Peri-implant diseases require an extensive approach that includes pre-operative risk assessment, patient education on oral hygiene, and ensuring sufficient tissue support and accurate implant placement. Treatment typically starts with comprehensive decontamination using mechanical debridement, chemical agents, and advanced therapies such as laser or photodynamic therapy. Depending on the severity of the disease and the extent of bone loss, surgical strategies are adapted, ranging from less invasive access surgery in initial stages to more intensive resective or regenerative procedures in advanced cases. The following article will present a holistic and systematic approach to managing periimplantitis.
Key points
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Peri-implantitis is a biofilm driven inflammatory condition affecting the soft and hard tissues around dental implants. Unlike peri-mucositis, it is irreversible. It progresses more aggressively than periodontitis due to the lack of a natural protecting barrier.
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Identifying and managing risk factors such as poor oral hygiene, periodontal disease, smoking, diabetes, and hyperfunction are essential in preventing peri-implantitis.
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Oral hygiene training and long-term maintenance are crucial for preventing and effectively managing peri-implantitis.
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The initial non-surgical management of peri-implantitis includes comprehensive implant decontamination via mechanical debridement, which can be combined with chemical agents, localized antibiotics, laser therapy, and photodynamic therapy.
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The choice of surgical method depends on the extent of bone loss and the bone defect shape. Early-stage disease may be treated with access surgery and implantoplasty, while advanced stages might require tissue resection and possibly regenerative surgery.
Introduction
Peri-implant diseases collectively describe inflammatory conditions affecting both the soft and hard tissues surrounding dental implants, primarily driven by the formation of peri-implant biofilms. The 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases and Conditions differentiates between 2 major categories of peri-implant disease: peri-implant mucositis and peri-implantitis.
Peri-implant mucositis is a reversible inflammatory condition confined exclusively to the soft tissues around the implant. It manifests with symptoms such as redness, swelling, and bleeding upon probing. Importantly, if identified early and managed appropriately, peri-implant mucositis can be resolved without any associated loss of bone around the implant site.
Peri-implantitis, on the other hand, represents a more severe state of inflammation which extends beyond the soft tissues to involve the bone surrounding the implant. This condition is marked by progressive bone loss and, if left untreated, it could precipitate the failure of the implant.
Several articles have attempted to evaluate the overall prevalence of Periimplantitis, all of which pointed out the difficulty of determining prevalence accurately considering the existing difference between researchers in determining the indicators by which the diagnosis of Periimplantitis is determined. Despite this, several different meta-analyses showed a prevalence of between 19% to 34% at the patient level, and between 12% to 20% at the implant level, a level of prevalence that indicates that Periimplantitis is a very common disease that requires broad and deep consideration.
The risk factors linked to the exacerbation of peri-implantitis encompass a previous history of severe periodontitis, inadequate plaque control, and lack of consistent post-implantation care. Associations with factors like smoking, diabetes, the presence of submucosal cement, absence of peri-implant keratinized mucosa, occlusal overload, the presence of titanium particles in peri-implant tissues, bone compression necrosis, local thermal overheating during implant placement, micromotion of the implant, biocorrosion of the implant materials and poorly positioned implants that compromise oral hygiene are recognized.
Interestingly, peri-implantitis and periodontitis, while similar, exhibit distinct differences especially in their bacterial involvement during disease maturation. The transition from a healthy implant site to one characterized by peri-implantitis involves a pathogenic shift and a notable decline in the diversity of commensal flora. Advanced bacteriologic studies show that both conditions harbor similar periodontopathic bacteria, indicating some overlap at the microbial level. However, specific disparities exist; peri-implantitis is typified by a microbial milieu dominated by anaerobic gram-negative bacteria, opportunistic organisms, and anaerobic gram-positive non-saccharolytic rods. Prominent pathogenic species such as Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Fusobacterium nucleatum, and Prevotella intermedia have been implicated in the progression and exacerbation of peri-implantitis.
Periimplantis lesions also manifest several other distinct characteristics compared to periodontal lesions, due to the several specific anatomic and biological features of dental implants versus natural teeth. Periimplantitis progresses in a nonlinear and accelerating manner, which is generally faster than the progression of periodontitis. This rapid progression is linked to the unique responses of the tissues surrounding implants.
Natural teeth are enveloped by a periodontal ligament that provides a buffering and limiting architecture against the spread of infection. In contrast, peri-implant lesions lack this structure, which means there is no natural barrier to halt the progression of inflammation. This absence leads to more direct and aggressive bone loss reaching up to the bone crest, a feature less common in periodontitis until it reaches severe stages. ,
The immune response in Periimplantitis is more intense with a greater infiltration of inflammatory cells, and in particularly plasma cells, macrophages, and neutrophils, extending deeply into the tissues. This results in a more extensive diseased area compared to periodontitis.
Lastly, the peri-implant lesions, especially under conditions of persistent biofilm presence and ineffective removal, show a tendency toward “spontaneous” progression with further bone degradation, characterizing an advanced and challenging stage of the disease that tends to be more severe than that typically seen in periodontitis.
