Professional Documents
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Wismeijer
ITI
Treatment
Guide
Volume 13
Treatment
N. Donos, S. Barter, D. Wismeijer
Guide
Authors:
L. J. A. Heitz-Mayfield
G. E. Salvi
Volume 13
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Preface
Treatment
Guide
For many years now, the use of dental implants in every-
day clinical practice has been established as one of the
most predictable treatment options for the successful
restoration of missing teeth.
Editors: Authors:
Nikolaos Donos, DDS, MS, FHEA, FDSRCS, PhD Lisa J. A. Heitz-Mayfield, Prof, BDS, MDSc, Odont Dr
Director of Research Specialist private practice
Professor, Head and Chair, Periodontology & 4 McCourt Street
Implant Dentistry West Leederville
Director of Centre for Oral Clinical Research Western Australia 6007
Institute of Dentistry Australia
Barts and The London School of Medicine Email: heitz.mayfield@iinet.net.au
and Dentistry
Turner Street Adjunct Professor
London E1 2AD International Research Collaborative –
United Kingdom Oral Health and Equity
Email: n.donos@qmul.ac.uk Faculty of Sciences
The University of Western Australia
Stephen Barter, BDS, MSurgDent, RCS 35 Stirling Highway, Crawley
Honorary Senior Clinical Lecturer 6009 Perth, WA
Centre for Oral Clinical Research Australia
Institute of Dentistry Email: lisa.heitz-mayfield@uwa.edu.au
Barts and The London School of Medicine
and Dentistry Professor Periodontics
Turner Street The University of Sydney Dental School
London E1 2A 2 Chalmers St
United Kingdom Surry Hills NSW 2010
Email: s.barter@qmul.ac.uk Australia
Email: lisa.heitzmayfield@sydney.edu.au
Daniel Wismeijer, Professor, PhD, DMD
Oral Implantology and Prosthetic Dentistry Giovanni E. Salvi, Professor, Dr med dent, Dr h c, MSc
Private Practice Vice Chairman and Graduate Program Director
Zutphensestraatweg 26 Department of Periodontology
6955 AH Ellecom University of Bern
Netherlands School of Dental Medicine
Email: Danwismeijer@gmail.com Freiburgstrasse 7
3010 Bern
Switzerland
Email: giovanni.salvi@zmk.unibe.ch
Mauricio G. Araújo, Prof. Dr., DDS, MSc, PhD Eduardo R. Lorenzana, BS, DDS, MS
Head, Periodontics and Implant Dentistry Private practice (Periodontics)
Research Unit 3519 Paesano’s Parkway, Suite 103
Department of Dentistry San Antonio, TX 78231-1266
State University of Maringá United States of America
Av. Colombo, 5790 – Zona 7 Email: drlorenzana@yahoo.com
87020-900 Maringá – PR
Brazil Flavia Matarazzo, Prof. Dr., DDS, MSc, PhD
Email: odomar@hotmail.com Department of Dentistry
State University of Maringá
Paolo Casentini, DDS, Dr Med Dent Av. Colombo, 5790 – Zona 7
Private practice 87020-900 Maringá – PR
Studio Dr Paolo Casentini Brazil
(Implantology, Oral Surgery, Periodontology, Email: flamatarazzo@gmail.com
Esthetic Dentistry)
Via Anco Marzio 2 Ausra Ramanauskaite, Dr med dent, PhD, DDS
20123 Milano (MI) Department of Oral Surgery and Implantology
Italy Centre for Dentistry and Oral Medicine (Carolinum)
Email: paolocasentini@fastwebnet.it Johann Wolfgang Goethe University Frankfurt
Theodor-Stern-Kai 7
Matteo Chiapasco, MD 60596 Frankfurt am Main
Professor, Unit of Oral Surgery Germany
Department of Biomedical, Surgical, Email: ramanauskaite@med.uni-frankfurt.de
and Dental Sciences
University of Milan Andrea Roccuzzo, Dr, DDS
Via della Commenda 10 Resident Department of Periodontology
20122 Milano School of Dental Medicine
Italy University of Bern
Email: matteo.chiapasco@unimi.it Freiburgstrasse 7
3010 Bern
Jason R. Gillespie, BS, DDS, MS Switzerland
Private practice (Prosthodontics) Email: andrea.roccuzzo@zmk.unibe.ch
105 W El Prado Dr
San Antonio, TX 78212-2024 Research Associate Department of
United States of America Oral and Maxillofacial Surgery
Email: jrgillespiedds@sbcglobal.net Copenhagen University Hospital (Rigshospitalet)
Blegdamsvej 9
2100 Copenhagen
Denmark
1 Introduction................................................................................................. 1
L. J. A. Heitz-Mayfield, G. E. Salvi
7 Peri-Implant Mucositis............................................................................... 47
L. J. A. Heitz-Mayfield, G. E. Salvi
8 Peri-Implantitis........................................................................................... 53
L. J. A. Heitz-Mayfield, G. E. Salvi
8.1 Pathogenesis................................................................................................................... 54
8.1.1 Preclinical Experimental Models..................................................................................................................... 54
