AO/AAP consensus on prevention and management of peri‐implant diseases and conditions: Summary report

Abstract

Background

The exponential increase in dental implant use has led to a parallel rise in peri‐implant diseases (PID), adversely affecting implant therapy success and patient quality of life. Efforts have been made by the dental community to understand systemic, behavioral, and site‐level risk factors involved in the etiologies and pathogenesis of PID and conditions and to develop standardized treatment protocols for the management of these clinical entities. The 2024 Academy of Osseointegration/American Academy of Periodontology (AO/AAP) consensus aimed to integrate the best available evidence and expert opinion into a unified framework for the prevention and management of PID and conditions.

Methods

Focused questions were previously addressed in eight systematic reviews that were grouped into two main topics. Group 1 evaluated systemic and local risk factors/indicators for the development of peri‐implant mucositis and peri‐implantitis, peri‐implant soft tissue deformities, as well as prosthetic factors associated with peri‐implant marginal bone loss. Group 2 focused on therapeutic strategies for the management of PID, encompassing nonsurgical debridement, implant surface decontamination methods, and surgical interventions (both nonreconstructive and reconstructive). Structured consensus discussions were held during an on‐site meeting in Oak Brook, Illinois (August 14–16, 2024) to inform evidence‐based recommendations.

Results

A plethora of systemic, behavioral, and local factors may play a pivotal role in the onset and progression of PID and conditions. Key systemic and behavioral risk factors include history of periodontitis, smoking, uncontrolled diabetes, poor microbial biofilm control, and obesity, while implant malposition, unfavorable prosthetic factors, and suboptimal peri‐implant soft tissue phenotypical features are relevant site‐related factors. Peri‐implant mucositis may be effectively managed with nonsurgical debridement and control of risk factors. This possibly represents the first step of treatment of peri‐implantitis, whereas more advanced cases require individualized surgical approaches, ranging from flap‐for‐access, resective, reconstructive, or soft tissue augmentation procedures. Supportive peri‐implant maintenance is essential for long‐term peri‐implant tissue stability and health.

Conclusions

An evidence‐based flow diagram combined with expert opinion was generated for clinicians to manage PID and conditions, emphasizing early risk factor identification, tailored treatment protocols, and continued maintenance to optimize long‐term implant therapy outcomes.

INTRODUCTION

The global use of dental implants has surged significantly over recent decades, providing substantial functional and aesthetic benefits to over one million patients annually around the world. ¹ , ² , ³ This widespread adoption, however, has concurrently heightened the incidence of long‐term peri‐implant biological complications, creating a growing public health concern. ⁴ , ⁵ , ⁶ In essence, peri‐implant diseases (PID) are primarily biofilm‐mediated inflammatory conditions that compromise the integrity of both soft and hard peri‐implant tissues around implants. ⁷ , ⁸ , ⁹ Specifically, peri‐implant mucositis is a reversible inflammatory lesion of the peri‐implant mucosa, in the absence of marginal bone loss (MBL) beyond the initial biological bone remodeling. ¹⁰ Clinically, this is characterized by bleeding on gentle probing, and variable presence of erythema, swelling, and/or suppuration (SUP), ⁹ and can evolve into peri‐implantitis if not properly addressed. ⁹ , ¹⁰ Peri‐implantitis is characterized by a persistent inflammation of the peri‐implant mucosa and subsequent loss of supporting bone ⁹ that can jeopardize implant stability and long‐term success. ¹¹ When compared with periodontitis, bone loss associated with peri‐implantitis tends to progress faster, following a nonlinear accelerating pattern. ⁹ , ¹² Additionally, peri‐implant conditions that may mimic or share certain clinical features with biofilm‐associated PID are also a major concern in contemporary clinical practice. ¹³ For example, a suboptimal peri‐implant soft tissue phenotype ¹⁴ may predispose to the occurrence of peri‐implant soft tissue dehiscences (PSTD), ¹⁵ which may result in partial exposure of the transmucosal prosthetic components or even the implant surface, compromising esthetics and increasing the risk for the onset and a more rapid progression of PID. ¹⁶ , ¹⁷ , ¹⁸

Epidemiological studies have reported that peri‐implant mucositis affects approximately 43%–47% of implant patients, whereas peri‐implantitis is observed in 20%–22% of patients. ¹⁹ , ²⁰ , ²¹ , ²² , ²³ These findings underscore an imperative need for early identification of risk factors and the formulation of preventive strategies prior to implant placement. ¹² , ²⁴ Peri‐implant biofilms are considered the primary etiological factor in the onset and progression of PID. ⁹ However, a robust body of scientific evidence has delineated various systemic conditions, behavioral aspects, and site‐specific characteristics as possible risk factors/indicators for PID development, such as previous history of periodontitis, ²⁵ , ²⁶ , ²⁷ diabetes and obesity, ⁷ , ⁸ smoking, ²⁸ , ²⁹ and heavy alcohol consumption, ²⁹ , ³⁰ as well as lack of enrollment in a preventive maintenance program. ³¹ Furthermore, recent studies have highlighted the influence of surgical variables, such as implant malposition, as a risk factor for the onset and progression of PID. ³² , ³³ , ³⁴ , ³⁵ Additionally, prosthetic parameters, such as abutment height ³⁶ , ³⁷ or restorative emergence angle and profile, ³⁸ , ³⁹ , ⁴⁰ have been linked to increased risk for peri‐implant MBL. Conversely, certain prosthetic design modifications appear to offer a protective effect by facilitating oral hygiene, reducing peri‐implant inflammation ⁴¹ , ⁴² and subsequently MBL. ⁴³ An in‐depth understanding of these variables is essential for proper case selection and optimal implant treatment planning aimed at minimizing the risk of PID ² , ²¹ as well as conditions such as PSTD. ¹⁵ , ⁴⁴ , ⁴⁵

Implant therapy should be substantiated on a preventive mindset ³³ , ⁴⁶ due to the lower predictability of achieving success when treating PID compared to periodontal diseases, such as periodontitis. ⁶ , ⁴⁷ , ⁴⁸ Nonetheless, once the disease is established, therapeutic strategies can be broadly categorized into nonsurgical and surgical approaches. ⁶ , ⁴⁹ Nonsurgical therapy primarily involves debridement using various devices, with possible adjuncts such as antiseptics ⁵⁰ or antibiotics, ⁵¹ each demonstrating a variable degree of efficacy. ⁵² Nonsurgical debridement remains the primary approach for the treatment of peri‐implant mucositis, ²⁴ , ⁴³ although its effectiveness may vary significantly. ⁵³ , ⁵⁴ Addressing other contributing factors (e.g., smoking, improper prosthetic design, deficient oral hygiene) is also a necessary step of treatment. ⁵³ , ⁵⁵ , ⁵⁶ Evidence suggests that adjunctive therapies, while beneficial for biofilm reduction, may not provide significant advantages over debridement alone for long‐term outcomes. ⁵⁷ , ⁵⁸ , ⁵⁹ , ⁶⁰

Surgical interventions are generally subdivided into nonreconstructive and reconstructive techniques, with the common goals of achieving effective implant surface decontamination, reducing peri‐implant pocket depth, and, in some cases, obtaining bone reconstruction. ⁴⁹ , ⁶¹ , ⁶² , ⁶³ , ⁶⁴ Nonreconstructive surgeries, such as flap‐for‐access and osseous resective surgeries, aim to provide access to facilitate biofilm removal and implant surface decontamination, as well as pocket depth reduction, though disease resolution still remains a challenge in some cases. ⁶⁵ , ⁶⁶ , ⁶⁷ In contrast, reconstructive surgeries aim to obtain bone gain and restore peri‐implant bone architecture ⁶⁸ , ⁶⁹ either alone or in combination with simultaneous soft tissue augmentation. ³⁴ , ⁷⁰ , ⁷¹ , ⁷² These techniques have shown potential in achieving greater pocket depth reduction and peri‐implant bone gain, but have also shown limited impact on reducing signs of mucosal inflammation and preventing disease recurrence. ⁴³ , ⁶⁵ , ⁷³ , ⁷⁴ Adjunctive pharmacotherapy, such as the use of antiseptics ⁷⁵ , ⁷⁶ or antibiotics, ⁷⁷ , ⁷⁸ has also been proposed in conjunction with surgical therapy, but there is limited evidence supporting their added value. ⁷⁹

A central challenge across all PID treatment modalities is achieving adequate decontamination of the implant surface. ⁸⁰ This is due to the intricate macroscopic design and microscopic surface features of most modern implants. ⁸¹ In pursuit of optimal decontamination protocols, various approaches have been investigated to eradicate biofilms without compromising the implant surface integrity or its reosseointegration potential. ⁷⁹ , ⁸² , ⁸³ Multiple studies have compared the efficacy of diverse decontamination methods, such as the use of curettes, ultrasonic devices, pharmacotherapeutics (e.g., chlorhexidine and citric acid), air‐polishing systems, implantoplasty, antimicrobial photodynamic therapy (aPDT) and lasers, either as monotherapies or in combination. ⁵⁴ , ⁶⁵ , ⁷⁸ , ⁷⁹ , ⁸⁴ , ⁸⁵ All of these methods have demonstrated a variable degree of effectiveness with regard to complete biofilm removal; therefore, no “gold standard” method has been identified yet. ⁶ , ⁶¹ , ⁸⁰

The goal of this consensus was to synthesize the most relevant available evidence regarding the epidemiology, risk factors/indicators, and management of PID and conditions. This evidence, together with expert opinion, aimed to develop a framework for clinicians to make informed decisions to prevent the occurrence of PID by identifying key risk factors and, if the disease is already established, achieve predictable treatment outcomes.