Ultimately, peri-implant lesions are characterized by more severe and rapid disease progression, a lack of natural protective barriers, and a more aggressive inflammatory response compared to periodontal lesions. This makes Periimplantitis a particularly persistent and difficult-to-manage condition requiring stringent preventive and active therapeutic measures.
The Biofilm-Mediated Inflammation and Bone Dysregulation (BIND) hypothesis has been proposed, explicating the biological mechanisms whereby inflammatory progression in peri-implantitis is dictated by the interplay among various risk factors, genetic predispositions, bacterial diversity, and immune responses, alongside the susceptibility of the local tissue environment.
Thus, maintaining an equilibrium among the bacterial composition and mitigating known risk factors is essential for the prolonged health of peri-implant sites, often described in literature as multi-stability. Hence, the development of peri-implant diseases, particularly Periimplantitis, originates fundamentally from a disruption of this balance by unduly emphasizing one of the originally balanced factors, which results in pathologic outcomes both in the soft and hard tissues surrounding the implant ( Fig. 1 ). Effective management of Periimplantitis thus focuses on restoring and sustaining a balanced microbial ecology from one hand, and managing the risk factors systematically from the other hand, to ensure long-term implant success and stability. This holistic approach requires a comprehensive treatment strategy that not only addresses immediate microbial concerns but also considers long-term preventive measures to ensure multi-stability and peri-implant health.
Although some of the risk factors for Periimplantitis may not be changed, or the possible exogenic effect on them may be very complex over time, such as the composition of the periopathogenic bacteria in the oral cavity, most other risk factors can and should be characterized, identified, and controlled in a didactic and systematic manner.
The aim of this article is to present a systematic approach to Periimplantitis. It included a comprehensive treatment protocol and algorithm, together with diagnostic and interventional measures, specified for the different stages of treatment—before implant installation, during implant installation, and after implant installation.
Stage 1—before implant installation
The approach to Periimplantitis should begin at the stage of pre-operative evaluation with a mapping and treatment of possible risk factors for Periimplantitis. These include, among others, poor oral hygiene, history of periodontal disease, smoking, diabetes and occlusal hyperfunction.
All patients should promptly undergo oral hygiene training and be informed about the necessity of participating in a long-term oral hygiene maintenance program. Patients with inadequate oral hygiene must show improved performance prior to dental implant treatment. Additionally, the long-term economic implications of participating in the oral hygiene maintenance program should be discussed with the patients.
Patients with periodontal disease must receive treatment for their condition before implant placement. It has been shown that both severity (Stage) and rate of progression (Grade) of the periodontal disease are risk indicators for the develop Periimplantitis. Yamazaki and colleagues have reported that Periimplantitis was most common in patients with stage 4 and grade C periodontitis prior to implant installation. Therefore, it is imperative to control and reduce the severity of periodontal disease before implant placement. Implants placed near teeth affected by uncontrolled periodontal disease are highly susceptible to Periimplantitis and early implant failure. Hence, periodontal patients should be informed that periodontitis is a chronic condition that necessitates strict, long-term follow-up and may require repeated periodontal or regenerative treatments. ,
Smoking and diabetes are is widely recognized as significant etiologic factors for Periimplantitis. Their effect on the long-term outcomes of dental implants in general, and as risk factor for Periimplantitis specifically, is covered widely in another article of this issue (Mark Wang and colleagues, The effect of medical status on Long-term survival of dental implants ). For the scope of our article, we will emphasize that it is essential to ensure smoking cessation and glycemic control (HgA1C <8%) prior to proceeding with implant installation.
The inter-maxillary occlusal relationship and function play a very significant factor in implant supported dentistry. In the context of Periimplantitis we will emphasise on bruxism. Although the direct relationship between bruxism and the incidence of periimplantitis has not been proven, it has been shown that when pathologic overload (>12 kg/mm2) is applied on dental implants prior to osseointegration, it may result in peri-implant bone loss. Hence, bruxism must be taken into consideration when planning an immediate loading procedure ( Boxes 1–6 ).
