Periodontology 2000 - 2024 - Berglundh - Etiology Pathogenesis and Treatment of Peri Implantitis A European Perspective

Received: 3 October 2023 | Revised: 19 December 2023 | Accepted: 22 December 2023
DOI: 10.1111/prd.12549
REVIEW ARTICLE
Etiology, pathogenesis and treatment of peri-implantitis: A

European perspective
Tord Berglundh1 | Andrea Mombelli2 | Frank Schwarz3 | Jan Derks1

1
Department of Periodontology, Institute of Odontology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
2
Division of Regenerative Dental Medicine and Periodontology, University Clinics of Dental Medicine, University of Geneva, Geneva, Switzerland
3
Department of Oral Surgery and Implantology, Goethe University, Carolinum, Frankfurt, Germany
Correspondence
Tord Berglundh, Department of Abstract
Periodontology, Institute of Odontology,
Peri-
implantitis is a plaque-
associated pathological condition occurring in tissues
The Sahlgrenska Academy at University
of Gothenburg, Box 450, SE 405 30 around dental implants. It is characterized by inflammation in the peri-implant mucosa
Gothenburg, Sweden.
and progressive loss of supporting bone. Over the last 30 years, peri-implantitis has
Email: tord.berglundh@odontologi.gu.se
become a major disease burden in dentistry. An understanding of the diagnosis, etiol-
ogy and pathogenesis, epidemiology, and treatment of peri-implantitis must be a cen-
tral component in undergraduate and postgraduate training programs in dentistry. In
view of the strong role of European research in periodontology and implant dentistry,
the focus of this review was to address peri-implantitis from a European perspective.
One component of the work was to summarize new and reliable data on patients
with dental implants to underpin the relevance of peri-implantitis from a population
perspective. The nature of the peri-implantitis lesion was evaluated through results
presented in preclinical models and evaluations of human biopsy material together
with an appraisal of the microbiological characteristics. An overview of strategies and
outcomes presented in clinical studies on nonsurgical and surgical treatment of peri-
implantitis is discussed with a particular focus on end points of therapy and recom-
mendations presented in the S3 level Clinical Practice Guideline for the prevention
and treatment of peri-implant diseases.
KEYWORDS
dental implants, peri-implantitis, treatment
1 | I NTRO D U C TI O N the terms “peri-implant infection” or “peri-implant lesion” to describe

pathologic conditions in peri-implant tissues, the consensus report
Peri-
implantitis was introduced as a term at the first European from session IV of the European Workshop presented definitions for
Workshop on Periodontology, held in Ittingen, Switzerland in peri-implant disease, peri-implant mucositis, and peri-implantitis. 2
1
February 1993. While studies published prior to 1993 often used It was stated that peri-implant disease was a collective term for
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2 BERGLUNDH et al.
inflammatory reactions in the tissues surrounding an implant. While treated patients also increased during the same period and the aver-
peri-implant mucositis was a term for a reversible inflammatory con- age number of installed implants per patient appeared to have de-
dition in the soft tissues surrounding an implant, peri-implantitis creased over time. Data from epidemiological research on patients
described inflammatory reactions with loss of supporting bone with dental implants in Sweden support this observation. Thus, the
in the tissues surrounding a functioning implant. Subsequent mean numbers of implants per patient in 1990 and in 2003 were 6.2
European Workshops addressed peri-implant diseases as a central and 4.0, respectively.11–13 Currently, the mean number of implants
3–8
part of clinical research in implant dentistry. The 2017 World per patient in Sweden is around 2.4.
Workshop on Classification of Periodontal and Peri-implant diseases The actual number of annually installed implants, however, is
and Conditions in Chicago, organized by the European Federation probably of limited value as it does not reflect the number or pro-
of Periodontology and the American Academy of Periodontology, portion of subjects with dental implants from a population perspec-
distinguished between disease definitions and case definitions for tive. In this context, the access to reliable registry data is relevant.
peri-implantitis.9 While case definitions are intended to serve as The Swedish Quality Registry on Caries and Periodontal Diseases
guidelines for the clinical assessment of the condition, disease defi- (SKaPa) is a unique national registry with a high degree of complete-
nitions are descriptive and present the typical characteristics of the ness. The registry is based on data from electronic patient records
disease. Thus, peri-implantitis is a plaque-associated pathological representing about 8 million subjects. Annual reports from the
condition occurring in tissues around dental implants. It is charac- SKaPa registry provide information on dental status including den-
terized by inflammation in the peri-implant mucosa and subsequent tal implants. The 2022 report14 covered about 3.3 million subjects
progressive loss of supporting bone.9,10 >20 years and 155.000 individuals of these had ≥1 dental implants.
Over the last 30 years, peri-implantitis has become a major dis- While the overall prevalence of subjects with dental implants in
ease reality in dentistry. The condition should therefore be consid- Sweden amounted to 4.7%, there was a large difference between
ered a disease from a population perspective rather than a biological age groups (Figure 1). Thus, 10%–13% of subjects aged >70 years
complication in the field of implant dentistry. An understanding of had dental implants, whereas the corresponding proportion of sub-
the diagnosis, etiology and pathogenesis, epidemiology, and treat- jects 40–60 years old varied between 3% and 5%. Although based
ment of peri-implantitis must be a central component in undergrad- on a smaller subject sample, data from The Fifth German Oral Health
uate and postgraduate training programs in dentistry. In view of the Study indicated that 8% of subjects aged 65–74 years in 2014 had
strong role of European research in periodontology and implant den- dental implants.15,16
tistry, the focus of this review was to address peri-implantitis from a Concomitant with an increase in the overall proportion of sub-
European perspective. One component of the work was to summa- jects with dental implants from 2.1% to 4.7% over the last 10 years,
rize new and reliable data on patients with dental implants to under- information derived from SKaPa suggested a shift in the average
pin the relevance of peri-implantitis from a population perspective. number of dental implants per individual. While the proportion of
The nature of the peri-implantitis lesion was evaluated through subjects with only one implant increased from 40% to 47%, the pro-
results presented in preclinical models and evaluations of human portion of subjects with >5 implants decreased from 19% to 11%.
biopsy material together with an appraisal of the microbiological From a population perspective, subjects with dental implants con-
characteristics. Finally, an overview of strategies and outcomes pre- stitute a well-defined group of individuals at risk for peri-implantitis.
sented in clinical studies on nonsurgical and surgical treatment of Based on the Swedish data on subjects with dental implants (almost
peri-implantitis was made. 5% of all adults), the number of individuals at risk for peri-implantitis
in European countries and elsewhere is large and should not be
overlooked.
2 | TH E R E LE VA N C E O F
PE R I - I M PL A NTITI S A S A D I S E A S E
E NTIT Y—A P O PU L ATI O N PE R S PEC TI V E 2.2 | Prevalence of peri-implantitis
2.1 | Prevalence of patients with dental implants The occurrence of peri-implantitis has been evaluated in several
cross-sectional studies. Given the large variation between stud-
Assessments of patients at risk for peri-implantitis should be consid- ies regarding the number and type of patients, function time, and
ered from a population perspective. The estimated number of an- case definitions used for identifying peri-
implantitis, prevalence
nually installed dental implants is often used to provide information figures ranging from 1% to 47% were reported.17 Weighted mean
on the global application of the technique in the replacement of lost values obtained from meta-
analyses of studies varied between
teeth. While the accuracy of such estimates may vary, national num- 20% and 22%.17,18 Not only did the different reports on the preva-
bers based on state subsidies for dental care provide information of lence of peri-implantitis exhibit a large variation in case definitions
high reliability. Data from the Dental and Pharmaceutical Benefits including thresholds of bone loss around implants, evaluations
Agency (TLV) in Sweden revealed that the number of installed dental were also often made on small and selected patient samples rep-
implants was twice as large in 2022 than in 2012. The number of resenting university/hospital clinical settings. Appraisals of the
|
BERGLUNDH et al. 3
F I G U R E 1 Proportion of individuals
with dental implants in Sweden. Data from
the Swedish Quality Registry for Caries
and Periodontal Disease.
prevalence of peri-implantitis should ideally be based on large and et al. 26 and also highlighted in the consensus report from the 2017
randomly selected population samples originating from different World Workshop9 and the connected review by Schwarz et al.10 The
clinical settings. In a nationwide clinical study in Sweden, Derks risk for peri-implantitis was especially high for patients with poor
13
et al. examined 596 patients representing a random sample from a plaque control and who did not attend regular maintenance pro-
registry-based cohort. Analysis of data on the clinical status of peri- grams during follow-up. The consensus report also stated that the
implant tissues and radiographs at 9 years after implant-supported current evidence on diabetes and tobacco smoking as risk factors
restorative therapy revealed peri-implantitis (≥1 implants presenting for the disease was inconclusive. It should be pointed out, however,
with bleeding on probing and bone loss >0.5 mm) in 45% of the pa- that in a statistical analysis, the potential effect of smoking may
tients. Moderate/severe forms of the disease (≥1 implants present- be masked by other and stronger factors, such as history of peri-
ing with bleeding on probing and bone loss >2.0 mm) were detected odontitis. Among risk factors related to the implant or the implant-
in 14.5% of patients. It should be noted that the average amount of supported prosthesis, access for oral hygiene has been emphasized
bone loss in sites with moderate/severe peri-implantitis was 3.5 mm, to be an important component. Studies by Serino & Ström27 and by
corresponding to about 30% of the initial bone support. The results Rodrigo et al. 22 demonstrated that implants not accessible for oral
13
presented by Derks et al. on the prevalence of peri-implantitis cor- hygiene measures had an elevated risk for peri-implantitis. Other
roborate data presented in other European cross-sectional studies. studies have shown that the extent of therapy, that is, the number of
13
Thus, when applying the case definitions used by Derks et al. to placed implants, was a risk factor for peri-implantitis.13 Data on the
19 20
the datasets described by Koldsland et al., Roos-Jansåker et al., importance of other factors, such as type of retention (cemented
Mir-Mari et al., 21 and Rodrigo et al., 22 the prevalence of moderate/ or screw-retained) or dimensions of the keratinized mucosa remain
severe peri-implantitis varied between 16% and 20%. In this context inconclusive.10
it is interesting to note that the data presented on the prevalence of
peri-implantitis appear to be consistent with those reported for peri-
odontitis. Both diseases present with an overall occurrence of about 3 | TH E PE R I - I M PL A NTITI S LE S I O N
40% in randomly selected adult populations, while severe forms of
the diseases affect a smaller proportion of about 10%. 23,24 Although peri-implantitis sites exhibit clinical characteristics similar
Potential risk factors or risk indicators for peri-
implantitis to those of periodontitis, for example, visible signs of inflammation,
were also assessed in studies investigating the occurrence of dis- bleeding on probing, and radiographic bone loss, there are evident
ease. Using a retrospective approach, several patient- and implant- differences in the patterns of disease progression. Studies have
19,25
specific risk factors were identified. Koldsland et al. and Derks shown that untreated peri-implantitis progresses in a nonlinear, ac-
et al.13 reported that patients with a history of periodontitis pre- celerating pattern and at a rate, which is faster than that of perio-
sented with an increased risk for peri-implantitis. This observation dontitis.9,10,13,28 While the reasons for the differences in the pattern
was confirmed in a recent systematic review presented by Carra of disease progression are not fully understood, differences in the
|
4 BERGLUNDH et al.
structure and composition of the local host response between peri- illustrated by the frequently observed high numbers of osteoclasts
odontitis and peri-implantitis should be emphasized. on the peri-implant crestal bone.38
3.1 | Preclinical in vivo models 3.2 | Human biopsy material
Pioneer experimental work using well-established preclinical in vivo The advantage of analyzing both hard and soft tissue components
models showed important differences between periodontitis and in specimens from preclinical studies is obvious. While ethical limi-
peri-implantitis lesions. 29,30 While the combination of a subgingival/ tations in most cases prevent analysis of hard tissue components
submucosal placement of ligatures and plaque accumulation re- in human biopsy material obtained from sites with peri-implantitis,
sulted in bone loss and the formation of a large area of infiltrated advanced techniques can still be applied to detect phenotypic
connective tissue (ICT) in the gingiva/peri-implant mucosa at teeth and functional characteristics of cells in peri-
implantitis lesions.
and implants, bone loss was more pronounced around implants. In Evaluations of human biopsy material with preserved tissue ori-
addition, peri-implantitis lesions, in contrast to periodontitis lesions, entation for section-based analyzes were predominantly based on
extended to the bone crest. Following the removal of ligatures dur- immunohistochemical preparations and, in few cases, morphologic
ing the experimental procedure, periodontal tissues responded with techniques. Other investigations applied procedures, in which the
a “self-limiting” process resulting in a protective zone of connective tissue samples were homogenized and subsequently analyzed using,
tissue with remaining periodontal ligament fibers that separated the for example, RT-PCR, western blot, or transcriptome profiling. An
ICT from the crestal bone. At peri-implantitis sites, however, such overview of European studies reporting on results from analysis of
a self-limiting process failed to occur due to the lack of periodontal human biopsy material and presenting with clear case definitions for
fibers. Similar observations were made in experimental studies by peri-implantitis is presented in Table 1.
31 32
Marinello et al. and Schou et al. The observation of the lack of Results from assessments of the cellular compositions and other
a self-limiting process in peri-implantitis sites opened for a new ap- characteristics of human peri-
implantitis lesions have been pre-
proach in experimental preclinical models. In a study by Zitzmann sented in reviews.10,40 Comparisons were, in most studies, made
33
et al., experimental peri-implantitis was established and, when between peri-implantitis specimens and tissue samples representing
about 40% of the bone support was lost, all ligatures were removed. other types of conditions, for example, periodontitis, peri-implant
It was reported that in the absence of ligatures and with an ongo- mucositis, and healthy peri-implant mucosa or gingiva. The most
ing plaque formation over several months, “spontaneous” progres- conspicuous characteristic of tissues collected from sites with peri-
sion of disease occurred with additional breakdown of peri-implant implantitis was the observation of large inflammatory cell infiltrates
bone. The “spontaneous progression” model was subsequently used that dominated the specimen area.41–48 In studies evaluating dif-
to examine differences in disease progression between implants ferences between peri-implantitis and periodontitis samples, the
with different surface characteristics. Data from numerous such ex- lesion was consistently larger at peri-implantitis sites and extended
perimental studies consistently demonstrated that size of the ICT apical to the pocket epithelium. While plasma cells were the pre-
and bone loss were more pronounced at sites representing implants dominant cell type of both lesions, the densities of plasma cells, mac-
with modified surfaces than implants with nonmodified, turned sur- rophages, and neutrophil granulocytes were significantly larger at
faces.34–37 The “spontaneous progression” model was also applied peri-implantitis than at periodontitis sites.44,46–48 In a study on the
38
by Carcuac et al. in a comparison between experimental periodon- activation status of macrophages in the ICT, it was reported that the
titis and peri-implantitis. It was reported that bone loss was greater number of macrophages undergoing M1-polarization was higher in
around implants than around teeth and that peri-implantitis lesions peri-implantitis than in periodontitis lesions.49 Findings from studies
occupied larger areas of the connective tissue and extended closer on the functional characteristics of cells demonstrated that peri-
to the crestal bone when compared to periodontitis lesions. Carcuac implantitis lesions presented with different mRNA signatures50 and
et al.39 took the model a step further by analyzing spontaneous pro- higher mRNA levels for specific cytokines, for example, TNF-a, IL-8,
gression of experimental peri-implantitis at an early stage without a CCR5, and CXCR3 than periodontitis lesions.51
preceding period of extensive tissue breakdown. Crestal bone loss The differences between periodontitis and peri-implantitis le-
was, again, greater around implants with modified surfaces than im- sions detected in studies on human biopsy material corroborate
plants with turned, nonmodified surfaces. data presented in preclinical research. Taken together, the dif-
Results from preclinical studies have contributed to the under- ferences in structure and in densities of key inflammatory cells
standing of the nature of peri-implantitis lesions and the reason for of the ICT between the two types of lesions reflect the charac-
a faster disease progression than is typical for periodontitis. It is teristics of a dysregulated local host response in peri-implantitis.
evident that peri-implantitis lesions are poorly encapsulated since This is evidenced by (i) the lack of an epithelial lining between the
a protective, “self-limiting” zone of healthy connective tissue that submarginal biofilm and the ICT in the pocket area, (ii) the large
separates the infiltrate from the crestal bone is lacking. The ad- spread of the ICT apical to the pocket epithelium and toward the
vanced and perpetuating nature of peri-implantitis lesions is further crestal bone, and (iii) the increased and continuous recruitment of
TA B L E 1 European studies describing the peri-implant lesions—human biopsy material.
Case definition for

