Chapter 7: Peri-Implantitis: Basics and Beyond

2 CE Hours

By: Dr. Madhumietha Arumugam, B.D.S., M.D.S.

Learning objectives ŠŠ Define peri-implantitis and peri-implant mucositis. ŠŠ Contrast differences between peri-implantitis and peri-implant ŠŠ Discuss the prevalence of peri-implantitis and peri-implant mucositis. mucositis. ŠŠ Outline the histology of peri-implant tissues. ŠŠ Describe the management strategies for peri-implantitis. ŠŠ List the grades of classification of peri-implantitis. ŠŠ Explain Cumulative Interceptive Supportive Therapy for peri- ŠŠ Identify the risk factors associated with peri-implantitis. implantitis. ŠŠ Explain etiopathogenesis of peri-implantitis. ŠŠ Summarize the clinical implications of peri-implantitis and the ŠŠ Discuss the steps involved in obtaining the diagnosis of peri- importance of implant maintenance. implantitis. Introduction Dental implants have seen a big boom in the field of , and defined as an inflammatory process affecting the tissues around an have emerged as a new vista in the arena of full mouth rehabilitations. osseointegrated implant in function, resulting in loss of supporting . It has been estimated that 2 million implants will be installed annually Peri-implant mucositis is defined as reversible inflammatory changes of and this number is expected to rise in the coming years. Hence, the the peri-implant soft tissues without any bone loss [3]. maintenance of the dental implants becomes an important matter Prevalence of peri-implantitis and peri-implant mucositis of subject. Akin to the natural teeth, implants emerge through the The sixth European workshop of on peri-implant and are susceptible to plaque formation and disease diseases has stated that peri-implant mucositis occurs in about 80 [1, 2]. progression in the susceptible host percent of subjects (50 percent of sites) restored with implants, and Definitions peri-implantitis in between 28 percent and 56 percent of subjects (12– The latest consensus about peri-implant diseases, reached in the seventh 40 percent of sites) [4]. This course will explore in detail the histology European Workshop on Periodontology has affirmed the definitions of peri-implant tissues, classification, risk factors, microbiology, of peri-implantitis and peri-implant mucositis. Peri-implantitis was etiopathogenesis, and management of peri-implantitis.

Histology of peri-implant tissues The soft tissue surrounding healthy osseointegrated dental implants ‘biological barrier,’ and protects the zone of from shares anatomic and functional features with the gingiva around teeth. factors released from plaque and the oral cavity. The connective tissue The outer surface of the peri-implant mucosa is lined by a stratified can be divided into an inner zone and an outer zone. keratinized oral that is continuous with a junctional The inner zone is 50-100 µm wide with collagen fibers aligned parallel epithelium attached to the titanium surface by a basal lamina and by to the implant surface. The outer zone consists of collagen fibers in hemi-desmosomes. The peri-implant epithelium is a keratinized, multi- various directions and is highly vascularized [5]. layered squamous epithelium with four layers: ●● Stratum basale with cylindrical or cubical mitotic active cells. The biologic width of an implant can be defined as the distance ●● Stratum spinosum. from most coronal extension of the to the ●● Stratum granulosum. alveolar bone. The average biologic width around an implant is ●● Stratum corneum. ~3mm, consisting of 1.8mm of junctional epithelium and 1.05mm of connective tissue attachment [6]. Supracrestal implant surface The junctional epithelium is separated from the alveolar bone by with an apical coronal expansion of at least 3 mm is essential for the collagen-rich connective tissue, which is ~3 to 4mm. This forms a development of a stable biologic width.

Classification of peri-implantitis Various authors have classified peri-implantitis for ease of classifications are listed below. Spiekermann (1995) has classified peri- communication and management. Some of the commonly used implantitis into four classes such as follows [7]: CLASS I Slight horizontal bone loss with minimal peri-implant defect. CLASS II Moderate horizontal bone loss with isolated vertical defect. CLASS III Moderate horizontal/vertical bone loss with circular bony defects. CLASS IV Advanced bone loss with broad, circumferential vertical defects as well as loss of buccal and/or palatal bony wall.

Schwarz et al. (2007) have classified the bone defects that occur in Class II – supra alveolar bone defects. Generally, a combination of peri-implantitis [8]. They classified bone defects as: Class I –intra class I and class II defects is observed at one implant. Class I was osseous bone defects. further classified as:

Dental.EliteCME.com Page 96 CLASS 1A Buccal or oral dehiscence defects with position of the implant body within or beyond the envelope. CLASS 1B Buccal or oral dehiscence defects with semi-circular bone resorption to the middle of the implant body (position of the implant body within or beyond the envelope). CLASS 1C Dehiscence defects with circular bone resorption under maintenance of the buccal or oral compact layer (position of the implant body within or beyond the envelope). CLASS 1D Circular bone resorption with buccal and oral loss of compact bone layer (position of the implant body within or beyond the envelope). CLASS 1E Circular bone resorption under maintenance of the buccal and oral compact layer.