8.1.2 Human Histopathology................................................................................................................................... 54
8.1.3 Peri-Implantitis Bony-Defect Configuration.................................................................................................... 55
8.3 Re-Evaluation.................................................................................................................. 61
11 Conclusions................................................................................................ 83
L. J. A. Heitz-Mayfield, G. E. Salvi
12.2
Peri-Implant Mucositis Associated with Misfit of a Cemented Restoration.................... 91
G. E. Salvi
12.7
Surgical Management of Peri-Implantitis: Open-Flap Debridement with
Seven-Year Follow-up After Treatment......................................................................... 109
L. J. A. Heitz-Mayfield
12.9
Surgical Management of Peri-Implantitis:
Reconstructive Surgical Treatment With Three-Year Follow-up After Treatment......... 127
L. J. A. Heitz-Mayfield
12.10 R
econstructive Treatment of a Peri-Implantitis Defect at an Implant
in a Mandibular Molar Site............................................................................................ 131
M. Roccuzzo
12.12
Reconstructive Treatment of Peri-Implantitis with Long-Term Follow-up (7 Years)..... 141
A.-M. Roos Jansåker
12.13 P
eri-Implantitis Modified by the Presence of Submucosal Excess Cement:
Reconstructive Therapy and a Ten-Year Follow-up....................................................... 145
G. E. Salvi
12.14
Surgical Treatment of Peri-Implantitis in the Posterior Mandible Associated
with Hard- and Soft-Tissue Reconstruction................................................................... 149
P. Casentini
12.15 S
urgical Management of Peri-Implantitis: Removal of Implant Due to
Recurrent Infection Using an Implant-Retrieval Tool.................................................... 157
L. J. A. Heitz-Mayfield
12.16 T
reatment of Advanced Peri-Implantitis by Implant Removal Followed by
Bone Reconstruction and New Implant Placement...................................................... 160
P. Casentini, M. Chiapasco
12.17
Occlusal Load—a Factor for Implant Failure?.............................................................. 174
N. U. Zitzmann
13 References............................................................................................... 179
L. J. A. Heitz-Mayfield, G. E. Salvi
The use of osseointegrated implants has become a rou- Before undertaking implant therapy, patients and clini
tine procedure in clinical practice for the replacement cians need to carefully weigh the risks for the occur-
of missing teeth with removable or fixed dental prosthe- rence of mechanical/technical complications (Salvi and
ses. Outcomes from long-term studies indicate that im- Brägger 2009; Heitz-Mayfield and Brägger 2015) and
plant-supported restorations are a predictable treatment biological complications (Heitz-Mayfield and coworkers
method for the management of fully and partially eden- 2018a).
tulous patients (Buser and coworkers 2012; Wittneben
and coworkers 2014; Derks and coworkers 2016a; Prior to the commencement of implant therapy, patients
Morton and coworkers 2018; Pjetursson and coworkers should be informed by dental professionals that compli-
2018; Sailer and coworkers 2018). However, interven- cations may occur, relating to the surrounding hard and
tions involving procedures for the surgical placement soft tissues of the implant (biological complications) and
and restoration of implants are associated with risks of to the implant-supported prosthesis (Abrahamsson and
complications. coworkers 2017). In addition, clinicians should be prop-
erly trained to prevent surgical and prosthetic complica-
The process of osseointegration may be jeopardized by tions and should be able to diagnose and manage them
several factors, such as surgical trauma during prepar- correctly. While patients must be properly informed and
ation of implant recipient sites and premature loading. instructed on how to prevent complications, clinicians
As a consequence, tissue necrosis may result during the must understand the causes of such complications in
early phases of healing, and patients may experience so- order to make the correct diagnosis and implement the
called “early” complications over a period of three to six appropriate treatment.