Authors Population peri-implantitis Methods Main findings
41
Sanz et al. 12 subjects PD >3 mm Soft tissue biopsies • PI samples showed higher numbers of inflammatory cells (predominantly plasma cells
BERGLUNDH et al.
1991 • Six with PI BOP+ LM and TEM and mononuclear cells) and transmigrating cells in the oral and sulcular epithelium
• Six healthy controls MBL <2 mm compared to healthy controls
• PI: Sixty-five percent of the connective tissue was replaced by the ICT versus 8.2% in
the healthy group
Cornelini et al.186 15 subjects Evidence of MBL Soft tissue biopsies • Healthy sites had no ICT, regular distribution of vessels
2001 • 10 implants with PI PD >5 mm LM, IHC • PI sites had ICT, mostly lymphocytes and plasma cells. Few neutrophils
• 10 healthy implants BOP/SOP+ VEGF, and factor VIII • Expression of VEGF lower in healthy sites than in PI sites
Swelling
Gualini & 16 subjects Evidence of MBL Soft tissue biopsies • In PiM, the inflammatory infiltrate was well defined in the area lateral to the pocket
Berglundh42 • Six with PI BOP/SOP+ LM, IHC epithelium, while in PI sites, the pocket epithelium appeared ulcerated, and the ICT
2003 • 10 with PiM CD3, CD4, CD8, CD19, and extended adjacent to it
elastase • The ICT of PI lesions was three times larger than the one found in PiM sites
• PI contained significantly higher proportions of B cells (CD19+) and elastase-positive
cells compared to PiM
Berglundh et al.43 Six subjects Advanced MBL Soft tissue biopsies • The apical portion of pocket epithelium thin and ulcerated
2004 • 12 implants with PI BOP/SOP+ LM • The ICT extended apically of the pocket epithelium
• Most of the ICT was occupied by plasma cells and PMNs
• Few but large vascular units occupied the marginal portion of the lesion, while
numerous small vessels could be found in the area lateral to the pocket epithelium
Bullon et al.187 10 subjects PD >5 mm Soft tissue biopsies • Multilayered para-keratinized oral epithelium in PI and AG
2004 • Five with PI Evidence of MBL LM and IHC • Thin nonkeratinized junctional epithelium partly ulcerated in PI
• Five with AG BOP+ CD1a, CD3, CD20, CD34, factor • Oral epithelium: Significantly less CD1a and CD34 but more VEGF and blc2 in PI than
VIII, VEGF, and oncoproteins in AG sites
bcl2 and p53 • Sulcular and junctional epithelium: Significantly more CD34, Factor-VIII, and VEGF in
PI than in AG sites
Roediger et al.188 48 subjects PD >4 mm Soft tissue biopsies • mRNA expression of collagen type IV was upregulated in PI compared to CP
2009 • 16 with PI Evidence of MBL RT-PCR and gene-ontology • No differences in mRNA levels of integrin b 1 and integrin b 4 between PI and CP
• 16 with CP BOP+ Collagen type IV, integrin b 1, • mRNA levels of integrin a 6 were upregulated in PI (5.3-fold more) and in CP (11.6-fold
• 16 healthy controls integrin b 4, integrin a 6, and more) compared to healthy controls
HPRT1
Venza et al.51 135 subjects PD ≥5 mm Soft tissue biopsies • Significantly higher levels of TNF-a, IL-8, CCR5, and CXCR3 in PI than in CP sites
2010 • 53 with PI CAL ≥2 mm RT-PCR and Western blot.
• 82 with CP MBL <4 implant TNF-a, IL-1a, IL-6, IL-8, MCP-I,
threads CCR1, CCR2, CCR3, CCR4,
CCR5, CXCR1, CXCR2, CXCR3,
PDGF-A , and TGF-a
|5
(Continues)
6
TA B L E 1 (Continued)
|
Case definition for

50
Becker et al. 14 subjects PD ≥3 mm Soft tissue biopsies • PI and CP exhibit significantly different mRNA signatures
2014 • Seven with PI MBL >3 mm Transcriptome analysis
• Seven with CP
Carcuac & 80 subjects PD ≥7 mm Soft tissue biopsies • PI lesions showed larger ICT area than CP sites
Berglundh44 • 40 with PI BOP/SOP+ LM and IHC • PI exhibited higher levels of CD138, CD68, and MPO-positive cells than CP
2014 • 40 with CP MBL ≥3 mm CD3, CD20, CD138, CD68, and • PI lesions had larger densities of vascular structures in the area lateral to the ICT than
MPO within the ICT
Konermann 25 subjects PD >4 mm Soft tissue biopsies • The ICT in peri-implantitis sites was occupied predominantly by plasma cells
et al.45 • 21 with PI CAL >3 mm LM, IHC • Thin and elongated vascular vessels were observed in PI sites
2016 • Two healthy peri- BOP+ TRAP, CD3, RANK, RANKL, OPG, • Healthy controls demonstrated lower densities of CD3-, OPG-, RANK-, RANKL-, and
implant controls and TNF-a TNF-a-positive cells than PI sites
• Two healthy
periodontal controls
Galindo-Moreno 30 subjects PD >5 mm Soft tissue biopsies • The ICT was more pronounced in PI than in CP.
et al.46 • 15 with PI BOP+ LM and IHC • Higher proportions of plasma cells in PI.
2017 • 15 with CP MBL >3 mm CD45, CD68, CD38, MPO, and • Abundant monocytes/macrophages and neutrophil granulocytes near the pocket
CD34 epithelium were found in both groups.
• Similar densities of CD34-positive cells were noted in both groups.
• CD38-positive cells were more pronounced in the lamina dura of PI than CP
Ghighi et al.189 31 subjects PD ≥5 mm Soft tissue biopsies • CD3, TIMP-2 levels were increased in PI compared to CP
2018 • 11 with PI BOP+ multiplex immunoassay, LM + IHC • Higher levels of IL-1β, IL-10, CD3, CD20, and CD68 were found in PI than in healthy
• 10 with CP Evidence of MBL Cytokines, Matrix controls
• 10 healthy controls metalloproteinases, TIMP, • Levels of IL-17, TIMP-2, Matrix metalloproteinase-2, Matrix metalloproteinase-8,
RANKL, OPG, CD68, CD20, Matrix metalloproteinase-12, and Matrix metalloproteinase-13 were increased in PI
CD3, IL-10, MPO, OPG, RANKL, and CP compared to healthy controls
and TIMP-2
Kasnak et al.47 37 subjects CAL ≥5 mm Soft tissue biopsies • 8-OHdG-and PARK7/DJ-1-positive cells spread in all epithelial layers of PI and CP
2018 • 12 with PI PD ≥5 mm IHC samples, but only in the basal layer of healthy controls
• 13 with CP BOP/SOP+ 8-OHdG, PARK7/DJ-1, NFE2L2/ • NFE2L2/NRF2-stained cells spread in all epithelial layers in all groups
• 13 healthy controls MBL ≥3 mm NRF2, and KEAP1 • A more pronounced ICT was found in PI samples compared to CP ones
• Proportions of 8-OHdG-positive cells in the epithelium were higher in PI and CP than
in healthy controls
• Number of PARK7/DJ-1-positive cells elevated in PI and CP compared to healthy
samples
Lucarini et al.190 48 subjects PD >5 mm Soft tissue biopsies • PI sites. Ulcerated pocket epithelium and a large ICT
2019 • 16 with PI BOP+ LM, IHC • PI showed significantly higher levels of VEGF, CD34, and CD44 compared to the other
• 16 with PiM Evidence of MBL VEGF, CD34, and CD44 groups
• 16 healthy controls • PD was positively correlated to VEGF, CD34, and CD44
BERGLUNDH et al.
Case definition for