METHODS

A consensus meeting was jointly organized by the American Academy of Periodontology (AAP) and the Academy of Osseointegration (AO) to critically evaluate and synthesize the most relevant evidence with the purpose of addressing critical questions regarding risk assessment and management of PID. The objective of this meeting was to develop an evidence‐based framework to identify risk factors/indicators, both at patient and site levels, as well as to propose comprehensive treatment recommendations and decision‐making tools for the management of PID and their sequelae.

This event, held in Oak Brook (Illinois, USA) from August 14–16, 2024, brought together a panel of international leading experts with extensive clinical and research experience in both PID risk assessment and management. Participants were divided into two groups. Group 1 focused on defining subject‐ and site‐level risk profiles associated with the onset and progression of PID and peri‐implant associated defects, while Group 2 was given the task of developing risk‐stratified treatment protocols based on current scientific evidence and clinical best practices.

Systematic assessment of evidence

To ensure a robust and systematic approach, each group was assigned four focused research questions, which were addressed through systematic reviews (SR) that were conducted by a designated leader in collaboration with other experts before the consensus meeting took place. Meta‐analyses (MA) were performed whenever feasible. The results of these SR served as the foundation for the consensus discussions and deliberations.

Expert opinion‐based consensus

At the consensus meeting, the main methodological aspects and findings of each SR were initially presented in a plenary session by the group chairs. The available evidence was categorized as:

1. High quality: evidence from high‐quality studies, both statistically significant (p < 0.05) and clinically relevant (odds ratio [OR] > 2).

2. Moderate quality: evidence from two or more low‐strength studies with consistent findings or a single moderate‐quality study that was either statistically significant (p < 0.05) or clinically relevant (OR > 2).

3. Low or unknown quality: lacking or low‐level relevant evidence, which led to recommendations primarily based on expert opinion.

A more detailed description of the quality‐of‐evidence categories can be found in the Group 1 paper. ⁸⁶

Panel members critically appraised the presented evidence and contrasted it with their experiential knowledge. Evidence from the SR was used to formulate questions by the respective group chairs, which were presented to the panel of experts in a plenary session. In this session, 44 experts (including the chairs) voted on their level of agreement with the presented statements. The degree of consensus was classified based on the agreement of the panelists (whether they agreed, disagreed, remained neutral, or abstained) according to the following grading system: unanimous (100% agreement), strong consensus (>95% of the participants), consensus (75%–95%), simple majority (50%–74%), or no consensus (<50%). This grading system was used to classify the recommendations, which later were employed to construct the clinical translation outcomes of this meeting, as previously stated: risk assessment tools ⁸⁶ and charts for clinical decision‐making ⁸⁷ .

RESULTS

A summary of the consensus plenary session is presented hereby, grouped by the original focused questions and answers based on the most relevant evidence contained in the SR from both working groups, as well as other relevant focused questions regarding the management of PID. For each focused question, a brief summary of the main findings of each individual SR is presented. ⁸⁸ , ⁸⁹ , ⁹⁰ , ⁹¹ , ⁹² , ⁹³ , ⁹⁴ , ⁹⁵ Expert opinions, when pertinent, and the results of the consensus are subsequently reported. This information was employed by members of Group 1 to identify key risk factors/indicators and propose clinical recommendations for risk management ⁸⁶ and by members of Group 2 to formulate flow diagrams to guide clinical decision‐making when managing PID and establishing personalized maintenance protocols ⁸⁷ .

Group 1 topic: Risk factors for peri‐implant diseases

Evidence search strategy

Four SR with subsequent MA were performed to address (1) patient‐related systemic diseases and conditions, (2) surgical‐ and implant‐related factors, (3) prosthetic design‐related factors, and (4) soft tissue‐related factors that may play a role in the onset and/or progression of PID:

1. Galarraga‐Vinueza et al. 2025—Prevalence, incidence, systemic, behavioral, and patient‐related risk factors and indicators for PID: The aim of this SR was to assess the overall incidence and prevalence of PID as well as the influence of systemic, behavioral, and patient‐related risk factors and indicators for PID. A total of 102 studies met the eligibility criteria. ⁸⁸

2. Monje et al. 2025—Surgical and implant‐related factors and onset/progression of PID: The aim of this SR was to identify and analyze surgical and implant‐related factors that play a role in the onset/progression of PID. A total of 33 studies were included. ⁸⁹

3. Lin et al. 2025—The influence of prosthetic design‐related factors on peri‐implant MBL: The aim of this SR was to evaluate the effect of prosthetic design‐related variables on peri‐implant MBL. Clinical studies with follow‐ups of 12 months or greater and reporting MBL associated with any possible component of the implant–abutment connection or prosthetic design were included, identifying a total of 93 studies. ⁹⁰

4. Tavelli and Barootchi 2025—Prevalence, incidence, and risk and protective factors for soft tissue dehiscences at implant sites in the absence of disease: The aim of this SR was to evaluate the prevalence and incidence of PSTD in absence of PID and to identify risk and protective factors. A total of 221 studies were selected. ⁹¹

Further methodological information regarding the conduction of each systematic review can be found within the original publications. ⁸⁸ , ⁸⁹ , ⁹⁰ , ⁹¹

Focused Question 1: Risk markers for peri‐implant mucositis

1. Summary of the scientific evidence—Galarraga‐Vinueza et al. 2025 ⁸⁸

   MA on peri‐implant mucositis reported a 5‐year, 10‐year, and 20‐year patient‐level incidence of 46% (95% CI 25%–68%), 61% (95% CI 56%–65%), and 53% (95% CI 36%–65%), respectively. Local and systemic factors can influence the risk of peri‐implant mucositis. Behavioral, patient‐related, and systemic risk markers that were considered included smoking, history/active periodontitis, diabetes mellitus, and obesity. Smoking significantly affects mucosal barrier function, immune response, and peri‐implant sulcus microbiota, with a notable association with peri‐implant mucositis (OR 1.47; 95% CI 1.06–2.07; I ² = 63.7%) in active or former smokers (<10 years after quitting). History of periodontitis and active periodontitis were significantly associated with peri‐implant mucositis presenting an effect summary of (OR 1.68; 95% CI 1.04–2.74; I ² = 80.1%) and (OR 3.12; 95% CI 2.51–3.89; I ² = 0.0%), respectively. No significant association was observed for diabetes mellitus (OR 1.54; 95% CI 0.9–2.64; I ² = 82.3%; Egger test p = 0.004), but obesity (OR 3.29; 95% CI 1.75–6.17; I ² = 1.93%; Egger test p = 0.716) was identified as a significant risk marker for mucositis. These findings underscore the multifactorial etiology of PID.

2. Expert opinions based upon the plenary voting outcomes: Peri‐implant mucositis

   • ‐
     Soft tissue phenotype plays a role in the risk for peri‐implant mucositis: consensus (83% agreed, 5% neutral, 12% abstained)
   • ‐
     Obesity is associated with a higher risk for peri‐implant mucositis: simple majority (61% agreed, 29% neutral, 10% disagreed)
3. Evidence‐based risk markers for peri‐implant mucositis

   • ‐
     Current or former smoking (<10 years of quitting): high risk (statistically and clinically significant; consensus was not reached)
   • ‐
     History of periodontitis: high risk (statistically and clinically significant; consensus was reached)
   • ‐
     Active periodontitis: high risk (statistically and clinically significant; consensus was not reached)
   • ‐
     Thin soft tissue phenotype: moderate risk (statistically and clinically significant; consensus was reached)
   • ‐
     Obesity and/or metabolic syndrome: moderate risk (statistically and clinically significant; consensus was not reached)
   • ‐
     Alcohol consumption (>7 U/week in women, >14 U/week in men): low risk (statistically and clinically not significant; consensus was not reached)
4. Evidence‐based clinical considerations for peri‐implant mucositis

   • ‐
     Consider delayed implant placement using a surgical guide, using a flapless approach when feasible.
   • ‐
     Consider soft tissue augmentation prior to or during implant placement in sites of high esthetic demand and those presenting unfavorable phenotypical features.
   • ‐
     Consider smoking status when planning implant treatment. Strongly recommend smoking cessation prior to implant placement and provide support for quitting. Regular follow‐ups and thorough plaque control strategies are critical in smokers.
   • ‐
     Periodontitis patients should undergo thorough periodontal treatment and achieve disease stability before implant placement. Long‐term maintenance programs and frequent monitoring are key to manage the risk of recurrence.
   • ‐
     Weight monitoring and healthy lifestyle promotion should be part of implant therapy for patients with obesity and/or metabolic syndrome, with peri‐implant maintenance being especially relevant in these patients.

