J Clin Periodontol 2008; 35 (Suppl. 8): 292–304 doi: 10.1111/j.1600-051X.2008.01275.

Peri-implant diseases: diagnosis Lisa J. A. Heitz-Mayfield

Centre for Rural and Remote Oral Health,
The University of Western Australia, 35

and risk indicators Stirling Highway, Crawley, WA 6009,

Australia

Heitz-Mayfield LJA. Peri-implant diseases: diagnosis and risk indicators. J Clin

Periodontol 2008; 35 (Suppl. 8): 292–304. doi: 10.1111/j.1600-051X.2008.01275.x

Abstract
Background: Peri-implant diseases include peri-implant mucositis, describing an
inflammatory lesion of the peri-implant mucosa, and peri-implantitis, which also
includes loss of supporting bone.
Methods: A literature search of the Medline database (Ovid), up to 21 January 2008
was carried out using a systematic approach, in order to review the evidence for
diagnosis and the risk indicators for peri-implant diseases.
Results: Experimental and clinical studies have identified various diagnostic criteria
including probing parameters, radiographic assessment and peri-implant crevicular
fluid and saliva analyses. Cross-sectional analyses have investigated potential risk
indicators for peri-implant disease including poor oral hygiene, smoking, history of
periodontitis, diabetes, genetic traits, alcohol consumption and implant surface. There
is evidence that probing using a light force (0.25 N) does not damage the peri-implant
tissues and that bleeding on probing (BOP) indicates presence of inflammation in the
peri-implant mucosa. The probing depth, the presence of BOP, and suppuration should
be assessed regularly for the diagnosis of peri-implant diseases. Radiographs are
required to evaluate supporting bone levels around implants. The review identified Key words: diagnosis; peri-implantitis; peri-
strong evidence that poor oral hygiene, a history of periodontitis and cigarette implant mucositis; review; risk factor
smoking, are risk indicators for peri-implant disease. Future prospective studies are
required to confirm these factors as true risk factors. Accepted for publication 20 May 2008

