Increased Levels of Dissolved Titanium Are Associated With Peri‐Implantitis – A Cross‐Sectional Study

Background: Peri‐implantitis represents a disruption of the biocompatible interface between the titanium dioxide layer of the implant surface and the peri‐implant tissues. Increasing preclinical data suggest that peri‐implantitis microbiota not only triggers an inflammatory immune response but also causes electrochemical alterations of the titanium surfaces, i.e., corrosion, that aggravate this inflammatory response. Thus, it was hypothesized that there is an association between dissolution of titanium from dental implants, which suggests corrosion, and peri‐implantitis in humans. The objective of this study is to compare levels of dissolved titanium in submucosal plaque collected from healthy implants and implants with peri‐implantitis. Methods: Submucosal plaque from 20 implants with peri‐implantitis and 20 healthy implants was collected with sterile curets from 30 participants. Levels of titanium were quantified using inductively coupled plasma mass spectrometry and normalized for mass of bacterial DNA per sample to exclude confounding by varying amounts of plaque per site. Statistical analysis was performed using generalized estimated equations to adjust for clustering of implants per participant. Results: Implants with peri‐implantitis harbored significantly higher mean levels of titanium (0.85 ± 2.47) versus healthy implants (0.07 ± 0.19) after adjusting for amount of plaque collected per site (P = 0.033). Conclusions: Greater levels of dissolved titanium were detected in submucosal plaque around implants with peri‐implantitis compared with healthy implants, indicating an association between titanium dissolution and peri‐implantitis. Factors triggering titanium dissolution, as well as the role of titanium corrosion in the peri‐implant inflammatory process, warrant further investigation.     

A Novel Approach for Enhanced Nanoparticle‐Sized Bone Substitute Adhesion to Chemically Treated Peri‐Implantitis–Affected Implant Surfaces: An In Vitro Proof‐of‐Principle Study

Background: The objective of this study is to evaluate micro and nano‐hydroxyapatite (NHA) blended clot adhesion to citric acid–conditioned peri‐implantitis–affected surfaces. Methods: Forty hopeless implants with peri‐implantitis designated for removal were included in this study. Implants were divided into eight groups of five each: group 1 (G1) test areas were coated with hydroxyapatite of a microparticle size (MHA); group 2 (G2) test areas were coated with NHA; group 3 (G3) implants were coated with MHA after surface conditioning using citric acid; group 4 (G4) samples were treated in the same manner as in G3 except for the use of NHA; group 5 (G5) samples were coated without surface treatment with MHA mixed with whole human blood; group 6 (G6) implant samples were treated in the same manner as in G5 except for the use of NHA; group 7 (G7) implant samples were treated in the same way as in G5 plus surface conditioning using citric acid; and group 8 (G8) samples were treated in the same manner as in G7 except for the use of NHA. All implants in all groups were agitated for 3 minutes in phosphate‐buffered saline. All samples were prepared for scanning electron microscopy evaluation. Results: G1 and G2 non‐etched implants coated with MHA or NHA sizes were devoid of any bone particle adhesion to the peri‐implantitis–affected surfaces. Contrary to the lack of microparticle adhesion to the root surface that was seen in G3, G4 acid‐treated and NHA‐coated samples revealed nearly complete coverage of the peri‐implantitis–affected parts by the graft material. G5 non‐etched, clot‐blended MHA showed some areas of clot‐blended graft adhesion covering 6.7% of the examined surfaces. G6 non‐etched, clot‐blended NHA showed NHA retention within the fibrin strands in areas where the implant surface pores were exposed (24.3%). G7 acid‐treated and clot‐blended MHA‐treated implant surfaces showed partial coverage of the implant surface with detached fibrin clot–blended graft material (31.4%). G8 acid‐treated and NHA clot‐blended graft‐coated implants showed complete coverage of the implant surface by the clot‐blended graft material (93.4%). Conclusion: Peri‐implantitis–affected surface conditioning with citric acid improves NHA‐blended clot adhesion to titanium implant surfaces.     