Focused Question 2: Risk markers for peri‐implantitis

1. Summary of the scientific evidence: Patient‐related factors—Galarraga‐Vinueza et al. 2025 ⁸⁸

   MA revealed a weighted mean 5‐year, 10‐year, and 20‐year incidence of peri‐implantitis of 12% (95% CI 7%–19%), 14% (95% CI 9%–20%), and 22% (95% CI 11%–36%), respectively. Higher incidence rates were observed in patients with a history of periodontitis, complete edentulism, and erratic compliance for in‐office maintenance visits. Smoking, diabetes mellitus, and alcohol consumption significantly increase peri‐implantitis risk. Smoking negatively influences mucosal barriers, immune function, and peri‐implant sulcus microbiota (OR 2.27; 95% CI 1.68–3.06; I ² = 65.2%; Egger test p = 0.4827). Diabetes mellitus was significantly associated with peri‐implantitis (OR 2.31; 95% CI 1.59–3.32; I ² = 9.88%; Egger test p = 0.2835). Alcohol consumption was also identified as a significant risk indicator for peri‐implantitis (OR 2.07; 95% CI 1.49–2.85; I ² = 0.00%; Egger test p = 0.271); however, evidence supporting this association remains limited compared to the aforementioned factors.

   Periodontitis and peri‐implantitis share some etiological factors, immunoinflammatory pathways, and pathogenesis mechanisms. Thus, both active periodontitis and history of periodontitis can increase the risk for peri‐implantitis. A history of periodontitis and active periodontitis were significantly associated with peri‐implantitis (OR 2.92; 95% CI 2.05–4.13; I ² = 61.4% and OR 4.05; 95% CI 3.06–6.35; I ² = 1.4%, respectively). Higher peri‐implantitis rates were reported in longitudinal studies in patients with a history of periodontitis. Preventive strategies addressing key systemic factors are essential to mitigate the risk of PID development.

2. Summary of the scientific evidence: Surgical and implant‐related factors—Monje et al. 2025 ⁸⁹

   The available evidence, which was presented as a narrative review due to the heterogeneity of the included studies, underscores that local surgical and implant‐related parameters critically influence both the onset and the progression of peri‐implant diseases, particularly in patients with a history of periodontitis. Notably, improper implant positioning—whether in the buccolingual, mesiodistal, or apicocoronal dimensions—has been consistently associated with a markedly elevated risk of peri‐implantitis, with investigations reporting an OR as high as 48.2 for malpositioned implants. In addition, implants placed too subcrestally have been linked to increased occurrences of peri‐implant mucositis (with OR around 5.33 in periodontally compromised individuals), and those positioned excessively far from adjacent anatomical landmarks (distance of ≥6 mm from the midfacial cementoenamel junction [CEJ] of the adjacent tooth) appear to further predispose to peri‐implantitis, with OR up to 8.5.

   Beyond these three‐dimensional position factors, the characteristics of the peri‐implant soft tissues also play an essential role in the onset and progression of PID, with studies showing correlation between a thicker crestal soft tissue profile and a lower risk of PID, whereas others demonstrate a beneficial effect of adjunctive soft tissue grafting. With respect to implant‐specific design, data derived from comparative studies did not display superiority for any implant macro‐ or microdesign characteristics regarding the onset and progression of PID. However, a diminished distance from the prosthetic margin to the crestal bone has emerged as a potential risk factor, thereby suggesting a rationale for the preferential use of tissue‐level implants or transmucosal abutments in select cases. All of these factors become more relevant in patients who have a predisposition to PID development due to a history of periodontitis or active periodontitis.

3. Expert opinions based upon the plenary voting outcomes: Peri‐implantitis

   • ‐Uncontrolled or poorly controlled diabetes mellitus is associated with a higher risk of peri‐implantitis: consensus (95% agreed, 2.5% neutral, 2.5% abstained).
   • ‐Depression and consumption of antidepressants are associated with a higher risk of peri‐implantitis: consensus (93% agreed, 2% neutral, 5% abstained).
   • ‐History of periodontitis is a risk factor for peri‐implantitis: consensus (90% agreed, 5% neutral, 5% abstained).
   • ‐Inadequate mesio‐distal interimplant distance is a risk of peri‐implantitis: consensus (93% agreed, 2% neutral, 5% abstained).
   • ‐Implant macro‐ and microdesign may influence the risk of onset/progression of peri‐implantitis: consensus (93% agreed, 2% neutral, 5% abstained).
   • ‐Peri‐implant mucositis is a predisposing factor of peri‐implantitis: consensus (80.5% agreed, 2.5% disagreed, 17% abstained).
   • ‐Soft tissue phenotype plays a role in the risk for peri‐implantitis: consensus (80.5% agreed, 2.5% disagreed, 17% abstained).
   • ‐Obesity is associated with a higher risk for peri‐implantitis: no consensus (44% agreed, 31% neutral, 20% disagreed, 5% abstained).
   • ‐Implants placed in sites that underwent bone augmentation are more susceptible to peri‐implantitis: no consensus (36.5% agreed, 12% neutral, 46.5% disagreed, 5% abstained).
   • ‐Hypertension is associated with a higher risk for peri‐implantitis: no consensus (34% agreed, 32% neutral, 34% abstained).

4. Evidence‐based risk markers for peri‐implantitis

   • ‐Implant malposition: high risk (statistically and clinically significant; consensus was reached)
   • ‐History of periodontitis: high risk (statistically and clinically significant; consensus was reached)
   • ‐Active periodontitis: high risk (statistically and clinically significant; consensus was reached)
   • ‐Uncontrolled diabetes: high risk (statistically and clinically significant; consensus was reached)
   • ‐Current or former smoker: high risk (statistically and clinically significant; consensus was reached)
   • ‐Interimplant distance <3 mm: moderate risk (clinically significant; consensus was reached)
   • ‐Implant platform >6 mm apical to adjacent tooth midfacial CEJ: moderate risk (statistically and clinically significant; consensus was reached)
   • ‐Placement of implant in limited width of bone: moderate risk (statistically and clinically significant; consensus was reached)
   • ‐Close proximity of the implant abutment/prosthetic interface to the bone: moderate risk (statistically and clinically significant; consensus was reached)
   • ‐Obesity and/or metabolic syndrome: moderate risk (statistically not significant and clinically significant; consensus was reached)
   • ‐Depression or antidepressant medication: moderate risk (statistically not significant and clinically significant; consensus was reached)

5. Evidence‐based clinical considerations for peri‐implantitis

   • ‐Proper implant treatment planning should be performed.
   • ‐Guided implant placement surgery is beneficial, especially in complex scenarios.
   • ‐Interimplant distance of >3 mm and implant platform <6 mm apicocoronal distance from the adjacent tooth midfacial CEJ should be respected in the absence of transmucosal abutments.
   • ‐When placing implants in sites with limited bone width, future bone remodeling as well as narrow diameter implants should be considered during treatment planning.
   • ‐Tissue‐level implants or transmucosal abutments may contribute to prevent MBL.
   • ‐Periodontitis patients should receive thorough periodontal treatment and achieve periodontal stability before implant placement. Personalized maintenance programs including frequent monitoring are essential to prevent periodontitis recurrence.
   • ‐For diabetic patients, collaboration with the patient's primary care provider is essential as glycemic levels should be well controlled in the context of implant therapy. Regular follow‐ups and strict oral hygiene protocols are critical in uncontrolled or poorly controlled diabetics.
   • ‐Smoking cessation is strongly recommended prior to initiating implant therapy. Regular follow‐ups and strict oral hygiene protocols are critical in smokers.
   • ‐Weight monitoring and healthy lifestyle promotion should be part of dental care, including implant therapy.
   • ‐Signs of depression or chronic stress should be detected and appropriate treatment, including referrals to mental healthcare professionals, should be implemented accordingly. Implant therapy should be delayed until amelioration of symptoms, and frequency of maintenances should be increased in these patients.

Focused Question 3: Risk markers for peri‐implant MBL after functional loading

1. Summary of the scientific evidence—Lin et al. 2025 ⁹⁰

   Following the connection of a transmucosal component (e.g., healing abutment or final prosthetic restoration), physiologic remodeling of the peri‐implant marginal bone may occur as part of the establishment of the supracrestal soft tissue dimension. However, this process may be influenced by a variety of factors, which may lead to additional peri‐implant MBL. Marginal bone level changes during the initial physiologic bone remodeling (12 months after loading) ⁹ can be multifactorial, including but not limited to prosthetic design variables, surgical planning, and biofilm accumulation.

   Adequate buccal and lingual bone thickness can act as a protective factor against MBL. Thus, clinicians should ensure optimal prosthetically driven implant positioning, leaving the implant circumferentially encased in sufficient bone, as well as with sufficient primary stability. Moreover, adequate mesiodistal distance between the implant and adjacent teeth/implants and proper apicocoronal position of the implant platform are also essential to facilitate the fabrication of restorations that minimize the risk for MBL and PID. Key protective prosthetic design considerations include emergence profiles, abutment height, and implant platform characteristics. A transmucosal abutment height of ≥2 mm is normally associated with an adequate supracrestal tissue height and an optimal restorative emergence profile. This can facilitate effective oral hygiene, which becomes especially critical for patients with limited manual dexterity, poor oral hygiene habits, or a history of periodontitis, among other factors addressed in previous sections of this article.