Forum and Rosen (2012) have classified peri-implantitis as early, moderate, and advanced based on the probing depth and the amount of bone loss [9]. It is as follows: Early PD ≥ 4 mm ( and/or suppuration on probing). Bone loss < 25 percent of the implant length. Moderate PD ≥ 6 mm (bleeding and/or suppuration on probing). Bone loss 25 to 50 percent of the implant length. Advanced PD ≥ 8 mm (bleeding and/or suppuration on probing) Bone loss > 50 percent of the implant length.

Risk factors associated with peri-implantitis A plethora of risk factors have been implicated in the etiopathogenesis [14, 15]. Glycated hemoglobin, or HbA1C, diabetic control is an of peri-implant diseases, enlisted below: important factor when assessing the relationship between ●● Plaque – Peri-implant diseases have been implicated with and peri-implantitis. High blood glucose level can impact tissue microbiota resembling that of and periodontitis. High repair and host defence mechanisms, as diabetic control affects proportions of anaerobic gram-negative rods, motile organisms, function [16]. As a result, diabetes can disrupt collagen and spirochetes have been denoted, but this association does not homeostasis in the and is associated with necessarily prove a causal relationship. Healthy peri-implant neutrophil dysfunction and imbalance of . Thus, sulcus is characterized by high proportions of coccoid cells, a the tissue repair ability and defensive mechanisms of diabetic low ratio of anaerobic/aerobic species, a low number of gram- patients to the insult of are impaired [17]. Additional negative anaerobic species, and low detection frequencies for prospective cohort studies are needed to clarify the association periodontopathogens [10]. Implants with peri-implantitis reveal between diabetes and peri-implantitis. a complex microbiota encompassing conventional periodontal ●● Residual cement – Many recent studies have confirmed residual such as A. actinomycetemcomitans, P. gingivalis, cement to be a risk factor for peri-implant diseases [18]. The presence T. forsythia, P. micra, C. rectus, F. nucleatum, P. intermedia, of residual cement makes the subgingival space more prone for plaque [19] T. denticola, and [10]. Other species, such as accumulation and progression of peri-implant diseases . Hence it Pseudomonas aeruginosa, Enterobacteriaceae species, C. albicans, has been advised to evaluate both clinically and radiographically for or staphylococci are also frequently detected around implants. any residual cement left after the placement. These organisms are uncommon in the subgingival area but have ●● Genetic traits – Genetic variations have been implicated with been associated with refractory periodontitis. High proportions of peri-implantitis, especially IL-1 gene polymorphism. However, Staphylococcus aureus and S. epidermidis on oral implants have conflicting results exist and future prospective studies are been reported. Recently, presence of Candida species has been needed to establish the relationship. A systematic review with isolated from failing peri-implant sites [11].. twenty-seven relevant articles found no consensus among the [20] ●● History of periodontitis – Substantial evidence suggests that studies reviewed . However another study on IL-1RN gene patients with a history of periodontitis show an increased risk for polymorphism concluded that it is associated with peri-implantitis [21] . peri-implant diseases compared with non-periodontitis patients [12]. and may represent a risk factor . Implants placed in patients suffering from ●● Occlusal overload – Non-axial occlusal load can be very have a tendency for greater crestal bone level changes and destructive to implants and are considered less tolerable to them probing pocket depth. The consensus report of the sixth European compared to teeth because of a lack of a periodontal ligament. [22, 23] workshop on periodontology has confirmed that history of Finite element studies suggested that the occlusal load is periodontitis is a major risk factor for peri-implantitis [4]. concentrated at the implant marginal bone. Bone remodels in ●● Smoking – Smoking has been considered a major risk factor for response to the strain. Excessive stress can cause micro fracture peri-implantitis [4]. A systematic review reported five retrospective within bone and eventual bone loss. This has been confirmed by a and one prospective study showing an association of smoking and recent systematic review, which suggested that occlusal overload [24] peri-implantitis. They showed a significant increase in marginal was positively associated with peri-implant marginal bone loss . bone loss in smokers compared with non-smokers [13].. ●● Potential risk factors – Research has emerged regarding an [25] ●● Diabetes – Diabetes has been implicated to be a risk factor for array of potential risk factors that need further exploration . peri-implantitis with limited evidence [4]. Systematic reviews state Rheumatoid arthritis with concomitant connective tissue disease [26] [27] [28] that the current evidence does not allow a definitive conclusion , increased time of loading , alcohol consumption , and [29] that diabetic patients have a higher incidence of peri-implantitis implant surface have been shown to be risk factors for peri- implantitis with limited evidence. Etiopathogenesis of peri-implantitis is a complex reaction of the body in response to an accumulation on teeth, clinical signs of inflammation appear. Even infectious agent, antigen challenge, or injury. An accumulation during early stages of inflammation, considerable tissue damage of microbes at the peri-implant/mucosal margin leads to a local occurs. Thus, the cells in the inflammatory lesion cause considerable inflammatory response, and within ten to twenty days of plaque tissue damage in their effort to combat the invading .

