Professional Documents
Culture Documents
Nada Muller
Norbert Cionca
Authors affiliations:
Andrea Mombelli, Nada Muller, Norbert Cionca,
School of Dental Medicine, Division of
Periodontology and Oral Pathophysiology,
University of Geneva, Rue Barthelemy-Menn 19,
CH-1205, Geneva, Switzerland
Corresponding author:
Andrea Mombelli
School of Dental Medicine
Division of Periodontology and Oral
Pathophysiology
University of Geneva
Rue Barthelemy-Menn 19
CH-1205 Geneva, Switzerland
Tel.: +41 22 379 40 30
Fax: +41 22 379 40 32
e-mail: andrea.mombelli@unige.ch
probing depths and bone loss, differences in treatment methods and aftercare of patients, and
Date:
Accepted 09 June 2012
To cite this article:
Mombelli A, Muller N, Cionca N. The epidemiology of
peri-implantitis
Clin. Oral Implants Res. 23(Suppl. 6), 2012, 6776
doi: 10.1111/j.1600-0501.2012.02541.x
Abstract
Aim: To review the literature on the prevalence and incidence of peri-implantitis.
Methods: Out of 322 potentially relevant publications we identified 29 articles concerning 23
cases.
Results and conclusions: All studies provided data from convenience samples, typically from
patients who were treated in a clinical center during a certain period, and most data were crosssectional or collected retrospectively. Based on the reviewed papers one may state that the
prevalence of peri-implantitis seems to be in the order of 10% implants and 20% patients during 5
10 years after implant placement but the individual reported figures are rather variable, not easily
comparable and not suitable for meta-analysis. Factors that should be considered to affect
prevalence figures are the disease definition, the differential diagnosis, the chosen thresholds for
dissimilarities in the composition of study populations. Smoking and a history of periodontitis have
been associated with a higher prevalence of peri-implantitis.
67
et al. 2011). The inflammation causes bleeding and/or suppuration upon gentle probing
with a blunt instrument. The marginal tissue
may be swollen or red, these characters are,
however, not always clearly visible. Unless
the access to the lesion is obstructed, a periodontal probe can be advanced 4 mm or more
into the peri-implant sulcus. Pain is usually
not recorded. The typical bone defect is crater-like, runs all around the implant, and is
strictly demarcated. As perfect osseointegration is maintained apically to the defect,
bone destruction can progress without any
notable signs of implant mobility. Mobility
therefore indicates complete loss of osseointegration and is a sign of total failure (Mombelli & Lang 1998).
Using the experimental gingivitis model
(originally described by Loe et al. 1965), a
cause and effect relationship between biofilm
formation on implants and peri-implant mucositis can be demonstrated (Pontoriero et al.
1994; Zitzmann et al. 2001). An attractive
extrapolation of these findings is the hypothesis that bacterial biofilm on implant surfaces causes peri-implantitis, and that the
removal of these bacteria is the remedy. Beneficial effects of mechanical debridement and
systemic antibiotics in cases diagnosed with
peri-implantitis supported this hypothesis
early (Mombelli & Lang 1992). However,
based on all data available up to 2008, it was
concluded that the predictability of such
treatment was limited and influenced by factors not yet fully understood (Claffey et al.
2008; Lindhe et al. 2008; Renvert et al. 2008).
As we have pointed out in a recent article on
the role of biofilms in peri-implant diseases
(Mombelli & Decaillet 2011), one needs to
consider the possibility that bacterial periimplant infections may also arise occasionally as a consequence of non-microbial
events favoring the emergence of a pathogenic microbiota. As an example, the fracture
of an implant can give rise to a secondary
bacterial infection, and thus provoke purulent peri-implant disease. Another example is
peri-implant infection due to submucosal
persistence of luting cement, where the presence of a foreign body gives rise to a bacterial
infection. In one study (Wilson 2009) excess
dental cement was associated with clinical
and/or radiographic signs of peri-implant disease in 81% of 39 cases. Once the excess
cement was removed, the clinical signs of
disease disappeared in 74%. The differential
diagnosis of peri-implantitis should therefore
include the search for a specific underlying
cause, even if suppuration, or the presence of
a biofilm points to a bacterial infection.