BERGLUNDH et al.
48
Dionigi et al. 80 subjects PD ≥7 mm Soft tissue biopsies • PI had significantly higher densities of CD68-, MPO-, and iNOS-positive cells than CP
2020 • 40 with PI BOP/SOP+ LM and IHC sites
• 40 with CP MBL ≥3 mm y-H2AX, CHK2, 8-OHdG, CD68, • Cellular densities for all markers were significantly higher in the inner ICT than in the
MPO, iNOS, NOX2, and outer ICT zone, both in PI and CP
PAD4-MPO • PI showed significantly higher levels of y-H2AX-, iNOS-, NOX2-, MPO-, and PAD4/
MPO-positive cells within the NCT area than that of CP
Fretwurst et al.49 14 subjects BOP/SOP+ Soft tissue biopsies • Heterogeneity of macrophage polarization in both PI and CP
2020 • Seven with PI Evidence of MBL LM, IHC, immunofluorescence • Higher numbers of CD68-positive cells in PI compared to CP
• Seven with CP CD68, iNOS, and CD206 • Higher levels of macrophages in M1 form in PI compared to CP
• Similar levels of macrophages in M2 form in the two groups
Galárraga- Four subjects BOP/SOP+ Soft and bone tissue biopsies LM • The mean defect length was 4.7 mm, the bone density was 85.5%, and the mean
Vinueza • Five implants with PI PD ≥6 mm bone-to-implant contact was 74%
et al.191 MBL ≥3 mm • Two samples showed a chronic inflammatory infiltrate
2020 • One sample revealed signs of osteoclastic activity, three samples showed inactive
crestal bone activity and one site showed active bone formation
• The residual bone was mainly cortical showing areas with small vessels and areas of
lamellar bone
• Secondary osteons were frequently present, while osteoclasts were sporadically seen
as well as cancellous bone which was located mostly in the apical portions of the
specimens
Mijirtsky et al.192 40 subjects PD ≥5 mm Soft tissue biopsies • The ICT of PI samples showed plasma cells 45%, lymphocytes 7%, PMN 6%, collagen
2019 • 20 with PI BOP/SOP+ LM, IHC, immunofluorescence, fibers 15%, fibroblasts 8%, and blood vessels 12%
• 20 healthy controls Exposure of ≥2 TEM, and RT-PCR • Levels of ROX, Osterix, and b catenin genes were downregulated in PI samples
implant threads • ROS production (NOX4 and NADPH oxidase) was upregulated in PI samples
Radiographic bone
loss
Fretwurst 15 subjects BOP/SOP+ Soft tissue biopsies • There were no significant differences in the number of positive cells in PI lesions
et al.193 • Seven with PI around MBL >2/3 of the LM, IHC between ceramic and titanium implants
2021 titanium-implants implant length CD3, CD20, CD138, and CD68 • The ICT was predominantly occupied by plasma cells, followed by T lymphocytes, B
• Eight with PI around lymphocytes, and macrophages
ceramic implants
Galárraga- 20 subjects BOP/SOP+ Soft tissue biopsies • CD68-positive density was about 14.36% of the ICT in PI sites
Vinueza 20 implants with PI PD ≥6 mm LM, IHC • CD80-and CD206-positive cells (M1 and M2 macrophages) occupied 7.07% and
et al.194 MBL ≥3 mm CD68, CD80, and CD206 5.22% of the ICT, respectively
2021 • The M1/M2 ratio was 1.56
• A positive correlation between CD68, M1 levels, and PD was observed
Abbreviations: AG, Aggressive periodontitis; BOP, Bleeding on probing; CAL, Clinical attachment level; CP, Chronic periodontitis; ICT, Infiltrated connective tissue; IHC, Immunohistochemistry; LM, Light
microscopy; MBL, Marginal bone level; PD, Probing depth; PI, Peri-implantitis; PiM, Peri-implant mucositis; SOP, Suppuration on probing; TEM, Transmission electron microscopy.
|7
|
8 BERGLUNDH et al.
beyond the lateral borderline of the ICT adds to the overall pic-
ture of an extensive tissue reaction at sites with peri-implantitis.
Since the dental implant is a metal device predominantly made of
titanium, it has been suggested that the presence of a foreign ma-
terial at peri-implantitis sites may influence the local host response.
Although studies have reported on the presence of metal particles
in soft tissue samples from peri-implantitis sites, 52–54 it remains un-
clear whether such findings are specific for diseased peri-implant
tissues since relevant comparisons to matching specimens repre-
senting healthy peri-implant tissues are lacking. In addition, assess-
ments of metal microparticles in peri-implant soft tissues require
the use of appropriate techniques to verify the type of material
(e.g., titanium) and to detect small-sized particles of 1–2 μm, for ex-
ample, μ-PIXE (micro proton-induced X-r ay emission), synchrotron
radiation, or SEM-EDX.
Data from studies evaluating human biopsy material obtained
from sites with peri-implantitis may vary depending on the severity
of the condition and case definitions used when recruiting patients.
One of the upsides of the histological evaluation of tissue samples
is the preservation of anatomy and orientation of tissue structures.
The detection of target cells in well-controlled locations is thereby
facilitated. Technical limitations of using cell markers of primarily
phenotypical characteristics with, for example, immunohistochem-
istry, however, must be considered. On the other hand, assessments
of mRNA expression of key elements in the lesion require the use of
homogenized tissue samples, in which the orientation of the tissue
structure is lost. Ideally, future analysis of human peri-implantitis
specimens should apply novel “omics” techniques (e.g., proteomics,
transcriptomics) in combination with a spatial visualization approach.
Although such techniques are currently available, their use needs to
F I G U R E 2 Section prepared from human biopsy obtained from a be balanced between meaningful and feasible sample sizes and the
site with severe peri-implantitis. Pocket epithelium (PE), inner (ICT-
extensive resources that are required. Future techniques should also
1) and outer (ICT-2) zones of ICT, and non-infiltrated connective
tissue (NCT) area. From Dionigi et al.48 aim at preserving the area that encompasses the interface between
the inflamed peri-implant tissues and the biofilm residing in the
pocket. The analysis of host–parasite interactions has the potential
neutrophils and macrophages to the ICT. Thus, the main features to provide further understanding of the role of microorganisms as
of peri-implantitis lesions illustrate an active and perpetuating the main etiological factor in peri-implantitis.
process of inflammation with few, if any, signs of inactivity. The
nonlinear and accelerating pattern of disease progression in peri-
implantitis described above, may, to a high degree, be explained by 4 | MICROBIOLOG IC AL CHAR AC TERISTIC S
these lesion characteristics. OF PERI-I MPL ANTITIS
In an extended analysis of biopsy material obtained from 80
subjects with severe peri-implantitis or periodontitis, Dionigi et al. Early on in the development of oral implantology, it was observed
reported that both types of lesions presented with higher densi- that bone loss around implants could sometimes be associated with
ties of inflammatory cells in an “inner zone” (ICT-1) adjacent of the classic signs of infection in the soft tissues including redness, swell-
48
pocket epithelium than in an “outer zone” of the lesion (ICT-2) ing, and pus formation.55 Pus is the result of the immune system
(Figure 2). The authors also made observations on cellular charac- responding to an infection, usually caused by bacteria. One might
teristics in the non-infiltrated connective tissue area (NCT) lateral have thought that this alone would have persuaded the dental com-
to the ICT. Thus, the NCT compartment in peri-implantitis speci- munity that infections around implants could be a serious threat and
mens contained higher densities of y-H2AX-, iNOS-, NOX2-, MPO-, that an antimicrobial approach to preventing implant failure would
and PAD4/MPO-positive cells, that is, markers for DNA damage, be worthwhile. However, the extent to which infection contrib-
antimicrobial nitric oxide, and formation of NETs, than found in utes to the phenomenon of peri-implant bone loss in general has
periodontitis samples. The finding of tissue reactions spreading remained controversial ever since.56 As evoked in previous chapters
|
BERGLUNDH et al. 9
in Periodontology 2000,57,58 several lines of evidence suggest that composition of the peri-implant microbiota in health and disease.
bacteria colonizing implant surfaces play an essential part in the Most investigators used methods originally developed for evaluating
pathogenesis of peri-implantitis: the subgingival microbiota in periodontal pockets at natural teeth
and primarily looked for so-called putative periodontal pathogens.
• Experiments in humans have shown that the unrestrained accu- In these studies, bacteria ubiquitous in chronic periodontitis, such as
mulation of bacterial plaque on implants over several days induced Fusobacterium spp. and P. intermedia were also regularly detected in
a local inflammation in the adjacent mucosa (called “experimental specimens from peri-implantitis.75 Organisms that are less common
59–61
peri-implant mucositis”), similar to the effect of dental plaque in chronic periodontitis, such as Aggregatibacter actinomycetemcomi-
on gingiva (called “experimental gingivitis”62). In both situations, tans,76 were less frequently identified.
signs of inflammation were diminished once the bacterial deposits Analysis using different methods have shown that the submuco-
were removed.63 sal microbiome in peri-implant diseases is (i) mixed, (ii) rather variable,
• Microbiota harvested from diseased peri-implant sites showed and (iii) in most cases dominated by various Gram-negative anaerobic
quantitative and qualitative differences from the microbiota at im- bacteria.75 According to a recent systematic review,77 meta-analyses
plant sites with a healthy mucosa, as discussed in more detail below. for species analyzed in at least two independent studies revealed the
• In preclinical in vivo studies, subgingival placement of ligatures to- following taxa to be associated with peri-implantitis (compared to
gether with plaque formation resulted in changes in the composi- “non-peri-implantitis”): the Gram-negative anaerobes Fusobacterium
tion of the local microbiota and in the destruction of peri-implant nucleatum, Porphyromonas gingivalis, Prevotella intermedia, and
64–67
tissues. Tannerella forsythia, the spirochete Treponema denticola, and the Gram-
• Treatment protocols of peri-implantitis aiming at removing bac- positive bacterium Staphylococcus epidermidis. With regard to the lat-
terial deposits from implants have shown positive clinical results, ter, it has long been speculated that this organism might be responsible
albeit to varying degrees, as reviewed in the next section. for a microbiologically distinct form of peri-implant infection. In fact,
• The lack of maintenance programs and poor compliance (i.e., per- S. epidermidis, a common symbiont living on the human skin and mu-
sistence of bacterial deposits due to poor oral hygiene) after im- cosa, is also linked to other forms of suppurative infections of indwell-
plant therapy increase the risk for peri-implantitis.68–70 ing devices that have little resemblance to the periodontitis-like lesions
commonly encountered around oral implants.
Preliminary evidence implicating certain types of microorgan- Several studies have shown that there is a difference in the com-
isms in peri-implantitis came from microscopic examination of position of the peri-implant microflora found in deep and shallow
specimens collected around implants with advanced pocketing. pockets,78 reflecting differences in the ecological conditions that are
While spirochetes were not detected in specimens from implant also known from the situation around natural teeth.75 Pockets with
sites with healthy peri-implant tissues, they were found in large a probing depth of ≥5 mm can be considered as protected habitats
numbers at diseased sites.71,72 Since electron microscopy had for putative pathogens and can be an indicator of risk of peri-implant
shown that these bacteria invaded periodontal tissues in necro- disease.
tizing ulcerative gingivitis,73 one wondered what significance this Classical microbiology is largely based on the study of the prop-
might have with regard to peri-implantitis. A study using bacterial erties of pure cultures of microorganisms grown under laboratory
culture methods published in 198774 showed that 41% of the or- conditions that are not representative of their life in nature. In the
ganisms cultured from implants with peri-implant probing depths wild, bacteria live in mixed communities called biofilms that adhere
>5 mm and bone loss were Gram-negative anaerobic rods. Among to environmental surfaces. However, the data discussed above, even
these organisms, Fusobacterium spp. and Prevotella intermedia were from studies using the latest molecular technologies, are based on
frequently identified at high levels. The presence of spirochetes samples obtained using biofilm-
destroying methods. Information
and other motile organisms was corroborated microscopically but on the spatial organization of the naturally grown biofilm in human
could not be further studied using the techniques available at the peri-implant disease is sparse and little is known about the behav-
time. On the other hand, only very few bacteria, mostly identified iors of suspected pathogens, specifically when adhering to im-
as Gram-positive cocci, were detected at implants without symp- plant surfaces.79 On a larger scale, biofilm infections are not only
toms. These results suggested that the condition henceforth re- a dental problem. As recognized in orthopedic implant research,80
ferred to as “peri-implantitis” appeared to be a site-specific disease they contribute to severe complications, increased use of antibiotic
process involving bacteria previously connected to chronic peri- treatments, and development of antibiotic-
resistant microorgan-
odontitis around teeth. isms. When discussing the sometimes frustrating results of treating
Over the course of almost four decades, further studies using oral peri-implantitis, one should keep in mind the difficult-to-treat
classic and newly emerging microbiologic methods have confirmed biofilm-
associated infections of indwelling devices, which often
and extended early findings. Technologies including checkerboard cause distress, increased morbidity, and high costs. There is a need
DNA–DNA hybridization, qPCR, fluorescence in situ hybridization, to improve the diagnosis of oral and non-oral biofilm infections to
and 16S rRNA gene-based PCR were used to further study the enable earlier detection and treatment to the benefit of our patients.
|
10 BERGLUNDH et al.
5 | TR E ATM E NT O F PE R I - I M PL A NTITI S therapy,93–95 studies on treatment of peri-implantitis have typically