Effects of an Erbium:Yttrium‐Aluminum‐Garnet Laser and Ultrasonic Scaler on Titanium Dioxide‐Coated Titanium Surfaces Contaminated With Subgingival Plaque: An In Vitro Study to Assess Post‐Treatment Biocompatibility With Osteogenic Cells

Background: Effects of conventional ultrasonic scaler versus an erbium:yttrium‐aluminum‐garnet (Er:YAG) laser on titanium surfaces contaminated with subgingival plaque from patients with peri‐implantitis are evaluated in terms of: 1) plaque and biocorroded titanium oxide coating removal; 2) surface change induction; and 3) residual biocompatibility toward osteoblasts. Methods: Subgingival plaque‐coated titanium disks with a moderately rough surface were fixed with ethanol and treated with an ultrasonic scaler (metal tip) or Er:YAG laser (20.3 or 38.2 J/cm²) in non‐contact mode. Fluorescent detection of residual plaque was performed. Disk surface morphology was evaluated by scanning electron microscopy. Viability, attachment, proliferation, and differentiation of Saos‐2 osteoblasts on new and treated disks were assayed by propidium iodide/DNA stain assay and confocal microscopic analysis of cytoskeleton, Ki67, expression of osteopontin and alkaline phosphatase, and formation of mineralized nodules. Results: Both methods resulted in effective debridement of treated surfaces, the plaque area being reduced to 11.7% with the ultrasonic scaler and ≤0.03% with the Er:YAG laser (38.2 J/cm²). Ultrasound‐treated disks showed marked surface changes, incomplete removal of the titanium dioxide (TiO₂) layer, and scanty plaque aggregates, whereas the Er:YAG laser (38.2 J/cm²) completely stripped away the plaque and TiO₂ layer, leaving a micropitted surface. Both treatments maintained a good biocompatibility of surfaces to Saos‐2 osteoblasts. Air‐water cooling kept disk temperature below the critical threshold of 47°C. Conclusion: This study shows that an ultrasonic scaler with metal tip is less efficient than high‐energy Er:YAG irradiation to remove the plaque and TiO₂ layer on anodized disks, although both procedures appear capable of restoring an adequate osseoconductivity of treated surfaces.     

Exfoliative Cytology and Titanium Dental Implants: A Pilot Study

Background: Oral exfoliative cytology is a diagnostic method that involves the study of cells exfoliated from the oral mucosa. Ions/particles released from metallic implants can remain in the peri‐implant milieu. The aim of the present study is to assess the presence of metal particles in cells exfoliated from peri‐implant oral mucosa around titanium dental implants. Methods: The study comprised 30 patients carrying titanium dental implants, who had neither a metallic prosthesis nor metal restorations in neighboring teeth. Individuals undergoing orthodontic therapy and those who had oral piercing were also excluded from the study. The study sample included patients with and without peri‐implantitis. Cytologic samples of the peri‐implant area were collected. Samples of the marginal gingiva on the contralateral side of the implant were taken from the same individuals to serve as control. Cytologic analysis was performed using light microscopy. Titanium concentration was determined using inductively coupled plasma‐mass spectrophotometry. Results: Metal‐like particles were observed inside and outside epithelial cells and macrophages in cytologic smears of peri‐implant mucosa of both patients with and without peri‐implantitis. No particles were found in the control cytologic samples. The concentration of titanium was higher in the peri‐implantitis group compared with the group without peri‐implantitis; no traces of titanium were observed in controls. Conclusions: Regardless of an inflammatory response, ions/particles are released from the surface of the implant into the biologic milieu. Exfoliative cytology is a simple technique that may be used to detect metal particles in cells exfoliated from the peri‐implant mucosa.     

