Introduction

Peri‐implant diseases are defined as any kind of inflammatory reaction in the tissues surrounding the implants’ [1], whereas peri‐implantitis was introduced as an inflammatory process on hard and soft tissue resulting in pathological pocket formation and loss of supporting bone [2].

The wide range in prevalences of peri‐implantitis varying between 2.7 and 47.1% of implants [1, 3, 4] can be attributed to the missing of exact diagnostic parameters, differences in study population, disease dentition, and implant micro‐ and macrostructures. An effective strategy for treating this disease is required, as otherwise a debilitating condition around the affected implants will result in risk of further loss of function and esthetics.

The development of an adherent biofilm on the implant surface plays an important role in the multifactorial etiology of peri‐implantitis [2]. One key factor in the initiation and progress of peri‐implant diseases is the presence of a bacterial biofilm; therefore, the elimination of the established biofilm from the implant surface and prevention of adhesion of a new biofilm are the main objectives in the treatment of peri‐implant mucositis and peri‐implantitis [5]. Thus, incomplete decontamination of the implant surface could be the biggest obstacle in maintaining the remaining peri‐implant bone [6].

When referring to peri‐implant inflammation, peri‐implantitis is an irreversible progressive inflammation of the surrounding bone [7]. For the classification of peri‐implantitis and corresponding peri‐implant bone lesions, a classification of different defect morphologies – especially focused on the various therapeutic options – is recommended. If there is a combination of bleeding/suppuration with an increasing probing depth compared to previous examinations, or probing depths of ≥6 mm and radiological detectable bone resorption beyond the initial bone level after implant placement, this is referred to as peri‐implantitis [8]. In the absence of initial radiological findings, bone resorption ≥3 mm apical to the intrabony part of the implant is considered indicative of peri‐implantitis [9]. Furthermore, intrabony defects (Class I) are distinguished from horizontal supracrestal defects (Class II). The supracrestal portion is defined as the distance between the transition from the smooth to the machined implant portion and the peri‐implant crestal alveolar bone [10]. Intrabony defects can be divided into purely vestibular or oral dehiscence defects (Class Ia), vestibular or oral dehiscence defects with additional semicircular portions (Class Ib), vestibular or oral dehiscence defects with additional circular bone resorption (class Ic), and circular bone resorption with vestibular and oral dehiscence defects (class Id) or with bilaterally preserved compact bone (class Ie). Horizontal and intrabony defects mostly occur together. According to current data, 55.3% of peri‐implant bone defects are a combination of Class Ie and Class II [11].

Patient age, gender, gene polymorphisms, cardiovascular disease, rheumatoid disease, osteoporosis, condition of residual dentition, implant design, and surface as well as implant site and type of restoration are possible risk factors for peri‐implant disease. Several clinical protocols for treatment of peri‐implantitis have been suggested, including mechanical debridement, the use of antiseptics and local or systemic antibiotics [12, 13], surgical access [14–16], and regenerative [17–20] or resective surgical procedures [21–24]. Yet, re‐osseointegration as desired goal in implant dentistry has not been achieved after treatment of infected treated implants in long term clinical trials until current days [25].

Among all clinical approaches to treat peri‐implantitis, the non‐surgical treatment involving mechanical debridement with local or systemic antimicrobials as adjuncts has not been effective to resolve peri‐implantitis since it cannot provide an adequate access to remove infected tissues around affected implants, especially in advanced lesions [26]. Yet, in a randomized clinical trial mechanical therapy reduced bleeding and plaque accumulation indexes after a six‐month follow‐up [27]. Hence, the non‐surgical approach as a preparatory phase has been recommended before any surgical intervention to treat PI since it can reduce inflammation and biofilm accumulation improving the preoperative conditions of the surgical area [28]. Compared to the non‐surgical approach, peri‐implantitis surgical intervention has been claimed as a more effective therapy since it provides an adequate access to decontaminate the infected implant. Removing biofilm accumulation and granulation tissue around implants can reduce the risk of further disease progression since the local etiological factors are eliminated [29].