months following implant placement. These complica-
tions are rare, but they may lead to implant loss. Volume 13 of the ITI Treatment Guide series aims to pro-
vide a comprehensive overview on implant supportive
Once osseointegration and the healing of the soft tis- care and peri-implant diseases (peri-implant mucositis/
sues are established, so-called “late” complications may peri-implantitis) including their classification, etiolo-
also occur when implants are restored and in function. gy, prevalence, risk factors, prevention, diagnosis, and
The most frequent biological complications are bio- management.
film-initiated peri-implant diseases (peri-implant muco-
sitis and peri-implantitis). Less common complications The theoretical chapters of this ITI Treatment Guide are
include medication-related complications, peri-implant complemented by clinical case presentations illustrating
mucosal disorders, peri-implant oncological disorders, various biological complications and their step-by-step
material allergies, or complete loss of osseointegration management.
and implant failure. Technical or mechanical complica-
tions related to the components and materials of the
implant-supported prosthesis are more frequent than
biological complications and can themselves lead to bio-
logical complications.
L. J. A. Heitz-Mayfield, G. E. Salvi
Following the completion of osseointegration and soft- In 2017, at the World Workshop on Classification of
tissue healing after implant placement, peri-implant dis- Periodontal and Peri-Implant Diseases and Conditions,
eases may develop if a biofilm is allowed to accumulate new disease definitions and case definitions were pre-
(Salvi and Ramseier 2015). This is in accordance with sented for peri-implant health, peri-implant mucositis,
the observation that peri-implant diseases are initiated and peri-implantitis (Berglundh and coworkers 2018a).
by the presence of similar etiological factors to those This was the first time that implant conditions were ad-
involved in the development of periodontal diseases dressed as part of the World Workshop Classification, the
(Heitz-Mayfield and Lang 2010). previous World Workshop having been held in 1999.
Fig 2 Peri-implant mucositis at implant site 12. Bleeding following gentle
probing of the peri-implant sulcus.
L. J. A. Heitz-Mayfield, G. E. Salvi
In order to make appropriate treatment choices for the In order to diagnose peri-implant diseases the clinician
effective management of patients with peri-implant dis- must assess both the peri-implant soft-tissue conditions
eases, a correct diagnosis is required. In 2017, the World (to detect signs of inflammation) and the peri-implant
Workshop for the Classification of Periodontal and Peri- marginal bone levels. A correct diagnosis cannot be
Implant diseases presented case definitions for peri-im- made from a radiograph alone. A clinical assessment of
plant health, peri-implant mucositis, and peri-implantitis tissue conditions should always be made.
(Berglundh and coworkers 2018a). These case definitions
have been proposed for universal reference to avoid the
ongoing ambiguity and confusion that previously existed
in this field.
Fig 1 Peri-implant infection as seen by the pres- Fig 2 Suppuration and bleeding following digital
ence of a draining sinus (white arrow) on the labial palpation on the buccal aspect of implant site 45.
peri-implant mucosa of implant site 12. The drain-
ing sinus was detected by visual inspection.
Detection of the presence of soft-tissue inflammation A metal or plastic periodontal probe can be used to
should include: perform peri-implant probing and a light probing force
(approximately 0.25 Ncm) is recommended (Figs 3a-b).
• Visual inspection to identify erythema, edema, or Peri-implant probing depths at four to six sites per im-
presence of a draining sinus (Fig 1) plant should be assessed and recorded in order to identi-
• Digital palpation to detect presence of suppuration fy changes in probing depths over time. It is recognized
(Fig 2) that there might be no access for probing of multiple
• Probing of the peri-implant sulcus to detect bleed- sites per implant due to the position of the implant in
ing or suppuration on probing (Berglundh and co- relation to the prosthesis contours. Where access for
workers 2018a) (Fig 3) probing at an implant is lacking, the prosthesis should be
removed, if possible, in order to assess the peri-implant
soft-tissue status (Serino and coworkers 2013).
a b
Figs 3a-b Probing of the peri-implant sulcus to assess the peri-implant tissue status. A plastic (a) or metal (b) periodontal probe can be
used with a light probing force (approximately 0.25 N).
Recording of the peri-implant mucosal margin in rela- of the peri-implant mucosal margin over time. Clinical
tion to a fixed reference point (such as the crown margin photographs are also useful for assessing changes in
or incisal edge) is also valuable for detecting migration peri-implant mucosal levels over time.
Fig 5a Periapical radiograph showing marginal bone levels Fig 5b Periapical radiograph at five years following restoration of
at the time of placement of the implant-supported prosthesis. the implants showing progressive marginal bone loss at the three
Marginal bone levels are at or above the level of the first im- implants.
plant thread on all implants.