Peri-implant disease following success-
ful integration of an endosseous implant
is the result of an imbalance between
bacterial load and host defence. Peri-
implant diseases may affect the peri-
implant mucosa only (peri-implant
mucositis) or also involve the support-
ing bone (peri-implantitis), (Zitzmann &
Berglundh 2008). Correct diagnosis of
peri-implant disease is critical for appro-
priate management of peri-implant dis-
ease. Bleeding on probing (BOP) is
always present with peri-implant
disease (Zitzmann & Berglundh 2008).
Other clinical signs of disease may
Conflict of interest and source of
funding statement
The author declares no conflict of interest.
The 6th European Workshop on Perio-
dontology was supported by an unrestricted
educational grant from Straumann AG.
292
include suppuration, increased probing
depths relative to baseline, mucosal
recession, a draining sinus (fistula)
and peri-implant mucosal swelling/
hyperplasia. If undiagnosed, peri-
implant disease may lead to complete
loss of osseointegration and implant
loss.
This review excludes post-operative
complications and early implant loss. In
this paper, diagnostic parameters rele-
vant to peri-implant diseases are
reviewed with the aim of providing
guidelines for clinical practice and
future research. The review also aims
to identify potential risk factors asso-
ciated with peri-implant diseases.
Material and Methods
Search strategy
A literature search was performed of the
Medline database (Ovid) from 1 January
Journal compilation r 2008 Blackwell Munksgaard
1950 to 21 January 2008. The search
strategy used included the terms ‘‘peri-
implantitis or peri-implant mucositis or
peri-implant disease$ or peri-implant
infection$ or peri-implant complica-
tion$ or peri-implant bone loss’’ OR
‘‘dental implant$ and diagnosis’’ OR
‘‘endosseous implant$ and diagnosis’’
OR ‘‘dental implant$ and risk’’ OR
‘‘endosseous implant$ and risk’’. The
search was limited to the English
language and resulted in 1113 articles.
Titles and abstracts were screened
and the full text of publications report-
ing on peri-implant diseases (peri-
implantitis or peri-implant mucositis)
were obtained (138). All levels of
evidence were included. Case reports
were included if 10 or more patients
were reported with a follow-up of
at least 6 months. In addition, the refer-
ence lists of review papers were hand
searched.
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Results
Diagnosis of peri-implant diseases
Peri-implant probing
Probing depth/attachment level chan-
ges. The periodontal probe is an essen-
tial tool for diagnosis of peri-implant
disease. Experimental peri-implantitis
studies have shown that an increase in
probing depth over time is associated
with attachment and bone loss (Lang
et al. 1993, Schou et al. 1993a, b).
Lang et al. (1994) and Schou et al.
(2002) demonstrated that periodontal
probing using a light probing force
(0.2–0.3 N) is a reliable tool for diag-
nosing peri-implant health and disease.
In health the probe tip identified the
apical extent of the barrier epithelium.
Experimental marginal inflammation
around implants resulted in an increas-
ing probe penetration as the degree of
inflammation increased. Even mild
inflammation around implants was asso-
ciated with an increased probe penetra-
tion. Penetration of the probe up to
1.6 mm into the connective tissue
occurred in the peri-implantitis lesion.
Probing force. In a clinical study of
healthy peri-implant tissues, evaluation
of tissue resistance to peri-implant prob-
ing at different force levels (0.25, 0.5,
0.75, 1.0 and 1.25 N) showed that the
peri-implant tissues are sensitive to
force variation. Radiographic evaluation
revealed that the probe tip was in close
proximity to the peri-implant marginal
bone when forces of 0.5 N and greater
were used (Mombelli et al. 1997). Ericsson
& Lindhe (1993) also observed in an
experimental study that in healthy peri-
implant mucosa a probing force of 0.5 N
resulted in the probe tip, penetrating the
connective tissue and being in close
proximity to the marginal bone.
In the past, probing around implants
has been suggested to have the potential
to cause damage to the peri-implant
mucosal seal and has not been routinely
performed. However, Etter et al. (2002),
in an experimental study, evaluated the
healing following standardized peri-
implant probing using a force of
0.25 N and observed complete reforma-
tion of the mucosal seal after 5 days.
Thus, probing using a conventional
periodontal probe with a light pressure
of 0.25 N will not cause damage to the
peri-implant tissues and is recom-
mended for evaluation of peri-implant
tissues. There are no data regarding
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Journal compilation r 2008 Blackwell Munksgaard
the influence of probe material (metal
versus plastic) or design on peri-implant
probing.
BOP. Presence of bleeding on gentle
probing (0.25 N) is a useful parameter
for diagnosis of mucosal inflammation.
An experimental study showed healthy
peri-implant sites had absence of BOP
while there was increased BOP at muco-
sitis (67%) and peri-implantitis (91%)
sites (Lang et al. 1994). The prognostic
value of BOP was investigated in a
prospective clinical study evaluating
progressive attachment loss in patients
with peri-implantitis (Jepsen et al.
1996). A minimum threshold of
1.0 mm loss of probing attachment was
chosen to classify a site as positive for
breakdown 6 months following baseline
recordings. After 6 months, 6% of
all sites (in 19% of the implants) and
28% of the patients had experienced
further peri-implant attachment loss.
BOP was characterized by a high nega-
tive predictive value. Thus, absence of
BOP was an indicator for stable peri-
implant conditions.
This was confirmed in a prospective
clinical study evaluating the prognostic
value of BOP for monitoring peri-
implant mucosal tissue conditions dur-
ing supportive periodontal therapy
(SPT) (Luterbacher et al. 2000). This
study showed that any site bleeding at
more than half of the recall visits over a
2-year period had disease progression.
Thus, the positive predictive value (of
X50% BOP) was 100%. It was of note
that this was greater than the corre-
sponding positive predictive value of
BOP for teeth of 40% in this study
population. The negative predictive
value of BOP, to indicate peri-implant
stability, varied between 50% and 64%
for a threshold BOP frequency of
420% (Luterbacher et al. 2000). Thus,
BOP is considered a valuable parameter
for diagnosing peri-implant disease.
Peri-implant crevicular fluid (PICF) and
saliva analysis
The correlation of biochemical markers
of inflammation with clinical para-
meters of healthy peri-implant tissues
and implants showing signs of peri-
implant disease has been the focus of
recent research. Levels of biochemical
mediators secreted into the PICF have
been studied with the aim of identifying
a diagnostic marker to monitor peri-
Peri-implant diseases 293
implant health. Markers in PICF includ-
ing cytokines, enzymes, and proteases
have been investigated. More recently
saliva samples, with the advantage of
being non-invasive and simpler to col-
lect than PICF, have been evaluated
(Table 1).
While this body of evidence indicates
potential for diagnostic tests for peri-
implant disease, prospective longitudi-
nal studies are required to correlate
disease progression with biochemical
markers. The search for a sensitive
diagnostic test to detect reversible
changes before the clinical changes of
peri-implant disease continues. This is
perhaps not surprising considering there
are to date no biochemical diagnostic
tests clinically available for perio-
dontitis progression.
Microbial diagnostic testing
Luterbacher et al. (2000) evaluated a
microbiological test in combination
with BOP, for monitoring peri-implant
tissue conditions over a 2-year recall
period. At each recall visit a microbio-
logical sample was taken at one implant
and one tooth site to identify the pre-
sence of specific bacteria Aggregatibac-
ter actinomycetemcomitans, Prevotella
intermedia, Porphyromonas gingivalis
and Treponema denticola. Presence or
absence of BOP was also recorded. Over
the 2-year period the percentage of
recall visits with positive bacteriological
tests (for one or more of the species) and
positive BOP was calculated. Peri-
implant probing depths were monitored
in order to identify peri-implant disease
progression. The addition of the micro-
biological test results were reported to
enhance the prognostic characteristics of
BOP alone for identifying disease pro-
gression at implants.
Radiographic evaluation
Radiographic techniques including
panoramic tomography and intra-oral
radiography using long cone parallelling
techniques have been widely used to
monitor marginal bone levels at
implants and diagnose interproximal
bone loss (Kullman et al. 2007). The
distance from a fixed reference point
(e.g. implant shoulder or implant–abut-
ment junction) to the inter-proximal
bone level is recorded at baseline and
monitored longitudinally.
While a panoramic tomograph allows
the entire implant to be visualized,
294 Heitz-Mayfield

Table 1. Investigations to identify potential diagnostic biochemical markers for peri-implant disease in peri-implant crevicular fluid (PICF) or saliva
Author/year Study sample Study design Sample/marker Findings