Different surgical approaches to treat peri‐implantitis have been evaluated including resective therapy, implantoplasty, bone recontouring, and regenerative techniques with adjuncts such as bone filler particles and membranes [5]. All these techniques depend especially on the configuration of the peri‐implant bone defect and the treated region and aim to either fill up bony defects by so‐called regenerative approaches or to provide effective access to osseodisintegrated areas for adequate daily oral hygiene by resective measures [30]. Regeneration, however, is not appropriate in many cases either due to an unfavorable defect morphology or due to patient‐related factors like continuous heavy smoking or incompliance regarding oral hygiene, leaving the resective intervention as a more reliable alternative [23, 24]. For an effective resective, peri‐implantitis therapy comprises a discreet osteoplasty of the marginal peri‐implant bone, an implant surface modification called implantoplasty through the removal of exposed threads, and antibacterial decontamination of the implant surface are key factors. Using resective techniques the main aim is to create a predominantly horizontal defect and therefore allow for better access during intervention and – importantly – during maintenance later on. Implant surface roughness and the size of initial peri‐implant lesion seem to have an influence on the progression rate of peri‐implantitis [31]. Studies have shown that implant and abutment surface roughness significantly influence the type and quantity of microbiota supra‐ and subgingivally [32]. Therefore, the commonly accepted rationale of implantoplasty consists of mechanical removal of implant threads (or any rough implant surface) using sequential drills [33], thus yielding a smooth‐finished implant structure that will reduce biofilm accumulation [34]. This has been found to influence the outcome of peri‐implantitis treatment in terms of extent and/or severity of residual peri‐implant inflammation [35]. Successful clinical and radiographic outcomes of peri‐implantitis treatment have been reported in literature when a resective procedure was combined with implantoplasty [23, 24, 26].

However, none of them has been proven superior to the others concerning peri‐implantitis resolution in long term. The combined resective and implantoplasty approach has shown favorable results in some studies [20, 23, 24, 29, 36]. The mechanical removal (grinding) of the implant threads and the rough implant surface, rendering thus a relatively “smooth” implant surface can be performed either at the parts of the implant, where due to defect anatomy only a limited potential for bone regeneration and/or re‐osseointegration after healing is expected, e.g. the supra‐bony and dehiscence‐aspects of the implant or on the whole exposed rough implant surface [37].

Both implantoplasty approaches aim to reduce biofilm accumulation by smoothening the rough exposed implant surface, since numerous studies have shown that a rough surface can protect biofilm from shear forces carried out by mechanical debridement [38, 39], thus allowing biofilm growth and persistence as a local factor for progession of peri‐implantitis.1 Regarding that, the smoothening and decontamination of the exposed implant surface will provide a more favorable area for soft tissue adaptation during the healing process. In vitro studies have also reported that a smooth surface enhances fibroblast adherence and consequently can help to get peri‐implant soft tissue health [36].

Unpleasantly, implantoplasty may cause perforation of the implant body, destruction of the implant‐abutment connection, overheating of the implant during grinding causing thermal damage to the surrounding bone, or induction of mucosal staining and/or increased risk for late inflammatory reactions due to titanium particle deposition [40], generated from the grinding procedure. Furthermore, reduction of the implant mass (implant diameter) at its coronal aspect, occasionally also involving the implant collar [41, 42], may compromise implant strength and lead to an increased rate of late mechanical complications, like for example implant collar deformation, loosening of the supra‐structure, fixation‐screw fracture and implant fracture. Altogether this may lead to recurrent peri‐implant biological complications and/or require explantation.

Treatment

Patient‐specific treatment of peri‐implant inflammation is a synoptic treatment concept with attention to individual risk factors in order to prevent the development or renewed progression of peri‐implant infections and anti‐inflammatory, if possible reconstructive treatment of the peri‐implant lesion. The aimed success of implant treatment is only possible, if in the long‐term biological, technical, and esthetic complications can be avoided. Biologically, the absence of peri‐implant mucositis, peri‐implantitis, and the establishment of stable soft tissue conditions is necessary, especially during maintenance therapy after active treatment of peri‐implant infections. Biological complications at implants differ in frequency and severity in patients with and without periodontitis. Thus, the implementation of a careful anti‐infective periodontal therapy with reduction of inflammatory signs and probing depth values before treatment of implantoplasty is mandatory.