L. J. A. Heitz-Mayfield, G. E. Salvi
4.1.1 Microbial Profiles at Healthy at implant and tooth sites; however, the bacterial load
was higher at tooth sites compared with implant sites
Implant Sites (Fürst and coworkers 2007).
Peri-implant microbiomes have been studied using var-
ious microbiological identification techniques including Additional studies employing molecular detection meth-
culture analysis, microscopy, DNA probe analysis, and ods found that titanium and zirconia abutment surfaces
molecular techniques such as 16S pyrosequencing and are rapidly colonized by a bacterial community similar to
Illumina sequencing. As molecular techniques become that found at adjacent teeth (de Freitas and coworkers
more sophisticated, our understanding of the diversity 2018; Raffaini and coworkers 2018).
and role of the peri-implant microbiome continues to
expand.
4.1.2 Microbial Profiles at Diseased
Microbiota associated with healthy peri-implant con-
Implant Sites
ditions have been evaluated in cross-sectional studies,
characterizing their composition as being predominately Overwhelming evidence indicates that, similar to periodon-
composed of gram-positive facultative cocci and rods, tal diseases, peri-implant diseases are associated with bac-
but also containing small numbers and low proportions terial biofilms predominately composed of gram-negative
of gram-negative anaerobic rods (Leonhardt and cowork- anaerobic taxa (Koyanagi and coworkers 2010; Kumar and
ers 1999; De Boever and De Boever 2006; Fürst and co- coworkers 2012; Tamura and coworkers 2013; Apatzidou
workers 2007). and coworkers 2017; Sanz-Martín and coworkers 2017;
Al-Ahmad and coworkers 2018). Furthermore, the sever-
Moreover, in partially edentulous patients treated for ity of peri-implantitis has been shown to be correlated
periodontitis and enrolled in supportive care, biofilm with substantial changes in the submucosal microbiome,
formation on newly placed implants occurs rapidly, and with increasing levels of dysbiosis as severity increases
the remaining dentition acts as a reservoir for bacterial (Kröger and coworkers 2018). Dysbiosis is a term used to
colonization of implant sites (Leonhardt and coworkers characterize microbial shifts with bacterial taxa normally
1999; Mombelli and coworkers 1995; van Winkelhoff associated with health becoming under-represented and
and coworkers 2000; De Boever and De Boever 2006; outcompeted by bacterial taxa associated with disease.
Quirynen and coworkers 2006; Fürst and coworkers Microbial shifts in the oral cavity may result from an im-
2007; Salvi and coworkers 2008). balance between the bacterial challenge and the inflam-
matory response in a susceptible host.
Fürst and coworkers (2007) assessed the pattern of bac-
terial colonization at implants in periodontally treated In contrast to biofilms detected at healthy peri-implant
patients with good levels of plaque control for up to sites, the microbiome at sites characterized with peri-im-
three months following implant placement. Biofilm sam- plant disease has been described as similar to that asso-
ples were collected from the sulci of transmucosal heal- ciated with periodontitis (Mombelli and Decaillet 2011;
ing abutments from 14 subjects. A total of 40 bacterial Charalampakis and coworkers 2012).
species were analyzed by means of DNA-DNA checker-
board hybridization and compared with bacteria colo- However, in a study using 16S pyrosequencing it was re-
nizing adjacent tooth sites. Biofilm formation occurred ported that the peri-implant microbiome differed signifi-
within 30 minutes after implant placement. Between cantly from that found at tooth sites, both in health and
30 minutes and seven days, only one bacterial species, disease (Kumar and coworkers 2012). In that study,
Veillonella parvula, yielded higher bacterial loads at im- peri-implantitis was characterized as a microbially het-
plant sites compared with adjacent tooth sites. At three erogeneous infection with less complexity compared to
months, the composition of bacterial species was similar that of periodontitis (Kumar and coworkers 2012).
Using DNA-DNA checkerboard analysis, Persson and and disease may be observed. Studies evaluating pa-
Renvert (2014) investigated the presence of 78 bacterial tient-specific microbiomes, using molecular techniques,
species in the biofilm at 166 implants diagnosed with indicate that peri-implant microbiomes are both com-
peri-implantitis and 47 with peri-implant health. Of the plex and diverse (Dabdoub and coworkers 2013; Zhuang
78 bacterial species, 19 were found at higher counts at and coworkers 2016; Yu and coworkers 2019; Heuer and
implants with peri-implantitis compared with healthy coworkers 2012).
implants. In that study, a cluster of bacteria including
P. gingivalis, Staphylococcus aureus, S. anaerobius, S. in-
termedius, S. mitis, T. forsythia, and T. socranskii were 4.1.3 Microbial Profiles in
found to be associated with peri-implantitis (Persson
Edentulous Patients with
and Renvert 2014).