Spontaneous progression of peri-implantitis at different types of implants. An experimental study in dogs. I: clinical and radiographic observations

Aim: The aim of the present study was to analyze tissue reactions to plaque formation following ligature removal at commercially available implants exposed to experimental peri‐implantitis. Material and methods: Six Labrador dogs about 1 year old were used. All mandibular premolars and the three anterior premolars in both sides of the maxilla were extracted. After 3 months four implants representing four different implant systems with different surface characteristics – implant group A (turned), B (TiOblast), C (sandblasted acid‐etched; SLA) and D (TiUnite) – were placed in a randomized order in the right side of the mandible. Three months after implant installation experimental peri‐implantitis was initiated by placement of ligatures in a submarginal position and plaque accumulation. At week 12, when about 40–50% of the supporting bone was lost, the ligatures were removed. During the subsequent 24‐week period plaque accumulation continued. Radiographic and clinical examinations were performed during the ‘active breakdown’ period (plaque accumulation and ligatures) and the plaque accumulation period after ligature removal. The experiment was terminated at week 36. Results: The bone loss that took place during the ‘active breakdown’ period varied between 3.5 and 4.6 mm. The additional bone loss that occurred during the plaque accumulation period after ligature removal was 1.84 (A), 1.72 (B), 1.55 (C) and 2.78 mm (D). Conclusion: Spontaneous progression of experimentally induced peri‐implantitis occurred at implants with different geometry and surface characteristics. Progression was most pronounced at implants of type D (TiUnite surface).     

Antimicrobial Agents Used in the Treatment of Peri‐Implantitis Alter the Physicochemistry and Cytocompatibility of Titanium Surfaces

Background: Chemotherapeutic agents (ChAs) are considered an integral part of current treatment protocols for the decontamination of titanium implants with peri‐implantitis, based on their antimicrobial effect. Despite the proven antimicrobial effect of ChAs on titanium‐bound biofilms, previous studies have elucidated an unexpected disassociation between bacterial reduction and biologically acceptable treatment outcomes. In this study, the authors hypothesize that ChAs residues alter titanium physicochemistry and thus compromise cellular response to decontaminated surfaces. Methods: Grit‐blasted acid‐etched titanium disks were contaminated with multispecies microcosm biofilms grown from in vivo peri‐implant plaque samples. To simulate implant decontamination, the contaminated disks were burnished with 0.12% chlorhexidine, 20% citric acid, 24% EDTA/1.5% NaOCl, or sterile saline and assessed surface physicochemical properties. Sterile untreated surfaces were the controls. The biologic effects of decontamination were assessed via cell proliferation and differentiation assays. Results: Bacterial counts after decontamination confirmed that the ChAs were antimicrobial. X‐ray photoelectron spectroscopy invariably detected elemental contaminants associated with each ChA molecule or salt that significantly altered wettability compared with controls. Notably, all surfaces with ChA residues showed some cytotoxic effect compared with controls (P <0.05). Increased cell counts were consistently found in the saline‐treated group compared with chlorhexidine (P = 0.03). Interestingly, no association was found between antimicrobial effect and cell counts (P >0.05). Conclusions: ChA‐specific residues left on the titanium surfaces altered titanium physical properties and adversely affected the osteoblastic response irrespective of their observed antimicrobial effect. Chlorhexidine may compromise the biocompatibility of titanium surfaces, and its use is not recommended to detoxify implants. Sterile saline, citric acid, and NaOCl‐EDTA may be proposed for use in the treatment of peri‐implantitis. Contrary to previous studies that recommended the selection of ChAs for the decontamination of titanium implants according to their antimicrobial effects, the present study demonstrated that the restoration of the biocompatibility of contaminated titanium surfaces is also contingent on the preservation of titanium material properties.     

Can degradation products released from dental implants affect peri‐implant tissues?