Page 97 Dental.EliteCME.com Accumulation of plaque in the gingival crevice aggravates the Advanced peri-implant mucositis shows ulcerated pocket epithelium inflammatory reaction over time, and consequently, irreversible tissue with apical proliferation and subepithelial connective tissue degeneration. destruction occurs. Degradation of connective tissue is followed by There is presence of micro or macro abscess formation. start epithelial migration and bone resorption, which marks the borderline producing prostaglandins (PG), cytokines and matrix metalloproteinases between gingivitis/mucositis and periodontitis/peri-implantitis [30]. (MMPs). TNF-α and IL-1 stimulate fibroblasts to produce MMPs and Peri-implant disease goes through the following stages: 1. Early peri- PG. TNF-α, IL-1, and PGs stimulate osteoclasts to initiate crestal bone implant mucositis, 2. Established peri-implant mucositis, 3. Advanced resorption. It further progresses to peri-implantitis where progressive peri-implant mucositis, and finally 4. Peri-implantitis. Early peri- dense infiltration of cells in lateral and apical direction takes place. It has implant mucositis is characterized by changes caused by supragingival been noted that continued apical proliferation and ulceration of epithelium [10]. plaque that cause alterations in junctional epithelium and with loss of collagen proceeds to peri-implant bone resorption subepithelial connective tissue. Junctional epithelium shows lateral The increased susceptibility for bone loss around implants may relate proliferation and is stimulated to produce IL-8. Histopathology to the absence of inserting collagen fibers into the implant, as is the shows increased polymorphonuclear leukocytes, macrophages, case with a . A self-limiting process exists in the tissues around T , plasma cells and increased vessel permeability. natural teeth that results in a protective connective tissue capsule of the Established peri-implant mucositis shows junctional epithelium with supracrestal of the tooth that separate the lesion from the lateral and apical proliferation and formation of pocket epithelium with alveolar bone in contrast to peri-implantitis. Such a self-limiting process mild degeneration. Dense inflammatory infiltration further increases does not occur in peri-implant tissues and the lesion usually extends with increase in polymorphonuclear leukocytes, macrophages and to the bony crest, which is different than the periodontitis lesions [31]. lymphocytes. Macrophages release IL-1, IL-6, IL-8, IL-12, and TNF-α Another distinct feature in studies on experimentally induced peri- in response to bacterial LPS. implantitis was that following ligature removal, there was spontaneous continuous progression of the disease with additional bone loss. All implants appear to be susceptible to peri-implantitis [32, 33]. Diagnosis of peri-implantitis Diagnosis of peri-implantitis is essential in order to treat and maintain It has been noted that suppuration associated with intense infiltration the dental implants. The sixth European workshop of periodontology containing polymorphonuclear leukocytes, B cells, macrophages, and on peri-implant diseases gave a consensus on the salient features to be plasma cells have been observed in sites taken from failed implants considered for diagnosis of peri-implantitis [4]. They are as follows: due to peri-implantitis [34]. Changes in the parameters of the attachment ●● Probing is essential for diagnosis of peri-implant diseases. level lead to the next step in investigation to perform additional ●● Conventional probing using a light force (0.25 N) does not damage radiographic examinations. the peri-implant tissues. Radiographic examination: Periapical radiographic examinations ●● indicates the presence of inflammation in the are considered essential to determine the diagnosis of peri-implantitis. peri-implant mucosa. Immediate post-implant placement periapical radiograph is considered ●● Bleeding on probing may be used as a predictor for loss of as the baseline to which the subsequent radiographs are compared to tissue support. establish the diagnosis. The periapical radiographs should be taken ●● An increase in probing depth over time is associated with the loss perpendicular to the implant body and ensured that the threads of of attachment and supporting bone. the implant are clearly demarcated. Usually ~1.5mm bone loss one ●● The probing depth, the presence of bleeding on probing and year after loading and ~0.2mm bone loss in the subsequent years is suppuration should be assessed regularly for the diagnosis of peri- considered normal. Other radiographic examinations including cone implant diseases. beam computed tomography (CBCT) can be used to examine the ●● Radiographs are required to evaluate supporting bone levels location of progressing attachment loss. Consequently, digital image around implants. analysis has expanded into implantology to monitor peri-implant bone ●● Analysis of peri-implant crevicularfluid (PICF) is not a clinically healing and gain or loss of alveolar bone density. useful diagnostic parameter for peri-implant disease. Implant mobility: Implant mobility is a finding associated with implant The American Academy of Periodontology has devised the steps to be failure, as the presence of mobility usually coincides with complete loss followed in its recent academy report on peri-implantitis [25]. of osseointegration. However, perceived implant mobility may relate to Probing, bleeding, and suppuration: Dental professionals should the restoration and/or abutment components that have loosened, which probe the implant after the installation of the final restoration, with a may or may not lead to crestal bone loss without loss of integration. A force of 0.25N, parallel to the implant, and the probing depth should loose implant-supported prosthesis may contribute to the accumulation be measured from the base of the sulcus to the gingival crest. The level of plaque, which may lead to the development of peri-implant mucositis of the crestal soft tissue can be measured using a fixed reference point and/or peri-implantitis, and as such, this should be corrected. Primary on the restoration and should be noted as the clinical attachment level implant stability is an important measure of osseointegration and many or the relative attachment level. The extent of probe penetration is devices which make use of this principle can be used as a diagnostic tool influenced by an array of factors such as probing force and angulation, for peri-implantitis. Periotest or Dental Fine Tester has been used in the probe tip diameter, roughness of the implant, inflammation of the past for the same; however, these methods have been criticized for their and the firmness of the marginal tissues. Hence, careful lack of resolution, poor sensitivity, and susceptibility to being influenced evaluation of the probing depth is crucial. Plaque assessment and by the operator. Resonance frequency analysis (RFA) is a novel clinical, mucosal assessment can aid in evaluation of the peri-implant disease non-invasive quantitative assessment tool for determining the stability process. A change in the parameters is essential to determine the and presumed osseointegration of implants. This system utilizes a basic diagnosis. vibration theory and is applied to design a transducer that can be excited using a steady state and frequency waveform; its response is measured Bleeding on gentle probing indicates soft tissue inflammation. [35] Presence of exudation/suppuration indicates pathological changes that to determine the implant stiffness in the surrounding tissues . demand further investigation.