For a successful long‐term treatment of peri‐implant inflammation, particularly from the patient point of view, it is essential to design the prosthetic restoration as similar as possible to the natural appearance of the teeth with corresponding good oral hygiene characteristics to satisfy the patient optically and functionally; often, this can only be achieved by restoring the lost tissue dimensions.

The extent to which the crown‐to‐implant length ratio has an influence on the survival, on the marginal bone level, or on prosthetic complications in the absence of augmentation is controversially discussed. Some reviews concluded that no negative influences exist [43, 44]. In contrast, other systematic reviews observed a higher incidence of prosthetic complications such as abutment loosening or fractures, mainly in posterior jaw regions. Restoration of near‐original dimensions of hard and soft tissues can minimize these risks in the long term [45]. Moreover, the esthetic result is significantly improved, and the ability to maintain oral hygiene, thus ensuring the prevention of inflammatory processes [46].

If peri‐implantitis develops despite consideration of these recommendations, the causal therapy of existing risk factors needs to start with the utmost priority; this includes smoking cessation, control of diabetes mellitus, and specific oral hygiene instructions. Localized plaque‐induced inflammation should be eliminated by non‐surgical mechanical plaque removal, optimization of oral hygiene skills, and inclusion in a regular maintenance therapy program [47]. To enable an efficient plaque removal is the primary goal [48]. Home‐based oral hygiene can be carried out using manual or electric toothbrushes and appropriate interdental brushes [49].

Peri‐implantitis with a maximum of 75% mean bone loss can more often result in implant loss depending on implant position, prosthetic importance, inflammation, oral hygiene access, and implant type. An implant with mean bone loss of 25–50% is 8.86 times more likely to fail than an implant with mean bone loss <25%. Moreover, 1 mm of additional mean bone loss increases the risk of failure by 74%. The removal of the affected implant is usually indicated after clinical and radiological diagnosis (Figures 14.1–14.8), as well as very low Resonance Frequency Analysis (RFA) values or very high Damping Capacity Analysis (DCA) values, deep tapping sounds, mobility, and large probing values as indicators for insufficient osseointegration [47]. In all other cases, the peri‐implant inflammation must permanently be brought back to a stagnation phase, beginning with a non‐surgical treatment phase and the adjustment of all oral hygiene parameters.

The systematic and continuous prevention and treatment of peri‐implant diseases is based on the original CIST concept (cumulative interceptive supportive therapy or antiseptic cumulative supportive therapy) according to Mombelli and Lang [50, 51]. The CIST concept is a step‐by‐step model divided into four treatment steps. Depending on the diagnostic course, the modular therapy guide initially includes hygiene instructions and professional dental cleanings (part A), followed by chlorhexidine rinses, gel applications (part B) and systemic antibiotic medication (part C), and finally subsequent surgical interventions with either resective or regenerative treatment approaches (part D) (Figures 14.9–14.15). However, especially in the further development of patient‐specific treatments, the existing risk factors must be recognized and adjusted, and the evaluation of each treatment step must not be made according to rigid consideration of probing values, but according to the change in probing values over time [52, 53].

Non‐surgical treatment of peri‐implantitis can be expected to reduce bleeding on probing, but results in a limited improvement in probing values [54]. When adjuvant irrigation solutions or antibiotics were used, such as minocycline products and tetracycline derivatives, the effectiveness was shown by improved bleeding on probing values and reduced probing depths [13,55–57] (Figure 14.11). However, the administration of systemic antibiotics should be avoided for non‐surgical procedures [14, 58]. The adjuvant use of Nd:YAG and Er:YAG lasers in addition to mechanical therapy resulted in only short‐term success, which lasted a few months in terms of bleeding on probing and probing depths reduction [59, 60].

Six weeks after the non‐surgical procedure, a surgical, mechanical debridement including chemical de‐ contamination of the implant surface should be performed. Access flaps, resective therapy approaches with or without implantoplasty, or augmentative procedures can be used in this operative intervention. The decisive factors in surgical treatment planning in this context are bony defect morphology and position of the affected implant – either inside or outside the esthetic area (Figures 14.12–14.14). In principle, augmentative measures for intrabony components such as bowl‐shaped defects (class Ie [61]) and three‐ or four‐walled bone defects can achieve improved clinical, radiological therapeutic, and anti‐inflammatory results. The remaining bony defect morphologies are usually treated with resective procedures optionally combined with implant surface modification.