2. Expert opinions based upon the plenary voting outcomes: MBL

   • ‐
     Transmucosal angle >30° increases the risk for MBL: consensus (92% agreed, 8% disagreed).
   • ‐
     Convex implant abutment profile increases the risk for MBL in bone level implants: consensus (92% agreed, 5% neutral, 3% disagreed).
   • ‐
     Transmucosal abutment height ≥2 mm decreases the risk for MBL: consensus (85% agreed, 5% neutral, 5% disagreed, 5% abstained).
   • ‐
     When the implant–abutment/prosthetic interface is in close proximity to the crestal bone it leads to MBL: consensus (83% agreed, 5% neutral, 5% disagreed, 7% abstained).
   • ‐
     Concave implant abutment profile decreases risk for MBL in bone level implants: consensus (78% agreed, 16% neutral, 5% disagreed, 1% abstained).
   • ‐
     Platform‐switched abutments lower the risk for MBL: consensus (85.3% agreed, 9.8% disagreed, 4.9% abstained).
   • ‐
     Splinted implants are associated with a higher risk for MBL: consensus (80% agreed, 10% disagreed, 7.5% neutral, 2.5% abstained).
3. Evidence‐based risk markers for MBL

   • ‐
     Platform‐matched abutments: high risk (statistically and clinically significant; consensus was reached).
   • ‐
     Transmucosal abutment height <2 mm: high risk (statistically and clinically significant; consensus was reached).
   • ‐
     Transmucosal emergence angle >30° in bone level implants: high risk (statistically significant; consensus was reached).
   • ‐
     Residual submucosal cement: high risk (statistically and clinically significant; consensus was not reached).
   • ‐
     Splinted implant restorations: moderate risk (statistically significant; consensus was reached).
4. Evidence‐based clinical considerations for MBL

   • ‐
     In bone‐level implants, an implant placed too shallow may compromise the ability of the restorative clinician to provide an implant‐supported prosthesis with favorable features, including a transmucosal abutment height of at least 2 mm.
   • ‐
     Interimplant distance should be ≥3 mm.
   • ‐
     Screw‐retained implant‐supported prostheses are preferred. If a crown needs to be cemented, zinc oxide or glass ionomer cements should be used to facilitate radiographic identification and excess cement must be removed.

Focused Question 4: Risk markers for peri‐implant soft tissue dehiscences/discrepancies

1. Summary of the scientific evidence—Tavelli and Barootchi 2025 ⁹¹

   PSTD are an emerging clinical concern, especially in patients with high esthetic expectations, as even minor exposure of the implant/abutment can significantly impact the perceived success of treatment. The primary goal of this SR was to assess the prevalence and incidence of soft tissue dehiscence (“recession”) at implant sites in the absence of PID, defined as follow or as defined in the individual studies:

   • ‐
     PSTD: apical position of the peri‐implant soft tissue margin in relation to the CEJ of the homologous contralateral tooth
   • ‐
     Mucosal recession (MREC): presence of a mucosal cleft that exposes the implant shoulder, prosthetic abutment, or implant surface
   • ‐
     Apical shift of the mucosal level (ASML): progressive apical shift of the soft tissue margin over time compared to the position of the mucosal level at crown delivery

   Mean incidence of PSTD was reported at 33.3% within 1 year, 38.3% between 3–5 years, and 64.5% beyond 5 years. MREC incidences ranged from 47.8% within 1–3 years to 45.7% in 3–5 years. ASML incidence was 15.3% within the first year and 35.1% after 5 years. The statistical analysis revealed that limited mucosal thickness, lack of soft tissue augmentation, inadequate keratinized mucosa width and interproximal MBL were risk factors for PSTD, MREC, and ASML. Similarly, soft tissue augmentation, adequate mucosal thickness, adequate keratinized mucosa width, digitally guided implant therapy, and bone grafting at the time of implant placement were protective factors against these conditions. Preventive strategies targeting these contributing factors are vital to mitigate soft tissue defects and enhance patient‐reported outcomes.

2. Expert opinions based upon the plenary voting outcomes: Peri‐implant soft tissue dehiscence/discrepancies

   • ‐
     Thin peri‐implant mucosa or inadequate keratinized mucosa width increases the risk for PSTD: strong consensus (95% agreed, 2.5% neutral, 2.5% abstained)
   • ‐
     Improperly positioned implants increase the risk for PSTD: consensus (90% agreed, 2.4% neutral, 7.6% abstained).
   • ‐
     Placing implants in the presence of inadequate or limited keratinized mucosa width increases the risk for PSTD: consensus (80.5% agreed, 5% neutral, 5% disagreed, 9.5% abstained)
   • ‐
     Immediate implant placement increases the risk for PSTD: no consensus (26% agreed, 4% neutral, 70% disagreed)
3. Evidence‐based risk markers for PSTD

   • ‐
     Facially positioned implant: high risk (statistically and clinically significant; consensus was reached)
   • ‐
     Convex emergence profile: high risk (statistically and clinically significant; consensus was reached)
   • ‐
     Buccal bone dehiscence: high risk (statistically and clinically significant; consensus was not reached)
   • ‐
     Keratinized mucosa width <2 mm: high risk (statistically and clinically significant; consensus was reached)
   • ‐
     Thin facial mucosa: high risk (statistically and clinically significant; consensus was reached)
   • ‐
     Interproximal MBL: high risk (statistically and clinically significant; consensus was not reached)
   • ‐
     Facially positioned (proclined sagittal implant angle): moderate risk (statistically significant; consensus was reached)
   • ‐
     Immediate implant placement: moderate risk (statistically significant; consensus was not reached)
   • ‐
     More than 5 years in function: moderate risk (statistically and clinically significant; consensus was not reached)
4. Evidence‐based clinical considerations for PSTD

   • ‐
     Dental implants should be placed in a favorable 3D position.
   • ‐
     Computer‐assisted guided implant placement is recommended.
   • ‐
     Thin buccal bone and dehiscences should be identified and addressed, if necessary, prior to or simultaneously with implant placement.
   • ‐
     Delayed implant placement could minimize the effect of some risk factors.
   • ‐
     Soft tissue augmentation with implant placement or prior to final restoration can significantly reduce the risk of esthetic complication.
   • ‐
     A flapless surgical approach should be considered.
   • ‐
     For long‐term mucosal stability, attempt to maintain interproximal bone level.

Group 2 topic: Management of PID and other implant‐related complications

Evidence search strategy

To establish an evidence‐based consensus on the management of PID and other implant‐related complications, four SR were conducted. Each review focused on different aspects of treatment of PID, including (1) nonsurgical treatment of peri‐implant mucositis, (2) implant surface decontamination strategies, and (3) nonreconstructive and (4) reconstructive surgical therapy for peri‐implantitis.

1. Lin et al. 2025—Treatment of peri‐implant mucositis: The aim of this SR was to evaluate whether adjunctive treatment modalities offer a therapeutic benefit when used in combination with conventional peri‐implant debridement for the management of peri‐implant mucositis. A total of 25 articles (for a total of 24 clinical trials) were included. ⁹²

2. Ravida et al. 2025—Efficacy of decontamination methods for biofilm removal from dental implant surfaces and reosseointegration: The aim of this SR was to assess the efficacy of different implant surface decontamination methods in removing bacterial biofilm from dental implants and their effect on reosseointegration potential. Different types of studies (animal and in vitro studies, ex vivo/in situ experiments) were included that evaluated various decontamination methods (curettes, ultrasonic tips, air‐powder abrasive devices, lasers, aPDT, chemical solutions, and electrolytic cleaning), amounting to a total of 121 studies that met the eligibility criteria. ⁹³

3. Saleh al. 2025—Efficacy of nonreconstructive surgical treatment of peri‐implantitis: The aim of this SR was to compare the effectiveness of two nonreconstructive surgical treatment modalities (i.e., access flap and osseous resective surgery) for the treatment of peri‐implantitis, including a total of 15 eligible studies (all randomized controlled trials [RCT]). ⁹⁴

4. Barootchi et al. 2025—Surgical reconstructive therapy for peri‐implantitis: The aim of this SR was to evaluate the effectiveness of reconstructive surgical therapy for the treatment of peri‐implantitis. A total of 40 publications (18 RCT and 22 non‐RCT) were included in this SR. ⁹⁵

Further methodological information regarding the conduction of each systematic review can be found within the original publications. ⁹² , ⁹³ , ⁹⁴ , ⁹⁵

Focused Question 1: Treatment of peri‐implant mucositis

1. Summary of the scientific evidence—Lin et al. 2025 ⁹²

   The SR by Lin et al. evaluated whether adjunctive treatments such as air polishing, antimicrobial photodynamic therapy (aPDT), lasers, antibiotics, local antimicrobials, and probiotics provide additional benefits beyond conventional debridement to treat peri‐implant mucositis. The findings indicate that debridement alone effectively reduces probing depth (PD) and bleeding on probing (BOP). Adjunctive therapies were found to have limited clinical impact. Probiotics, particularly Lactobacillus reuteri, showed a modest short‐term reduction in BOP in nonsmokers, but their long‐term efficacy remains uncertain. In contrast, adjunctive treatments failed to show meaningful improvements in smokers and electronic cigarette users. Air‐polishing devices and aPDT yielded inconsistent results across studies, and routine laser use did not demonstrate significant clinical benefits over debridement alone.