reported on changes of clinical and radiographic parameters. In fact,
5.1 | Concepts the variables probing depth and bleeding on probing were described
in almost 90% of all studies on the management of peri-implant dis-
At the 2017 World Workshop on the Classification of Periodontal eases during the last 10 years, primarily as mean values of changes
and Peri-Implant Diseases and Conditions, the bacterial etiology occurring pre-versus post-therapy.96
9
of peri-
implant mucositis and peri-
implantitis was highlighted. Within the periodontal field, the importance of tangible end
Interventional research has demonstrated the causal link between points of active therapy has been widely studied.97 In addition to
the accumulation of bacterial plaque and subsequent development end points evaluated in the long term (e.g., need for retreatment
61,63,81
of peri-implant inflammation, that is, peri-implant mucositis. and tooth loss) and patient-reported oral health-related quality-of-
The overall understanding of disease development is that of a step- life, the concept of pocket closure, that is, shallow probing depth
wise model, by which peri-implant mucositis will initially develop and the absence of bleeding on probing, is strongly associated with
upon plaque accumulation and may, subsequently, progress into periodontal stability. The relevance of residual pocketing at implant
82
peri-implantitis. The model proposes that peri-implantitis is always sites following surgical therapy of peri-implantitis was evaluated by
preceded by peri-implant mucositis. Bacterial plaque thereby rep- Carcuac et al.90 The authors found that residual probing depth ≥6 mm
resents a necessary component of disease development according at 1 year was a strong indicator of disease recurrence (odds ratio 7.4)
to the “sufficient component cause” model described by Rothman when compared to more shallow pocketing (<6 mm). This finding
83
in 1976. Much like the relationship between bacterial plaque and speaks to the concept of the deepened pocket acting as a protected
periodontitis, the validity of a similar pathway for peri-implantitis is habitat for a microbial biofilm as outlined in Section 4.
supported by data from, both, observational and interventional re- The predictive value of bleeding on probing at implant sites has
search. As pointed out above, subgroups of implant-carrying individ- also been assessed. Thus, Karlsson et al.,98 in a 3-year follow-up
uals not attending regular supportive care have been shown to suffer study on 70 subjects diagnosed with peri-implantitis at ≥1 of their
a significantly higher burden of peri-implant diseases, including the implants, found that disease progression (additional bone loss
occurrence of peri-implantitis.84–86 Secondly, and more importantly, >2 mm) was more likely to occur at implant sites presenting with
anti-infective approaches applied in the management of established multiple bleeding spots (hazard ratio 7.1) when compared to no or
peri-implantitis, that is, establishment of patient-performed plaque only isolated bleeding. The negative predictive value of bleeding on
control combined with decontamination of implant surfaces, has probing was particularly high (95%). A corresponding analysis fol-
conceptually been shown to arrest disease progression also in stud- lowing active therapy of peri-implantitis resulted in similar findings.
ies with long-term follow-up periods.87–91 The negative predictive value (for complete absence of bleeding on
As a consequence of the understanding of peri-implantitis as probing) and subsequent disease recurrence (additional bone loss
a disorder driven by bacterial plaque, the S3 level Clinical Practice >0.5 mm) in a 2-year evaluation by Carcuac et al.99 was 78%. In an
Guideline developed by the European Federation of Periodontology early European study on short-term changes of peri-implant attach-
for the prevention and treatment of peri-implant diseases is very ment levels in a patient population under maintenance care, Jepsen
92
much centered on this factor. Thus, management of peri-implantitis et al.100 reported an almost identical negative predictive value of
should include an initial nonsurgical step, during which bacterial de- 82%.
posits are to be removed/reduced through supra-and submarginal Collectively, these data support the concept that meaning-
instrumentation. Following an evaluation of the healing response to ful short-term end points for the active therapy of peri-implantitis
nonsurgical treatment modalities and in case of residual signs of dis- should correspond to what has been proposed for periodontal care.
ease, a surgical step is recommended. Also here, decontamination In other words, therapeutic efforts should aim for shallow peri-
of the implant surfaces, following flap elevation, is the key thera- implant probing depths and reduction or elimination of bleeding
peutic component. The treatment of peri-implantitis encompasses on probing. It should be noted that recent data has suggested that
adequate self-performed and professionally delivered oral hygiene the two parameters, that is, peri-implant probing depth and possi-
measures during all steps of therapy, including the period upon com- ble bleeding upon probing, are closely interlinked.101,102 Also, after
pletion of active treatment. Regular supportive peri-implant care surgical therapy of peri-implantitis, the probability of bleeding on
represents the final step of the sequential approach. probing was found to be low at sites with shallow probing (≤5 mm;
<40%), while the corresponding likelihood at sites with deep pock-
eting (≥7 mm) was high (>70%).103 Consequently, the S3 level Clinical
5.2 | End points of therapy Practice Guideline by the European Federation of Periodontology
for the prevention and treatment of peri-implant diseases92 recom-
In the clinical setting, peri-
implantitis is characterized and diag- mended end points of successful surgical therapy to include shallow
nosed through visual inspection, peri-implant probing, and radio- probing (≤5 mm), the absence of suppuration on probing, and only
graphic evaluation.9 In line with reports on outcomes of periodontal minimal bleeding on probing (≤1 point).
|
BERGLUNDH et al. 11
5.3 | Nonsurgical therapy of peri-implantitis or reduction of bleeding scores were noted following the adminis-
tration of probiotics. In view of the overall evidence and following
The clinical efficacy of nonsurgical treatment of peri-implantitis careful consideration of potential benefits and harms, particularly
has recently been evaluated in three systematic reviews.104–106 A associated with the administration of systemic antibiotics, the S3
total of 15 RCTs, mainly conducted in European countries, were level Clinical Practice Guideline suggested not to use any of the
107–120
included. Numerous adjunctive and alternative methods for aforementioned adjunctive measures in the nonsurgical treatment
plaque removal and/or implant surface decontamination were evalu- of peri-implantitis.92 Table 2 presents an overview of selected
ated, including mechanical, physical, photomechanical/−thermal (i.e., European studies on nonsurgical therapy of peri-implantitis.
laser application) as well as chemical treatment approaches. Control
interventions were defined as cleaning approaches that did not aim
at any mechanical or physical decontamination, except for the re- 5.4 | Surgical therapy of peri-implantitis
moval of hard deposits (i.e., scalers or sonic/ultrasonic devices with
or without saline irrigation).104–106 European contributions to the scientific evidence on the effect of
Various laser devices, used either as monotherapy (i.e., Er:YAG surgical therapy of peri-implantitis have been extensive. Virtually,
laser, Nd:YAG laser) or in combination (diode laser, Er,Cr:YSGG laser) all datasets cited by the recently published S3 level Clinical Practice
with chlorhexidine irrigation were commonly associated with sim- Guideline for the prevention and treatment of peri-implant dis-
ilar reductions of probing depth and bleeding scores as respective eases92 were generated in European countries (Table 3). The first re-
control groups.104 Significant benefits for test groups were only reports originated from Germany,128–130 Italy,131,132 and Sweden,133,134
ported in two studies employing 3-micron lasers, with limited fol- mostly in the form of case series with limited sample sizes. From
low-up periods of 6 months.108,109,120 Accordingly, laser application 2010 and onward, randomized controlled trials135–140 evaluating effi-
used either as an adjunct or monotherapy was suggested not to be cacy of different surgical protocols have been consistently published.
used for nonsurgical treatment of peri-implantitis in the S3 level One key aspect that these early studies highlighted was the im-
Clinical Practice Guideline presented by the European Federation of portance of implant surface characteristics on the outcomes of ther-
Periodontology in 2023.92 apy, as had been suggested in preclinical in vivo evaluations.141,142 In
The efficacy of submucosal Instrumentation using glycine a pivotal such clinical study, Roccuzzo et al.132 found that, 12 months
powder-based air polishing was evaluated in two RCTs.111,112,114 following surgical treatment, reduction of peri-implant probing depth
Even though one study reported on significantly greater reductions was greater at implants with a sandblasted and acid-etched (SLA®)
of bleeding scores following air polishing monotherapy versus con- surface (mean reduction 3.4 mm) when compared to TPS-surface im-
trol treatment at 6 and 12 months, the overall quality of evidence plants (2.1 mm). Corresponding results for bleeding on probing were
was low. The S3 level Clinical Practice Guideline therefore suggested also noted with considerably higher residual bleeding at 1 year (57%
not to use air polishing in nonsurgical treatment of peri-implantitis.92 vs. 15%) at tissue plasminogen activator (TPS)-surface implants. The
The adjunctive use of chemical surface decontamination approaches importance of implant surface characteristics explains why clinical
evaluated in the literature encompassed antimicrobial photody- studies in the field typically account for implant categories/brands
namic therapy (aPDT, low level lasers: 635/670 nm; photosensitizers: that are included.135,143 This aspect, along with technical details such
toluidine/methylene blue) as well as a desiccant gel (i.e., hydroxy- as the possibility to remove the implant-borne restoration during the
benzenesulphonic/hydroxymethoxybenzene and sulfuric acid). Both surgical procedure, distinguishes surgical therapy of peri-implantitis
procedures were associated with some improvements in reductions with its periodontal counterpart. However, many of the clinical
105
of probing depth over respective control groups at 6 months. Due questions and the overall scientific approach, have otherwise been
to the very low overall quality of evidence, it was, however, sug- similar. As such, interventional studies addressed (i) the efficacy of
gested not to use aPDT nor a desiccant antiseptic gel in nonsurgical different decontamination protocols, (ii) the potential benefit of anti-
peri-implantitis therapy.92 septics/antimicrobials, and (iii) reconstructive treatment modalities.
The administration of local antimicrobials, systemic antibiotics All these domains have already been extensively evaluated within
as well as probiotics was evaluated as an adjunct to conventional the periodontal field,93,95,144,145–147 while corresponding evidence for
106
nonsurgical treatment of peri-implantitis. More specifically, four the surgical management of peri-implantitis is only emerging.
studies analyzed the efficacy of local antimicrobials, such as mino- The effectiveness of surgical therapy of peri-implantitis, in
121–124
cycline microspheres and chlorhexidine chips. Three studies general, was recently evaluated in a systemic review solicited by
looked into systemic antibiotics, notably amoxicillin + metronidazole the EFP. While Karlsson et al.148 could not identify direct compar-
117,125,126
or just metronidazole. Two studies evaluated the potential isons of surgical interventions with other standard therapies (e.g.,
benefits of Lactobacillus reuteri probiotics.113,127 Local antimicrobi- nonsurgical treatment), the overall effect of access flap surgery
als moderately improved probing depth reduction, while systemic and/or pocket elimination was estimated through meta-analyses.
antibiotics had a more obvious effect on reduction of both probing Based on 18 study arms, surgical therapy resulted in a standardized
depths and bleeding scores, particularly at sites with an initial pock- mean reduction of probing pocket depth of 2.2 mm and in a gain of
eting of >6 mm. No adjunctive effects on either pocket reduction marginal bone level of 0.2 mm (Figure 3). These data, originating
12
TA B L E 2 Selected European studies on nonsurgical therapy of peri-implantitis.

|
Patients/ Inclusion criteria: Mean PD at

Study Treatment groups implants peri-implantitis baseline Outcomes Comments
120
Alpaslan Yayli et al. Titanium curettes 17/17 PD 4–6 mm & BOP/SOP and 4.1 mm PD red: 0.5 mm • Smokers excluded
2022 AB− bone loss 2–3 mm BOP red: 11.3% • Oral hygiene instructions
RCT AS− • No details on removal of implant-supported
6 months Titanium curettes 16/16 4.1 mm PD red: 0.9 mm prosthesis provided (all cemented)
Turkey Photodynamic therapy BOP red: 26.2% • No details on local anesthesia provided
AB− • MBL changes not reported
AS−
Titanium curettes 17/17 4.5 mm PD red: 1.2 mm
Er,Cr:YSGG laser BOP red: 48.8%
AB−
AS−
Schwarz et al.108 Plastic curettes 10/16 PD ≥4 mm and BOP and SOP 5.5 mm PD red: 0.7 mm • Smokers excluded
2005 AB− and bone loss BOP red: 22.0% • Oral hygiene instructions
RCT AS+ REC: 0.1 mm • Local anesthesia
6 months Er:YAG laser 10/16 5.4 mm PD red: 0.8 mm • No details on removal of implant-supported
Germany AB− BOP red: 52.0% prosthesis provided
AS− REC: 0.1 mm • MBL changes not reported
Schwarz et al.109 Plastic curettes 10/20 PD >7 mm and BOP and SOP 4.5 PD red: 0.2 mm • Smokers excluded
2006 AB− and bone loss CAL change: 0.1 mm (gain) • Oral hygiene instructions
RCT AS+ • Local anesthesia
12 months Er:YAG laser 10/20 4.6 mm PD red: 0.5 mm • No details on removal of implant-supported
Germany AB− CAL change: 0.3 mm (gain) prosthesis provided
AS− • MBL changes not reported
Merli et al.114 Ultrasonic 16/16 PD 5–8 mm and BOP/SOP and 4.4 mm PD red: 0.2 mm • Oral hygiene instructions
2020 bone loss exceeding initial BOP red (out of four sites): 0.4 • Implant-supported prosthesis removed
RCT bone remodeling REC: 0.1 mm • No local anesthesia used
6 months MBL change: 0.2 mm (gain) • No details on ultrasonic tip provided
Italy Ultrasonic 16/16 5.0 mm PD red: 0.5 mm
Desiccant material BOP red (out of four sites): 0.5
REC: 0.3 mm
MBL change: −0.1 mm (loss)
Ultrasonic 16/16 5.1 mm PD red: 0.1 mm
Air polishing BOP red (out of four sites): 0.7
REC: 0.3 mm
Desiccant material BOP red (out of four sites): 0.8
Air polishing REC: 0.2 mm
BERGLUNDH et al.