Dental Implants
An additional comparison of the microbial biofilm in It was hypothesized that full-mouth tooth extraction
both periodontal and peri-implant health and disease may lead to the elimination of all hard and non-shed-
was reported by Zhuang and coworkers (2016). In that ding surfaces, and subgingival habitats in the oral cavity,
study, bacterial samples of 22 patients with healthy and thereby favoring the disappearance of pathogenic bac-
diseased implant sites as well as with healthy and dis- teria (Danser and coworkers 1994; Danser and cowork-
eased periodontal sites were analyzed in order to quan- ers 1997).
tify the presence of 6 pathogens (Zhou and coworkers
2016; Zhuang and coworkers 2016). Although within In 1987, a first study using microscopic, immunochem-
the same patient, detection frequencies were higher at ical, and cultural methods challenged this hypothesis
diseased tooth and implant sites compared with healthy (Mombelli and coworkers 1987). The bacterial composi-
sites, putative pathogens were detected at all sites irre- tion in 5 edentulous patients with healthy peri-implant
spective of health status (Zhuang and coworkers 2016). conditions was compared with that in 7 edentulous pa-
In that patient sample, P. gingivalis and Fusobacterium tients presenting both healthy and diseased peri-implant
nucleatum were not associated with peri-implantitis conditions (Mombelli and coworkers 1987). Implants
(Zhuang and coworkers 2016). displaying signs of peri-implantitis harbored signifi-
cantly elevated proportions of gram-negative bacteria,
Using Illumina sequencing, Sanz-Martín and coworkers including black-pigmented Bacteroides, compared with
(2017) investigated microbial differences at sites charac- non-diseased implants in both patient groups (Mombelli
terized by peri-implant health or peri-implantitis. Overall, and coworkers 1987).
diseased peri-implant sites presented a higher diversity
compared with that observed at healthy sites. More specif- Later, quantitative polymerase chain reaction (qPCR)
ically, diseased peri-implant sites were primarily colonized was used to monitor microbiological changes following
by Bacteroides, Spirochetes and Synergistetes, whereas full-mouth tooth extraction in 9 patients (Van Assche
healthy peri-implant sites mostly harbored Proteobacteria and coworkers 2009). The results showed that, follow-
and Actinobacteria (Sanz-Martín and coworkers 2017). ing a period of six months of edentulism, periodontal
The relative abundance of the genera Porphyromonas, pathogens could still be detected at low concentrations
Treponema, Filifactor, Fretibacterium, Synergistetes, and in the saliva and on the tongue (Van Assche and cowork-
Tannerella was significantly higher in peri-implantitis ers 2009).
sites compared with healthy implant sites. On the other
hand, bacteria such as Streptococcus, Veillonella, Rothia, In a follow-up study, the levels of the microbiota were
and Haemophilus displayed a significantly higher relative monitored following a period of edentulism and up to
abundance at healthy compared with peri-implantitis sites one year after abutment connection (Quirynen and Van
(Sanz-Martín and coworkers 2017). Assche 2011). The outcomes of that study indicated
that pristine submucosal habitats around implants were
Collectively, the outcomes of the studies presented colonized within ten days, suggesting that bacteria as-
above indicate that, depending on the diagnostic tech- sociated with periodontitis and peri-implantitis remain
nique applied, significant differences in microbial load in the oral cavity following full-mouth tooth extraction
and diversity between teeth and implants both in health (Quirynen and Van Assche 2011).
a b
Figs 2a-b Implant site 46 has lost osseointegration after 18 years in function. This is not diagnosed as peri-implantitis, as there are no
signs of marginal bone loss or clinical signs of inflammation (bleeding on probing and/or suppuration). The implant was mobile. There is
a thin radiolucent line on the radiograph surrounding implant 46. While the etiology for the loss of osseointegration is unknown, excessive
occlusal load is considered likely.