Eley et al. 15 subjects Cross-sectional PICF Total enzyme activities had good diagnostic
(1991) Each with two to six Protease specificity and sensitivity as predictors of
implants clinical parameters
The figures were especially high for elastase-
like activity as a marker of bone reduction
Niimi & Ueda 63 implants Cross-sectional PICF volume Increased PICF volume at implants with high
(1995) gingival index and plaque index
Kao et al. 12 subjects Cross-sectional PICF Level of IL-1b at peri-implantitis sites was
(1995) Interleukin-1b (IL-1b) three times that at healthy sites
Boutros et al. 30 subjects Cross-sectional PICF Levels of neutrophil elastase, myeloperoxidase
(1996) 73 implants Neutral protease, neutrophil and b-glucuronidase were significantly higher
elastase, myeloperoxidase, b- around failing implants compared with
glucuronidase levels successful implants
Panagakos 13 subjects Cross-sectional PICF Increased levels of IL-1b in sites with peri-
et al. (1996) 50 implants: healthy, IL-1b implantitis
early peri-implantitis and
advanced peri-
implantitis
Jepsen et al. 25 subjects Prospective PICF Significant differences NPE (36% versus 12%)
(1996) 54 implants longitudinal (two Neutral proteolytic enzyme scores between patients with progressive peri-
sampling (NPE) activity (Periocheck) implantitis and those with stable peri-implant
occasions, 6 conditions. NPE-test was characterized by high
months apart) negative predictive value
Teronen et al. Seven patients, seven Cross-sectional MMP-8 (collagenase -2) MMP-8 was present in elevated amounts in the
(1997) implants with peri- PICF from peri-implantitis sites
implantitis
Six control patients with
healthy implant sites
Salcetti et al. 21 subjects with failing Cross-sectional PICF Significant elevations in levels of PGE2, IL-1
(1997) implant sites Prostaglandin E2 (PGE2), IL-1b b, and PDGF in mouths with failing implant
Eight subjects with and IL-6 transforming growth sites as compared with mouths with healthy
healthy sites factor b (TGF-b) platelet- control implants
derived growth factor (PDGF)
Aboyoussef 29 patients Cross-sectional PICF No difference in levels of PGE2 and MMP
et al. (1998) 37 healthy implants IL-1 b between healthy implant and early peri-
37 implant early peri- PGE2 implantitis
implantitis MMP IL-1 b increased six-fold in early peri-
implantitis samples
Rühling et al. 20 subjects Prospective PICF Low positive predictive value (8%)
(1999) 42 implants longitudinal (two Aspartate aminotransferase High negative predictive value (92%) for
sampling (AST) progressive attachment loss
occasions, 6 Sensitivity 15% Specificity 83%
months apart) Conclusion: limited clinical value
Paolantonio 81 subjects Cross-sectional PICF A significant difference in AST activity existed
et al. (2000) 81 implants (27 peri- AST between health and peri-implantitis and
implantitis; 27 mucositis; mucositis and peri-implantitis. When the
27 healthy) threshold for a positive AST test was set
4or 5 0.4 U/ml, a sensitivity 5 0.81 and a
specificity 5 0.74 were found in the detection
of peri-implantitis; positive predictive value
61% negative predictive value 88%
Fiorellini 20 subjects Cross-sectional PICF Statistically significant association of increased
et al. (2000) 59 implants AST AST activity with positive bleeding on
probing, increased probing depth, and
increased gingival index
Ataoglu 14 subjects Cross-sectional PICF NE activity and IL-1b levels in PICF may be
et al. (2002) 42 implants IL-1b, tumour necrosis factor-a used to measure implant health status of
(TNF-a) levels neutrophil patients who do not smoke
elastase (NE) activity
Hultin 17 subjects Cross-sectional PICF Elastase activity was higher at implants with
et al. (2002) 98 implants (45 with Elastase activity lactoferrin IL- peri-implantitis than at control implants
peri-implantitis) 1b concentrations
19 control subjects with
healthy implants

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Journal compilation r 2008 Blackwell Munksgaard
 Peri-implant diseases 295

Table 1. (Contd.)
Author/year Study sample Study design Sample/marker Findings

Murata et al. 16 patients Cross-sectional PICF IL-1b levels in PICF from peri-implantitis sites
(2002) 34 implants: six peri- Osteocalcin deoxypyridinoline were significantly higher than levels from peri-
implantitis IL-1b implant mucositis (po0.05) and healthy
Eight peri-implant implant sites (po0.01)
mucositis
20 healthy
Plagnat et al. Eight subjects Cross-sectional PICF In comparison with the clinically healthy
(2002) 11 implants with peri- Phosphatase activity (ALP) implants, total amounts of ALP, EA, a2M were
implantitis Elastase activity (EA) significantly higher in PICF collected around
Seven subjects a2-macroglobulin (a2M) implants with peri-implantitis
11 healthy control
implants
Kivelä-Rajamäki 72 samples Cross-sectional PICF Elevated MMP-8 and LN-5 g2-chain fragment
et al. (2003b) LN-5 g2-chain levels in PICF can reflect the active phase of
MMP-8 (collagenase-2) the inflammatory peri-implant disease
Kivelä-Rajamäki 13 subjects Cross-sectional PICF Levels of MMP-8 and MMP-7 were
et al. (2003a) 72 samples MMP-7 (matrilysin-1) significantly elevated in diseased PICF
MMP-8 (collagenase-2) compared with healthy PICF
Ma et al. (2003) 12 subjects Cross-sectional PICF Gelatinase B is associated with peri-implant
46 implant Gelatinase B bone loss
Liskmann et al. 24 subjects Cross-sectional PICF Total amounts of myeloperoxidase were
(2004) 64 implants Myeloperoxidase significantly higher at implants with
inflammatory lesions
Yalçn et al. 24 implants PDX3 mm Cross-sectional PICF PI, GI, PPD and implant crevicular fluid (ICF)
(2005) Peri-implant mucositis Prostaglandin E2 levels were levels of prostaglandin E2 were statistically
24 implants PDo3 mm evaluated using a commercially significantly higher in the test group (po0.05).
available enzyme immunoassay In the test group, gingival index and probing
kit depths were statistically significantly related
with PICF prostaglandin E2 levels (po0.05)
Liskmann et al. 30 subjects Cross-sectional Saliva IL-6 significantly elevated in peri-implant
(2006) Pro-inflammatory cytokine IL-6 disease group as compared with healthy group
Anti-inflammatory cytokine IL- IL-10 only detected in peri-implant disease
10 group
Paknejad et al. 12 subjects Cross-sectional PICF AST activity was significantly associated with
(2006) 17 implants (peri- AST and alkaline phosphatase the amount of bleeding on probing
implantitis) (ALP)
13 subjects
17 implants (healthy
peri-implant tissues)
Strbac et al. 19 subjects Cross-sectional PICF Higher amount of cathepsin K (protease
(2006) 40 implants Cathepsin K levels expressed by osteoclasts) associated with
peri-implantitis