68 |
Results
Included studies
The initial search yielded 321 potentially relevant publications. Two hundred and eighty
nine of them, however, failed to satisfy the
study selection criteria. The main reason for
non-inclusion was that articles did not concern at least 20 human subjects with dental
osseointegrated implants. The second most
frequent reason was that cases with periimplant pathology were selected deliberately.
Of the 32 articles that seemed to meet all
study selection criteria five additional ones
were excluded during data extraction: One
(Feloutzis et al. 2003) was not about peri-implantitis; one (Laine et al. 2006) selected
patients with or without peri-implantitis
intentionally; three (Lekholm et al. 1986,
1996; Merickse-Stern et al. 2001) did not provide peri-implantitis prevalence data. Two
additional studies, one not initially identified
(Astrand et al. 2004), and one becoming available shortly after the search (Dierens et al.
2012), were added.
For the final evaluation 29 articles, reporting data from 23 studies could be included.
They are listed in Table 1 and are presented
narratively below in alphabetic order. The
selected studies all reported data from convenience samples, typically all patients treated
in a clinical center during a certain period
and satisfying certain inclusion criteria.
Case definition
Study 1 (Astrand et al. 2004): This prospective split-mouth study included 28 patients
treated in the maxilla with a total of 150
implants of two different types in five centers. Twenty-five percent were smokers, 29%
had a history of periodontal disease. After
3 years two implants of each type were lost.
Peri-implantitis, defined as infection including pus and bone loss, was found at 5%
implants in an undisclosed number of subjects. Six of the seven implants with peri-implantitis were found in patients with a
history of periodontitis, and all implants had
the same implant surface (TPS).
Study 2 (Baelum & Ellegaard 2004): This
case series included all 258 implants inserted
in 128 subjects in a private periodontal practice during 14 years. Ten-year data were presented for 19 two-stage, and 41 one-stage
implants. All patients had received extensive
periodontal treatment prior to implant placement and were maintained at a high standard
of oral hygiene. Sixty-five percent were
smokers at the time of implant placement.
Ten-year survival rates were 97% and 78%,
depending on implant type. After 10 years,
21% of the two-stage and 40% of the onestage implants showed bone loss 1.5 mm,
but only 5% and 14% at the 3.5 mm threshold. Twenty-three percent of the two-stage
and 25% of the one-stage implants showed
probing depth > 5 mm. Ninety percent of the
two-stage and 69% of the one-stage implants
showed BOP. The description was on the
level of the implant. The frequency of periimplantitis could not be determined due to
lack of composite disease definition and
according data.
Study 3 (Bragger et al. 2001): This case series includes 48 patients with 103 implants
examined after 45 years of function (105
implants were placed, two were lost early).
69 |
Comments
References
Study design
I type
Disease definition
Risk factors
Follow-up
Astrand
et al.
(2004)
Prospective
split-mouth
Branemark, ITI
TPS
SUP plus BL n
25% smok
29% PCP
3 yrs
C: nd
I: 5%
Baelum &
Ellegaard
(2004)
Prospective
case series
Astra, ITI
PPD, BOP, BL
No composite
disease definition
65% smok
014 yrs
nd
Bragger
et al.
(2001)
Retrospective
case series
ITI
5 yrs
C: 10%
I: 10%
Bragger
et al.
(2005)
Prospective
case series
ITI
812 yrs
24 instances of
peri-implantitis
Lee et al.
(2012)
Retrospective
case series
Straumann
TPS, SLA
50% PCP
8 yrs
Prospective
case series
Undisclosed
49% smok
6 m5 yrs
C: 37% PCP,
17% PHP
I: 27% PCP,
13% PHP
C: 3%
I: 1.4%
Periimplantitis as part of
biological complication.
Includes C from Bragger et al.
(2001)
54% for C with residual
pockets
Corbella
et al.
(2011)
Dierens
et al.