| Diagnostic measure | Description |
|---|---|
| Oral Hygiene | Characterization of patient’s level of oral hygiene and his level of willingness to commit to an oral hygiene maintenance plan |
| Periodontitis | Characterization of the level of periodontal disease the patient suffers from |
| Smoking | To check if the patient smokes and if he is ready to stop smoking |
| Diabetes Mellitus | To check whether the patient suffers from diabetes Verification of fasting glycemic values Verification of updated HbA1C value |
| Occlusion and Function | Characterization the occlusal relationships and check whether the patient suffers from bruxism |
| Intervention | Description |
|---|---|
| Oral Hygiene | Explanation regarding the importance of oral hygiene maintenance plan Oral hygiene training Oral Hygiene performance assessment Professional mechanical plaque removal |
| Periodontitis | Professional periodontal treatment until periodontal disease resolution and control |
| Smoking | Advising patients regarding professional smoking secession programs |
| Diabetes Mellitus | Balance HbA1C levels below 7% |
| Occlusion and Function | Balance occlusal load below 12 kg/mm2 |
| Diagnostic measure | Description |
|---|---|
| Tissue phenotype |
|
| Occlusion |
|
| Intervention | Description |
|---|---|
| Tissue phenotype (bone) | Achieve adequate bone volume and peri implant envelope (2 mm buccal, 1 mm lingual/palatal) |
| Tissue phenotype (soft tissue) | Plan soft tissue regeneration program prior to rehabilitation |
| Occlusion |
|
| Diagnostic Measure | Description |
|---|---|
| Clinical examination |
|
| Radiographic assessment |
|
| Post treatment assessment |
|
| Intervention | Description |
|---|---|
| Mild bone loss |
|
| Moderate bone loss |
|
| Severe bone loss |
|
| Treatment failure |
|
Stage 2—during implant installation
Before addressing the treatment of periimplantitis, it is essential to highlight the proactive measures that can be implemented during the implant planning and installation stages to minimize the risk of developing periimplantitis.
Peri-implant envelope phenotype
The phenotypes of both soft tissue and bone play critical roles in the susceptibility to and management of Periimplantitis. ,
The gingival tissue forms a biological seal around the implant, which is essential for preventing bacterial invasion into the peri-implant crevice. If this soft tissue environment is compromised, the seal may become inadequate, increasing the vulnerability of the implant site to infections and subsequent inflammatory responses.
Gingival phenotypes, categorized as Type A (thin) and Type B (thick), play a critical role in peri-implant health. Type A phenotype, with gingival thickness typically ranging from 0.5 to 1.0 mm, may predispose individuals to increased risk of peri-implant soft tissue complications like recession and peri-implantitis due to its vulnerability. Conversely, Type B phenotype, characterized by gingival thickness exceeding 1.0 mm (often 1.5–2.0 mm or more), offers better protection against such complications owing to its robust nature. ,
Furthermore, inadequate width of attached gingival and keratinized tissues around implants has been linked to increased peri-implantitis risk. Notably, findings suggest that width of less than 2 mm of keratinized tissue, coupled with a minimum of 1 mm of attached gingival tissue, elevates the likelihood of peri-implantitis occurrence.
Interestingly, contrasting perspectives have emerged, suggesting that diligent oral hygiene practices may mitigate the impact of keratinized and attached gingival tissue thickness and width on peri-implantitis development.
Bone phenotype involves factors such as density, volume, and architectural integrity. The interplay between bone phenotype and peri-implantitis risk is pivotal in treatment planning.
Narrow bone width, typically less than 6 mm, may lead to bone resorption and compromised soft tissue adaptation, creating an environment conducive to bacterial infiltration and peri-implantitis development. Specifically, regardless of the implant diameter, when the bone envelope is less than 1 mm on the lingual or palatal side and 2 mm on the buccal side, studies indicate a heightened susceptibility to Periimplantitis.
In cases where there is a deficiency in the peri-implant tissue envelope, the optimal timing for tissue augmentation depends on the type of tissue involved. Bone tissue regeneration can be carried out either before or during implant placement, depending on the feasibility of achieving initial implant stability. Soft tissue augmentation may also be performed prior to implant installation but is typically conducted after implant placement and prior to the restorative phase. This sequence allows the soft tissues to stabilize and mature around the implant optimizing gingival aesthetics.
Positioning and distribution
Implant placement should follow the guidelines established by Tarnow and colleagues, requiring a minimum distance of 2 mm from adjacent teeth and 3 mm from neighboring implants.
This allows for sufficient biologic space and adequate blood supply essential for the implant health, proper distribution of mechanical forces between teeth and implants, and optimal rehabilitation that enables effective cleaning.
Ng and colleagues found that implant proximity to adjacent teeth less than 1 mm increases peri-implantitis risk due to inflammation and bone resorption, caused by poor hygiene access and improper prosthetic contour. Schuldt Filho and colleagues reported implants with less than 3 mm inter-implant distance are 3 times more likely to develop peri-implantitis, with 48.48% of these cases affected.
The decision regarding the number of implants required to rehabilitate an edentulous segment of jaw is based upon a multitude of factors including the extent and function of the dentition to be restored, the type of restoration planned, the characteristics of the opposing dentition, and the occlusal forces involved. ,
Implants should be positioned to achieve optimal occlusal force distribution and create ideal conditions for successful rehabilitation. Although not universally superior in aesthetic or biomechanical terms when compared to cemented restorations, screw-retained restorations may have advantageous characteristics in the context of peri-implantitis prevention. They simplify maintenance, reduce the risk of adhesive residue accumulation in subgingival areas, and minimize bacterial leakage at the interface of the restoration components. Consequently, implants should be positioned to enable straightforward screw retention, either via a unified insertion pathway for all implants or through angle adjustments using multi-unit abutments.
Adequate spacing and distancing between implants can also help prevent the spread of existing diseases among implants ( Fig. 2 ).