119
Roccuzzo et al. Titanium curettes and 12/12 PD >5 mm and BOP/SOP and 5.3 mm PD red: 1.5 mm • Oral hygiene instructions
BERGLUNDH et al.
2022 stainless-steel bone loss ≥2 mm BOP red: 0% • Local anesthesia

RCT curettes MBL change: 0.0 mm • Implant-supported prosthesis not removed
6 months Titanium curettes and 13/13 5.4 mm PD red: 1.3 mm • Treatment repeated in both groups at
Switzerland stainless-steel BOP red: 8.4% baseline, 7, and 14 days
curettes MBL change: 0.0 mm
Diode laser
Renvert et al.110 Titanium curettes and 17/17 PD ≥4 mm and BOP/SOP and 4.0 mm PD red: 0.0 mm • Oral hygiene instructions
2009 rubber cups bone loss <2.5 mm BOP red (out of four sites): 0.3 • Local anesthesia
RCT Ultrasonic scaler and 14/14 4.3 mm PD red: 0.4 mm • No details on removal of implant-supported
6 months rubber cups BOP red (out of four sites): 0.5 prosthesis provided
Sweden • Dedicated ultrasonic tip (Vector)
Karring et al.195 Carbon curettes 11/11 PD ≥5 mm and BOP and bone 6.3 mm PD red: 0.0 mm • Oral hygiene instructions
2005 loss ≥1.5 mm BOP red: −9.8% (worsening) • Local anesthesia not provided
RCT (split mouth) MBL change: −0.3 (loss) • No details on removal of implant-supported
6 months Ultrasonic 11/11 5.8 mm PD red: −0.1 mm (worsening) prosthesis provided
Denmark BOP red: 27.2% • Dedicated ultrasonic tip (Vector)
MBL change: −0.3 (loss)
Sahm et al.111 Carbon curettes 15/19 PD ≥4 mm and BOP/SOP and 4.0 mm PD red: 0.5 mm • Oral hygiene instructions
2011 0.1% CHX digluconate bone loss ≤30% following BOP red: 11.0% • Local anesthesia
RCT irrigation + implant placement REC: 0.0 mm • No details on removal of implant-supported
6 months submucosal 0.1% CAL change: 0.5 mm (gain) prosthesis provided
Germany CHX digluconate gel
application
Air polishing (glycine 15/22 3.8 mm PD red: 0.6 mm
powder) BOP red: 43.5%
REC: 0.2 mm
CAL change: 0.4 mm (gain)
John et al.112 Carbon curettes 13/18 PD ≥4 mm and BOP/SOP and 3.9 mm PD red: 0.4 mm • 12-month follow-up of Sahm et al.111
2015 0.1% CHX digluconate bone loss ≤30% following BOP red: 16.6% • Oral hygiene instructions
RCT irrigation + implant placement REC: 0.1 mm • Local anesthesia
12 months submucosal 0.1% CAL change: 0.5 mm (gain) • No details on removal of implant-supported
Germany CHX digluconate gel prosthesis provided
application
Air polishing (glycine 12/18 3.7 mm PD red: 0.5 mm
powder) BOP red: 41.2%
REC: 0.1 mm
CAL change: 0.6 mm (gain)
|13
(Continues)
14
|

118
Polymeri et al. Ultrasonic 19/19 PD ≥5 mm and BOP/SOP and 8.0 mm PD red: 1.5 mm • Oral hygiene instructions
2022 Carbon curettes bone loss ≥3 mm BOP red: 10% (approximated) • Local anesthesia
RCT AB− • Implant-supported prosthesis not removed
3 months AS+ • No details on MBL or REC changes provided
Netherlands Ultrasonic 18/18 7.4 mm PD red: 2.3 mm • Dedicated ultrasonic tip (PEEK)
Carbon curettes BOP red: 15% (approximated)
AB+
AS+
De Waal et al.115 Air polishing 29/64 PD ≥5 mm and BOP/SOP and 5.8 mm PD red: 1.4 mm • Oral hygiene instructions
2021 (erythritol-based bone loss ≥2 mm BOP red: 39.2% • No details on removal of implant-supported
RCT powder) CAL change: 1.0 mm (gain) prosthesis provided
3 months Ultrasonic MBL change: 0.0 • No details on local anesthesia provided
Netherlands AB−
AS+
Air polishing 28/68 5.6 mm PD red: 1.7 mm
(erythritol-based BOP red: 38.6%
powder) CAL change: 1.0 mm (gain)
Ultrasonic MBL change: 0.1 (loss)
AB+
AS+
Hentenaar et al.116 Air polishing 38/63 PD ≥5 mm and BOP/SOP and 4.8 mm PD red: 0.5 mm • Oral hygiene instructions
2021 (erythritol-based bone loss ≥2 mm BOP red: 8.3% • Implant-supported prosthesis not removed
RCT powder) MBL change: 0.0 mm • Local anesthesia (if required)
3 months Hand instruments • Dedicated ultrasonic tip (PEEK)
Netherlands AB−
AS+
Hand instruments BOP red: 8.1%
AB− MBL change: 0.1 (loss)
AS+
Blanco et al.117 Ultrasonic 16/34 PD ≥6 mm and BOP/SOP and 6.3 mm PD red: 0.9 mm • Oral hygiene instructions
2022 Stainless steel curette bone loss ≥3 mm BOP red: 20.5% • Implant-supported prosthesis removed
RCT AS+ REC: 0.7 mm • Local anesthesia
12 months AB− CAL change: 0.5 mm (gain)
Spain MBL change: 1.0 mm (gain)
Stainless steel curette BOP red: 34.7%
AS+ REC: 1.2 mm
AB+ CAL change: 1.7 mm (gain)
MBL change: 2.2 mm (gain)
BERGLUNDH et al.
BERGLUNDH et al.

196
Schär et al. Titanium curette 20/20 PD 4–6 mm and BOP and bone 4.4 mm PD red: 0.4 mm • Oral hygiene instructions
2013 Air polishing (glycine loss 0.5–2 mm BOP red: 50% • No details on removal of implant-supported
RCT powder) REC: 0.3 mm prosthesis provided
6 months AS+ CAL change: 0.2 mm (gain) • Local anesthesia
Switzerland AB+ • Local antibiotics (control group)
Titanium curette 20/20 4.2 mm PD red: 0.5 mm
Air polishing (glycine BOP red: 44%
powder) REC: 0.2 mm
Photodynamic therapy CAL change: 0.2 mm (gain)
AS+
AB−
Laleman et al.113 Ultrasonic 10/10 PD 4–6 mm and BOP and bone 5.5 mm PD red: 1.3 mm • Oral hygiene instructions
2020 Titanium curette loss 1–3 mm BOP red: 34% • No details on removal of implant-supported
RCT Air polishing prosthesis provided
6 months Placebo drops • Local anesthesia
Belgium AS− • Dedicated ultrasonic tip (PEEK)
AB− • Local application of placebo/probiotic drops
Ultrasonic 9/9 5.2 mm PD red: 1.0 mm and subsequent use by patients
Titanium curette BOP red: 28%
Air polishing
Probiotic drops
AS−
AB−
Abbreviations: AB, systemic antibiotics; AS, local antiseptics; BOP, bleeding on probing; CAL, clinical attachment level; CHX, chlorhexidine; MBL, marginal bone level; PD, probing depth; RCT, randomized
control trial; RCT, randomized controlled trial; REC, soft tissue recession; SOP, suppuration on probing.
|15
16
TA B L E 3 Selected European studies on surgical therapy of peri-implantitis.

|
Patients/ Inclusion criteria: Mean PD at Decontamination

Study Treatment groups implants peri-implantitis baseline protocol Outcomes Comments
Wohlfahrt Access flap 16/16 PD ≥5 mm and BOP and 6.5 mm Titanium curettes. PD red: 2.0 mm • Diabetes and smoking
et al.138 AB+ osseous defect ≥4 mm EDTA and saline BOP red (sites): 0.6 not exclusion criteria
2012 AS− MBL change: 0.1 mm (gain) (uncontrolled diabetes not
RCT Access flap and bone graft 16/16 6.5 mm PD red: 1.7 mm allowed)
12 months AB+ BOP red (sites): 0.4 • Interventions prior to
Norway AS− MBL change: 2.0 mm (gain) surgery: hygiene phase
also reported in: • Implant-supported
Andersen prosthesis removed for
et al.197 surgery
2017 • Submerged healing for
6 months following surgery
Jepsen et al.160 Access flap 26/26 PD ≥5 mm and BOP/SOP 6.3 mm Titanium brush. PD red: 2.6 mm • Diabetes and smoking
2016 AB+ and radiographic intra- Hydrogen peroxide BOP red: 44.9% not exclusion criteria
RCT AS+ osseus defect ≥3 mm 3% and saline MBL change: 0.9 mm (gain) (uncontrolled diabetes not
12 months Access flap and bone graft 33/33 (verified at surgery) 6.3 mm PD red: 2.8 mm allowed)
Multi-center AB+ and defect with BOP red: 56.1% • Interventions prior to
(Europe) AS+ circumference ≥270 MBL change: 3.6 mm (gain) surgery: mechanical
degrees instrumentation and oral
hygiene instructions
• Handling of implant-
supported prosthesis not
reported
• Transmucosal healing
Renvert Access flap 20/20 PD ≥5 mm and BOP/SOP 6.7 mm Titanium curettes. PD red: 2.5 mm • Diabetes and smoking
et al.162 AB+ and osseous defect Hydrogen BOP: 35.0% no BOP at 1 year not exclusion criteria
2018 AS+ ≥3 mm peroxide 3% and MBL change: 0.2 mm (gain) (uncontrolled diabetes not
RCT Access flap and bone graft 21/21 6.5 mm saline PD red: 3.6 mm allowed)
12 months AB+ BOP: 47.6% no BOP at 1 year • Interventions prior to
Sweden AS+ MBL change: 0.7 mm (gain) surgery: None/not reported
reported
BERGLUNDH et al.