(2012)
Dvorak
et al.
(2011)
Crosssectional
C:
28
I:
150
C:
128
I:
258
C:
48
I:
103
C:
89
I:
160
C:
60
I:
117
C:
61
I:
244
C:
50
I: 59
C:
177
I:
828
C:
212
I:
578
C:
662
I:
3413
C:
62
I:
227
Branemark
Nobel
Nobel, 3i,
Intra-lock
Branemark
Progressive BL. No
composite disease
definition
Nobel,
Zimmer,
Mathys,
Straumann,
Friadent
ITI
53% PCP
5 yrs
C: 3%
I: 1%
SUP plus BL
29% smok
815 yrs
C: 19%
I: 17%
ITI
15% PCP
10 yrs
C: nd
I: 29% PCP, 6%
PHP
Astra Tech,
Branemark,
Straumann, 3i
8.4 yrs
C: 1147%
I: 537%
Branemark
19% smok
Undisclosed
C: 12%
I: 7%
Ankylos
19% smok,
72% PCP
211 yrs
C: 11%
I: nd
Straumann
TPS
Antibiotic/surgical
therapy according to
the CIST protocol
37% PCP
10 yrs
Straumann
SLA
36% smok,
68% PCP
5 yrs
C: 11% PHP,
27% moderate
PCP, 47% severe
PCP
C: nd
I: 6%
Crosssectional
Ferreira
et al.
(2006)
Crosssectional
Fransson
et al.
(2005)
Retrospective
case series
Gatti et al.
(2008)
Prospective
case series
Gruica
et al.
(2004)
Prospective
case series
Karoussis
et al.
(2003)
Prospective
case series
Koldsland
et al.
(2010)
Crosssectional
Maximo
et al.
(2008)
Prospective
case series
Rinke et al.
(2011)
Retrospective
case series
Roccuzzo
et al.
(2012)
Prospective
case series
Rodrigo
et al.
(2011)
Prospective
case series
70 |
C:
180
I:
292
C:
53
I:
112
C:
109
I:
372
C:
113
I:
374
C:
89
I: nd
C:
101
I:
228
C:
22
I: 68
26%
osteoporosis,
9%
osteopenia
14% PCP
1622 yrs
C: 6%
I: 5%
6 yrs
C: 24%
I: 13%
Mean
loading
time
42.5 m
5 yrs
C: 9%
I: 7%
C: 28%
I: 12%
Table 1. (continued)
Peri-implantitis
Incidence/
prevalence
Comments
Different levels of severity
assessed on C and I level
References
Study design
I type
Disease definition
Risk factors
Follow-up
RoosJansaker
et al.
(2006b)
Rutar et al.
(2001)
Retrospective
case series
C:
218
I:
999
C:
45
I: 64
C:
nd
I: 39
C:
55
I:
131
C:
46
I:
116
C:
112
I:
304
Branemark
BL 3 threads
following 1st year
plus BOP+/SUP
914 yrs
C: 16%
I: 7%
ITI
26% smok,
no
maintenance
care
38% smok
510 yrs
C: nd
I: 23%
322 yrs
C: nd
I: 13%
Retrospective
case series
Schmidlin
et al.
(2010)
Simonis
et al.
(2010)
Retrospective
case series
Wahlstrom
et al.
(2010)
Retrospective
case series
Zetterqvist
et al.
(2010)
Prospective
RCT
Retrospective
case series
16% smok,
26% PCP
10 yrs
C: nd
I: 38% PCP,
11% PHP
Astra Tech
Nobel
11% smok,
all PCP
5 yrs
C: 4%
I: nd
5 yrs
C: 1%
I: <1%
3i
Abbreviations:
BL: Bone loss, BOP: Bleeding on probing, C: Case, I: Implant, smok: Smoking, nd: Not determined, PCP: Periodontally compromised patient, PHP: Periodontally healthy patient, PPD: Pocket probing depth, SUP: Suppuration, yrs: Years, m: Months
BOP+,
suppuration,
recession
and
PPD > 5 mm. Smokers had larger numbers of
affected implants than non-smokers (Fransson et al. 2008). In 182 subjects, 419 of 1070
examined implants exhibited peri-implantitis-associated vertical bone loss > 2 mm.