Dental.EliteCME.com Page 98 RFA values are represented by a quantitative unit called the implant Secondary diagnostics: Besides these main criteria for diagnosis of stability quotient (ISQ) on a scale from 1 to 100 and are measured peri-implantitis, various other factors have been used to study the disease using the Osstell device. RFA values for successfully osseointegrated process of peri-implantitis. These include bacterial culturing, inflammatory implants have been reported to be in the range of 57 to 82 ISQ with a markers, and genetic diagnostics. Further studies are needed to establish mean of 69 ISQ after one year [36]; values under 50 ISQ should be seen relationship between these factors and peri-implantitis. as critical and should be evaluated further for peri-implantitis.

Differences between peri-implantitis and peri-implant mucositis In order to effectively treat peri-implant diseases, dental professionals Management of peri-implantitis must determine the differences between peri-implantitis and peri- A systematic review on treatment of peri-implantitis has confirmed that implant mucositis. The contrasting differences between peri-implantitis mechanical combined with antiseptic/antibiotic therapy, and peri-implant mucositis are listed below. the Er: YAG or regenerative techniques may be used for treating peri-implantitis [37]. There has been a plethora of strategies tried and Peri-implant mucositis Peri-implantitis tested for the management of peri-implantitis. They are detailed below. Reversible + - Mechanical debridement Local debridement of hyperplastic peri-implant tissues using hand Plaque accumulation + + or ultrasonic plastic instruments has been suggested to be one of Bleeding on probing + + the most important management strategies for peri-implantitis. The + (+) recommendation is to avoid metallic or hard instruments when touching the abutment/implant surface. This is to minimize surface Pocket formation - + damages and roughening, which can favor plaque adhesion, and Suppuration - + has been based on several in vitro investigations and randomized [38, 39, 40] Swelling (+) + controlled trials . However, it should be noted that implant surfaces are abraded by bristles as well and that roughening Redness + + of the surface by different maintenance methods has not yet been Bone resorption - + shown to increase the amount of mineralized deposits on abutments or Implant mobility - (+) their adherence to implant surfaces.

Surface decontamination and conditioning A nonspecific decrease of the total bacterial load in the peri-implant rinsing also establishes adequate surface pocket, together with a suppression of specific pathogens, may deconditioning. It has been suggested that infected surfaces of be enough to re-establish equilibrium between the peri-implant Hydroxyapatite-coated (HA) implants should be cleaned with citric microbiota and the host defense. If perfect procedures can acid (pH 1) for 30 seconds to one minute. Burnished hydrogen prevent massive recolonization of treated sites, implants may remain peroxide has not been found to be superior to saline in removing stable over prolonged periods after such therapy, even though the bacterial endotoxins. It has been proposed that an altered HA coating surfaces of the implants may not be biocompatible enough to allow a be removed or that titanium plasma-sprayed surfaces be cleaned with direct re-apposition of bone. Surface decontamination has been seen as ultrasonic or air-powder abrasives [40]. Sonic scalers with plastic tips an important technique for treatment of peri-implantitis. Studies have were found to be as effective as or more effective than burnished saline shown that titanium alloy implants can be decontaminated with citric controls in removing endotoxins from implant surfaces. Randomized acid, stannous , -HCl, chlorhexidine gluconate, controlled studies have shown that air-powered abrasives can clean a , chloramine T, sterile water, plastic sonic scaler tip rough implant surface of bacteria and organic materials [41]. However, and air powder abrasive unit. it is not known whether air-powered abrasives can effectively clean narrow infrabony defects, as the contact profile angle may be too acute Various mechanical and chemical techniques have been proposed for to deliver an effective spray to the implant surface. In addition, such an cleaning infected implant surfaces. Low-speed rotary instruments can acute angle of the air-powered abrasive instrument may induce emboli be used for removing the plasma-sprayed layer from rough surfaces. in the bone marrow spaces. Indeed, several authors have advised Additional application of chlorhexidine gel for five minutes on the against the risk of embolism induced by pressurized air when using mechanically cleaned implant surface has been recommended to air-powered abrasives. provide topical disinfection.

