Peri-implantitis is a plaque-associated pathological condition occurring around dental implants that results in a breakdown of the supporting tissues [1•, 2••]. Clinically, peri-implantitis-affected sites exhibit bleeding on probing (BOP) and/or suppuration (Supp), increased probing depths (PDs), and/or recession of the peri-implant mucosal margin in addition to radiographic bone loss compared to previous examination [1•]. Untreated disease progresses in nonlinear accelerating pattern and finally leads to a loss of the implant [3••, 4]. As the number of patients undergoing restorative therapy through dental implants increases, peri-implantitis is considered to be a major and growing problem in dentistry [4].

The primary goal of peri-implantitis treatment has been established as a resolution of the inflammation and a prevention of further bone loss [5]. To achieve these treatment endpoints, it is currently accepted that surgical approaches that allow adequate access to the contaminated implant surface are required [6,7,8]. Indeed, numerous peri-implantitis surgical treatment protocols have been proposed, which basically can be categorized into two main modalities: non-augmentative and augmentative.

The aim of this narrative review is to provide an overview of various peri-implantitis surgical treatment strategies with regard to their indications, performance, and efficacy.

Non-augmentative Approaches

Open Flap Debridement

In order to achieve the resolution of inflammation and arrest further bone loss, decontamination of the implant’s surface is of critical importance [9]. Open flap debridement (OFD) is a surgical technique aimed at gaining access to the implant surfaces to facilitate decontamination.


The surgery consists of the following steps:

  • Access to the lesion

  • Removal of granulation tissues

  • Decontamination of the implant surface

  • Suturing with or without apical flap positioning

During OFD surgery, implant surface is mechanically debrided with titanium or plastic curettes or titanium brushes, with or without the adjunctive application of antimicrobials (Table 1) [8, 11,12, 13, 15]. The effectiveness of different decontamination approaches has been assessed in randomized clinical investigations (RCTs) [10••, 13, 14]. Particularly, significantly greater reductions of initial PD values as well as stable bone levels were obtained at implant sites debrided with titanium brushes compared with those cleaned with plastic curettes or an air-abrasive device [13]. Repeated applications of local antibiotics (minocycline) led to superior therapeutic outcomes (i.e., greater PD reductions and increased marginal bone levels) compared with those in the placebo group [14]. In contrast to the abovementioned decontamination approaches, the additional use of a diode laser provided comparable treatment outcomes to those of mechanical debridement alone (i.e., plastic curettes and cotton pellets soaked in sterile saline) [10••]. It should, however, be noted that all of the abovementioned controlled clinical investigations involved a follow-up period limited to 6 months and thus do not permit an assessment of the long-term impacts of the implant surface decontamination method on the treatment outcomes following OFD. Regarding the rationale for adjunctive systemic antibiotic therapy, as demonstrated by a 1-year follow-up controlled clinical investigation, prescribing systemic antibiotics did not lead to improved therapeutic outcomes, as compared with those in the control group [12].

Table 1 Studies reporting on open flap debridement therapy

Outcomes of the Therapy

Peri-implantitis management with the OFD approach significantly reduced inflammation signs (BOP, PD values, and Supp) compared with the baseline situation [8, 10••, 11, 12, 13]. However, a postoperative soft tissue recession of 1.9 to 1.8 mm occurred after 1 year and 5 years, respectively [8, 11].

Treatment success, defined as PD ≤ 5 mm, no BOP, no Supp, and no bone loss ≥ 0.5 mm, after 6 months was achieved in 33% of the implants mechanically treated with titanium brushes, whereas lower values were noted for the sites where debridement was performed with plastic curettes or an air-abrasive device (22% and 27%, respectively; p < 0.05) [13]. According to the same definition, success was obtained in 47% of patients with postoperative antibiotics and 25% without systemic antibiotic prescription after 1 year; however, no significant difference was found between the groups (p = 0.2) [12]. Contrarily, disease resolution (defined as PD < 5 mm, no BOP/Supp, and no bone loss) was more frequently noted at the sites treated with locally repeated minocycline applications (intraoperatively, after 1 month, 3 months, and 6 months) compared to the controls (test 66.7%, control 36.3% of the implants) [14]. Over a 5-year follow-up, treatment success (the absence of PD ≥ 5 mm with concomitant BOP and Supp and the absence of additional bone loss) was yielded in 63% of the patients that adhered to a regular supportive therapy [11].