Indications

Surgical access flaps and resective treatment approaches are indicated for supracrestal bone defects (horizontal bone resorption) with exposed implant threads [62, 63]. Resective treatment of peri‐implant inflammation can recontour the bone and reduce probing values. This can be performed with or without smoothening of the implant surface. Peri‐implant bone defect morphology can limit the angulation of the bur and, thus, affect the outcome of implantoplasty. Concerns have also been raised regarding biological and mechanical complications associated with implantoplasty [64].

In the esthetic region, an access flap with a strictly intrasulcular incision preserving the soft tissue is preferred, whereas in the posterior region, an apically repositioned flap can be used [62]. In esthetic regions with moderate bone loss and shallow bone defects, the combination of surgical debridement with a free connective tissue graft is a recommended option to achieve significant clinical improvement while avoiding the high risk of recession (Figures 14.16–14.21) [15, 20]. Especially in posterior areas, resective treatment with implantoplasty leads to improved clinical and radiological results after a three‐year follow‐up compared to the resective approach without implantoplasty (STM: 1.64 ± 1.29 versus 2.3 ± 1.45 mm) [23, 24].

Surgical Procedure

The aims of resective surgery are reducing pocket probing depths and gaining a soft tissue morphology that enhances good self‐performed oral hygiene and peri‐implant health. The therapeutical approach of peri‐implantitis with suprabony defects surrounding rough implants comprises several aspects [65]: (i) removal of supragingival bacterial plaque, (ii) surgical approach with access flap, (iii) removal of granulation tissue and detoxification of the exposed implant surface, (iv) correction of the anatomical architecture of the bone, (v) modification of the roughness of implant surface, (vi) establishment of an efficient plaque control regime (Figures 14.22–14.28) [48, 66].

Implantoplasty can be performed at the surgical peri‐implantitis treatment. Implantoplasty is done on the exposed implant threads by polishing and smoothing implant surface in order to reduce bacterial recolonization [34, 67]. Removal of the threads and surface polishing can generally be performed using different sequences of instruments. While Chan et al. [68] and Ramel et al. [33] described the use of diamond burs followed by an Arkansas stone, Sahrmann et al. [69] suggested the use of a rough carborundum stone followed by an Arkansas stone and – like Chan et al. [68] – silicon polishers. Beyond that, several other sequences of instruments for implantoplasty have been proposed [23, 70]. They vary in different ways that might potentially influence the mechanical stability of the instrumented implant [71, 72]. Firstly, the invasiveness or quickness of abrasion that depends on the rotational speed and the coarseness of the instrument is likely to have an effect: the quicker the abrasion the less material loss will be controllable. Secondly, instruments with unchangeable morphology like diamonds might not perfectly adapt to the implant surface while abrasive stones can be trimmed in order to fit perfectly. However, diamonds might have a smaller diameter and therefore might be less prone to injure neighboring teeth, which should be considered as a potential damage during instrumentation [69].

The so‐called “modified” implantoplasty technique [26] forming a bottleneck format beginning from the most apical part of the exposed implant body is commonly performed following a sequence of steps and burs (Figures 14.29–14.33). First, a bud‐shaped diamond bur (grit size 106 μm) at 120,000 rpm is used to smoothen the exposed threads and to perform a “platform switch” area in the exposed apical part of the implant. In this step, the smoothing procedure is mainly restricted to the threads and does, obviously, not affect the core diameter of the implants. A waist shape, narrowing the medial region of the exposed implant body is achieved by using football‐shaped fine (grit size 46 μm) and extra‐fine (grit size 25 μm). Afterward, the rough surface is polished at 40,000 rpm with flame‐shaped fine (grit size 46 μm) and extra fine (grit size 25 μm) diamond burs (8379 314.021; 379EF 314.023, Gebr. Brasseler GmbH & Co. KG, Lemgo, Germany) [73] (Figure 14.34). Flame or ellipse‐shaped carbide burs (30 mm length) can be used with normal (12 cutting edges) and ultra‐fine (30 cutting edges) finishing grades (Figure 14.35). Damage of the neighboring teeth, however, is a rather frequent finding with a prevalence of one‐third of all cases. That is why football‐shaped burs should only be used carefully in situations with good accessibility [74]. The smoothening of the surface is finalized with Arkansas stone torpedo‐ or round‐shaped white aluminum oxide burs at 40,000 rpm (601.314, extra fine, grit 420; Gebr. Brasseler GmbH & Co. KG) (Figure 14.36) [75]. The final polishing of the implant’s waist‐like surface is done using a mini‐point‐shaped abrasive‐impregnated silicone polisher (Greenie) until the smoothened areas look evenly machined macroscopically (Figure 14.36). The complete burs sequence is performed under copious irrigation with sterile saline. Using this technique, the median implant diameters in tissue‐level or bone‐level implants are normally reduced by about 0.10–0.20 mm. The surface modification with a sequence of burs leads to smoother surfaces compared to diamond sonic tips. Followed by Arkansas stones, equivalent final surface roughness could be detected in both implantoplasty procedures. In cases of narrow‐diameter implants, it could be helpful to use sonic devices as a more conservative method with less structure loss [64]. Bone recontouring can be performed with a spherical bur under copious irrigation (Figures 14.37–14.46).