Antimicrobial therapy To improve the resistance to mechanical load, almost all implants However, its bactericidal effect in vivo at low concentrations (0.12 today have a roughened surface in the area where osseointegration percent to 0.2 percent), coupled with crevicular fluid dilution and is supposed to occur. These surfaces can become contaminated by the apparent protective function of serum, may render chlorhexidine bacteria as a consequence of peri-implantitis. Mechanical debridement weakly bactericidal or even ineffective. Metronidazole has been on such surfaces has a limited effect and can certainly not remove all found to be effective at the tested concentrations of 25 percent in bacteria. Adjunctive chemical agents have thus been recommended to gel form [40]. Local application of tetracycline fibers has also been enhance the treatment effect. proposed as an effective adjunctive treatment for failing implants. A randomized controlled trial proved that minocycline microspheres In case of suspected infectious complications and peri-implantitis, can be effectively used for treating for peri-implantitis [42]. If systemic adjunctive subgingival irrigation of the pocket with 0.12% to 0.2% antibiotic therapy is considered, it has been suggested that it be guided chlorhexidine two to time times per day for ten days to three weeks by bacterial culturing and sensitivity tests. However, it is unknown has been suggested as an efficient local disinfectant[41] . Chlorhexidine whether the results of such diagnostic tests would actually influence is believed to be the antimicrobial agent of choice. the course of the therapy.

Page 99 Dental.EliteCME.com Bacteria associated with failing implants have been found to be The effect of combination therapy, including systemic amoxicillin sensitive to the following antibiotics: penicillin G, amoxicillin, and metronidazole and local debridement, has also been suggested for combination of amoxicillin and metronidazole, and amoxicillin- peri-implantitis treatment. The combination of systemic antimicrobial clavulanate, respectively. Bacteria around implants may form therapy and mechanical debridement has shown to result in the to protect themselves from the host. Dental plaque is a typical resolution of the peri-implantitis lesion, resolution of recession of the example of . Although biomaterial centered for marginal peri-implant mucosa, and a minor additional apical shift of implants placed in the maxillofacial region are rarely associated with the base of the bone defect. conspicuous biofilms, such deposits have been shown to protect the Use of for implant surface detoxification embedded bacteria from antibiotic. In case of suppurative peri-implant Various laser systems have been tried and tested for implant surface , the use of specific systemic antibiotics against anaerobic decontamination. It is known that photosensitization and soft lasers microorganisms is generally recommended. In particular, it has been can eliminate bacteria from different implant surfaces (i.e., machined, proposed that the administration of a combination of antibiotics sandblasted/acid-etched, flame-sprayed, and HA-coated) in one minute. such as amoxicillin and metronidazole, be employed for ten days. The most widely used lasers for implant surface detoxification has been This protocol is derived directly from the treatment of refractory Er:YAG laser. Nd:YAG and Ho:YAG lasers are not suitable for use in periodontitis and is specifically targeted against Actinobacillus decontamination of implant surfaces, irrespective of the power output. actinomycetemcomitans. Systemic ornidazole (1000 mg for ten days) With the Er:YAG and CO2 laser, the power output must be limited so as together with chlorhexidine subgingival irrigation can also be used for to avoid surface damage. The GaAIAs laser seems to be safe as far as the treatment of failing implants. The possibility of using nonsteroidal possible surface alterations are concerned. Various randomized control anti-inflammatory drugs for inhibiting peri-implant bone loss in cases trials have been performed to compare mechanical debridement and of peri-implantitis has been proposed. Even though preliminary animal Er:YAG laser for implant decontamination [43, 44]. These studies have results seem to be promising, such therapy may not be indicated for shown no statistical differences between the probing attachment levels, the treatment of an acute phase. probing pocket depths and recession levels between the methods, yet effective improvement in the parameters individually.

Occlusal therapy When centric or lateral premature contacts or interference have suggested. It has also been reported that if overload etiology is suspected, been detected, occlusal adjustment has been recommended. Dental the clinician should remove the prosthesis with the hope of improving professionals should evaluate the fit of the prosthesis and the abutment. the situation. A systematic review by Carl Misch has shown a positive When parafunctional activity is suspected, night-guard therapy has been correlation between occlusal overload and peri-implant bone loss [45].