The proportion of affected implants varied
between 30% and 52% in different jaw positions and the most common position was the
lower front region (Fransson et al. 2009).
Study 9 (Gatti et al. 2008): Sixty-two partially edentulous patients were consecutively
enrolled in this study. One hundred and
twenty-nine implants were placed in 26
patients with a history of severe periodontitis, 26 implants in seven subjects with a history of mild periodontitis, and 72 in 29
periodontally healthy subjects. Patients
requiring periodontal treatment were treated
prior to implantation. At 5 years, six
patients, two from each group, had dropped
out. In the severe periodontitis group, two
implants in one patient failed due to peri-implantitis, and two implants in another patient
were successfully treated for peri-implantitis.
The criteria to define peri-implantitis were
loss of > 2 mm of marginal bone from the
last radiographic assessment, in the presence
of pus or another sign of infection and
PPD > 5 mm. Patients affected by severe or
moderate periodontitis had lost 2.6 mm periimplant bone over 5 years on average;
healthy subjects lost 1.2 mm.
71 |
72 |
Study 16 (Roccuzzo et al. 2012): One hundred and one partially edentulous subjects
were examined 10 years after implant placement and fixed prosthodontic therapy.
Twenty-eight periodontally healthy subjects
received 61 implants. Thirty-seven subjects
with moderate periodontal disease, and 36
subjects with advanced periodontal disease,
received 95 and 90 implants, respectively. At
the end of active periodontal treatment,
patients were asked to follow an individualized supportive periodontal therapy program.
The diagnosis and treatment of peri-implant
biological complications was carried out
according to cumulative interceptive supportive therapy (CIST) (Mombelli & Lang 1998).
Eighteen implants were removed due to biological complications (two, seven, nine
implants in the three groups, respectively).
During the 10 years, antibiotic and/or surgical therapy was performed in 11%, 27%, and
47% cases, respectively, significantly more in
severely compromised than healthy patients
(P = 0.002). At the final examination, the percentage of implants with at least one site
with a PPD > 5 mm was, respectively, 2%,
16%, and 27%, with a statistically significant
difference between healthy and compromised
subjects.
Study 17 (Rodrigo et al. 2011): Five years
after implant loading, clinical and radiographical variables were recorded in 22 implant
patients of a private clinic. Patients were not
included if presenting with untreated periodontitis, inappropriate periodontal maintenance, or with a systemic or local disease.
Thirty-six percent were smokers, 68% were
periodontally treated. Each subject received
at least one post-extraction immediate
implant (34 implants in total) and one
delayed implant (34 implants). During the
follow-up period, 9 of the 22 participants
(40%) showed signs of biological complications: mucositis (PPD > 3 mm, BOP+,
without significant bone loss) was diagnosed at 13 (20%) implants, peri-implantitis
(PPD > 3 mm, BOP+, vertical bone loss years
15 > 3x the standard deviation of repeated
measures) at four (6%) implants. There was
no difference between groups. Once these
conditions were diagnosed they were immediately treated according to the CIST protocol, with success in all cases except one,
where one delayed implant showed signs of
persisting peri-implantitis (deep PPD and progressing loss of bone).
Study 18 (Roos-Jansaker et al. 2006a,b,c):
Two hundred and eighteen subjects with 999
implants (71% partially edentulous, 26% current smokers) were examined clinically and
Discussion
Prospective studies with clinical and radiological baseline data reflecting the status
after initial healing and remodeling, with an
appropriate sampling frame, adequate sample
size and sampling method would be needed
to determine the incidence of peri-implantitis
correctly. Such studies are currently unavailable. All included publications provided data
from convenience samples, typically from
patients who were treated in a clinical center
during a certain period, and most data were
cross-sectional or collected retrospectively.
Convenience samples may not be representative of the general target population for oral
2012 John Wiley & Sons A/S
73 |
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