limitations including image resolution
and distortion are well known (Åkesson
et al. 1993, De Smet et al. 2002). Further
limitations of conventional radiography
include the inability to monitor facial
and lingual/palatal bone levels, low sen-
sitivity in the detection of early bone
changes and the underestimation of
bone loss (Brägger et al. 1988, De
Smet et al. 2002). The use of computer-
assisted image analysis such as sub-
traction radiography may improve the
diagnostic accuracy of radiographs as it
allows detection of small changes in
bone density (Nicopoulou-Karayianni
et al. 1997).
Recently, multi-slice computer tomo-
graphy (CT) and cone beam volume
r 2008 The Author
Journal compilation r 2008 Blackwell Munksgaard
imaging have been used in implant
dentistry offering the advantage that
osseous structures can be represented
in three planes, true to scale and without
overlay or distortion. In a recent experi-
mental study in pig mandibles, Mengel
et al. (2006) evaluated the accuracy and
quality of the representation of prepared
peri-implant defects by intra-oral radio-
graphy, panoramic radiography, CT and
cone beam radiography. Both CT and
cone beam imaging techniques provided
accurate three-dimensional representa-
tions of the peri-implant bone defects.
The CT scans showed a slight artefact
immediately adjacent to the implant
while the cone beam scans showed the
better imaging quality.
Implant mobility
Mobility of an implant indicates com-
plete lack of osseointegration and the
implant should be removed. Mobility is
therefore not useful for early diagnosis
of peri-implant diseases.
Suppuration
The presence of pus is the result of
infection and an inflammatory lesion.
In a report of 218 patients who were
examined for biological complications
at existing implants 9–14 years after
implant placement, the presence of pus
was identified as explanatory for peri-
implantitis resulting in a bone level at
296 Heitz-Mayfield
X3 threads (Brånemark implants)
(Roos-Jansåker et al. 2006b). Similar
data were presented by Fransson et al.
(2008) in a larger group of subjects with
at least one implant with progressive
bone loss.
Risk indicators for peri-implant
diseases
In order to identify a true risk factor for
peri-implant disease prospective long-
itudinal studies are required. Only few
such studies have been reported. Retro-
spective and cross-sectional studies can
identify risk indicators for disease and
have thus been included in this review.
In the current review, ‘‘risk’’ refers to a
factor which is associated with peri-
implant disease. Most studies only
report implant loss (either early or late
loss). Although implant loss following
successful osseointegration (late loss) is
likely to be the result of peri-implant
disease, only studies where peri-implant
mucositis or peri-implantitis (BOP, sup-
porting bone loss) were clearly
described were included.
Cross-sectional analyses in the stu-
dies included in this review investigated
the following factors: history of perio-
dontitis, diabetes, genetic traits, poor
oral hygiene, smoking, alcohol consump-
tion, absence of keratinized mucosa
and implant surface.
History of periodontitis
Peri-implant diseases may take years to
develop, as is the case with perio-
dontitis. Therefore, long-term prospec-
tive clinical studies are the most
appropriate to identify risk factors.
Many patients who lose teeth due to
periodontitis are treated using implant-
retained reconstructions. An increasing
number of clinical studies reporting on
the occurrence of peri-implant disease
have suggested that this patient group
may be more susceptible to peri-implant
disease due to host-related factors. A
number of recent systematic reviews
have addressed the question of whether
patients with a history of periodontitis
have an increased risk of peri-implant
disease (Van der Weijden et al. 2005,
Schou et al. 2006, Karoussis et al. 2007,
Quirynen et al. 2007).
Van der Weijden et al. (2005) eval-
uated the long-term (X5 years) success
of implants placed in partially edentu-
lous patients with a history of perio-
dontitis. Of the four selected papers, two
were controlled clinical trials comparing
the success of implants in periodontitis
and non-periodontal patients (Hardt
et al. 2002, Karoussis et al. 2003). The
remaining two studies evaluated the
success rate of implant placement in
periodontitis patients only (Mengel
et al. 2001, Leonhardt et al. 2002). The
authors concluded that the outcome of
implant therapy in terms of loss of
supporting bone and implant loss may
be different in periodontitis patients
compared with individuals without a
history of the disease.
The systematic review by Schou et al.
(2006) included prospective and retro-
spective cohort studies with at least a 5-
year follow-up comparing the outcome
of implant treatment in individuals with
periodontitis associated and non-perio-
dontitis-associated tooth loss. The same
studies included in the review by Van
der Weijden et al. (2005), Hardt et al.
(2002) and Karoussis et al. (2003) were
identified including a total of 33 patients
with tooth loss due to periodontitis and
70 patients with non-periodontitis-asso-
ciated tooth loss. The authors performed
a meta-analysis, and concluded that
there was a significantly increased inci-
dence of peri-implantitis and increased
peri-implant marginal bone loss in indi-
viduals with periodontitis-associated
tooth loss.
A further review by Karoussis et al.
(2007) used a systematic approach to
identify 15 prospective studies regard-
ing the short term (o5 years) and
long-term (X5 years) prognosis of
osseointegrated implants placed in perio-
dontally compromised partially dentate
patients [note the authors described
Rosenberg et al. (2004) as a prospective
study although it was retrospective]. The
authors found no statistically significant
differences in both short- and long-term
implant survival between patients with a
history of chronic periodontitis and
periodontally healthy individuals. How-
ever, the authors found that patients with
a history of chronic periodontitis may
exhibit significantly greater long-term
probing pocket depth, peri-implant mar-
ginal bone loss and incidence of peri-
implantitis compared with periodontally
healthy subjects.
Quirynen et al. (2007) performed a
systematic review investigating a rela-
tionship between susceptibility to perio-
dontitis and peri-implantitis, with
implant outcome as the primary outcome
variable, and SPT and implant surface
Journal compilation r 2008 Blackwell Munksgaard
roughness as confounding factors. The
heterogeneity of the 16 studies included
in this systematic review excluded the
possibility of a meta-analysis.
Five papers compared patients with
different degrees of periodontitis (Hardt
et al. 2002, Karoussis et al. 2003, Evian
et al. 2004, Rosenberg et al. 2004,
Mengel & Flores-de-Jacoby 2005).
Four of these papers reported a higher
incidence of late implant loss and/or
marginal bone loss in patients with a
history of periodontitis. This difference
was most obvious when implants with a
very rough surface were used (Karoussis
et al. 2003, Evian et al. 2004, Rosenberg
et al. 2004) or when SPT was not
organized (Hardt et al. 2002). Included
in the systematic review were another
10 papers, which only reported the out-
come of implants in patients with a
history of periodontitis (Tables 2 and 3).
Tables 2 and 3 summarize studies
included in the systematic reviews as
well as additional clinical studies inves-
tigating history of periodontitis as a risk
indicator for peri-implant infection.
Only studies which report on either
marginal bone levels, probing depths,
attachment level, BOP or peri-implantitis
are included.
Conclusion
The studies identified in these four sys-
tematic reviews have considerable
variations in study design, length of
follow-up, definition of patient popula-
tions with respect to periodontal status,
outcome measures and SPT regimens. In
addition lack of reporting on occurrence
of peri-implantitis and confounding fac-
tors such as smoking and differences in
timing of baseline measurements make
it difficult to draw robust conclusions.
However, the systematic reviews indi-
cate that subjects with a history of
periodontitis are at greater risk for
peri-implant disease.
Diabetes
Diabetes is a systemic disease which
results in a wide range of mechanisms
that may delay wound healing and
increase a patient’s susceptibility to
infection or implant loss (Fiorellini &
Nevins 2000).
While the association between dia-
betes and implant loss has been
addressed in systematic reviews by
Kotsovilis et al. (2006) and Mombelli
& Cionca (2006) there is only one study
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 Peri-implant diseases 297