This study aimed to assess the literature available on the effects, on peri‐implant tissues, of degradation products released from dental implants as a consequence of therapeutic treatment for peri‐implantitis and/or of wear‐corrosion of titanium. A literature review of the PubMed medline database was performed up to December 31, 2016. The following search terms were used: “titanium wear and dental implant”; “titanium corrosion and dental implant”; “bio‐tribocorrosion”; “peri‐implantitis”; “treatment of peri‐implantitis”; “titanium particles release and dental implant”; and “titanium ion release and dental implant”. The keywords were applied to the database in different combinations without limits of time period or type of work. In addition, the reference lists of relevant articles were searched for further studies. Seventy‐nine relevant scientific articles on the topic were retrieved. The results showed that pro‐inflammatory cytokines, infiltration of inflammatory response cells and activation of the osteoclasts activity are stimulated in peri‐implant tissues in the presence of metal particles and ions. Moreover, degenerative changes were reported in macrophages and neutrophils that phagocytosed titanium microparticles, and mutations occurred in human cells cultured in medium containing titanium‐based nanoparticles. Debris released from the degradation of dental implants has cytotoxic and genotoxic potential for peri‐implant tissues. Thus, the amount and physicochemical properties of the degradation products determine the magnitude of the detrimental effect on peri‐implant tissues.     

Erbium,Chromium:Yttrium‐Scandium‐Gallium‐Garnet Laser Effectively Ablates Single‐Species Biofilms on Titanium Disks Without Detectable Surface Damage

Background: Increasing evidence implicates biofilms, consisting of species such as Porphyromonas gingivalis (Pg), in the etiology of peri‐implantitis. Multiple approaches to ablate biofilms on failing implants have been proposed and include use of lasers, most recently the erbium, chromium:yttrium‐scandium‐gallium‐garnet (Er,Cr:YSGG) laser. The purpose of this study is to establish an in vitro single‐species biofilm model on implant surfaces and determine power settings of the Er,Cr:YSGG laser that remove biofilm without causing physical damage to disks. Methods: Single‐species biofilms consisting of Pg strain 381 were grown on titanium disks, including: 1) sandblasted, large‐grit, acid‐etched (SLA); 2) calcium phosphate nano‐coated (CaP); 3) anodized; or 4) machined surfaces. Power settings from 0 to 1.5 W using an Er,Cr:YSGG laser equipped with radial firing tip were used. Biofilm formation/removal was quantitated using confocal and scanning electron microscopy. Surface changes in temperature, microroughness, and water contact angle were analyzed. Results: Results show confluent Pg biofilm coating all disk surfaces. The laser removed biofilms from all surfaces, with CaP and SLA surfaces requiring power setting of 1.0 to 1.5 W for ablation of bacteria coating the disks. Within this power range, and with water spray, there were no changes in surface temperature, surface roughness, or contact angle on any surfaces tested. Conclusion: The Er,Cr:YSGG laser with radial firing tip and water spray was able to effectively ablate ≥95% of biofilm on all types of tested titanium surfaces, using clinically relevant power settings, without causing measurable physical changes to surfaces.     

A Novel Rat Model of Polymicrobial Peri‐Implantitis: A Preliminary Study

Background: Peri‐implantitis is a complex polymicrobial biofilm‐induced inflammatory osteolytic gingival infection that results in orofacial implant failures. To the best knowledge of the authors, there are no preclinical in vivo studies in implant dentistry that have investigated the inflammatory response to known microbial biofilms observed in humans. The aim of this study is to develop a novel peri‐implant rat model using an established model of polymicrobial periodontitis. Methods: Wistar rats were used for the study of experimental peri‐implantitis. One month after extraction of maxillary first molars, a titanium mini‐implant was inserted. Two months after implant healing, implants were uncovered, and abutment fixing was done using cyanoacrylate to prevent abutment loosening. Rats were separated into two groups (group A: polymicrobial‐infected and group B: sham‐infected). One week after healing of abutments, rats were infected with Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia for 12 weeks. Bacterial colonization, bone resorption, and implant inflammation were evaluated by polymerase chain reaction (PCR), microcomputed tomography, and histology, respectively. Results: Three rats with four implants in the infection group and two rats with three implants in the sham‐infection group were analyzed. PCR analysis revealed presence of bacterial genomic DNA, and infection elicited significant immunoglobulin (Ig)G and IgM antibody responses, indicating bacterial colonization/infection around implants. Infection induced an enhanced mean distance from implant platform to the first bone‐to‐implant contact, extensive peri‐implantitis with advanced bone resorption, and extensive inflammation with granulation tissue and polymorphonuclear leukocytes. Conclusions: To the best knowledge of the authors, this is the first study to develop a novel rat model of polymicrobial peri‐implantitis. With modifications to improve implant retention it could offer significant advantages for studies of initiation and progression of peri‐implantitis.     