Resective Therapy

Resective peri-implantitis therapy involves reducing or eliminating pathological peri-implant pockets, apical positioning of the mucosal flap, or recontouring of the bone with or without implantoplasty [16]. The indication of this surgical approach includes the presence of horizontal bone loss with exposed implant threads in non-aesthetic areas [16].


The following steps should be followed during resective peri-implantitis therapy (Fig. 1):

  • Access to the defect

  • Removal of inflamed tissues

  • Decontamination of the implant surface

  • Performance of resective therapy by means of osseous recontouring with or without implantoplasty

  • Apical positioning of the mucosal flap

Fig. 1
figure 1

A clinical case of resective peri-implantitis therapy combined with implantoplasty. a Presurgical view following the removal of a suprastructure. b Radiographic view. Marginal bone loss present around implants 14 and 16. c Implantoplasty performed at supracrestally exposed implant sites. d Suturing. e Intraoral view after 6 months

Mechanical debridement combined with antibacterial agent application (e.g., chlorhexidine gluconate (CHX), hydrogen peroxide, sterile saline, phosphoric acid, or antibiotic gel) is the most common method for decontaminating implant surfaces [15, 17,18,19,20,21,22,23,24,25] (Table 2). Clinical comparative studies have shown that the adjunctive use of phosphoric acid or CHX application with or without cetylpyridinium chloride was not superior to control methods (e.g., sterile saline alone) [17,18,19,20, 22]. Adjunctive systemic antibiotics regimens had no impact on disease resolution (i.e., PD ≤ 5 mm, no BOP/Supp, bone loss ≤ 0.5 mm) in implants with nonmodified surfaces, whereas they had a positive effect on treatment success on implants with modified surfaces [20]. Over a 3-year period, however, the increased treatment success by systemic antibiotics at nonmodified surfaces was not sustained [19].

Table 2 Studies reporting on the treatment outcomes following resective therapy

Implant surface modification, or implantoplasty, was suggested to be used as an adjunct to the resective therapy of peri-implantitis [24, 25]. Implantoplasty is aimed at removing supracrestally exposed rough implant surfaces, which, in turn, would be less prone to plaque accumulation and, ultimately, the recurrence of infection [24, 25, 27,28,29]. Clinically, the advantage of implantoplasty compared to resective therapy alone in terms of BOP, PD reduction, and marginal bone preservation was demonstrated in a 3-year comparative clinical investigation (Table 2) [24]. Nevertheless, compared to the control sites, adjunctively performed implantoplasty leads to significant postoperative soft tissue recession (1.64 mm vs. 1.94 mm, respectively) [24].

Outcomes of the Therapy

Surgical resective peri-implantitis treatment was found to be effective in reducing signs of peri-implant soft tissue inflammation and decreased probing depths in the short term [16, 30]. According to the similar definitions used by different authors, resective therapy yielded success in 14% of implants after 6 months [21] and in 75% of implants after 3 years [26] (Table 2). Over a 5-year period, healthy conditions (PD < 4 mm and no BOP or Supp) were found in 60% of implants for patients enrolled in a 6-month recall system [15].

The characteristics of implant surfaces were demonstrated to be among the prognostic factors for the successful treatment of peri-implantitis following resective treatment [19, 20]. Over 3 years, treatment success (no bone loss > 0.5 mm, PD ≤ 5 mm, and no BOP or Supp) was more frequently observed for implants with nonmodified surfaces compared to implants with modified surfaces (61% vs. 23%, respectively) [19]. In addition, retrospective data demonstrated significantly higher PD and BOP reduction as well as greater crestal bone preservation for the implants with nonmodified surfaces 2 to 10 years after the resective therapy [31]. Factors, such as the preoperative presence of Supp, bone loss > 7 mm, and PD > 8 mm, as well as residual PDs ≥ 4 mm following resective peri-implantitis therapy, were found to be associated with the reduced therapeutic success and increased the risk of further disease progression [15, 21].

Augmentative Approaches

Augmentative Therapy

In addition to resolving infection, augmentative therapy for peri-implantitis is aimed at (1) regenerating the bone defect, (2) achieving re-osseointegration, and (3) limiting the recession of peri-implant soft tissue [32]. Indications of this surgical approach involve the presence of intrabony defects with a minimum depth of 3 mm, three- or four-wall-contained defects, and the presence of keratinized mucosa [32].