Table 2. Clinical studies comparing patients with a history of periodontitis with control (non-periodontitis) patients
Study Study design Subjects Implant surface Follow-up SPT Findings
implant (N)

Watson et al. Prospective Seven patients chronic Hydroxyapatite 3–4 years 6 monthly Periodontitis patients: five
(1999) cohort study periodontitis (HA) coated clinical exam, yearly implants had bone loss 44 mm
19 non-periodontitis patients 33 implants radiographic follow- over 4 years and were diagnosed
Heavy smokers excluded up as failing
(X20/day) Non-periodontitis patients:
None of these patients had
implants with bone loss 44 mm
Brocard et al. Prospective 440 patients – subgroup of 147 TPS surface Up to 7 years regular Implants in periodontally
(2000)n,w case series patients (33.5%) treated for 1022 implants in SPT maintained patients: cumulative
periodontal disease total group success rate (CSR) 74.7%
132 smokers in total group Implants in systemically healthy
patients CSR 88.8%
Hardt et al. Retrospective 25 patients with a history of Turned surface 5 years SPT not Periodontitis patients: 64% had
(2002)w,z,§ cohort study periodontitis (defined by age- reported peri-implant bone loss 42 mm
related bone score) Non-periodontitis patients: 24%
25 non-periodontitis patients had peri-implant bone loss
Smoking history not reported 42 mm
Regression analysis revealed a
statistically significant
relationship between the age
related bone score and the peri-
implant bone level change
Karoussis et al. Prospective Eight patients who had lost teeth TPS hollow 10 years regular SPT Significant difference in
(2003)n,w,z,§ cohort study due to chronic periodontitis (CP) screw implants incidence of peri-implantitis:
45 patients who had lost teeth 28.6% in CP patients
due to other reasons 5.8% non-periodontitis patients
Smokers included Success (PD45 mm, BOP-)
71.4% in CP patients
94.5% in non-periodontitis
patients
Rosenberg Retrospective 151 patients with history of Turned surface Up to 13 years Peri-implantitis defined as
et al. (2004)n,w cohort study periodontitis (tooth loss due to HA coated SPT – 3 monthly failure occurring after 1 year of
periodontitis)
923 implants SLA loading
183 periodontally healthy (tooth TPS Patients with history of
loss not caused by periodontitis) Acid etched periodontitis: 25.6% of implants