Surgical therapy Surgical procedures for the treatment of complications and “failing” control and eliminate the favorable environment for anaerobic bacteria implants have been advocated by several authors, particularly after such as deep pockets. This may be accomplished either with resective unsuccessful antimicrobial treatment and progressive marginal procedures such as bone resection and apically repositioned flaps or bone loss. Early perforations of the mucoperiosteum covering a with regenerative procedures such as guided bone regeneration [GBR], submerged implant, often caused by decubital ulcers related to autologous, or allogenic bone grafts. inadequate relief of the denture on the implant site, can be treated Bone grafts with excision of the bordering mucosa, full-flap coverage of the Numerous bone graft materials have been used to aid in the perforation, and adequate relief of the denture. For some implant reconstruction of bone defects. These range from allografts to systems, it is also possible to replace a standard cover screw with xenografts and alloplasts. a smaller one. Hyperplastic mucositis refractory to increased oral hygiene procedures, in the absence of other treatable conditions (for Autogenous bone grafts example, loose implant components that can be tightened after local These bone grafts are considered to be the “gold standard,” since the cleaning and sterilization of the abutment), is usually treated with graft is harvested from the donor itself. These grafts are osteoinductive. procedures. Chronic fistulae originating from infected Intraoral sources: soft tissues entrapped at the abutment junction level have been treated ●● Bone from extraction . by removing the abutment and interposed granulation tissue, cleaning ●● Edentulous ridges. the implant head, sterilizing the abutment, fitting a new silicon ring ●● Bone from within the jaw. (when present), surgically excising the epithelialized sinus tract (not ●● Newly formed bone in . always necessary), and properly reseating the abutment. Surgical ●● Bone removed from ostectomy and osteoplasty. revision of failing implants aims mainly at cleaning the abutment/ implant surfaces of bacteria through . Effective Extra oral sources: cleaning of the implant surface represents an important issue in the ●● Iliac autografts. treatment of failing implants. In fact, cleaning rough implant surfaces Allografts: is very difficult since bacteria are protected in micro irregularities or ●● Decalcified freeze-dried bone allograft (DFDBA). undercuts of the surface. For this reason, it seems wise to carry out ●● It is thought to have osteoinductive effect because it releases any surgical intervention under antibiotic coverage to maximize the BMPs. Schwartz et al. reported that variations in the amount of antibacterial effect. There is unanimous consensus that bacteria should bone formation induced by DFDBA may relate to the source and be eliminated from the surfaces of failing implants. Further, there is a processing of bone. belief that if endotoxins or other contaminants are left, there cannot be Alloplasts: biologic repair or re-osseointegration. ●● These grafts are synthetic and prepared from artificial sources. Resective and regenerative procedures Once the primary goal of surgical intervention of a bacteria-free implant surface has been achieved, it may be necessary for dental professionals to correct the anatomic conditions to improve plaque

Dental.EliteCME.com Page 100 Guided tissue regeneration and guided bone regeneration in peri-implantitis The concept of guided tissue regeneration is based on the principle of by anatomic variations of the bony defects and by barrier infections exclusion of fast growing epithelial and connective tissue cells paving and exposures. The combination of GBR and resorbable HA or the way for periodontal ligament cells osteoblasts, cementoblasts to freeze-dried bone has shown a statistically higher percentage of regenerate new bone. Nyman et al. put forward the concept of guided reosseointegration when compared to GBR alone [47]. Recombinant tissue regeneration in 1982. human bone morphogenetic protein-2 has been shown to have the potential to promote bone formation and reosseointegration in advanced The decision-making process regarding the use of resective or peri-implantitis bony defects, although the amount of bone to implant regenerative procedures may be influenced by the degree and/or contact in the reosseointegrated portion of bone was significantly lower morphology of the peri-implant tissue destruction. If the amount of lost than bone contact within the resident bone. It has been suggested that supporting bone is minimal, a resective approach may be preferable. microbial leakage at the abutment-implant junction might influence If a major portion of the supporting bone has been resorbed, forming a the outcome of GBR. In addition to sterilization of the abutment, craterlike defect with remaining wall structures, a regenerative technique disinfection of the internal part of the implant has been advocated, but has been recommended. Finally, if the destruction has reached the vents its effectiveness has not been proven. To improve the likelihood of bone of a hollow-cylinder implant, or if the dental professional determines regeneration, it has been recommended that the area be isolated from the the remaining supporting bone is insufficient to withstand the usual oral cavity with full-flap coverage of the barrier. A long-term follow-up loading conditions, the implant should be removed. After a flap is study has concluded that the use of regenerative procedures such as bone apically repositioned, it has been suggested that a surgical pack be graft techniques with or without the use of barrier membranes has been used to secure the position of the flap. No studies have been published reported with various degrees of success. Implants with peri-implant that substantiated such a procedure. Several randomized controlled defects that are treated with GBR had similar survival rates and crestal trials have investigated the possibility of regenerating new supporting [46, 47] bone levels compared with implants in native bone with survival rates bone around failing implants using barriers (GBR) . Partial bone [50] fill around failing implants using GBR alone or in combination with of 96.1 percent . However, it must be stressed that such techniques do not address disease resolution but rather merely attempt to fill the autogenous bone grafts or various types of allografts/alloplastic grafts osseous defect. There are strong recommendations against using HA or have been reported [48, 49]. Despite different antibiotic regimens, barriers usually required premature removal because of infections. It has allogenic freeze-dried bone to fill bone pockets around infected implant been shown that premature barrier exposure and removal is generally sites, warning of the potential consequences for the patient. In fact, associated with poor clinical outcomes. Although some case reports biomaterial-centered infections may bear catastrophic consequences have displayed a pronounced radiographic bone fill, such results should for the patient, such as acute localized suppurative osteomyelitis. be viewed with caution, since unsuccessful reports can be found as Biomaterial-centered infections are extremely resistant to antibiotics and well. Barriers are usually placed both in a completely submerged combined antibiotic/surgical therapy. Therefore, whenever a clinician fashion or adapted to a permucosal abutment. Many differences in feels uncertain with regard to the possibility of eliminating bacteria in bone regeneration among different studies can be explained partly an area of difficult access (i.e., vents of hollow implants, rough coatings, etc.), the solution of choice is implant removal. Cumulative Interceptive Supportive Therapy for implants Lang et al. in 2004 gave a strategy for supportive maintenance plan recall and assessment of plaque, bleeding, suppuration, pocket and for implant patients called Cumulative Interceptive Supportive radiological evidence of bone loss [51]. The CIST gave a clear-cut Therapy (CIST). He modified and devised a concept called the AKUT protocol for treatment of peri-implantitis depending on the probing concept, which is a concept of implant maintenance based on repeated depth and bone loss. It is as follows: Stage Result Therapy