Renvert Access flap 34/34 PD ≥5 mm and BOP/SOP 6.8 mm Titanium curettes, PD red: 2.3 mm • Diabetes and smoking
BERGLUNDH et al.
et al.164 AB+ and radiographic intra- rotating titanium BOP red: 1.0 not exclusion criteria
2021 AS+ osseus defect ≥3 mm brush. Hydrogen (Mean of 4 surfaces—0 = no; (uncontrolled diabetes not
RCT (verified at surgery) peroxide 3% and 1 = dot; 2 = line; and 3 = drop) allowed)
12 months and defect with saline REC: 0.9 mm • Interventions prior to
Multi-center circumference ≥270° MBL change: 1.3 mm (gain) surgery: mechanical
(Europe) Access flap and bone graft 32/32 6.7 mm PD red: 1.9 mm instrumentation and oral
and Membrane BOP red: 0.9 hygiene instructions
AB+ (Mean of 4 surfaces—0 = no; • Implant-supported
AS+ 1 = dot; 2 = line; and 3 = drop) prosthesis removed for
REC: 0.5 mm surgery, if possible
MBL change: 2.3 mm (gain) • Transmucosal healing
Derks et al.165 Access flap 67/74 PD ≥7 mm and BOP/SOP 8.5 mm Titanium curette, PD red: 3.7 mm • Diabetes and smoking
2022 AB+ and bone loss ≥3 mm rotating titanium BOP red: 49.6% not exclusion criteria
RCT AS− and osseous defect brush REC: 1.1 mm (uncontrolled diabetes not
12 months ≥3 mm MBL change: 1.1 mm (gain) allowed)
Multi-center Access flap and bone graft 66/73 8.8 mm PD red: 3.7 mm • Interventions prior to
(Europe) AB+ BOP red: 44.8% surgery: supramucosal
AS− REC: 0.7 mm cleaning and oral hygiene
MBL change: 1.1 mm (gain) instructions
• Implant-supported
prosthesis removed for
surgery, if possible (70% of
cases)
Carcuac Access flap and bone 27/47 PD ≥6 mm and BOP/SOP 7.9 mm Titanium curettes, PD red: 2.8 mm • Diabetes and smoking
et al.143 recontouring (if indicated) and marginal bone loss gauze with CHX BOP: 60.9% no BOP at 1 year not exclusion criteria
2016 AB+ ≥3 mm MBL change: 0.2 mm (gain) (uncontrolled diabetes not
2022 AS+ allowed)
RCT Access flap and bone 25/46 7.9 mm Titanium curettes, PD red: 3.4 mm • Interventions prior to
12 months recontouring (if indicated) gauze with saline BOP: 65.2% no BOP at 1 year surgery: supramucosal
Sweden AB+ MBL change: 0.5 mm (gain) cleaning and oral hygiene
also reported in: AS− instructions
Carcuac et al.99 • Implant-supported
2017 Access flap and bone 24/49 7.8 mm Titanium curettes, PD red: 2.2 mm prosthesis removed for
Carcuac et al.90 recontouring (if indicated) gauze with CHX BOP: 55.6% no BOP at 1 year surgery, if possible
2020 AB− MBL change: −0.7 mm (loss) • Transmucosal healing
AS+
Access flap and bone 24/37 7.8 mm Titanium curettes, PD red: 1.7 mm
recontouring (if indicated) gauze with saline BOP: 48.6% no BOP at 1 year
AB− MBL change: −1.0 mm (loss)
|
AS−
17
(Continues)
18
|

159
Isehed et al. Access flap 13/13 PD ≥5 mm and BOP/SOP 7.6 mm Titanium curettes, PD red: 4.0 mm • Diabetes and smoking
2016 AB− and marginal bone loss (median) ultrasonics, and BOP red: 20.0% not exclusion criteria
RCT AS− ≥3 mm gauze with saline MBL change: 0.2 mm (gain) (uncontrolled diabetes not
12 months Access flap and Emdogain 12/12 6.5 mm PD red: 2.5 mm allowed)
Sweden AB− (median) BOP red: 20.0% • Interventions prior to
also reported in: AS− MBL change: 0.7 mm (gain) surgery: not described
Isehed et al.198 • Implant-supported
2018 prosthesis removed for
surgery
Emanuel Access flap 13/14 PD ≥6 mm and BOP and Not Curettes, sonics, PD red: 1.6 mm • Diabetes and smoking
et al.169 AB− marginal bone loss reported ultrasonics, and BOP red: 14.3% not exclusion criteria
2020 AS− >2 mm saline MBL change: −0.1 mm (loss) (uncontrolled diabetes
RCT Access flap and bone graft 14/18 Not PD red: 2.9 mm not allowed; smoking >5
12 months with local AB reported BOP red: 38.9% cigarettes not allowed)
Israel AB− MBL change: 1.1 mm (gain) • Interventions prior to
AS− surgery: None/not reported
reported
• Healing protocol not
described
Roos-Jansåker Access flap and bone graft & 17/29 BOP/SOP and marginal 5.4 mm Titanium curettes, PD red: 2.9 mm • Diabetes and smoking not
et al.134 Membrane bone loss ≥1.8 mm Hydrogen BOP red: 57.7% exclusion criteria
2007 AB+ peroxide 3%, and MBL change:1.5 mm (gain) • Interventions prior to
Cohort study AS+ saline surgery: not described
12 months Access flap and bone graft 19/36 5.6 mm PD red: 3.4 mm • Implant-supported
Sweden AB+ BOP red: 67.9% prosthesis removed for
also reported in: AS+ MBL change:1.4 mm (gain) surgery
Roos-Jansåker • Transmucosal healing
et al.199
2011
Roos-Jansåker
et al. 200
2014
BERGLUNDH et al.

Roccuzzo Access flap and bone graft 71/71 PD ≥6 mm and crater-like 7.2 mm Titanium curettes, PD red: 2.9 mm • Diabetes and smoking not
BERGLUNDH et al.
et al.178 AB+ lesion titanium brush. BOP red: 53.2% exclusion criteria
2016 AS+ EDTA, CHX, and MBL change: not reported • Interventions prior to
Case series saline surgery: mechanical cleaning
12 months and oral hygiene instructions
Italy • Handling of implant-
also reported in: supported prosthesis not
Roccuzzo reported
et al.179 • Transmucosal healing
2021
Isler et al.161 Access flap and bone graft 26/26 PD ≥5 mm and BOP/SOP 5.4 mm Titanium curettes, PD red: 2.7 mm • Diabetes and smoking not
2018 and Membrane and osseous defect gauze with saline BOP red: 67.3% exclusion criteria
RCT AB+ ≥3 mm REC: 0.2 mm • Interventions prior to
12 months AS− CAL change: 2.6 mm (gain) surgery: mechanical cleaning
Turkey MBL change: 2.0 mm (gain) and oral hygiene instructions
also reported in: Access flap and bone graft 26/26 5.9 mm PD red: 2.2 mm • Implant-supported
Isler et al. 201 and Growth factors BOP red: 61.5% prosthesis removed for
2022 AB+ REC: 0.2 mm surgery
AS− CAL change: 2.0 mm (gain) • Submerged healing for
MBL change: 1.6 mm (gain) 6 months following surgery
La Monaca Access flap and bone graft 34/34 BOP/SOP and bone loss 5.9 mm Titanium curettes, PD red: 1.3 mm • Diabetes and smoking were
et al. 202 and Membrane ≥3 mm titanium brush, BOP red: 58.8% exclusion criteria
2018 AB+ ultrasonics, and MBL change: 0.5 mm (gain) • Interventions prior to
Case series AS+ air polishing. surgery: mechanical cleaning
5 years Hydrogen peroxide and oral hygiene instructions
Italy 3%, CHX 0.2%, • Implant-supported
tetracycline prosthesis removed for
hydrochloride, surgery
and saline • Transmucosal healing
Aghazadeh Access flap and bone 22/36 PD ≥5 mm and BOP/SOP 6.0 mm Titanium curettes. PD red: 2.0 mm • Diabetes and smoking
et al.136 graft (autologous) and and bone loss ≥2 mm Hydrogen peroxide BOP red: 44.8% not exclusion criteria
2012 Membrane 3%, CHX 0.2%, MBL change: 0.2 mm (gain) (uncontrolled diabetes not
RCT AB+ and saline allowed)
12 months AS+ • Interventions prior to
Sweden Access flap and bone graft 23/39 6.2 mm PD red: 3.1 mm surgery: mechanical cleaning
also reported in: (bovine) and Membrane BOP red: 50.4% and oral hygiene instructions
Aghazadeh AB+ MBL change: 1.1 mm (gain) • Handling of implant-
et al.183 AS+ supported prosthesis not
2020 reported
Aghazadeh • Transmucosal healing
et al. 203
|
2022
19
(Continues)
20
|

Gonzalez Access flap and bone graft 43/43 PD >5 mm and BOP/SOP 6.4 mm Ultrasonics, PD red: 1.3 mm • Diabetes and smoking not
Reguerio and Membrane and bone loss ≥3 mm implantoplasty. BOP red: 58.8% exclusion criteria
et al. 204 AB− Orthophosphoric MBL change: 0.5 mm (gain) • Interventions prior to
2021 AS+ acid 37%, surgery: mechanical cleaning
Case series CHX 2.0%, and oral hygiene instructions
12 months gauze soaked • Implant-supported
Spain in piperacillin/ prosthesis removed for
tazobactam surgery, reseated 2 weeks
later
Hentenaar Access flap and bone 31/40 PD ≥5 mm and BOP/SOP 4.6 mm Scaler, gauzes PD red: 1.1 mm • Diabetes and smoking
et al.151 recontouring (if indicated) and bone loss ≥2 mm soaked in saline BOP red: 13.9% not exclusion criteria
2022 AB− MBL change: −0.1 mm (loss) (uncontrolled diabetes not
RCT AS− allowed)
12 months Access flap and bone 27/54 4.9 mm Scaler, air polishing PD red: 1.6 mm • Interventions prior
Netherlands recontouring (if indicated) BOP red: 18.2% to surgery: supra and
AB− MBL change: −0.2 mm (loss) submucosal instrumentation
AS− by air polishing or with
Air polishing ultrasonic instrument and
oral hygiene instructions
surgery, if possible
Toma et al. 205 Access flap 10/12 PD ≥5 mm and BOP/SOP 4.9 mm Plastic curettes, PD red: 0.7 mm • Diabetes and smoking
2014 AB− and bone loss ≥3 mm gauzes soaked in MBL change: −0.3 mm (loss) not exclusion criteria
Cohort study AS− saline (uncontrolled diabetes not
12 months Access flap 7/10 5.1 mm Air polishing PD red: 2.0 mm allowed)
Belgium AB− MBL change: 0.3 mm (gain) • Interventions prior to
AS− surgery: mechanical cleaning
Air polishing and oral hygiene instructions
reported
• BOP reduction not reported
BERGLUNDH et al.

De Tapia Access flap and bone graft 15/15 PD ≥6 mm and BOP/SOP 7.8 mm Ultrasonics. PD red: 2.9 mm • Diabetes and smoking not
BERGLUNDH et al.
et al.152 and Membrane and bone loss >30% Hydrogen peroxide BOP red: 54.0% exclusion criteria (heavy
2019 AB+ of implant length and 3% REC: 0.2 mm smoking not allowed)
RCT AS+ osseous defect ≥3 mm MBL change: 1.1 mm (gain) • Interventions prior to
12 months Access flap and bone graft 15/15 8.5 mm Ultrasonics, titanium PD red: 4.9 mm surgery: mechanical cleaning
Spain and Membrane brush. BOP red: 80.0% and oral hygiene instructions
AB+ Hydrogen peroxide REC: 0.6 mm • Implant-supported
AS+ 3% MBL change: 2.8 mm (gain) prosthesis removed for
• Implantoplasty at
supracrestally located
implant surfaces
• Dedicated ultrasonic tip
(teflon-coated)
Schwarz Access flap and bone graft 14/16 PD >6 mm and osseous 5.5 mm Plastic curettes, PD red: 2.0 mm • Diabetes and smoking
et al.135 and Membrane defect >3 mm gauzes soaked in BOP red: 60.1% not exclusion criteria
2011 AB− saline CAL changes: 1.5 mm (gain) (uncontrolled diabetes and
RCT AS− REC: 0.5 mm heavy smoking not allowed)
6 months Access flap and bone graft 10/19 5.1 mm Er:YAG laser PD red: 1.7 mm • Interventions prior to
Germany and Membrane BOP red: 55.0% surgery: mechanical cleaning
also reported in: AB− CAL changes: 1.3 mm (gain) and oral hygiene instructions
Schwarz AS− REC: 0.4 mm • Handling of implant-
et al.137 supported prosthesis not
2012 reported
Schwarz • Implantoplasty at
et al.140 supracrestally located
2013 implant surfaces
Schwarz • Transmucosal healing
et al.87 • MBL changes not reported
2017
Esposito Access flap 40/40 Signs of soft tissue 6.5 mm Various curettes, PD red: 1.0 mm • Diabetes and smoking not
et al. 206 AB− inflammation and ultrasonics BOP red (sites out of 4): 1.3 exclusion criteria
2013 AS− marginal bone loss MBL change: −0.1 mm (loss) • Interventions prior to
RCT Access flap 40/40 ≥3 mm 6.2 mm Various curettes, PD red: 1.1 mm surgery: Oral hygiene
12 months AB− ultrasonics, LAD BOP red (sites out of 4): 1.4 instructions, modification of
Multi-center AS− MBL change: 0.0 mm prostheses when indicated
(Europe) • Handling of implant-
supported prosthesis during
surgery not reported
|21
(Continues)
22
|

De Waal Pocket elimination 15 / 48 PD ≥5 mm and BOP/SOP 5.5 mm Gauze soaked in PD red: 1.8 mm • Diabetes and smoking not
et al.139 AB− and marginal bone loss saline BOP red: 22.5% exclusion criteria (insulin-
2013 AS− (placebo) ≥2 mm and implant Rinsing of implant MBL change: −0.3 mm (loss) dependent diabetes not
RCT function time ≥2 years surface with allowed)
12 months placebo solution • Interventions prior to
Netherlands Pocket elimination 15 / 31 6.6 mm Gauze soaked in PD red: 2.3 mm surgery: mechanical
AB− saline BOP red: 19.9% instrumentation and oral
AS+ Rinsing of implant MBL change: −0.7 mm (loss) hygiene instructions
surface with • Implant-supported
0.12% CHX and prosthesis removed for
0.05% CPC surgery, if possible (in all but
8 patients)
De Waal Pocket elimination 22 / 59 PD ≥5 mm and BOP/SOP 5.0 mm Gauze soaked in PD red: 2.1 mm • Diabetes and smoking not
et al. 207 AB− and marginal bone loss saline BOP red: 37.2% exclusion criteria (insulin-
2015 AS+ ≥2 mm and implant Rinsing of implant MBL change: 0 mm dependent diabetes not
RCT function time ≥2 years surface with allowed)
12 months 0.12% CHX and • Interventions prior to
Netherlands 0.05% CPC surgery: mechanical
Pocket elimination 22 / 49 4.7 mm Gauze soaked in PD red: 1.7 mm instrumentation and oral
AB− saline BOP red: 39.4% hygiene instructions
AS+ Rinsing of implant MBL change: −0.3 mm (loss) • Implant-supported
surface with 2% prosthesis removed for
CHX surgery, if possible (in all but
16 patients)
Englezos Pocket elimination 25 / 40 PD ≥6 mm and BOP and 9.5 mm Carbon curettes, PD red: 5.6 mm • Smoking not exclusion
et al. 208 AB+ bone level ≥3 mm PEAK ultrasonic BOP: 75% no BOP at 2 years criterion. No subjects with
2018 AS+ CHX MBL change: −0.2 mm (loss) diabetes included
Case series • Interventions prior
2 years to surgery: supra and
Belgium submucosal instrumentation
with ultrasonic and hand
instruments and oral hygiene
instructions
BERGLUNDH et al.