   The main findings of the review suggest that debridement alone leads to significant reductions in PD and BOP, reinforcing its role as the primary treatment for peri‐implant mucositis. Adjunctive treatments do not seem to provide consistent benefits as their additional effect is often negligible. For smokers and electronic cigarette users, no adjunctive therapy significantly improved clinical outcomes. Hence, the selected evidence does not support the routine use of adjunctive therapies in the management of peri‐implant mucositis. Conventional debridement as a monotherapy appears to be an effective and reliable intervention, along with proper maintenance and patient education, to control microbial biofilm accumulation and prevent recurrence and progression of peri‐implant mucositis. However, it was also observed that achieving complete resolution of peri‐implant mucositis is an elusive outcome.

2. Expert opinions based upon the plenary voting outcomes: Treatment of peri‐implant mucositis

   • ‐
     Antimicrobial mouth rinses containing hydrogen peroxide are not recommended as an adjunct in the treatment of peri‐implant mucositis: simple majority (54% agreed, 18% disagreed, 28% neutral).
   • ‐
     Antimicrobial mouth rinses containing iodine are not recommended as an adjunct in the treatment or peri‐implant mucositis: simple majority (65% agreed, 11% disagreed, 24% neutral).
   • ‐
     Subgingival irrigation with chlorhexidine is recommended as an adjunct to nonsurgical mechanical debridement for treating peri‐implant mucositis: no consensus (48% agreed, 36% disagreed, 16% neutral).
   • ‐
     Subgingival irrigation with hydrogen peroxide is not recommended as an adjunct to nonsurgical mechanical debridement for treating peri‐implant mucositis: simple majority (53% agreed, 17% disagreed, 30% neutral).
   • ‐
     Subgingival irrigation with iodine is not recommended as an adjunct to nonsurgical mechanical debridement: consensus (76% agreed, 10% disagreed, 14% neutral).
   • ‐
     Clinical evidence does not support the use of local delivery antibiotics as an adjunct to treat peri‐implant mucositis: simple majority (63% agreed, 27% disagreed, 10% neutral).
   • ‐
     Clinical evidence does not support the use of systemic antibiotics as an adjunct to treating peri‐implant mucositis: consensus (78% agreed, 6% disagreed, 16% neutral).
   • ‐
     Clinical evidence does not support the use of probiotics as an adjunct to treating peri‐implant mucositis: simple majority (53% agreed, 28% disagreed, 19% neutral).
   • ‐
     Lasers should be used as an adjunct in nonsurgical therapy to manage peri‐implant mucositis: no consensus (25% agreed, 45% disagreed, 30% neutral)
   • ‐
     Lasers should be used as an adjunct in treating medically compromised groups where other means of nonsurgical therapy may not be possible: no consensus (39% agreed, 44% disagreed, 17% neutral).

3. Clinical recommendations: Treatment of peri‐implant mucositis

   Peri‐implant mucositis should be primarily treated through an etiology‐based approach that is primarily, but not necessarily exclusively, based on nonsurgical debridement using implant‐safe instruments, such as titanium curettes, ultrasonic scalers, and air abrasion devices, to remove biofilm while avoiding damage to the implant fixture. If needed, adjunctive irrigation with chlorhexidine, hydrogen peroxide, or saline can be used to further reduce bacterial load and inflammation. For persistent cases, local antimicrobials like minocycline microspheres or doxycycline gel may be applied. When PD reach 6 mm with no bone loss beyond expected physiologic remodeling, laser therapy (e.g., Nd:YAG, CO₂, diode, Er,Cr:YSGG, or Er:YAG lasers) can be used as an adjunctive treatment, but not a monotherapy. Adjunct probiotics containing Lactobacillus and Bifidobacterium may help rebalancing the oral microbiome and reduce peri‐implant soft tissue inflammation in some instances. A structured maintenance program, including in‐office debridement every 3–4 months, can contribute to reduce the risk of disease recurrence or progression. During each visit, adjunctive treatments should be applied if necessary. Patient education is crucial, focusing on daily oral hygiene practices to prevent plaque buildup. This combination of professional intervention and rigorous at‐home care helps reverse the inflammation, prevent disease progression, and ensure long‐term peri‐implant health.

4. Clinical flow diagrams: Treatment of peri‐implant mucositis

   Figures 1 and 2 depict clinical flow diagrams pertaining to nonsurgical and adjunctive treatments to manage peri‐implant mucositis, extracted from the clinical translation paper of Group 2. ⁸⁷

FIGURE 1.

Flow diagram for nonsurgical treatment of peri‐implant mucositis (without flap elevation). BOP, bleeding on probing; CPC, cetylpyridinium chloride; OTC, over the counter; PD, probing depth. Reprinted with permission from Quintessence Publishing and the International Journal of Periodontics & Restorative Dentistry.

FIGURE 2.

Flow diagram for adjunctive therapies (antibiotics or probiotics) to nonsurgical treatment of peri‐implant mucositis. Reprinted with permission from Quintessence Publishing and the International Journal of Periodontics & Restorative Dentistry.

Focused Question 2: Nonsurgical treatment of peri‐implantitis

1. Summary of evidence

   No SR was carried out to respond the focused question regarding nonsurgical treatment of peri‐implantitis.

2. Clinical recommendations: Nonsurgical treatment of peri‐implantitis

   Nonsurgical, minimally invasive therapy should be considered as the first line of treatment for peri‐implantitis with the purpose of reducing microbial load and local inflammation while preserving the implant and surrounding bone. Debridement using implant‐safe instruments like titanium curettes, ultrasonic scalers with plastic or carbon tips, or air‐polishing devices is central to this approach, while other tools, such as a titanium brush, may be used when threads are exposed. Adjunctive therapies, such as chemical agents (e.g., chlorhexidine, hydrogen peroxide, saline, or iodine) and locally delivered or systemic antibiotics, may assist in reducing microbial load. Lasers (e.g., Nd:YAG, CO₂, diode, Er,Cr:YSGG, and Er:YAG) and aPDT may also be used for implant surface decontamination and to promote healing. Patient education is crucial to maintain adequate oral hygiene, emphasizing the use of interdental brushes, floss, and electric toothbrushes to control biofilm. Regular maintenance visits every 3–4 months are essential for monitoring and adjusting treatment plans. However, surgical intervention may be required if the condition does not improve or in cases of disease recurrence after successful nonsurgical therapy.

3. Clinical flow diagrams: Nonsurgical treatment of peri‐implantitis

   Figures 3 and 4 depict clinical flow diagrams pertaining to nonsurgical treatment for the treatment of peri‐implantitis, extracted from the clinical translation paper of Group 2. ⁸⁷

FIGURE 3.

Flow diagram for nonsurgical treatment of peri‐implantitis (without flap elevation). BOP, bleeding on probing; CHX, chlorhexidine; CPC, cetylpyridinium chloride; OTC, over the counter; PD, probing depth. Reprinted with permission from Quintessence Publishing and the International Journal of Periodontics & Restorative Dentistry.

FIGURE 4.

Flow diagram for adjunctive methods (antibiotics or probiotics) to nonsurgical treatment of peri‐implantitis. PD, probing depth. Reprinted with permission from Quintessence Publishing and the International Journal of Periodontics & Restorative Dentistry.

Focused Question 3: Peri‐implant surface decontamination methods and potential for reosseointegration

1. Summary of the scientific evidence—Ravida et al. 2025 ⁹³

   Evidence emanating from in vivo studies underscores that systemic antibiotics alone are ineffective to achieve sufficient implant surface decontamination, highlighting the importance of manual debridement to eliminate biofilm and resolve peri‐implant lesions. Reosseointegration, defined as the re‐establishment of bone‐to‐implant contact (BIC), can be attained following appropriate decontamination; reported BIC values vary widely (9%–85%), with vertical bone gains ranging from minimal (<1 mm) to over 2 mm. Notably, air‐polishing devices and controlled laser applications (e.g., Er:YAG and Er,Cr:YSGG lasers) frequently yield favorable reosseointegration outcomes, whereas high‐level evidence on the effect of implantoplasty, polyetheretherketone (PEEK) ultrasonic tips, and titanium brushes used as monotherapies is limited. Comparative studies (e.g., titanium brushes versus ultrasonic devices or air‐polishing devices versus plastic curettes) reveal no statistically significant superiority among decontamination methods in promoting vertical bone gain. Furthermore, adjunctive use of chemical agents (chlorhexidine, citric acid, hydrogen peroxide, sodium hypochlorite, EDTA) with manual debridement methods does not consistently enhance BIC or vertical bone gain over manual debridement alone.