Pocket depth (PD) <3mm, no No therapy. plaque or bleeding on probing. A Pocket depth (PD) <3mm, plaque Mechanical debridement, scaling, and polishing, oral hygiene instructions. and/or bleeding on probing. B PD 4-5 mm, radiologically Mechanical debridement, scaling & polishing, oral hygiene instructions, plus local anti- no bone loss or PD >5mm but no infective therapy 0.1 percent chlorhexidine twice daily for three to four weeks. cratering. C PD >5 mm, radiologically bone loss Mechanical debridement, scaling, and polishing, oral hygiene instructions, microbial <2mm. testing plus local and systemic anti-infective therapy. D PD >5 mm, radiologically bone loss Mechanical debridement, scaling and polishing, oral hygiene instructions, microbial >2mm. testing, local and systemic anti-infective therapy PLUS resective and regenerative .

Another commonly accepted protocol given by Zitmann et al. referred Schmage et al. gave a protocol for peri-implantitis treatment that followed to as systematic periodontitis therapy. The initial phase of the protocol the concept of CIST-protocol but recommended mechanical and local consists of oral hygiene instructions with an adjunct of local and systemic disinfective treatments at stage A and B. He recommended interventions anti-infective therapy as required. If non-surgical treatment fails, it has if probing depths exceeded 5 mm or are progressive, as well as if they been recommended to treat further with open flap debridement and occurred under any local inflammation signs[53] . Hence, following such resective/ regenerative surgery [52]. protocols can aid in long-term treatment and maintenance of dental implants.