558 implants Non-periodontitis patients: 5.4%
Periodontal health before of implants
implant placement
Smoking history not reported
Evian et al. Retrospective 77 implants placed in 77 Titanium Follow-up mean 943 Implant failure defined as
(2004)w case series patients treated for chronic HA coated days advanced bone loss, infection,
periodontitis (CP) Patients were pain
72 implants in 72 patients instructed to return CP patients – failure 21%
without a history of periodontal for regular SPT Non-periodontitis patients –
disease failure 8%
Implant failure due to peri-
implantitis significantly
associated with a history of
periodontal disease
Hänggi Retrospective Aggressive periodontitis 16 TPS 3 years Tendency for greater crestal
et al. (2005) case series CP33 Regular SPT bone loss at implants placed in
radiographic No periodontitis 19 patients diagnosed with
evaluation – 15 smokers aggressive periodontitis before
subgroup implant placement
Mengel & Prospective 15 treated for generalized Turned 3 years Peri-implantitis not reported
Flores-de- cohort study aggressive periodontitis (GAgP) surface1turned/ 3 monthly SPT Radiographic bone loss was
Jacoby 12 treated for generalized CP acid etched slightly greater at implants in
(2005)n,w 12 periodontally healthy surface patients treated for GAgP
Treated: All PD43 mm with no compared with CP and healthy
BOP patients
Non smokers Implant success: GAgP 95.7%
CP and healthy patients 100%

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Journal compilation r 2008 Blackwell Munksgaard
298 Heitz-Mayfield

Table 2. (Contd.)
Study Study design Subjects Implant surface Follow-up SPT Findings
implant (N)

Roos- Retrospective 94 partially dentate patients with Turned surface 9–14 years Peri-implantitis significantly
Jansåker case series a history of periodontitis No systematic SPT related to a history of
et al. (2006b) (430% of remaining teeth Patients returned to periodontitis
before implant placement with general practitioner
bone loss X4 mm) for SPT
Treated 62 partially dentate
patients with no periodontitis
history (430% of remaining
teeth before implant placement
with bone loss X4 mm)
Smokers included
Ferreira et al. Cross- 212 subjects Turned surface Mean loading time Multinomial logistic regression
(2006) sectional 30 had periodontitis (four or Acid etched 42.5  17.1 months analysis: outcome peri-
more teeth with one or more surface implantitis
sites PDX4 mm and Periodontal BOPX30% sites
CALX3 mm) affected; odds ratio (OR) 3.3
56 (26.4%)had healthy peri- [95% confidence interval (CI):
implant tissues 2.1–5.6]
137 (64.6%) had mucositis Diagnosis of periodontitis; OR
43 (7.44%) had peri-implantitis 3.1 (95% CI: 1.1–3.5)
Non smokers Other factors:
Uncontrolled diabetes; OR 1.9
(95% CI: 1.0–2.2)
Very poor plaque score; OR
14.3 (95% CI: 9.1–28.7)
Age 445 years OR 1.7(95% CI
1.3–2.8)
Gender (male); OR 2.7 (95% CI
2.1-6-3)
Mengel et al. Prospective Five Generalized aggressive GAgP: 36 10 years More bone loss and attachment
(2007) cohort study periodontitis (GAgP) implants SPT – 3 monthly loss at implants in GAgP
5 Periodontally healthy (PH) PH: seven compared with implants placed
Smokers excluded implants in PH patients
Turned surface Implant success (Albrektsson
et al. 1986 criteria):
GAgP: 83.3%
PH: 100%
Outcome variable peri-implant disease (described as marginal bone loss, BOP, probing measurements, suppuration, peri-implantitis). Listed in order of
year of publication.
n
Study included in systematic review Karoussis et al. (2007).
w
Study included in the systematic review Quirynen et al. (2007).
z
Study included in systematic review Schou et al. (2006).
§
Study included in systematic review Van der Weijden et al. (2005).
SLA, sandblasted and acid etched; SPT, supportive periodontal therapy; TPS, titanium plasma sprayed.

describing the association between dia-
betes and peri-implantitis.
Ferreira et al. (2006) in a recent
cross-sectional study including 212
non-smoking subjects in a Brazilian
population investigated the presence of
risk variables for peri-implant infection.
At the time of examination, all implants
had been in function between 6 months
and 5 years. Glycemic data at the time
of implant surgery were checked in
subjects’ files. For all subjects diag-
nosed with diabetes at the time of sur-
gery as well as for those who reported
having the disease at the time of evalua-
tion, a new exam was requested. Dia-
betes mellitus was diagnosed if an
individual had fasting blood sugar
X126 mg/dl or had been taking anti-
diabetic medicine over the past 2 weeks.
The prevalence of peri-implant mucosi-
tis and peri-implantitis were 64.6% and
8.9%, respectively. The prevalence of
periodontitis in these subjects was
14.2%. In multivariate analyses, the
risk variables associated with increased
odds for having peri-implant disease
included: gender, plaque scores, and
periodontal BOP. In addition presence
of periodontitis and diabetes were sta-
Journal compilation r 2008 Blackwell Munksgaard
tistically associated with greater risk
of peri-implantitis. The results showed
that poor metabolic control in sub-
jects with diabetes was associated with
peri-implantitis (Ferreira et al. 2006),
Table 1.
Genetic traits
Interleukin (IL)-1a, IL-1b and their nat-
ural specific inhibitor IL-1 receptor
antagonist (IL-1ra) play a key role in
the regulation of the inflammatory
response. The identification of genetic
polymorphisms as risk indicators for
r 2008 The Author
 Peri-implant diseases 299