Hallström Access flap 19/19 PD ≥5 mm and BOP/SOP 5.8 mm Curettes, gauzes PD red: 1.5 mm • Diabetes and smoking
BERGLUNDH et al.
et al.155 AB− and bone loss ≥2 mm soaked in saline BOP red: not reported not exclusion criteria
2017 AS− or bone level ≥3 mm MBL change: 0.3 mm (gain) (uncontrolled diabetes not
RCT Access flap 20/20 5.8 mm Curettes, gauzes PD red: 1.3 mm allowed)
12 months AB+ soaked in saline BOP red: not reported • Interventions prior to
Sweden AS− MBL change: 0.5 mm (gain) surgery: None/not reported
reported
Romeo Access flap and bone 10/20 PD >4 mm and BOP/SOP 5.8 mm Metronidazole gel, PD red: 2.2 mm • Diabetes and smoking not
et al.131,209 recontouring and and gauzes soaked BOP red: not reported exclusion criteria
2005 & 2007 Implantoplasty Evidence of horizontal in tetracycline CAL change: −0.4 mm (loss) • Interventions prior to
RCT AB+ peri-implant hydrochloride REC: 1.8 mm surgery: mechanical
2 years AS+ radiolucency MBL change: −0.0 mm instrumentation
Italy Access flap and 9/18 6.5 mm Metronidazole gel, PD red: 1.0 mm • Handling of implant-
bone recontouring gauzes soaked BOP red: not reported supported prosthesis not
AB+ in tetracycline CAL change: −1.5 mm (loss) reported
AS+ hydrochloride REC: 1.4 mm • Transmucosal healing
Lasserre Access flap and 15/20 PD ≥5 mm & BOP/SOP & 6.7 mm Curettes PD red: 3.9 mm • Smokers excluded
et al. 210 Implantoplasty bone loss ≥2 mm BOP change. 61.4% • Diabetes not exclusion
2020 AB− REC: 0.5 mm criterion
RCT AS+ CAL change: 3.5 mm (gain) • Interventions prior to
6 months MBL change: 0.3 mm (gain) surgery: mechanical
Belgium Access flap and 14/19 5.6 mm Curettes PD red: 3.3 mm instrumentation, oral
Air polishing Air polishing BOP change. 61.1% hygiene instructions
AB− REC: 0.5 mm • Implant-supported
AS+ CAL change: 2.7 mm (gain) prosthesis removed for
MBL change: 0.5 mm (gain) surgery, if possible
|23
(Continues)
|24