Implantoplasty commonly results in a smoothing of the sharp‐edged microstructure. However, it is also associated with the presence of irregular grooves and flat pits, which appear to be more uneven than the structure noted for machined surfaces. In particular, implantoplasty‐treated and machined surfaces are characterized by a comparable quantity (Wt%) of elements carbon (C), oxygen (O), sodium (Na), chloride (Cl), potassium (K), and silicon (Si), but a significantly different quantity of elements nitrogen (N), titanium (Ti) and aluminum (Al) [73]. Finally, the peri‐implant mucosa is thinned out and repositioned in a more apical direction, leaving the previously smoothened surface accessible for self‐conducted oral hygiene by the patient [20].

The remaining titanium particles in the tissue should be reduced by means of gauze exposure and excision of the granulation tissue after implantoplasty or, depending on the indication and diagnosis, implantoplasty should be limited to the supramucosal areas before flap formation, since the effect of tissue reactions to the remaining titanium with regard to progressive peri‐implant inflammation is currently unclear [62, 76]. It is recommended to remove the suprastructure before resective intervention, especially in case of implantoplasty; as hereby, the suprastructure can be adapted to as sufficient oral hygiene design before being reinserted [62]. Resective procedures with adjuvant systemic antibiotics did not result in significant clinical and radiological long‐term improvement [58]. Especially, implant position and design as well as the hygienic suitability of the prosthetic reconstruction should be critically evaluated preoperatively [47]. The question of open or closed healing [77] and the benefit of adjuvant systemic antibiotics [78] also cannot be clearly answered with the current state of literature. In cases of implant surface modifications and open flap debridement, there is no explicit need for a closed healing and suprastructure can be inserted directly after the surgical procedure [63].

Decontamination

The efficacy of titanium decontamination can be assessed using different protocols under consideration of surface changes in roughness, chemical composition, and wettability on the microimplant surface. Common protocols for decontamination are irrigation with 24% EDTA, 2% chlorhexidine (CHL), gauze soaked in 2% chlorhexidine (GCHL), gauze soaked in ultrapure water (GMQ), irrigation with citric acid (20%) or scaling (SC), use of titanium brushes (TiB) and implantoplasty (IP) [64]. All protocols resulted in changes in roughness, wettability, and chemical composition, yet gauze‐soaked chlorhexidine, scaling, titanium brushes, and implantoplasty presented the best decontamination outcomes. Changes in surface roughness were observed after all treatment protocols, but implantoplasty presented the smoothest and least hydrophilic surface [26]. In both initially smooth and rough implants, the lowest values of residual contamination were observed using gauze‐soaked chlorhexidine, scaling, titanium brushes, and implantoplasty. There was a statistically significant reduction in hydrophilia after implantoplasty, with no difference if implants were initially smooth or rough. Concurrently, the topographic implant changes are most effective in removing biofilm [34]. Almost no bacterial remnants could be observed after implantoplasty (Figures 14.47–14.52) [79]. In accordance, most effective decontamination protocols do not preserve the elemental integrity of the titanium surface, affecting the interaction of the implant with surrounding tissues [80]. The benefits of a combination of chemical disinfection and protocols with implantoplasty are still controversial [81].