Table 3. Clinical studies evaluating patients with a history of periodontitis

Study Study design Subjects Implant Follow-up SPT Findings
surface
Implant (N)

Ellegaard et al. Prospective 75 patients – all had TPS Tioblast – 3 years At 3 years: 24% of Tioblast and 12% of
(1997a)n cohort study experienced tooth loss Tioblast TPS – 5 years TPS implants had bone loss X1.5 mm
due to periodontitis SPT – 3 monthly At 3 years: 36% of Tioblast and 31% of
Treated before implant TPS implants bled on probing
placement After 5 years: 43% of TPS implants had
64% smokers bone loss X1.5 mm and 45% bled on
probing (excluding early failures)
Ellegaard et al. Prospective 24 periodontally TPS Up to 3 years At 3 years:
(1997b)n cohort (sinus compromised patients Tioblast Annual follow up bone loss X3.5 mm: 0–14% of implants
elevation/ 62.5% smokers SPT – 3 monthly PDX4 mm: 20–56% of implants
conventional BOP: 14–35% of implants
placement)
Yi et al. (2001)n Prospective 43 treated for advanced Turned 3 years Bone loss 40.5 mm in 81% implants
cohort periodontal disease 125 implants Individual SPT 0.5–2.0 mm bone loss in 19% implants
edentulous/ Smoking not reported programme for
partially each patient
dentate
Mengel et al. Prospective Five treated for Turned GCP – 3 years Increased probing depth and attachment
(2001)n,w,z cohort generalized aggressive GAgP – 36 GAgP-5 years loss in the GAgP group after 3 years
periodontitis (GAgP) implants SPT – 3 monthly compared with GCP
Five treated for GCP – 12 recall Bone loss at implants in the GAgP group
generalized chronic implants was significantly higher at 3 years than in
periodontitis (GCP) the GCP group
Smoking not reported
Leonhardt et al. Prospective 15 patients treated for Turned 10 years 61% implants with BOP
(2002)n,w,z cohort advanced periodontitis 57 implants Mean bone loss of 1.7  1.2 mm
Smoking not reported
Baelum & Prospective 140 treated periodontal Tioblast 10 years At 10 years:
Ellegaard (2004)n case series patients TPS SPT – 3 month Survival: TPS 78%, Tioblast 97%
(1 and 2 stage Smokers included Annual bone loss X3.5 mm: Tioblast 5%, TPS
implants) recordings 14%
PDX4 mm: Tioblast 75%, TPS 76%
PDX6 mm: Tioblast 23%, TPS 25%
BOP: Tioblast 69%, TPS 90%
Wennström et al. Prospective 51 subjects treated for Turned 5 years Bone loss: baseline – 5 years
(2004)n randomized- CP 17 smokers included surface Yearly recall Turned surface 0.33 mm
controlled Tioblast Tioblast 0.48 mm
trial
Ellegaard Prospective 68 treated periodontal Tioblast (109 Up to 10 years 27 of 262 implants had to be explanted due
(2006)z,n cohort patients conventional implants) SPT – 3 monthly to recurrent peri-implantitis
and sinus implant TPS (113 47% (TPS) and 17.5% (Tioblast) of
placement smokers implants) implants had bone loss X1.5 mm after 10
included Hollow screw years
implants
No comparison with a control (periodontally healthy) group. Listed in order of year of publication.
SPT, supportive periodontal therapy.

peri-implant infection has been investi-
gated in a number of clinical studies
with conflicting results.
Wilson & Nunn (1999) found no
association between implant failure or
bone loss and the IL-1 genotype.
A cross-sectional study on implant
recall patients with and without clinical
signs of peri-implantitis failed to find an
association between the IL-1 genotype
and peri-implantitis (Lachmann et al.
2007).
In a retrospective study, Feloutzis et
al. (2003) investigated the relationship
r 2008 The Author
Journal compilation r 2008 Blackwell Munksgaard
between specific IL-1 gene polymorph-
isms and peri-implant bone loss and
peri-implant mucosal inflammation in
both smokers and non-smokers. 31.1%
of the 90 Caucasian patients were IL-1
genotype positive. Patients were strati-
fied according to smoking history. There
were 14 heavy smokers (20 cigarettes
per day), 14 moderate smokers (5–19
cigarettes per day), 23 former smokers
(smoking cessation 45 years) and 39
non-smokers. Significant differences in
marginal bone loss between heavy smo-
kers and non-smokers were found for the
IL-1 genotype positive group but not for
the IL-1 genotype negative group. This
suggests that there is a synergistic effect
of smoking and the carriage of the IL-1
gene polymorphism resulting in an
increased risk for peri-implant bone loss.
Gruica et al. (2004) also investigated
the impact of the IL-1 genotype and
smoking status on peri-implant tissues
in a retrospective study of 292 implants
which had been in function for at least 8
years. Fifty-one implants in 34 patients
showed late biologic complications,
while 241 implants had survived
300 Heitz-Mayfield