Augmentative peri-implantitis treatment protocol includes the following steps (Fig. 2):

  • Access to the defect

  • Removal of inflamed tissues

  • Decontamination of the implant surface

  • Placement of the graft material (with or without a barrier membrane)

  • Adequate flap adaptation

Fig. 2
figure 2

Peri-implantitis therapy with an augmentative approach. a Intrabony circumferential defect at implant 46. b Intrabony defect fill with bone substitute and coverage with collagen membrane. c Suturing. d Intraoral view after 12 months

Implant surface decontamination methods applied during augmentative peri-implantitis treatment include mechanical debridement (i.e., plastic, titanium, or carbon curettes; titanium brushes; or air polishing), laser therapy (carbon dioxide and Er:YAG lasers), application of chemical agents (chlorhexidine digluconate, citric acid, minocycline, sterile saline, ethylenediaminetetraacetic acid (EDTA) 24%, or hydrogen peroxide), and their combinations (Table 3) [8, 33,34,35,36,37,38, 40]. As indicated in a recent systematic review, currently existing clinical, radiographic, and microbiological data do not favor any implant surface decontamination approach and fail to show the influence of a particular decontamination protocol on the long-term outcomes of peri-implantitis surgical therapy [41].

Table 3 Studies reporting on augmentative therapy of peri-implantitis

The impact of such factors as the healing pattern (i.e., submerged or nonsubmerged) or additional use of systemic antibiotics for the therapeutic outcomes of augmentative peri-implantitis therapy cannot be investigated because of the absence of comparative studies [42]. Nevertheless, whenever feasible, to facilitate protected physiological healing, clinicians are recommended to choose submerged postoperative wound closure [43].

Grafting Materials

Reconstruction of peri-implant bone defect can be performed by either the use of bone substitute material solely or in combination with a barrier membrane [42]. Bone replacement materials suggested for peri-implant bone defect fill include autogenous bone; alloplastic, xenogenic, and allogenic bone substitutes; and titanium granules [8, 33,34,35, 37, 38, 40, 44].

Findings of a comparative investigation pointed toward significantly better clinical and radiographic outcomes when using a xenograft over autogenous bone [34]. Superior clinical treatment outcomes were obtained at the implant sites where xenogeneic bone substitute was applied over alloplastic bone particles (i.e., hydroxyapatite) [33]. Furthermore, a significantly higher radiographic fill of peri-implant bone defect resulted was noted at the implant sites treated with titanium particles compared to the xenogenic bone substitute, although the clinical outcomes (i.e., PD and BOP changes) did not differ between the two treatment modalities [40]. It should be, however, elucidated that the findings of the aforementioned comparative investigations should be evaluated with caution since the compared bone fill materials (i.e., autogenous bone vs. xenograft, xenograft vs. titanium granules) exhibit different opacity properties, which may lead to the misinterpretation of the data.

The potential beneficial effect of the application of enamel matrix derivates (EMDs) into intrabony peri-implant defects of ≥ 3 mm depth was investigated over a 5-year period [45, 46]. After 1 year, significantly higher marginal bone levels and an increased prevalence of Gram-positive and Gram-negative aerobic bacteria compared with OFD alone were noted at the implant test sites [45]. However, over the 3-year and 5-year periods, the positive effect associated with the superior marginal bone level was not sustained, as a bone level gain of 1.3 mm was observed in the control group, and a gain of 1.4 mm was noted in the test group, with no significant difference between the two groups (p = 0.043) [46].

Conflicting data exist with regard to the rationale for using barrier membranes to improve augmentative treatment outcomes [33, 35, 44]. In particular, two studies did not observe beneficial effects from the adjunctive use of a barrier membrane over autogenous bone or alloplastic bone substitute alone after 3 years and 5 years, respectively [35, 44]. Contrarily, over a 4-year period, the use of a combination of xenogenic bone and a collagen membrane provided better clinical outcomes, in terms of BOP and PD reduction, than hydroxyapatite particles alone [33].

Outcomes of the Therapy

The overall efficacy of augmentative peri-implantitis therapy was assessed in a recent systematic review and meta-analysis [47]. Based on its findings, significant improvement in marginal bone levels (weighted mean difference (WMD) = 2.0 mm), clinical attachment gain (WMD = 1.8 mm), and reduction of the PD values (WMD = 2.8 mm) were obtained at peri-implantitis sites treated with adjunctive-augmentative measures [47]. Assessment of the potential beneficial effects of the augmentative therapy over the controls (i.e., open flap debridement) showed a significantly higher gain in marginal bone levels of 1.7 mm and defect fill (WMD = 57%), favoring augmentative measures [47]. Clinically, augmentative therapy resulted in significant postoperative soft tissue recession (WMD = 0.7 mm), and when compared to the control sites, the therapy failed to produce significant reductions in PD and BOP values [47].