Early intervention of peri‐implantitis and periodontitis using a mouse model

1 Background

Peri‐implantitis is an inflammatory response to bacterial biofilm resulting in bone loss and can ultimately lead to implant failure. Because of the lack of predictable treatments available, a thorough understanding of peri‐implantitis's pathogenesis is essential. The objective of this study is to evaluate and compare the response of acute induced peri‐implantitis and periodontitis lesions after insult removal.

2 Methods

Implants were placed in one‐month‐old C57BL/6J male mice eight weeks post extraction of their left maxillary molars. Once osseointegrated, ligatures were placed around the implants and contralateral second molars of the experimental groups. Controls did not receive ligatures. After one week, half of the ligatures were removed, creating the ligature‐retained and ligature‐removed groups. Mice were sacrificed at two time points, 5 and 14 days, from ligature removal. The specimens were analyzed via micro‐computed tomography and histology.

3 Results

By 5 and 14 days after ligature removal, the periodontitis group experienced significant bone gain, whereas the peri‐implantitis group did not. Histologically, all implant groups exhibited higher levels of cellular infiltrate than any of the tooth groups. Osteoclast numbers increased in peri‐implantitis and periodontitis ligature‐retained groups and decreased following insult removal. Collagen was overall more disorganized in peri‐implantitis than periodontitis for all groups. Peri‐implantitis experimental groups revealed greater matrix metalloproteinase‐8 and NF‐kB levels than periodontitis.

4 Conclusions

Implants respond slower and less favorably to insult removal than teeth. Future research is needed to characterize detailed peri‐implantitis disease pathophysiology.     

Biofilm as a risk factor in implant treatment

This article summarizes the microbiological findings at dental implants, drawing distinctions between the peri‐implant microbiome and the periodontal microbiome, and summarizes what is known regarding biofilm as a risk factor for specific stages of implant treatment. Targeted microbial analysis is reviewed as well as the latest results from open‐ended sequencing of the peri‐implant flora. At this time there remains a lack of consensus for a specific microbial profile that is associated with peri‐implantitis, suggesting that there may be other factors which influence the microbiome such as titanium surface dissolution. Therapeutic interventions to address the biofilm are presented at the preoperative, perioperative, and postoperative stages. Evidence supports that perioperative chlorhexidine reduces biofilm‐related implant complications and failure. Regular maintenance for dental implants is also shown to reduce peri‐implant mucositis and implant failure. Maintenance procedures should aim to disrupt the biofilm without damaging the titanium dioxide surface layer in an effort to prevent further oxidation. Evidence supports the use of glycine powder air polishing as a valuable adjunct to conventional therapies for use at implant maintenance visits. For the treatment of peri‐implantitis, nonsurgical therapy has not been shown to be effective, and while surgical intervention is not always predictable, it has been shown to be superior to nonsurgical treatment for decontamination of the implant surface that is not covered by bone.     