   Ex vivo, in situ, and in vitro investigations further delineate the efficacy of various tools in biofilm removal. Air‐polishing devices, Er:YAG laser at energy levels below 70 mJ/pulse, electrochemical cleaning, and cold atmospheric plasma have emerged as methods that achieve substantial biofilm reduction while inducing minimal surface alterations, although high‐level evidence is still limited. Other instruments such as titanium brushes, curettes, and ultrasonic tips often produce notable surface damage, flattening of peaks, or leave material remnants that may compromise implant fixture integrity.

   In summary, implant surface decontamination is indispensable for resolving peri‐implantitis lesions and enabling reosseointegration. Although reosseointegration is feasible with appropriate decontamination, no single method has demonstrated unequivocal clinical superiority regarding BIC or vertical bone gain when similar biomaterials and techniques are used. The ideal decontamination protocol should predictably and efficiently eliminate microbial biofilms and calculus deposits without releasing titanium particles or altering the implant's macro‐ and microtopography. Within the current evidence, electrolytic cleaning, air‐polishing devices, and Er:YAG laser therapy best capture these attributes, offering a balanced approach between effective biofilm removal and surface preservation.

2. Expert opinions based upon the plenary voting outcomes: Peri‐implant surface decontamination

   • ‐
     Evidence supports that there is no standard of care for surface decontamination of dental implants with peri‐implantitis: consensus (85% agreed, 12% disagreed, 3% neutral).
   • ‐
     Implantoplasty is an effective adjunct in managing supracrestal or subcrestal defects: simple majority (53% agreed, 25% disagreed, 22% neutral).

Focused Question 4: Non‐reconstructive surgical treatment of peri‐implantitis

1. Summary of the scientific evidence—Saleh et al. 2025 ⁹⁴

   Following unsuccessful nonsurgical therapy, both flaps for access with or without osseous resective surgical procedures have demonstrated some efficacy in managing peri‐implantitis. According to available evidence, both of these nonreconstructive approaches consistently reduce PD and BOP, with no significant differences between them. The only notable distinction was in the observed marginal bone levels, where the flap group showed less marginal bone changes than the flap with osseous resective surgery group. Specifically, a statistically significant difference of 0.58 mm at 6 months (p = 0.044) and 0.73 mm at 12 months (p < 0.001) was noted in favor of flap‐for‐access surgery. This difference is likely related to the primary goal of osseous resective surgery (i.e., eliminating unfavorable bony deformities, such as shallow crater defects, to achieve PD reduction). Despite the absence of direct comparative studies, both interventions effectively improved key clinical outcomes. Moreover, a weak inverse relationship between BOP reduction and smoking was observed. Also, patients with a history of periodontitis showed slightly greater marginal bone changes regardless of the type of surgery performed. These findings may infer that while nonreconstructive surgical interventions are effective in the treatment of peri‐implantitis, outcomes may largely vary depending on specific patient and site features.

2. Expert opinions based upon the plenary voting outcomes: Nonreconstructive surgical treatment of peri‐implantitis

   All the statements and results proceeding from the plenary voting have been grouped within other focused questions.

3. Clinical recommendations: Nonreconstructive surgical treatment of peri‐implantitis

   Flap for access without resective surgery

   Flap procedures allow for access to the implant surface for debridement and decontamination. A full‐thickness flap, with or without vertical releasing incisions, is often necessary for proper access. Afterward, the flap is repositioned and stabilized with sutures. Soft tissue modification, such as deepening the vestibule and/or widening the buccal band of keratinized mucosa, may be performed simultaneously or staged.

   Flap for access with resective surgery

   Combining flap for access and debridement with osseous resection may require larger flaps or modifications to flap design (e.g., vertical releasing incisions) to facilitate proper visualization. Osseous resective surgery is often indicated when peri‐implant bony defects are not favorable to attempt reconstruction of the missing peri‐implant bone. After debridement and osseous resection, the flap may be repositioned and stabilized with sutures, or instead, it may be apically positioned to maximize the chances of pocket depth reduction at the expense of greater implant fixture exposure after healing.

4. Clinical flow diagram: Surgical peri‐implantitis therapy (both reconstructive and nonreconstructive)

   Figure 5 displays a clinical flow diagram pertaining to the surgical treatment of peri‐implantitis, including reconstructive and nonreconstructive approaches, extracted from the clinical translation paper of Group 2. ⁸⁷

FIGURE 5.

Flow diagram for surgical treatment options of peri‐implantitis. OFD, open flap debridement; PD, probing depth; SRP, scaling and root planing. Reprinted with permission from Quintessence Publishing and the International Journal of Periodontics & Restorative Dentistry.

Focused Question 5: Reconstructive treatment of peri‐implantitis

1. Summary of the scientific evidence—Barootchi et al. 2025 ⁹⁵

   Selected evidence strongly supports the efficacy of reconstructive surgical approaches to treat some peri‐implantitis lesions with favorable anatomical configuration (e.g., contained defects). The review also found that while reconstructive approaches offer superior outcomes regarding PD reduction, marginal mucosa position improvement, and radiographic MBL gain, there were no significant differences in the resolution of BOP and SUP when compared to nonreconstructive modalities. A slight, yet statistically significant, relapse over time was observed for these clinical parameters regardless of the modality of treatment; however, this effect was lower after reconstructive therapy involving the use of either a particulate allograft or xenograft.

   Quantitative analyses demonstrated a significant overall reduction in PD after reconstructive surgery (mean = 2.88 mm; 95% CI 2.49, 3.28; p < 0.001). Notably, the adjunctive use of titanium brushes, allografts, and xenografts was associated with slightly greater improvements. Conversely, implant surface decontamination with agents such as hydrogen peroxide or ethylenediamine tetraacetic acid (EDTA) did not offer additional benefits over a rinse with sterile saline. In terms of radiographic outcomes, reconstructive therapies that involved the use of bone graft substitutes, specifically allogeneic and xenogeneic particulates, were associated with significant gains in radiographic MBL, for a mean increase of 1.14 mm and 0.43 mm, respectively. The application of barriers or membranes, though showing a positive trend (mean gain of 0.56 mm), was associated with a more modest impact. Additionally, baseline PD, MBL, and keratinized mucosa width were found to significantly predict improved outcomes, while defect morphology did not emerge as a critical determinant.

2. Expert opinions based upon the plenary voting outcomes: Reconstructive treatment of peri‐implantitis

   • ‐
     When feasible, reconstructive surgical therapy is preferable over nonreconstructive approaches: consensus (79% agreed, 0% disagreed, 21% neutral).
   • ‐
     Reconstructive therapy should be performed wherever the lesion morphology favors this (e.g., multiple bony walls for containment, infraosseous compartments, defects ≥3 mm in depth): strong consensus (97% agreed, 0% disagreed, 3% neutral).
   • ‐
     Submerging the implant should be pursued for reconstructive therapies whenever possible: consensus (82% agreed, 9% disagreed, 9% neutral).
   • ‐
     A membrane should be placed over the bone graft: consensus (79% agreed, 9% disagreed, 12% neutral).

3. Clinical recommendations: Reconstructive treatment of peri‐implantitis

   Reconstructive surgery may result in gain of lost bone and soft tissue around implants affected by peri‐implantitis. A full‐thickness flap, with or without vertical releasing incisions, should be used for access. After exposing the peri‐implant defect, granulomatous tissue should be removed and the implant surface decontaminated. Autogenous bone grafts or substitutes may be used to fill the infraosseous component of the defect, with or without the application of a barrier or membrane. The flap may be replaced or coronally displaced and stabilized with sutures.

   Bone loss is categorized as <25%, 25%–50%, or >50%. Defect types include supraosseous, infraosseous (one‐wall, two‐wall, or three‐wall), and combination defects. These factors should be considered when deciding the surgical treatment approach of peri‐implantitis.

   Simultaneous soft tissue augmentation should be considered in sites presenting unfavorable phenotypical features (e.g., thin peri‐implant mucosa). A submerged approach with primary closure may favor healing and increase the chance of achieving a superior clinical outcome compared to nonsubmerged approaches, but further research is warranted. Implant removal should be considered in sites presenting extensive peri‐implant bone loss and unfavorable bony architecture, recurrent peri‐implantitis, or implant mobility.

4. Surgical peri‐implantitis therapy flow diagram: Reconstructive treatment of peri‐implantitis

   Figure 5 displays a clinical flow diagram pertaining to the surgical treatment of peri‐implantitis, including reconstructive and nonreconstructive approaches, extracted from the clinical translation paper of Group 2. ⁸⁷

Focused Question 6: Surgical soft tissue management

1. Summary of evidence

   No SR was carried out to respond to the focused question regarding soft tissue management.