Alternative theories to explain the breakdown of peri-im- 4.2.1 Excessive Occlusal Load
plant tissues and the loss of osseointegration have
been proposed. Theories include excessive occlusal The hypothesis that excessive load may constitute an
load (Gotfredsen and coworkers 2001; Heitz-Mayfield etiologic or predisposing factor for peri-implantitis and
and coworkers 2004; Kozlovsky and coworkers 2007; progressive marginal bone loss still remains a matter of
Lima and coworkers 2019), foreign-body reaction theo- debate (Coli and coworkers 2017). While excessive load
ry (Albrektsson and coworkers 2019), and the presence may result in mechanical and/or technical complications
of titanium particles (Fretwurst and coworkers 2016; of the prosthesis or implant (Figs 2a-b), or in complete
Mombelli and coworkers 2018). Experimental peri-im- loss of osseointegration (Figs 3a-c), the evidence for ex-
plantitis models incorporating these factors have either cessive load and marginal bone loss is lacking. On the
not been established or have not demonstrated the eti- contrary, outcomes of preclinical experimental studies
ologic contribution of these factors to peri-implantitis. indicate that in the absence of peri-implant soft-issue
inflammation, neither static nor dynamic excessive load
While titanium particles and degradation products of ti- result in the induction of peri-implant marginal bone loss
tanium have been detected in oral tissues of patients (Gotfredsen and coworkers 2001; Heitz-Mayfield and co-
with peri-implant biological complications, there is in- workers 2004; Kozlovsky and coworkers 2007; Lima and
sufficient evidence to show a cause-and-effect relation- coworkers 2019).
ship between biocorrosion, the presence of titanium
particles, and peri-implant diseases (Mombelli and co-
workers 2018).
a b c
Figs 3a-c Fractured Implant site 11. A narrow-diameter TiZr tissue-level implant that fractured after ten years in function. No signs of clinical inflamma-
tion were observed. The patient had reduced posterior support and did not wear a nightguard, indicating that excessive occlusal load may have contributed
to fracture of the implant. There was a high crown-to-implant ratio allowing for significant leverage on the mechanical components. (a) Clinical photo-
graph of site 11 illustrating the implant fracture. No signs of clinical inflammation were present. (b) Radiographs showing the implant prior to fracture with
no marginal bone loss and (c) following implant fracture.
Excessive load may be applied to an implant via the pres- 10 years (Schmid and coworkers 2021). The results in-
ence of premature occlusal contacts, oblique forces to dicated that single implants supporting SCCs in poster-
the implant axis, bruxism, unfavorable crown-to-implant ior areas of the maxilla and mandible yielded a survival
ratios, or cantilever extensions. rate of 100% and were associated with minimal mar-
ginal bone level changes after a mean function time
An experimental study in dogs compared the effects of of 13.6 years (range: 10–19 years). The most frequent
excessive occlusal load on single titanium implants re- complication was loss of retention, noted on 3 occasions
stored with a cantilever extension with non-loaded and in 2 patients (Schmid and coworkers 2021).
normally loaded implants over a period of 6 months
(Lima and coworkers 2019). The results indicated that Hence, these results are in accordance with those of
excessive occlusal load applied to single implants with previous studies failing to report a detrimental effect of
moderately rough surfaces and restored with a canti- cantilever extensions on peri-implant marginal bone lev-
lever extension failed to induce loss of osseointegration els (Wennström and coworkers 2004; Hälg and coworkers
or significant changes in clinical, radiographic, or histo- 2008; Romeo and coworkers 2009; Zurdo and coworkers
logic parameters (Lima and coworkers 2019). Excessively 2009; Aglietta and coworkers 2012; de Freitas and co-
loaded implants, however, displayed a higher incidence workers 2018). Nevertheless, incidences of mechanical/
of technical complications (Lima and coworkers 2019). A technical complications were reported to be higher at
recent retrospective cohort study reported the outcomes implant-supported restorations with cantilever extensions
of biological and technical complications of 21 patients when compared with those without extension (Kreissl and
with 25 single implants supporting single crowns with a coworkers 2007; Salvi and Brägger 2009; Aglietta and co-
cantilever extension (SCCs) with a follow-up of at least workers 2009; Brägger and coworkers 2011).
L. J. A. Heitz-Mayfield, G. E. Salvi
Cross-sectional studies, while frequently cited, report A large cross-sectional study identified patients from the
widely diverging data for the prevalence of peri-implant Swedish population who had implants in situ for 9 years
diseases. (n > 24,716). 596 patients attended a clinical examin-
ation out of 900 invitees and the prevalence of moderate
In 1994, the consensus report of group 4 of the 1st to severe peri-implantitis (defined as presence of BoP,
European Workshop on Periodontology (EWP) defined suppuration and > 2 mm of peri-implant bone loss) was
peri-implantitis as an inflammatory process around os- 14.5% (Derks and coworkers 2016a).