Page 101 Dental.EliteCME.com Clinical implications for the Any dentist who deals with implants, either with its placement, ●● Mobility indicates complete loss of osseointegration and requires prosthetics, or maintenance, should be well aware of the pathological removal of the implant. process of peri-implantitis and should be well informed about its ●● Peri-implant probing and recording at annual intervals is essential to clinical implications in the day-to-day dental practice. The clinical determine the course of the disease and to help establish the diagnosis. implications of peri-implant diseases are summarized as follows [4]: ●● Baseline probing measurements should be recorded at the time of ●● The dentist should inform the patient that peri-implant tissues placement of implant super structure. respond to plaque in the same way as the periodontal tissues, and ●● Probing does not damage peri-implant tissues and at least one site per hence in the absence of adequate plaque control, diseases may implant should be established to record the relative attachment levels. develop in the tissues around the implant. ●● Baseline radiograph is considered mandatory and should be taken ●● Poor oral hygiene and subsequent plaque accumulation leads to at the time of placement of implant super structure to determine peri-implant diseases. the initial bone levels. ●● Patients with history of periodontitis should be informed about ●● When suspecting peri-implantitis, the clinician should take their increased risk for peri-implantitis. radiographs and confirm the bone loss to establish and confirm ●● Patients who smoke should be informed about their increased risk the diagnosis. for developing peri-implantitis. ●● Bacterial deposits must be removed in the treatment of peri- ●● Diabetic patients should be encouraged to maintain a normal range implant mucositis and peri-implantitis. blood glucose level and should be made aware of their increased ●● The clinician should be aware that peri-implantitis is difficult to risk for developing peri-implantitis. treat and the outcomes may not be predictable. ●● Bleeding on probing should be considered as an objective sign for ●● Clinicians should consider non-surgical mechanical therapy for the inflammation of peri-implant tissues and prolonged presence of which treatment of peri-implantitis and if that does not resolve the lesion, indicates increased risk for future bone loss and attachment loss. adjunctive antimicrobials and access flap surgery are recommended. ●● The clinician should be aware that suppuration and mobility are ●● In order to restore the hard-tissue defect, reconstructive surgery definite indicators of peri-implantitis. may be considered. Conclusion Prevention is better than cure. The implantologist must be aware generalize the results. Longitudinal studies on large subject samples of the importance of preventing peri–implantitis, should consider must be performed in order to confirm that factors associated with appropriate case selection, keep in mind the risk factors involved with peri-implant disease are indeed risk factors or indicators. Betterment the disease process, and make the patient aware of the importance in future clinical research will lead to the betterment of treatment and of implant maintenance. Future research should focus on the various management strategies and hence a better clinical practice. strategies for combatting peri-implantitis with larger samples to References 1. Serino, G., & Ström, C. (2009). Peri‐implantitis in partially edentulous patients: association with 21. Laine, M. L., Leonhardt, Å., Roos‐Jansåker, A. M., Peña, A. S., Van Winkelhoff, A. J., Winkel, E. 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Dental.EliteCME.com Page 102 39. Persson, G. R., Samuelsson, E., Lindahl, C., & Renvert, S. (2010). Mechanical non‐surgical treatment 47. Roos‐Jansåker, A. M., Renvert, H., Lindahl, C., & Renvert, S. (2007). Surgical treatment of peri‐ of peri‐implantitis: a single‐blinded randomized longitudinal clinical study. II. Microbiological implantitis using a bone substitute with or without a resorbable membrane: a prospective cohort results. Journal of clinical periodontology, 37(6), 563-573. study. Journal of clinical periodontology, 34(7), 625-632. 40. Karring, E. S., Stavropoulos, A., Ellegaard, B., & Karring, T. (2005). Treatment of peri‐implantitis by the 48. Schwarz, F., Sahm, N., Bieling, K., & Becker, J. (2009). Surgical regenerative treatment of peri‐ Vector® system. Clinical Oral Implants Research, 16(3), 288-293. implantitis lesions using a nanocrystalline hydroxyapatite or a natural bone mineral in combination with 41. Sahm, N., Becker, J., Santel, T., & Schwarz, F. (2011). Non‐surgical treatment of peri‐implantitis using a collagen membrane: a four‐year clinical follow‐up report. Journal of clinical periodontology, 36(9), an air‐abrasive device or mechanical debridement and local application of chlorhexidine: a prospective, 807-814. randomized, controlled clinical study. Journal of clinical periodontology, 38(9), 872-878. 49. Schwarz, F., Bieling, K., Latz, T., Nuesry, E., & Becker, J. (2006). Healing of intrabony peri‐implantitis 42. Renvert, S., Lessem, J., Dahlén, G., Renvert, H., & Lindahl, C. (2008). Mechanical and repeated defects following application of a nanocrystalline hydroxyapatite (Ostim™) or a bovine‐derived antimicrobial therapy using a local drug delivery system in the treatment of peri-implantitis: a randomized xenograft (Bio‐Oss™) in combination with a collagen membrane (Bio‐Gide™). A case series. Journal of clinical trial. Journal of periodontology, 79(5), 836-844. Clinical Periodontology, 33(7), 491-499. 43. Schwarz, F., Sculean, A., Rothamel, D., Schwenzer, K., Georg, T., & Becker, J. (2005). Clinical 50. Blanco, J., Alonso, A., & Sanz, M. (2005). Long‐term results and survival rate of implants treated with evaluation of an Er: YAG laser for nonsurgical treatment of peri‐implantitis: a pilot study. Clinical oral guided bone regeneration: a 5‐year case series prospective study. Clinical oral implants research, 16(3), implants research,16(1), 44-52. 294-301. 44. Schwarz, F., Bieling, K., Bonsmann, M., Latz, T., & Becker, J. (2006). Nonsurgical treatment of moderate 51. Lang, N. P., Berglundh, T., HeitzMayfield, L. J., Pjetursson, B. E., Salvi, G. E., & Sanz, M. (2004). and advanced periimplantitis lesions: a controlled clinical study. Clinical Oral Investigations, 10(4), 279- Consensus statements and recommended clinical procedures regarding implant survival and 288. complications. International Journal of Oral and Maxillofacial Implants, 19(SUPPL.), 150-154. 45. Misch, C. E., Suzuki, J. B., Misch-Dietsh, F. M., & Bidez, M. W. (2005). A positive correlation between 52. Zitzmann, N. U., Walter, C., & Berglundh, T. (2006). Ätiologie, Diagnostik und Therapie der and peri-implant bone loss: literature support. Implant dentistry, 14(2), 108-116. Periimplantitis–Eine Übersicht. Deutsche Zahnärztliche Zeitschrift, 61(12), 642-649. 46. Roos‐Jansåker, A. M., Renvert, H., Lindahl, C., & Renvert, S. (2007). Submerged healing following 53. Schmage, P. (2010). Befundorientiertes Behandlungskonzept bei periimplantären surgical treatment of peri‐implantitis: a case series. Journal of clinical periodontology, 34(8), 723-727. Infektionen. Parodontol, 21, 339-358. PERI-IMPLANTITIS: BASICS AND BEYOND Final Examination Questions Select the best answer for each question and mark your answers online at Dental.EliteCME.com.

1. Class II of Spikermann’s classification of peri-implantitis is 4. Chlorhexidine is believed to be the antimicrobial agent of choice. characterized as what? a. True. a. Slight horizontal bone loss with minimal peri-implant defect. b. False. b. Moderate horizontal/vertical bone loss with circular bony defects. 5. ______is better than a cure. c. Advanced bone loss with broad, circumferential vertical a. Health. defects as well as loss of buccal and/or palatal bony wall. b. Prevention. d. Moderate horizontal bone loss with isolated vertical defect. c. Surgery. d. Implantation. 2. History of periodontitis cannot be considered as a risk factor for peri-implantitis. a. True. b. False.

3. Dental professionals should probe the implant after the installation of the final restoration, with a force of 0.25N. a. True. b. False.

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