2. Expert opinions based upon the plenary voting outcomes: Surgical soft tissue management

   • ‐
     Soft tissue modification should be performed simultaneously with or following peri‐implantitis surgical therapy depending on the case scenario: consensus (94% agreed, 3% disagreed, 3% neutral).
   • ‐
     Indications for soft tissue modification differ between reconstructive and nonreconstructive peri‐implantitis surgery: simple majority (65% agreed, 16% disagreed, 19% neutral).
   • ‐
     When the primary therapeutic purpose is to increase the band of keratinized mucosa, clinicians may consider free gingival grafting: consensus (94% agreed, 0% disagreed, 6% neutral).
   • ‐
     When the primary therapeutic purpose is to increase the band of keratinized mucosa, clinicians may consider soft tissue substitutes as an alternative: simple majority (67% agreed, 16% disagreed, 17% neutral).
   • ‐
     When the primary therapeutic purpose is peri‐implant soft tissue volume augmentation (i.e., thickness and/or height), clinicians may consider autogenous connective tissue grafts: strong consensus (97% agreed, 0% disagreed, 3% neutral).
   • ‐
     When the primary therapeutic purpose is peri‐implant soft tissue volume augmentation, clinicians may consider soft tissue substitutes as an alternative: consensus (93% agreed, 7% disagreed, 0% neutral).
   • ‐
     When the primary therapeutic purpose is to deepen the vestibule, clinicians may consider autogenous soft tissue grafts: consensus (92% agreed, 4% disagreed, 4% neutral).
   • ‐
     When the primary therapeutic purpose is to deepen the vestibule, clinicians may consider soft tissue substitutes as an alternative: simple majority (66% agreed, 21% disagreed, 13% neutral).
   • ‐
     Autogenous connective tissue‐based modification should be considered the standard of practice for all soft tissue grafting procedures around dental implants: consensus (80% agreed, 13% disagreed, 7% neutral).
   • ‐
     When treating peri‐implantitis in the esthetic zone, connective tissue grafting may be considered in conjunction with surgical measurements: consensus (83% agreed, 10% disagreed, 7% neutral).

3. Clinical flow diagram: Surgical soft tissue management

   Figure 6 depicts a flow diagram pertaining to soft tissue augmentation for the treatment and prevention of peri‐implantitis, extracted from the clinical translation paper of Group 2. ⁸⁷

FIGURE 6.

Flow diagram illustrating key considerations regarding soft tissue reconstruction procedures for prevention and management of peri‐implantitis. CAL, clinical attachment level; CBCT, cone‐beam computed tomography. Reprinted with permission from Quintessence Publishing and the International Journal of Periodontics & Restorative Dentistry.

Focused Question 7: Supportive peri‐implant maintenance therapy

1. Summary of evidence—No SR performed

   No SR was carried out to respond to the focused question regarding peri‐implant maintenance therapy.

2. Expert opinions based upon the plenary voting outcomes: Supportive peri‐implant maintenance therapy

   • ‐
     Supportive peri‐implant maintenance therapy (SPiT) intervals should be more frequent for patients who have undergone interventions to treat peri‐implant mucositis: consensus (91% agreed, 6% disagreed, 3% neutral).
   • ‐
     SPiT intervals of 3–4 months should be recommended for patients with peri‐implant mucositis who are under active surveillance: consensus (88% agreed, 3% disagreed, 9% neutral).
   • ‐
     SPiT intervals of 5–6 months should be utilized for patients with peri‐implant mucositis who require less active surveillance: consensus (88% agreed, 9% disagreed, 3% neutral).
   • ‐
     SPiT intervals of 3–4 months should be recommended for patients who have undergone treatment for peri‐implantitis: consensus (94% agreed, 6% disagreed, 0% neutral).
   • ‐
     SPiT intervals should be reassessed following the first year of treatment: consensus (89% agreed, 7% disagreed, 4% neutral).
   • ‐
     A 5–6‐month SPiT interval is essential for maintaining tissue stability after peri‐implantitis treatment: consensus (94% agreed, 6% disagreed, 0% neutral).
   • ‐
     All SPiT should be tailored to the specific patient risk profile to maintain peri‐implant health: consensus (93% agreed, 7% disagreed, 0% neutral).
   • ‐
     Regular and effective patient‐delivered biofilm control through oral home care is a critical component of ongoing SPiT for prevention of PID and maintenance of implant health: consensus (93% agreed, 3% disagreed, 4% neutral).

3. Clinical recommendations: Supportive peri‐implant maintenance therapy

   SPiT is essential for maintaining long‐term peri‐implant health, especially after the treatment of peri‐implant mucositis and peri‐implantitis. SPiT intervals should be tailored based on the patient's overall risk profile: High‐risk patients, such as those with a history of periodontitis or poorly controlled diabetics, should visit every 3–4 months, while low‐risk patients may visit every 5–6 months, if their peri‐implant tissues are stable and no signs of disease recurrence are observed.

   SPiT should include peri‐implant tissue health monitoring, reinforcement of oral hygiene practices and professional microbial biofilm and calculus removal, if present. During visits, clinicians should use implant‐safe instruments and assess soft tissues and the implant–abutment interface, as well as perform radiographic monitoring of marginal bone stability. Signs of inflammation require immediate action, such as further debridement, use of antiseptics like chlorhexidine, or locally delivered antibiotics. Patient education and regular reassessment of risk profiles are fundamental components of SPiT, especially after the first year, to adjust SPiT visit intervals as needed.

4. Clinical flow diagrams: Supportive peri‐implant maintenance therapy 

   Figures 7 and 8 depict flow diagrams pertaining to supportive peri‐implant therapy for patients who received treatment for PID with or without soft tissue augmentation, extracted from the clinical translation paper of Group 2. ⁸⁷

FIGURE 7.

Flow diagram for supportive peri‐implant therapy after treatment of peri‐implant mucositis. Reprinted with permission from Quintessence Publishing and the International Journal of Periodontics & Restorative Dentistry.

FIGURE 8.

Clinical flow diagram for supportive peri‐implant therapy after treatment of peri‐implantitis. SPiT, supportive peri‐implant maintenance therapy. Reprinted with permission from Quintessence Publishing and the International Journal of Periodontics & Restorative Dentistry.

Additional consensus questions and voting results—No correspondence with a SR

• ‐Peri‐implant mucositis is a predisposition for the development of peri‐implantitis: strong consensus (97% agreed, 0% disagreed, 3% neutral).
• ‐Soft tissue phenotype plays a role in the risk for peri‐implant mucositis: consensus (94% agreed, 0% disagreed, 6% neutral)—the result is slightly different from Group 1 voting.
• ‐Titanium biomaterial degradation may play a role in PID initiation and/or progression: simple majority (61% agreed, 28% disagreed, 11% neutral)
• ‐Microbial biofilm is the primary etiologic factor for PID: consensus (91% agreed, 3% disagreed, 6% neutral).

Future research recommendations and gaps of knowledge

This consensus meeting identified several gaps of knowledge on the risk assessment for PID and conditions. The following recommendations for future research and further development of this field were made:

• ‐Conduct well designed longitudinal studies to identify new and evaluate the role of established risk factors.
• ‐Conduct properly sized RCT with a minimum follow‐up time of 12 months to determine the efficacy and effectiveness of different modalities (i.e., nonsurgical and surgical) for the treatment of PID and conditions, while considering patient‐specific factors, defect morphology, and other clinical variables such as implant surface characteristics, defect geometry, and healing modalities.
• ‐Clinical studies to investigate the efficacy of adjunctive therapies, including but not limited to laser therapy, aPDT, probiotics, systemic antibiotics, and biologic agents in the nonsurgical and surgical treatment of PID.
• ‐Determine the effect that implant surface characteristics (e.g., topography, surface alterations, and decontamination challenges) and prosthetic design features may have on the outcomes of PID therapy.
• ‐Studies to determine disease recurrence, peri‐implant tissue stability, and long‐term success rates after different peri‐implantitis treatments should be carried out.
• ‐Establish evidence‐based definitions for PID resolution accounting for a composite of relevant parameters.
• ‐Assess the cost‐effectiveness of different therapies for the treatment of PID by considering treatment duration, healing time, and long‐term maintenance. Explore criteria for deciding between implant retention and explantation in severe cases, considering bone loss extent, implant position, and patient prognosis.
• ‐Develop precise tools, with high sensitivity and specificity, to assess the presence of PID and monitor health.
• ‐Standardization of clinician‐ and patient‐reported outcomes: Establish standardized outcome measures for peri‐implantitis treatment, including radiographic bone level changes, soft tissue migration, disease resolution, patient satisfaction, and mucosal recession.

The expert panel also stressed the importance of integrating these recommendations in the curriculum of educational programs at both the predoctoral and graduate level as well as the implementation of policies regarding the availability of primary data from original studies published in scientific journals.

CONCLUSIONS—BASED UPON EVIDENCE AND EXPERT OPINION

Narrative format

Since their introduction in dentistry, osseointegrated implants have been extensively used to successfully rehabilitate fully or partially edentulous patients, with estimated trends for increasing demand in the following decade. Despite their therapeutic benefits, implant therapy is not exempt of complications, including the PID and conditions such as peri‐implant mucositis, peri‐implantitis, and PSTD. Peri‐implantitis represents a significant clinical challenge due to its rapidly progressive nature in many cases and the lack of standardized and predictable protocols to arrest it and treat its sequelae. Treatment of peri‐implantitis does not only increase dental care costs but can also severely compromise patients’ quality of life if it culminates in implant loss. Through a systematic assessment of the best available scientific evidence and extensive expert panel discussions, Group 1 identified a series of key systemic and local factors involved in the onset and progression of PID. Strong associations were found between PID and history of periodontitis, active periodontitis, smoking, uncontrolled diabetes, obesity, and excessive alcohol consumption. At the local level, factors such as implant malposition, inadequate mesiodistal interimplant distance, and suboptimal peri‐implant soft tissue phenotypical features were highlighted as key risk factors/indicators for PID and PSTD. These findings emphasize the importance of comprehensive pretreatment assessments and the implementation of tailored preventive strategies to optimize implant therapy success and reduce the risk for PID and PSTD.

