loss around implants in the absence of clinical signs of soft tissue inflammation is a rare event.
Prevalence
Multiple authors have studied the prevalence of peri‐implantitis and peri‐mucositis on implant level and patient level. Differences in inclusion criteria have led to a wide range of results. Recently, Derks et al. (2016) reviewed 588 patients and 2277 implants over nine years and found:
Patient level: Mucositis: 32% Peri‐implantitis: 45% Implant level: Mucositis: 35.1% Peri‐implantitis: 24.9%. Additionally, Pimentel et al. (2018) included 147 patients with 490 implants and found: Patient level: Mucositis: 80.9% Peri‐implantitis: 19.1% Implant level: Mucositis: 85.3%, peri‐implantitis: 9.2%.
Criteria for Diagnosis of Peri‐implantitis: Case Definition
According to the 2017 World Workshop (Schwarz et al. 2018), a diagnosis of peri‐implantitis will be based on the following:
- Presence of peri‐implant signs of inflammation: redness, swelling, line or drop of bleeding within 30 seconds following probing, and/or suppuration
- Increasing probing depth as compared with probing depth values compared with measurements obtained at placement of the prosthetic superstructure
- Radiographic evidence of bone loss following initial healing (one year following prosthetic superstructure delivery)
- In the absence of previous radiographs, radiographic bone loss ≥3 mm, and/or PD ≥6 mm in combination with bleeding on probing (BOP)
Additionally, clinical and radiographic examinations are necessary to evaluate peri‐implant health (Jepsen et al. 2015; Schwarz et al. 2018). Clinical evaluation of the peri‐implant soft tissue should include assessment of the patient’s oral hygiene and the presence or absence of bacterial biofilm and visual evaluation of dental implants should be completed at least once per year including probing with a light force (∼0.25 N). Implant health is indicated by a peri‐implant probing depth of ≤5mm and an absence of bleeding on probing. Radiographic analysis requires a baseline X‐ray, preferably with the suprastructure in place, and the reference point of the implant platform will allow assessment of changes in the bone level over time.
Risk Factors
History of Periodontitis
In a study involving 80 patients with peri‐implant mucositis followed for five years, Costa et al. (2012) found the overall incidence of peri‐implantitis to be 31.2% and that periodontitis patients had significantly higher odds of developing peri‐implantitis with an odd ratio ranging from 4.1 to 9 (Costa et al. 2012; Koldsland et al. 2011; Derks et al. 2016). Complete edentulism resulted in a significant reduction of bacteria related to periodontitis and peri‐implantitis, with the exception of Aggregatibacter actinomycetemcomitans, which might indicate that key pathogens can survive without pockets (Quirynen and Van Assche 2011).
The specific diagnosis and severity of the periodontal condition can also influence the risk for peri‐implantitis. The risk ratio for failure in patients with aggressive periodontitis is significantly higher when compared with healthy patients and those with chronic periodontitis (Monje et al. 2014). Additionally, the more severe the diagnosis and those with greater probing depths were at a greater risk (Daubert et al. 2015; Pimentel et al. 2018).
Implant Maintenance
Implant success depends largely on good plaque control and regular maintenance. The incidence of peri‐implantitis in non‐maintained patients is 44% while the incidence in maintained patients is 18% (Costa et al. 2012). Tan et al. (2017) found periodontally susceptible patients following a strict periodontal maintenance program had similar peri‐implant crestal bone loss as compared with periodontally non‐susceptible subjects over six years of follow‐up. This study highlights the benefits of a strict periodontal maintenance.
Number of Implants
The number of implants a patient has also affects their risk. Patients with ≥4 implants had a greater risk of developing peri‐implantitis (Derks et al. 2016; Pimentel et al. 2018).
Clinician Experience
Implants are more successful when placed by surgical specialists as those implants placed and restored by general dentist have a greater risk with an odds ratio of 4.3 (Derks et al. 2016).
Implant Brand
Peri‐implantitis risk also varied between manufacturers with Nobel: OR 3.8 Astra: OR: 3.6 Other: OR 5.6. (Derks et al. 2016).