Reimplantation of Dental Implants following Ligature‐Induced Peri‐Implantitis: A Pilot Study in Dogs

Objectives: This preliminary investigation aimed to evaluate the potential of contaminated implants to reosseointegrate into pristine sites and, in addition, to assess the potential of osseointegration of new implants in peri‐implantitis sockets in a canine model. Methods: All mandibular premolars were bilaterally extracted from two mongrel dogs. Following 12 weeks of healing, two dental implants were inserted on each hemiarch. Forty‐five days following implant placement, a silk ligature secured with cyanoacrylate was placed around the implants' cervical region in order to induce peri‐implantitis. After another 45 days from ligature placement, the implants were mechanically removed using counter rotation with a ratchet and were reimplanted without any decontamination (neither rinsing nor chemical or mechanical cleaning) in adjacent pristine zones. In sites where implants were removed, new, wider‐diameter implants were placed in the infected sockets. Forty‐five days following reimplantation surgery, the dogs were sacrificed; nondecalcified specimens were processed and toluidine blue stained for morphologic and morphometric (bone‐to‐implant contact [BIC]) assessment under an optical microscope. In dog 1 all the implants (both in the pristine and in the infected sites) survived and osseointegrated while in dog 2, six out of eight implants failed to osseointegrate and exfoliated. Overall, the mean BIC of all implants was 51.08% (SD 20.54). The mean BIC for the infected implants placed into pristine sites was 51.48% ± 26.29% (SD) and the mean BIC for the new implants in peri‐implantitis socket was 50.58% ± 14.27% (SD). Conclusions: Within the limitations of this preliminary investigation, especially the small number of animals, osseointegration seems to be achievable both in infected sites and around contaminated implant surfaces.     

Clinical Outcomes of Using Lasers for Peri‐Implantitis Surface Detoxification: A Systematic Review and Meta‐Analysis

The aim of this systematic review is to compare the clinical outcomes of lasers with other commonly applied detoxification methods for treating peri‐implantitis. An electronic search of four databases and a hand search of peer‐reviewed journals for relevant articles were conducted. Comparative human clinical trials and case series with ≥6 months of follow‐up in ≥10 patients with peri‐implantitis treated with lasers were included. Additionally, animal studies applying lasers for treating peri‐implantitis were also included. The included studies had to report probing depth (PD) reduction after the therapy. Results: Seven human prospective clinical trials and two animal studies were included. In four and three human studies, lasers were accompanied with surgical and non‐surgical treatments, respectively. The meta‐analyses showed an overall weighted mean difference of 0.00 mm (95% confidence interval = ?0.18 to 0.19 mm) PD reduction between the laser and conventional treatment groups (P = 0.98) for non‐surgical intervention. In animal studies, laser‐treated rough‐surface implants had a higher percentage of bone‐to‐implant contact than smooth‐surface implants. In a short‐term follow‐up, lasers resulted in similar PD reduction when compared with conventional implant surface decontamination methods.     

Treatment Outcome in Patients With Peri‐Implantitis in a Periodontal Clinic: A Retrospective Study

Background: The number of placed implants has grown during the past decade, and the prevalence of peri‐implantitis has increased. The purpose of the present study is to investigate the treatment outcome of peri‐implantitis and to identify factors influencing the treatment success rate. Methods: The study was conducted as a retrospective longitudinal study on a referral population. The material included 382 implants with peri‐implantitis in 150 patients. Peri‐implantitis was defined as presence of pocket depths ≥5 mm, bleeding at probing and/or suppuration, and the presence of implant radiographic bone loss ≥3 mm or bone loss comprising at least three threads of the implant. Variance analyses, χ² analyses, and logistic regression analysis were used for data analyses. Results: The mean age of the participants at baseline was found to be 64 years (range: 22 to 87 years). The mean ± SD follow‐up time was 26 ± 20 months, and the mean time between implant installation and baseline was 6.4 years (range: 1 to 20 years). Periodontal flap surgery with osteoplasty was the most common type of therapy (47%), and regenerative surgery procedures with bone substitute materials were chosen in 20% of the cases. The mean success rate at patient level was 69%. The results of the logistic regression analyses showed that the success rate was significantly lower for individuals with the diagnosis of severe periodontitis, severe marginal bone loss around the implants, poor oral hygiene, and low compliance. Conclusion: The effectiveness of the peri‐implantitis therapy was impaired by severe periodontitis, severe marginal bone loss around the implants, poor oral hygiene, and low compliance.     