Regidor Access flap and 19/19 PD ≥7 mm and 9.4 mm Titanium brush PD red: 4.4 mm • Diabetes and smoking
et al.167 Bone graft and BOP/SOP and bone BOP change: 67.3% not exclusion criteria
2023 Membrane loss ≥3 mm or bone REC: 0.1 mm (uncontrolled diabetes not
RCT AB+ level ≥3 mm MBL change: 1.2 (gain) allowed, smoking >10 cig/
12 months AS+ day not allowed)
Spain Access flap and 20/20 8.8 mm Titanium brush PD red: 4.2 mm • Interventions prior to
Bone graft BOP change: 66.2% surgery: mechanical
AB+ REC: 0.1 mm instrumentation, oral
AS+ MBL change: 0.9 mm (gain) hygiene instructions
Monje et al.166 Access flap and Bone graft 16/24 PD ≥6 mm and BOP/SOP 8.7 mm Titanium brush. PD red: 5.0 mm • Diabetes and smoking were
2023 AB+ and bone level ≥3 mm Hydrogen peroxide BOP red: not reported exclusion criteria
RCT AS+ 3%, saline REC: 2.0 mm • Interventions prior to
MBL change: 1.7 mm (gain) surgery: mechanical cleaning
Access flap and bone graft 17/24 8.6 mm Titanium brush. PD red: 4.6 mm and oral hygiene instructions
and Membrane Hydrogen peroxide BOP red: not reported • Implant-supported
AB+ 3% and saline REC: 1.8 mm prosthesis removed for
AS+ MBL change: 1.7 mm (gain) surgery, if possible
• Implantoplasty at
supracrestally located
implant surfaces
Polymeri Access flap and bone graft 11/11 PD ≥5 mm and BOP/SOP, 7.0 mm Titanium curettes. PD red: 3.6 mm • Smoking not exclusion
et al.163 (bovine, BioOss) bone loss ≥3 mm and Hydrogen peroxide BOP red: 54.5% criterion. No subjects with
2020 AB+ osseous defect ≥3 mm 3% and saline MBL change: 2.2 mm (gain) diabetes included
RCT AS+ • Interventions prior to
12 months Access flap and bone graft 13/13 7.1 mm Titanium curettes. PD red: 3.8 mm surgery: not described
Netherlands (bovine, Endobon) Hydrogen peroxide BOP red: 50.5% • Implant-supported
AB+ 3% and saline MBL change: 2.8 mm (gain) prosthesis removed for
AS+ surgery, if possible
Abbreviations: AB, Systemic antibiotics; AS, Local antiseptics; BOP, Bleeding on probing; CAL, Clinical attachment level; CHX, Chlorhexidine; CPC, Cetylpyridinium chloride; EDTA, 24%
ethylenediaminetetraacetic acid gel; LAD, Light-activated disinfection; MBL, Marginal bone level; PD, Probing depth; RCT, Randomized control trial; RCT, Randomized controlled trial; REC, Soft tissue
recession; SOP, Suppuration on probing.
BERGLUNDH et al.
|
BERGLUNDH et al. 25
F I G U R E 3 Adapted from Karlsson et al.148 See original publication for references. Standardized mean reduction of probing pocket depth
and changes in marginal bone level as reported in prospective observational studies or in select arms of randomized controlled trials on
access flap or pocket elimination procedures.
predominantly from European studies, suggested that surgical plus gauze soaked in saline) and additional mechanical/physical/an-
therapy aimed at decontamination of the implant surface was ef- timicrobial measures (Comparison 2).149
fective in reducing signs of peri-implant inflammation and in arrest- For Comparison 1, the meta-analysis, based on two stud-
ing disease progression. ies,150,151 revealed weighted mean differences for reductions
of bleeding and probing depth of 14% and 0.9 mm, respectively,
favoring the use of adjunctive and alternative (i.e., air polishing
5.4.1 | Efficacy of different with glycine powdered or erythritol-b ased powder and titanium
decontamination protocols brushes) over conventional implant surface decontamination
methods between 6 and 12 months following non-reconstructive
The cleaning and decontamination of exposed implant surfaces is a surgical therapy of peri-implantitis.149 Over a period of 2 years fol-
crucial component of the surgical management of peri-implantitis.92 lowing combined surgical therapy, an Er:YAG laser was associated
While the removal of mineralized deposits is commonly accom- with similar reductions of probing depth (1.1 mm vs. 1.5 mm) and
plished by means of curettes or scalers, numerous instruments and bleeding (75% vs. 55%) when compared to the conventional de-
protocols were proposed to facilitate the removal of the microbial contamination regimen.137
biofilm. A recent systematic review and meta-analysis evaluated the For Comparison 2, two RCTs investigated either the efficacy of
efficacy of either adjunctive (i.e., measures used subsequent to con- an Er:YAG laser used as an adjunct to a piezoelectric scaler, or the
ventional implant surface debridement) or alternative photo−/me- adjunctive effect of titanium brushes following mechanical debride-
chanical and physical measures for implant surface decontamination ment and chemical decontamination using 3% H2O2.152,153 The re-
in conjunction with various surgical protocols.149 More specifically, ported weighted mean differences for reductions of bleeding (12%)
these measures included implantoplasty, air polishing, ultrasonic and probing depth (0.6 mm) did not report benefit from the use of
devices, titanium brushes, and lasers, used either as mono-or com- either of the two decontamination protocols.
bination therapies. These interventions were compared with either Based on this limited clinical evidence and for reasons presented
standard instrumentation (e.g., scalers to remove hard deposits plus for nonsurgical therapy, air polishing and an Er:YAG laser were rec-
gauze soaked in saline) alone (Comparison 1), or with a combination ommended not to be used, while titanium brushes may be consid-
of standard instrumentation (e.g., scalers to remove hard deposits ered for surgical implant surface decontamination.92
|
26 BERGLUNDH et al.
5.4.2 | Adjunctive use of systemic antibiotics context represent contributions from Europe.136,138,159–167 While
some trials have performed head-to-head comparisons of different
The use of systemic antibiotics as an adjunct to surgical therapy of reconstructive techniques,161,163,166,167 in the majority of reports
peri-implantitis has so far been evaluated in two trials, both of them the efficacy of reconstructive methods was evaluated through
originating from Sweden.154 In 2017, Hallström et al.155 used azithro- comparisons to access flap surgery, that is, omission of the recon-
mycin in 20 subjects in the test group, while the 19 control patients structive technique. In this, the field is very much in line with peri-
were treated with access flap surgery alone. At 12 months after ther- odontal research.93
apy, the authors noted similar reductions in probing depth (control The primary end points of peri-implantitis therapy include shal-
1.5 mm; test: 1.3 mm) and marginal bone level (control 0.3 mm; test: low probing pocket depth and limited bleeding on probing, as illus-
0.5 mm). Subsequent conclusions were that this specific antibiotic trated in Figure 5 and outlined in Section 5.2.
regime did not provide any benefits. As summarized in two systematic reviews,156,168 reconstructive
90,99,143
In the second trial relevant in this context, Carcuac et al. methods, per se, have not been shown to provide any benefit in this
enrolled 100 patients and randomly allocated half of these to an context. This may be exemplified by the multicenter randomized con-
antibiotic regime consisting of 10 days of twice daily 750 mg amox- trolled trial presented by Jepsen et al.160 The authors included 64
icillin in conjunction with surgical therapy. Results were somewhat subjects with peri-implantitis and allocated these to either a control
different from those observed by Hallström et al.155 as reductions of (access flap surgery) or a test group (access flap surgery and bone
probing pocket depth (2.8/3.4 mm vs. 1.7/2.2 mm) and marginal bone replacement graft). At 12 months, the reduction in probing depth
level (0.2/0.5 mm vs. −0.7/−1.0 mm) at 12 months were more favor- was 2.6 and 2.8 mm, respectively. Reduction of bleeding on probing
able in the test than in the control group. The authors subsequently amounted to 45% and 56%. Similarly, Renvert et al.164 could not ob-
90,99
followed the patient sample for up to 5 years, reporting on more serve any benefit for a reconstructive approach in terms of primary
long-term outcomes. It was noted that the initially observed ben- outcomes. The authors combined a bone replacement graft and mem-
efits of the antimicrobial intervention did not persist beyond year brane in the test group and noted a reduction in probing depth of
1 (Figure 4). Consequently, the S3 level Clinical Practice Guideline 1.9 mm compared to a reduction of 2.3 mm in controls (access flap
for the prevention and treatment of peri-implant diseases published surgery). And finally, Derks et al.165 described 12-month reductions
92
by the EFP recommended not to use systemic antibiotics as an in both probing depth (3.7 mm vs. 3.7 mm) and in bleeding on probing
adjunct to surgical therapy of peri-implantitis, citing an overall low (50% vs. 45%) that were almost identical in both the control and test
quality of evidence. arms. The latter consisted of the addition of a bone replacement graft.
With the exception of the study by Derks et al.,165 radiographic
parameters, however, were consistently improved by reconstruc-
5.4.3 | Efficacy of reconstructive methods tive measures. Wohlfahrt et al.,138 Jepsen et al.,160 Isehed et al.,159
Renvert et al.,162,164 and Emanuel et al.169 all reported benefits in
93
Consistent with the periodontal literature, the most extensively test groups ranging from 0.5 to 2.7 mm of additional bone level gain.
evaluated question within the surgical domain relates to recon- It must be noted, however, that the clinical impact of this effect re-
156
structive techniques and their potential benefits. This treat- mains to be demonstrated. Also, radiographic evaluation of marginal
ment modality includes the use of either bone replacement grafts, bone levels following the application of a bone substitute material
membranes, bioactive agents, or combinations thereof that are may be difficult and subject to interpretation (Figure 5B).
applied into or on top of the peri-implant bony defect typically The effect of reconstructive measures on changes of soft tissue
135,157
resulting from the disease process. In addition to the basic levels, that is, soft tissue recession, has only rarely been evaluated.
treatment goals related to resolution of soft tissue inflammation, Two trials assessed recession at buccal implant sites up to 12 months
reconstructive methods are specifically aimed at (i) regeneration after surgery and found a 0.9 mm164 and 1.1 mm165 reduction of soft
of the bony defect, (ii) re-osseointegration, and (iii) the preserva- tissue height in control groups (access flap surgery). Interestingly,
158
tion of soft tissue height. Virtually, all controlled studies in this both studies reported less recession in test groups, with a consistent
F I G U R E 4 Five-year outcomes
following surgical therapy of peri-
implantitis therapy with or without
the adjunctive use of Amoxicillin (AB).
Data (90 implants in situ at the 5-year
evaluation) originate from the randomized
controlled trial reported by Carcuac
et al.90
|
BERGLUNDH et al. 27
benefit of 0.4 mm. As outlined above, the clinical relevance of this replacement graft, as illustrated in Figure 5C. The authors found that
benefit remains to be evaluated. Patient satisfaction at 12 months moderately rough implants fared rather well with a survival rate of
was generally high and not different across study groups in either of 80% and critical reductions in probing depth (3.9 mm) and bleeding
the two studies. on probing (63%). For implants with a titanium plasma-sprayed sur-
Long-
term evaluations of outcomes following reconstructive face, however, the proportion of implant loss was as high as 45%.
91
treatment of peri-implantitis are rare. Roccuzzo et al. reported These findings are underpinned by the obvious differences in clinical
10-year results following access flap surgery combined with a bone response observed already at 1 year.132 They are also in line with
(A)
(B)
(C)
F I G U R E 5 (A) Four-year clinical follow-up after surgical therapy of peri-implantitis. Note the reduction in probing pocket depth (scored
at four sites of the implant) at 1 and 4 years. Red color indicates bleeding on probing. (B) Four-year radiographic follow-up after surgical
therapy of peri-implantitis. The clinical images are shown in (A). (C) Clinical images illustrating the surgical intervention. The implant crown
was temporarily removed to facilitate access. Following decontamination of the implant surface by means of titanium curettes and a rotating
titanium brush under irrigation with saline, a bovine bone material was placed in the bony defect. After suturing, the implant crown was
reseated (transmucosal healing). Pre-and postsurgical status and radiographic appearance are illustrated in (A) and (B), respectively.
|
28 BERGLUNDH et al.
findings from preclinical in vivo evaluations141,142 indicating the dif- depths (Figure 6). This observation is in line with estimates from
ficulties in managing peri-implantitis at implants with rough/complex a systematic review presented by Karlsson et al.,148 in which the
surfaces characteristics. magnitude of probing depth reduction was directly related to ini-
tial values.
The quality of soft tissues, that is, the dimensions of kerati-
5.5 | Factors influencing treatment outcomes nized mucosa, as an indicator of treatment outcomes have been
evaluated in at least two European studies, reporting contradicting
Within the periodontal field, it has long been understood that tooth data. In a retrospective case series with a mean follow-up period of
position/morphology,170 defect configuration,171–173 and patient- 23 months, Monje et al.180 observed less favorable outcomes at im-
related parameters, such as level of infection control174 and tobacco plant sites with reduced dimensions of keratinized mucosa (<2 mm).
smoking,175 are all critical determinants of outcomes of surgical The difference, however, was only apparent at implants treated by
therapy. Also, the surgical approach, that is, the flap design, has reconstructive techniques (n = 31). Among the 104 implant sites
been suggested to be relevant for clinical outcomes.176,177 The cor- treated by resective/pocket elimination approaches, the height of
responding understanding of factors influencing outcomes of surgi- keratinized mucosa was not associated with outcomes. In general,
cal therapy of peri-implantitis is still limited. Some recent European also Ichioka et al.103 failed to identify a consistent effect of kerati-
studies, however, have addressed the question. nized mucosa on treatment outcomes following access-flap surgery
As already discussed above, follow-up data gathered over short- either without (control) or with (test) the addition of a bone replace-
and long-term periods demonstrated the importance of implant sur- ment graft (Figure 6). The statistical analysis revealed that probing
face characteristics on treatment outcomes. 88,90,91,99,132,143,178,179 depth at 12 months was, on average, 0.6 mm greater at sites with
In a secondary analysis of a randomized controlled trial on the ef- no (<0.5 mm) (Figure 7A) when compared to sites with (≥0.5 mm)
ficacy of a bone replacement graft, Ichioka et al.103 evaluated the keratinized mucosa (Figure 7B). This difference was not statistically
relevance of multiple background factors. The authors observed significant. The same study did, however, reveal a higher likelihood
a strong correlation between initial and final (12 months) probing (OR 5.2) of residual bleeding at implants without keratinized mucosa.
F I G U R E 6 Probing pocket depth (PD) at 12 months following surgical therapy of peri-implantitis therapy with or without the adjunctive
placement of a bone replacement graft (n = 136 implants in 129 patients) as reported by Ichioka et al.103 Note the differences in final probing
by smoking and plaque (at 6 weeks). Neither dimensions of keratinized mucosa nor defect configuration had a statistically significant effect
on outcomes. The statistical models are adjusted for smoking, plaque (at 6 weeks), keratinized mucosa at baseline, and defect configuration
assessed during surgery.
|
BERGLUNDH et al. 29
Data on the relevance of the configuration of the peri-implant following application of either autogenous bone or a bovine bone
bony defect are equally limited. Based on a prospective case material at 1 year.
series with a 5-year follow-u p, Roccuzzo et al.179 noted pro- While the importance of patient adherence is strongly high-
nounced improvements in clinical parameters, as illustrated by lighted in the S3 level Clinical Practice Guideline on the preven-
a mean reduction in probing depth of 3.9 mm. The magnitude of tion and treatment of peri-implant diseases,92 relevant scientific
improvement, in this dataset, was not dependent on the defect evidence is extremely limited.184 Hence, the reasoning strongly re-
135
type, classified according to Schwarz et al. A similar conclu- lies on the principles related to periodontal therapy. In one study,
sion was drawn by Ichioka et al.103 While the most shallow prob- Ichioka et al.103 observed that poor plaque control at 6 weeks sub-
ing at 12 months was recorded at defects classified as contained sequent to surgical therapy of peri-implantitis was associated with
(Figure 6), differences were small (<0.7 mm) and not statistically poorer outcomes at 12 months (Figure 6). In the same dataset, the
significant. In a third study, Monje et al.181 also failed to identify presence of plaque at 12 months was also strongly related (OR 3.7)
radiographic defect depth or the defect angle to be significant to the presence of residual bleeding. It must be noted, however, that
predictors of clinically assessed disease resolution. The authors participants in this study were generally highly compliant and under
did, however, observe more pronounced radiographic bone fill at strict maintenance during the observation period.
sites with narrower defect angles (<40°). Somewhat contradicting In a retrospective 5-year study including 21 patients, Cortellini
findings were presented by Schwarz et al.,182 who reported more et al.185 applied a minimally invasive surgical protocol to implant sites
favorable 6-m onth clinical improvements (reductions of probing affected by peri-implantitis. At the final examination, the authors re-
depth and clinical attachment level) at fully contained defects. ported an average reduction of probing depth of 3.9 mm and a corre-
Differences, however, were not maintained at the 12-m onth eval- sponding gain of radiographic bone levels of 2.5 mm. Due to the lack
uation. Agazadeh et al.183 reported that fully contained defects of controlled studies on surgical approaches, the effect of the type of
were associated with greater defect fill than other defect types surgical approach in accessing the peri-implant defect remains unclear.
(A)
(B)
F I G U R E 7 (A) Images illustrating a

case of peri-implantitis with absence of
keratinized mucosa on the buccal aspect
of the implant. (B) Images illustrating a
case of peri-implantitis with abundant
keratinized mucosa on the buccal aspect
of the implant.
|
30 BERGLUNDH et al.
6 | CO N C LU D I N G R E M A R K S diseases: consensus report of working group 4. J Clin Periodontol.

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C O N FL I C T O F I N T E R E S T S TAT E M E N T related to severity of the disease with different degrees of bone
The authors declare no potential conflicts of interest with respect to loss. J Periodontol. 2010;81(2):231-238.
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How to cite this article: Berglundh T, Mombelli A, Schwarz F,
treatment of peri- implantitis: clinical and radiographic out-
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2018;38(5):729-735. implantitis: A European perspective. Periodontol 2000.
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peri-implantitis with resective surgery. A 3-year clinical trial on
rough screw-shaped oral implants. Part II: radiographic outcome.
Clin Oral Implants Res. 2007;18(2):179-187.

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Received: 3 October 2023 | Revised: 19 December 2023 | Accepted: 22 December 2023

Etiology, pathogenesis and treatment of peri-­implantitis: A

Tord Berglundh1 | Andrea Mombelli2 | Frank Schwarz3 | Jan Derks1

1 | I NTRO D U C TI O N the terms “peri-­implant infection” or “peri-­implant lesion” to describe

Periodontology 2000. 2024;00:1–36. ﻿ wileyonlinelibrary.com/journal/prd | 1

3.1 | Preclinical in vivo models 3.2 | Human biopsy material

Case definition for

Case definition for

Case definition for

5 | TR E ATM E NT O F PE R I - ­I M PL A NTITI S therapy,93–95 studies on treatment of peri-­implantitis have typically

TA B L E 2 Selected European studies on nonsurgical therapy of peri-­implantitis.

Patients/ Inclusion criteria: Mean PD at

Patients/ Inclusion criteria: Mean PD at

2022 stainless-­steel bone loss ≥2 mm BOP red: 0% • Local anesthesia

Patients/ Inclusion criteria: Mean PD at

Patients/ Inclusion criteria: Mean PD at

TA B L E 3 Selected European studies on surgical therapy of peri-­implantitis.

Patients/ Inclusion criteria: Mean PD at Decontamination

Patients/ Inclusion criteria: Mean PD at Decontamination

Patients/ Inclusion criteria: Mean PD at Decontamination

Patients/ Inclusion criteria: Mean PD at Decontamination

Patients/ Inclusion criteria: Mean PD at Decontamination

Patients/ Inclusion criteria: Mean PD at Decontamination

Patients/ Inclusion criteria: Mean PD at Decontamination

Patients/ Inclusion criteria: Mean PD at Decontamination

Patients/ Inclusion criteria: Mean PD at Decontamination

F I G U R E 7 (A) Images illustrating a

6 | CO N C LU D I N G R E M A R K S diseases: consensus report of working group 4. J Clin Periodontol.

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Etiology, pathogenesis and treatment of peri-implantitis: A

1 | I NTRO D U C TI O N the terms “peri-implant infection” or “peri-implant lesion” to describe

Periodontology 2000. 2024;00:1–36. wileyonlinelibrary.com/journal/prd | 1

5 | TR E ATM E NT O F PE R I - I M PL A NTITI S therapy,93–95 studies on treatment of peri-implantitis have typically

TA B L E 2 Selected European studies on nonsurgical therapy of peri-implantitis.

2022 stainless-steel bone loss ≥2 mm BOP red: 0% • Local anesthesia

TA B L E 3 Selected European studies on surgical therapy of peri-implantitis.