Smoking
Smokers had greater risk for peri‐implantitis and for implant failure (Pimentel et al. 2018; Chen et al. 2013; Johnson and Hill 2004). The mechanism for this may be: smoking negatively influences oral microbial profile, suppresses the immune system, and alters microvascular environment, leading to disrupted healing (Johnson and Hill 2004). Factors relating to the greater risk with smokers include an altered oral microbial profile, reduced tissue oxygenation caused by carbon monoxide, vasoconstrictive properties of nicotine, and its cytotoxic effects on fibroblasts and PMNs (Johnson and Hill 2004; Liddelow and Klineberg 2011).
Microbiota
The most studied risk factor for peri‐implantitis has been the microbiota (Padial‐Molina et al. 2016). Zitzmann et al. (2001) demonstrated that once plaque deposits are from implants, the signs of inflammation in the peri‐implant tissue disappeared. There have been cases where the primary causative agent in peri‐implantitis was non‐bacterial, such as the presence of irritating excess cement under the implant crown or implant fracture. However, it has been shown that these causative agents create a different ecological environment that shifts the composition of the biofilm to a more pathogenic one that is harmful to the peri‐implant tissues (Mombelli and Décaillet 2011; Wilson 2009). Therefore, the ensuing tissue destruction and bone loss is still caused by the bacteria in the plaque biofilm that has accumulated on the implant surface (Canullo et al. 2016).
Various studies have been conducted to study the composition of this microbiota. Similar bacteria to those found in periodontal disease, such as Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, Tannerella Forsythia, and Treponema. denticola have been implicated (Mombelli and Décaillet 2011; Maximo et al. 2009). Additionally, a general shift from Gram‐positive coccoid species in health to anaerobic Gram‐negative rods in peri‐implantitis was seen (Padial‐Molina et al. 2016). Successful implants contained little amounts of cultivable bacteria and they had mostly Gram‐positive coccoid bacteria. Bacteria around implants with peri‐implantitis were found at high levels and mostly consisted of Gram‐negative anaerobic rods. More specifically, there was an abundance of Fusobacterium and P. intermedia (Mombelli et al. 1987). Peri‐implantitis biofilm represents a mixed infection, with a majority consisting of diverse anaerobic Gram‐negative bacteria (Mombelli and Décaillet 2011).
Earlier literature cites periodontal pathogens as the culprits behind peri‐implantitis. However, the methods of detection involve either bacterial cultures or DNA probe analysis. Both types of methods may be biased because they involve pre‐selection of bacteria for detection. Newer techniques such as metagenomics and 16S rRNA sequencing are beginning to elucidate new bacterial species beyond periodontopathogens. These include Streptococcus, Eubacterium, Filifactor alocis, Parvimonas micra, Staphylococcus, and more (Padial‐Molina et al. 2016; Tamura et al. 2013). There have also been a number of fungi and viruses detected at higher levels around implants with peri‐implantitis (Schwarz et al. 2018).
Treatment
It has been generally accepted that peri‐implantitis is caused by microbial infection. As a result, any treatment protocol for peri‐implantitis must include decontamination of the exposed contaminated implant surface. This said, decontamination is a difficult task that is complicated by the basic structure of the implant. Most modern implants have a medium rough surface structure in order to increase the bone‐implant contact area and facilitate osseointegration. This can complicate the management of infections deep inside the peri‐implant pocket, as increased surface area and surface roughness may facilitate microbial colonization and enhance biofilm formation.
Recent evidence suggests that the surface roughness and chemical composition of the implant surface can have an impact on plaque accumulation and thus contribute to the difficulty in reducing the bacterial load to a level necessary for resolution of peri‐implant inflammation (Teughels et al. 2006).
Nonsurgical Therapy
Non‐surgical treatment should always be done prior to surgical intervention as it allows the clinician to gauge the healing response and to assess the patient’s ability to perform effective oral hygiene.
Peri‐implant Mucositis
Similar to gingivitis, symptoms of peri‐implant mucositis can be reversed via improved oral hygiene or effective removal of excess cement or other foreign material. The treatment for peri‐implant mucositis often involves mechanical debridement alone. Schenk et al. (1997) found improved results after three months with scaling with rubber cup polishing; Strooker et al. (1998) found similar results using a carbon fiber brush with rubber cup polishing; and Thöne‐Mühling et al. (2010) used plastic curettes + ultrasonic scaling.
The use of 0.12% CHX was found to be similar compared with a placebo as an adjunct to non‐surgical therapy in patients with peri‐implant mucositis (Menezes et al. 2016
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