seointegrated implants characterized by bleeding on
probing and/or suppuration, pocket formation, and bone More recently, the prevalence of peri-implant mucositis
resorption beyond initial bone remodeling (Albrektsson and peri-implantitis was reported in a case-series study
and Isidor 1994). with a 21- to 26-year follow-up. In that study, 86 out of
294 patients rehabilitated with implants were re-exam-
Since then, following decades of clinical research in im- ined on average 23.3 years later. The results indicated
plant dentistry, the patient-based estimated weighted that 54.7% of patients were diagnosed with peri-implant
mean prevalence and range of peri-implant diseases have mucositis and 22.1 % with peri-implantitis (Renvert and
been reported in systematic reviews with meta-analy- coworkers 2018a).
ses (Mombelli and coworkers 2012; Derks and Tomasi
2015). The mean prevalence for peri-implant mucosi- In another large study assessing the electronic health re-
tis was reported at 43% (range: 19–65%), whereas for cords of patients treated in a dental school in the USA, a
peri-implantitis it was estimated at 22% (range: 1–47%) prevalence of peri-implantitis of 35% was reported using
(Derks and Tomasi 2015). In addition, outcomes from a threshold of > 2 mm bone loss (Kordbacheh Changi
cross-sectional studies (Aguirre-Zorzano and coworkers and coworkers 2019).
2015; Daubert and coworkers 2015; Dalago and cowork-
ers 2017; Konstantinidis and coworkers 2015; Rokn and In summary, a wide range of prevalence of peri-implant
coworkers 2017; Schwarz and coworkers 2017a) not in- diseases is apparent. The heterogeneity in reporting may
cluded in the systematic review by Derks and Tomasi be influenced by factors such as definitions and thresh-
(2015) reported a similar prevalence for peri-implantitis, olds used, time point of assessment, level of reporting
ranging from 12.9 to 26%. (i.e., implant- vs. patient-based), compliance of patient
sample with supportive periodontal therapy (SPT), and
characteristics of patient samples and implant recipient
sites, making comparisons among studies difficult.
The lack of clear thresholds defining peri-implant diseas- An additional factor observed in most studies reporting
es has resulted in numerous case definitions in studies on the prevalence of peri-implant diseases is that the
addressing disease prevalence. analyses are based on convenience patient samples
from universities or private practices with limited num-
The consensus report of the 8th European Workshop on bers of patients included, rather than on large randomly
Periodontology (EWP) in 2012 emphasized the impor- selected cohorts (Roos-Jansåker and coworkers 2006a;
tance of reporting the prevalence of peri-implant diseas- Tomasi and Derks 2012). This limitation may account
es at the patient-level, rather than at the implant-level for selection bias and impacts on external validity in
(Sanz and Chapple 2012). The lack of patient-based anal- terms of true prevalence of peri-implant diseases. Only
yses in some studies was highlighted in a systematic re- a limited number of studies reporting on the prevalence
view on the quality of studies reporting prevalence, inci- of peri-implant diseases have included both patients
dence, and risk factors of peri-implant diseases (Tomasi treated in private and University settings (Derks and co-
and Derks 2012). workers 2016a; Schwarz and coworkers 2017a; Renvert
and coworkers 2014) or analyzed a randomly selected
Furthermore, different thresholds for marginal bone population sample (Derks and coworkers 2016a).
loss assessment and reference time points from which
bone loss occurred have been used, making it difficult The results of a 10-year prospective study in patients
to compare study populations. This has also been re- treated for periodontitis, but not complying with regu-
flected in the systematic review by Derks and Tomasi lar supportive periodontal therapy (SPT), showed signifi-
(2015), where one study considered a threshold of 5 mm cantly higher proportions of implant sites with bleeding
marginal bone loss as a case definition reporting a 1% on probing (BoP), greater mean deepest probing depths
prevalence of peri-implantitis (Zetterqvist and coworkers (PD) at implant sites, and higher frequency of implants
2010), whereas in another study a threshold of 0.4 mm with ≥ 1 site with PD ≥ 6 mm compared with patients
marginal bone loss was used resulting in a 47% preva- compliant with regular SPT (Roccuzzo and coworkers
lence of peri-implantitis (Koldsland and coworkers 2010). 2014).