Peri-implant defect morphology has shown to impact upon the augmentative outcomes for the management of peri-implantitis [48]. Specifically, augmentation of circumferential peri-implant defects resulted in higher PD reduction and clinical attachment level (CAL) gain at 6 months and 12 months compared with the dehiscence-type defects [48]. Furthermore, treatment success (defined as PD < 5 mm, no BOP or Supp, and no further bone loss) was more frequently achieved for rough-surfaced implants versus moderately rough implants (14% vs. 58%, respectively) [37].

Combined Therapy

Combined peri-implantitis therapy includes implantoplasty (i.e., mechanical modification of the implant surface) performed at implant sites where no bone regeneration is expected (i.e., supracrestally and buccally exposed implant parts) followed by augmentation of the intrabony defect components [48]. This surgical approach might be applicable in the majority of peri-implantitis cases, as more than half of naturally occurring peri-implantitis sites (79%) have a combined configuration, including intrabony and suprabony components [49].


Combined peri-implantitis surgery comprises the following steps (Fig. 3):

  • Access to the defect

  • Removal of inflamed tissues

  • Decontamination of the implant surface

  • Implantoplasty performed at buccally and supracrestally exposed implant parts

  • Grafting of the intrabony defect (bone substitute + barrier membrane) with or without a connective tissue graft

  • Adequate flap adaptation

Fig. 3
figure 3

Combined peri-implantitis therapy. a Presurgical view following the removal of a suprastructure. Suppuration detected at implants placed in regions 15 and 16. b Raising of full-thickness flap and removal of granulation tissues. c Implantoplasty performed at the supracrestally and buccally exposed implant surfaces. d Intrabony defect at implant 16 filled with bone substitute. e Placement of collagen membrane over the bone substitute. f Suturing. g Clinical view after 6 months

With respect to the method of implant surface decontamination, over a 12-month period, the use of titanium brushes (i.e., mechanical debridement with an ultrasonic scaler + rinsing with 3% H2O2 + titanium brush) led to significantly better PD reduction (4.87 mm vs. 2.85 mm) and bone defect fill (2.61 mm vs. 1.17 mm) compared with the controls (i.e., mechanical debridement with ultrasonic scaler + rinsing with 3% H2O2) [28] (Table 4). Contrarily, during a 7-year follow-up period, Er:YAG laser application showed similar treatment outcomes to debridement with plastic curettes and cotton pellets soaked in sterile saline [27].

Table 4 Studies reporting on combined peri-implantitis therapy

For the reconstruction of the intrabony defects, xenogenic bone substitute or antibiotic impregnated allograft was used in conjunction with collagen membrane (Table 4) [29, 50, 51]. A concomitant soft tissue augmentation with a concomitant connective tissue graft placed on the buccal aspect performed with a combined peri-implantitis therapy after 6 months led to a mean gain in facial soft tissue height of 0.07 mm around 13 implant sites [50].

Outcomes of the Therapy

Compared with the baseline, combined peri-implantitis therapy significantly reduces BOP, PD, and Supp [27, 29, 51]. A significant reduction in intrabony defects, with a mean radiographic intrabony defect fill of 87 to 93%, was detected after 1 to 7 years [29, 51]. The rate of successful treatment (defined as the absence of PD ≥ 5 mm, no BOP/Supp, and no additional bone loss) was significantly higher for the patients whom titanium brushes were adjunctively used for decontaminating the implant surface (66.7% (10/15) vs. 23.1% (3/15)) [28]. Peri-implant tissue health (i.e., absence of BOP) was detected in 60% (9/15) of the patients 7 years after the combined therapy [27]. As indicated by the retrospective data, disease resolution (i.e., the absence of BOP and PD ≥ 6 mm) was obtained in 28% (11/39) of the patients at 6 months to 10 years following combined peri-implantitis therapy [52].


The disease severity, the defect’s regenerative potential, and patient expectations should be evaluated prior to choosing a surgical technique for peri-implantitis management. OFD with or without adjunctive resective measures may be indicated in the presence of horizontal bone loss. Implantoplasty as a part of peri-implantitis surgical therapy may improve soft tissue inflammatory status; however, it can lead to more extensive mucosal recession. At peri-implantitis sites exhibiting intrabony defects, augmentative measures should be favored. In more advanced cases with combined defect configurations, a combination of augmentative and resective measures may be feasible. Soft tissue volume grafting as an adjunct to surgical peri-implant therapy may be effective to overcome mucosa recession in the aesthetic zone.