This consensus also addressed treatment strategies to effectively manage PID. Selected evidence supports that manual debridement is the cornerstone for treating peri‐implant mucositis, and the first step to treatment of peri‐implantitis. Adjunctive therapies can be selectively applied based on patient‐specific risk profiles to obtain an additional therapeutic benefit. For the treatment of peri‐implantitis, nonreconstructive surgical interventions, such as flap for access to facilitate debridement with or without osseous resection, can predictably lead to significant reductions in PD and BOP, although MBL and PD reduction logically tend to be greater if osseous resection is performed. In cases of pronounced bone loss but in the presence of a favorable bony architecture, reconstructive procedures that incorporate bone grafts, barriers or membranes, and gentle implant surface decontamination techniques offer a promising avenue for the restoration of lost tissue architecture and reosseointegration. SPiT, including patient education and monitoring, is key to manage risk over time. The therapeutic recommendations derived from this consensus that combine risk factor identification with tailored nonsurgical and surgical interventions, as well as proper maintenance, provide a solid framework for the prevention and management of PID in contemporary practice.

Bullet point format

Risk factor assessment for PID

• Behavioral, systemic, and patient‐related factors:

  • Smoking: Current and recent former smokers (quit within the last 10 years) are at a high risk for developing PID.

  • History of periodontitis: A history of periodontitis has been consistently linked to an elevated risk for the onset and progression of PID.

  • Metabolic conditions: Uncontrolled diabetes (HbA1c > 7%) and obesity/metabolic syndrome significantly increase the risk of peri‐implant inflammation and bone loss.

  • Other systemic conditions: Excessive alcohol consumption and depression (and related medication use) contribute to an adverse immunoinflammatory response in the peri‐implant tissues.

• Local factors and prosthetic/design considerations:

  • Implant position and mesiodistal space: Implant malposition, particularly for those placed too buccally or excessively apical (>6 mm from adjacent teeth), and inadequate mesiodistal spacing (<3 mm) are strongly associated with an increased risk of peri‐implantitis.

  • Peri‐implant soft tissue phenotype characteristics: Thin mucosa and inadequate keratinized mucosa width (<2 mm) are key local risk factors for both mucosal inflammation and PSTD.

  • Prosthetic design factors: Platform‐matched abutments, a transmucosal abutment height <2 mm, splinted adjacent implants, and a transmucosal emergence angle exceeding 30° (particularly with convex abutment profiles) are linked to MBL, especially in bone‐level implants.

  • Other local variables: Factors such as residual submucosal cement, buccal bone dehiscence, immediate implant placement (noted as a moderate risk), and prolonged function (beyond 5 years) further predispose to the occurrence of soft tissue dehiscences and MBL.

Treatment of PID

• Nonsurgical therapy:

  • Mechanical Debridement: Remains the cornerstone for treating peri-implant mucositis, and first step of treating peri‐implantitis, effectively reducing PD and BOP.

  • Adjunctive therapies: Additional treatments (e.g., lasers, air‐polishing devices, pharmacotherapeutics) may offer modest benefits in select cases.

• Surgical therapy:

  • Nonreconstructive approaches: Flap‐for‐access and osseous resective surgeries are effective in predictably reducing pocket depth and BOP. While both methods yielded improvements, flap‐for‐access approaches typically result in less MBL.

  • Reconstructive approaches: For defects with pronounced bone loss but a favorable architecture, reconstructive surgery—incorporating bone grafts, barriers, membranes, and optimized implant surface decontamination—can result in reosseointegration and restoration of lost tissue architecture.

  • Implant surface decontamination: Although no single method has emerged as the gold standard, air‐polishing devices and some lasers (e.g., Er:YAG) have shown promise in achieving effective biofilm removal while preserving the implant's surface integrity.

• SPiT:

  • Individualized maintenance protocols: Regular, tailored SPiT (with intervals ranging from 3 to 6 months, depending on risk assessments) is essential to prevent disease recurrence.

  • Patient education: Emphasis on rigorous at‐home oral hygiene for proper biofilm control is critical for the long‐term success of implant therapy.

AUTHOR CONTRIBUTIONS

Hom‐Lay Wang, Paul Rosen: Conceptualization; original draft writing; visualization; review; supervision; AO/AAP Consensus Co‐Chairs, and final approval. Gustavo Avila‐Ortiz, Alberto Monje, Purnima Kumar, Tara Aghaloo, Joseph Kan: Writing–review and editing; AO/AAP Consensus Participants. Javier Calatrava: Writing–review and editing; final approval. Shayan Barootchi, Joseph P. Fiorellini, Maria Elisa Galarraga‐Vinueza, Purnima Kumar, Guo‐Hao Lin, Alberto Monje, Andrea Ravida, Muhammad H.A. Saleh, Lorenzo Tavelli: Lead authors of AO/AAP Consensus papers; Consensus Participants; review and final approval. AO/AAP Consensus Participants: Review and final approval. Tara Aghaloo, Joseph P. Fiorellini, Joseph Kan, and Purnima Kumar: Also served as AO/AAP subgroup co‐chairs.

AO/AAP CONSENSUS PARTICIPANTS

1. Tara Aghaloo, DDS, MD, PhD

2. Gustavo Avila‐Ortiz, DDS, MS, PhD

3. Shayan Barootchi, DMD

4. Martinna Bertolini, DDS, MS, PhD

5. Leandro Chambrone, DDS, MSc, PhD

6. Don Curtis, DMD

7. Joseph Fiorellini, DMD, DMSc

8. María Elisa Galarraga‐Vinueza, DDS, MSc, PhD

9. German Gallucci, DMD, PhD

10. Jeffrey Ganeles, DMD

11. Sukirth Ganesan, DDS

12. Mia Geisinger, DDS, MS

13. William Giannobile, DDS, MS, DMSc

14. Oscar Gonzalez‐Martin, DDS, MSc, PhD

15. Effie Ioannidou, DMD, MDSc

16. Joseph Kan, DDS, MS

17. Georgios Kotsakis, DDS, MS, PhD

18. Theofilos Koutouzis, DDS

19. Purnima Kumar, DDS, PhD

20. Bach Le, DDS, MD

21. Robert Levine, DDS

22. Guo‐Hao Lin, DDS, MS

23. Harriett McGraw, DDS

24. Steve Meraw, DDS, MS

25. Craig Misch, DDS, MDS

26. Sean Mojaver, DDS

27. Alberto Monje, DDS, MS, PhD

28. Rodrigo Neiva, DDS, MS

29. Joerg Neugebauer, DDS, PhD

30. Flavia Pirih, DDS, PhD

31. Paul Rosen, DMD, MS

32. Andrea Ravida, DDS, PhD

33. Muhammad Saleh, BSD MSD

34. Hector Sarmiento, DMD, MSc

35. Todd Schoenbaum, DDS, MS

36. Frank Schwarz, DMD

37. Amerian Sones, DMD, MS

38. Clark Stanford, DDS, PhD, MHA

39. Lambert Stumpel, DDS

40. Dennis Tarnow, DDS

41. Daniel Taub, DDS, MD

42. Lorenzo Tavelli, DDS, MS, PhD

43. Hom‐Lay Wang, DDS, MSD, PhD

44. Robert Vogel, DDS

CONFLICT OF INTEREST STATEMENT

Participants filed detailed disclosure of potential conflicts of interest relevant to the meeting topic, and these are kept on file. The authors receive, or have received, consulting fees and/or lecture compensation from the following companies: BioHorizons, Brasseler USA, Bredent Medical, Camlog, Dentsply Sirona, Geistlich, ITI, Nobel Biocare, Novabone LLC, Osteogenics, Osteology Foundation, Straumann, W&H, and ZimVie. Dr. Ioannidou is the editor‐in‐chief of the Journal of Periodontology. Dr. Kotsakis holds a patent for a dental irrigator (US‐2024390122‐A1) and is an associate editor of the Journal of Periodontology. Dr. Levine is currently employed by Geistlich Pharma North America. Dr. Pirih is an associate editor of the Journal of Periodontology. Dr. Schwarz is an executive board member of the Osteology Foundation. Dr. Stanford is the editor‐in‐chief of the International Journal of Oral & Maxillofacial Implants.

FUNDING INFORMATION

The authors received no specific funding for this work.

Wang H‐L, Avila‐Ortiz G, Monje A, et al. AO/AAP consensus on prevention and management of peri‐implant diseases and conditions: Summary report. J Periodontol. 2025;96:519–541. 10.1002/JPER.25-0270