Surgical Management of Peri-implantitis

The surgery consists of the following steps:

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].

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].

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

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, 17‐25] (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) [17‐20, 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].

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, 27‐29]. 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].

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

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, 33‐38, 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].

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].

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, 33‐35, 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].

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

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].

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].

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].