Microbiologic results after non-surgical erbium-doped:yttrium, aluminum, and garnet laser or air-abrasive treatment of peri-implantitis: a randomized clinical trial

Background: The purpose of this study is to assess clinical and microbiologic effects of the non‐surgical treatment of peri‐implantitis lesions using either an erbium‐doped:yttrium, aluminum, and garnet (Er:YAG) laser or an air‐abrasive subgingival polishing method. Methods: In a 6‐month clinical trial, 42 patients with peri‐implantitis were treated at one time with an Er:YAG laser or an air‐abrasive device. Routine clinical methods were used to monitor clinical conditions. Baseline and 6‐month intraoral radiographs were assessed with a software program. The checkerboard DNA–DNA hybridization method was used to assess 74 bacterial species from the site with the deepest probing depth (PD) at the implant. Non‐parametric tests were applied to microbiology data. Results: PD reductions (mean ± SD) were 0.9 ± 0.8 mm and 0.8 ± 0.5 mm in the laser and air‐abrasive groups, respectively (not significant). No baseline differences in bacterial counts between groups were found. In the air‐abrasive group, Pseudomonas aeruginosa, Staphylococcus aureus, and Staphylococcus anaerobius were found at lower counts at 1 month after therapy (P <0.001) and with lower counts in the laser group for Fusobacterium nucleatum naviforme (P = 0.002), and Fusobacterium nucleatum nucleatum (P = 0.002). Both treatments failed to reduce bacterial counts at 6 months. Porphyromonas gingivalis counts were higher in cases with progressive peri‐implantitis (P <0.001). Conclusions: At 1 month, P. aeruginosa, S. aureus, and S. anaerobius were reduced in the air‐abrasive group, and Fusobacterium spp. were reduced in the laser group. Six‐month data demonstrated that both methods failed to reduce bacterial counts. Clinical improvements were limited.     

Occurrence of peri‐implant diseases and risk indicators at the patient and implant levels: A multilevel cross‐sectional study

Background : High prevalence rates of peri‐implant diseases have been reported; however, the lack of standardization of definition criteria has lead to variations in the observed estimates. In addition, scarce data are available concerning patient and implant related factors associated to peri‐implantitis. The aim of this study was to determine the prevalence of peri‐implant diseases and their risk indicators at the patient and implant levels. Methods : One hundred forty‐seven patients with 490 dental implants were included. Dental implants were clinically and radiographically evaluated to determine their peri‐implant conditions. Patient‐related conditions and implant and prosthetic‐related factors were recorded. Multivariable Poisson regression was fitted and prevalence ratios (PR) were reported. Results : 85.3% of implants (95%CI 80.2 to 90.4) had mucositis and 9.2% (95%CI 4.7 to 13.7) had peri‐implantitis. 80.9% (95%CI 73.8 to 86.8), and 19.1% (95%CI 12.6 to 25.5) of patients had mucositis and peri‐implantitis. At the patient level, it was observed an increased probability of peri‐implantitis in individuals with pocket depths ≥6 mm (PR = 2.47) and with ≥4 implants (PR = 1.96). Smoking increased the probability of peri‐implantitis by three times (PR = 3.49). The final multilevel Poisson regression model at the implant level indicated that platform switching reduced the probability of peri‐implantitis (PR = 0.18) and implants in function for ≥5 years increased this probability (PR = 2.11). The final model including patient and implant level indicators demonstrated that higher time of function (PR = 2.76) and smoking (PR = 6.59) were associated with peri‐implantitis. C onclusion : Peri‐implant diseases are highly prevalent in the studied sample, and factors associated with the occurrence of peri‐implantitis were presence of pockets ≥6 mm, smoking, time of function, and type of platform.     