In a cross-sectional analysis of a randomly selected sam- Interestingly, patients who received implant-support-
ple of 588 Swedish citizens, peri-implantitis was defined ed prostheses following periodontal therapy displayed
as the presence of bleeding on probing (BoP) and/or sup- a higher rate of compliance with scheduled SPT ap-
puration and marginal bone loss of > 0.5 mm (Derks and pointments compared with patients who underwent
coworkers 2016a). In that study, a 45% patient-based periodontal therapy alone without receiving implants
prevalence of peri-implantitis was reported after 9 years (Cardaropoli and Gaveglio 2012).
of loading (Derks and coworkers 2016a). A threshold
of > 2 mm of marginal bone loss was defined as moder-
ate to severe peri-implantitis, resulting in a prevalence of
14.5% of patients (Derks and coworkers 2016a).
Patient-related factors associated with a lack of com- implants placed in pristine bone after a mean observa-
pliance with SPT were reported in a recent systematic tion period of at least ten years (Salvi and coworkers,
review (Amerio and coworkers 2020). Age, gender, and 2018). These differences, however, were not statistical-
socio-economic status were not found to be significant ly significant. Based on differences in characteristics of
predictors of patients’ compliance with SPT. While pa- patient samples, materials, and surgical protocols used
tients with a history of treated periodontitis were found for augmentation procedures and implant designs, the
to be more likely to comply with SPT, smokers were reported rates should be interpreted with caution (Salvi
associated with a low level of compliance. The results and coworkers 2018).
also indicated that the main patient-reported reasons
for non-compliance with SPT were lack of information In conclusion, it should be expected that the new classifi-
and motivation (Amerio and coworkers 2020). cation of peri-implant diseases and conditions introduced
at the 2017 World Workshop (Berglundh and coworkers
Finally, outcomes of a systematic review including eight 2018a) and outlined in Chapter 2 will help standardize
case series indicated that implants placed in augmented case definitions and minimize differences in reporting of
sites may yield higher rates of peri-implantitis (17.8 vs. epidemiologic data, thus providing a more globally con-
10.3%) and implant loss (3.6 vs. 2.5%) compared with sistent picture of the prevalence of peri-implant diseases.
a b c d
Peri-implant mucositis may be present for extended follow-up examination. Of the patients who developed
periods of time without progressing to peri-implantitis. peri-implantitis 81% presented with one or more im-
Conversion from peri-implant mucositis to peri-implanti- plants with detectable signs of bone loss (i.e. at least
tis in humans is impossible to study in an experimental 0.5 mm) within three years of delivery of the restoration.
set-up for obvious ethical reasons. Only 4% of patients experienced onset of peri-implanti-
tis five years from baseline.
The assessment of the shift from peri-implant muco-
sitis to peri-implantitis would require the detection of The results of this study clearly indicated that the on-
early signs of marginal bone loss. Longitudinal retro- set of peri-implantitis occurred early following implant
spective studies could be used to identify the time of loading and that the progression of the disease followed
onset of peri-implantitis by its pattern of progression in a non-linear accelerating pattern (Derks and cowork-
radiographs. ers 2016b) (Figs 1a-d and 2a-c). Left untreated, peri-
implantitis may progress rapidly, leading to complete
Such an assessment was undertaken in a retrospective loss of osseointegration (Fig 3). The progression of peri-
study including a random sample of 596 patients at- implantitis appears to be faster than that observed in
tending a nine-year clinical and radiographic follow-up periodontitis.
examination (Derks and coworkers 2016). Peri-implant
marginal bone loss could be assessed by comparing This in turn highlights the importance of early diagnosis
radiographs taken one year following delivery of res- of peri-implantitis and the implementation of therapeutic
toration (baseline) with those taken at the nine-year steps.
a b c
Figs 2a-c Implant site 36. Bleeding on probing and a peri-implant circumferential intrabony defect observed intrasurgically in 2010.
a b
The ITI Treatment Guide series is a compendium of evidence-based implant-therapy techniques for daily
practice. Written by renowned clinicians and supported by contributions from expert practitioners, the
ITI Treatment Guides provide a comprehensive overview of the various indicated treatment options. The
management of different clinical situations is discussed with an emphasis on sound diagnostics, evidence-
based treatment concepts, and predictable treatment outcomes with minimal risk to the patient.
Volume 13 of the ITI Treatment Guide series provides clinicians with the latest evidence-based information
regarding the prevention and management of peri-implant diseases. This information is based in part on
the proceedings of the 6th ITI Consensus Conference held in Amsterdam in 2018, as well as on a review
of the current literature. 17 clinical cases presented by experienced clinicians from all over the world
illustrate the diagnosis and treatment of peri-implant diseases.
The forthcoming Volume 14 of the ITI Treatment Guide series will address immediate implant placement
and restoration in partially edentulous patients.