Preventing and Treating Peri‐Implantitis: A Cost‐Effectiveness Analysis

Background: A large number of treatments for peri‐implantitis are available, but their cost‐effectiveness remains uncertain. This study evaluates the cost‐effectiveness of preventing and treating peri‐implantitis. Methods: A Markov model was constructed that followed each implant over 20 years. Supportive implant therapy (SIT) for managing peri‐implant mucositis and preventing development of peri‐implantitis was either provided or not. Risk of peri‐implantitis was assumed to be affected by SIT and the patient's risk profile. If peri‐implantitis occurred, 11 treatment strategies (non‐surgical or surgical debridement alone or combined with adjunct therapies) were compared. Treatments and risk profiles determined disease progression. Modeling was performed based on systematically collected data. Primary outcomes were costs and proportion of lost implants, as assessed via Monte Carlo microsimulations. Results: Not providing SIT and performing only non‐surgical debridement was both least costly and least effective. The next best (more costly and effective) option was to provide SIT and perform surgical debridement (additional 0.89 euros per 1% fewer implants lost). The most effective option included bone grafts, membranes, and laser treatment (56 euros per 1%). For patients at high risk, the cost‐effectiveness of SIT increased, whereas in low‐risk groups, a cost‐optimized strategy was cost‐effective. Conclusions: Although clinical decision‐making will be guided mainly by clinical condition, cost‐effectiveness analyses might add another perspective. Based on these findings, an unambiguous comparative effectiveness ranking was not established. However, cost‐effectiveness was predominantly determined by provision of SIT and initial treatment costs. Transferability of these findings to other healthcare systems needs further confirmation.     

Outcome of surgical treatment of peri-implantitis: results from a 2-year prospective clinical study in humans

Aim: The aim of the present study was to evaluate the outcome of a surgical procedure based on pocket elimination and bone re‐contouring for the treatment of peri‐implantitis. Material and methods: The 31 subjects involved in this study presented clinical signs of peri‐implantitis at one or more dental implants (i.e. ≥6 mm pockets, bleeding on probing and/or suppuration and radiographic evidence of ≥2 mm bone loss). The patients were treated with a surgical procedure based on pocket elimination and bone re‐contouring and plaque control before and following the surgery. At the time of surgery, the amount of bone loss at implants was recorded. Results: Two years following treatment, 15 (48%) subjects had no signs of peri‐implant disease; 24 patients (77%) had no implants with a probing pocket depth of ≥6 mm associated with bleeding and/or suppuration following probing. A total of 36 implants (42%) out of the 86 with initial diagnosis of peri‐implantitis presented peri‐implant disease despite treatment. The proportion of implants that became healthy following treatment was higher for those with minor initial bone loss (2–4 mm bone loss as assessed during surgery) compared with the implants with a bone loss of ≥5 mm (74% vs. 40%). Among the 18 implants with bone loss of ≥7 mm, seven were extracted. Between the 6‐month and the 2‐year examination, healthy implants following treatment tended to remain stable, while deepening of pockets was observed for those implants with residual pockets. Conclusion: The results of this study indicated that a surgical procedure based on pocket elimination and bone re‐contouring and plaque control before and following surgery was an effective therapy for treatment of peri‐implantitis for the majority of subjects and implants. However, complete disease resolution at the site level seems to depend on the initial bone loss at implants. Implants with no signs of peri‐implantitis following treatment tended to remain healthy during the 2‐year period, while a tendency for disease progression was observed for the implants that still showed signs of peri‐implant disease following treatment. To cite this article:
Serino G, Turri A. Outcome of surgical treatment of peri‐implantitis: results from a 2‐year prospective clinical study in humans.
Clin. Oral Impl. Res. 22 , 2011; 1214–1220.
doi: 10.1111/j.1600‐0501.2010.02098.x