without any biologic complications at Smoking as suppuration, fistula formation, peri-

all. An association between heavy smo-
kers
with a positive IL-1 genotype and
peri-implantitis was observed. Jansson
et al. (2005) also investigated the IL-1
genotype as a risk indicator for peri-
implant disease. Patients positive for IL-
1 genotype were not more prone to
implant loss (due to pain, mobility or
peri-implant infection); however, a sig-
nificant synergistic effect of IL-1 geno-
type and smoking was demonstrated.
Laine et al. (2006) investigated the
IL-1 gene cluster polymorphisms in
patients with peri-implantitis. The study
included 120 Caucasian individuals. A
total of 71 patients demonstrating peri-
implantitis at one or more implants and
49 control patients with healthy peri-
implant mucosa were recruited for the
study. The implants had been in func-
tion for at least 2 years. Significant
differences were found in the carriage
rate of allele 2 in the IL1-RN gene
between peri-implantitis patients and
controls. Logistic regression analysis
taking smoking, gender and age into
account confirmed the association
between the IL-1RN allele 2 carriers
and peri-implantitis [odds ratio (OR) 3;
95% confidence interval (CI) 1.2–7.6;
p 5 0.02]. Future prospective studies
involving large numbers of patients are
required to confirm this association.
The effect of cigarette smoking on
the peri-implant tissues has been docu-
mented in a number of studies. Strietzel
et al. (2007) published a systematic
review with meta-analysis, including
35 papers, to investigate if smoking
interferes with the prognosis of
implants, with and without augmenta-
tion procedures. As the definition of
smokers varied among studies (regard-
ing the number of cigarettes smoked
per day) any patient who smoked
was considered a smoker in this review.
This systematic review (Strietzel et al.
2007) also indicated significantly
enhanced risks of biologic complica-
tions among smokers compared with
non-smokers (Table 4). The following
six studies were included which
reported on the frequency of peri-
implant disease in smokers and non-
smokers.
Ataoglu et al. (2002) in a prospective
study, with at least 1-year follow-up
of 24 implants in 10 smokers and
18 implants in four non-smokers,
showed significantly increased inflam-
mation related clinical parameters in
smokers.
Gruica et al. (2004) in a retrospective
study of X8 years found that smokers
were at significantly higher risk to
develop peri-implant disease defined
implantitis and bone loss.
McDermott et al. (2003) in a retro-
spective study of up to 8 years found a
significantly higher risk for smokers to
develop peri-implant disease.
Haas et al. (1996) in a 22-month
retrospective study compared the pre-
sence of peri-implantitis in a group of
107 smokers and 314 non-smokers.
Smokers showed a higher score in the
bleeding index, mean peri-implant prob-
ing depth, degree of peri-implant muco-
sal inflammation, and radiographic bone
loss.
Attard & Zarb (2002) in a retrospec-
tive study of 16–18 years follow-up
reported smokers had a significantly
higher risk to develop peri-implant soft
tissue complications.
Weyant (1994) reported significantly
more peri-implant soft tissue complica-
tions in smokers compared with non-
smokers in a retrospective study of 2098
implants in 598 patients.
The systematic review by Strietzel
et al. (2007) also included studies report-
ing on the influence of smoking on
peri-implant marginal bone changes.
The following studies included showed
a significant increase in peri-implant
marginal bone loss in smokers compared
with non-smokers (Haas et al. 1996,
Lindquist et al. 1996, 1997, Carlsson
et al. 2000, Feloutzis et al. 2003,

Table 4. Clinical studies reporting on peri-implant disease in smokers and non-smokers and evaluating smoking as a risk indicator for
peri-implantitis
Study Study design Subjects Implants Follow-up Findings

Weyant Retrospective 598 patients HA coated and 4 years Significantly more soft tissue
(1994) cohort Partially dentate 42% uncoated 2098 complications in smokers soft tissue
Number of smokers not implants (15 different complications: 11.9% of smokers
reported types of cylinder 6.8% of non-smokers
implants) Bivariate analysis odds ratio (OR) 1.8 for
smoking
Haas et al. Retrospective 107 smokers TPS 22 month Smokers: significantly higher BOP, PD,
(1996) cohort 314 non-smokers Turned surface peri-implant mucosal inflammation, bone
loss
Attard & Retrospective 27 hypothyroid patients Turned surface 16–18 years Significantly higher risk for smokers to
Zarb (2002) cohort 29 control patients N 5 163 develop peri-implant soft tissue
complications
Ataoglu Prospective 10 smokers 42 implants At least 1 year Smokers: increased PD, modified plaque
et al. (2002) cohort Four non-smokers index, modified gingival index, and
crevicular flow rate
McDermott Retrospective 677 subjects (results TPS HA coated Up to 8 years Multivariate analysis for inflammatory
et al. (2003) cohort based on 677 implants) uncoated (median 13.1 complications (including peri-implantitis)
10.3% of patients were months) showed smoking was significant Hazard
smokers ratio: 3.26 (95% CI: 1.7–6.10)
69 of 677 implants had inflammatory
complications
Gruica et al. Retrospective 180 patients TPS At least 8 years Significantly greater risk for smokers to
(2004) 53 smokers develop peri-implantitis, draining sinus,
127 non-smokers suppuration and bone loss

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Journal compilation r 2008 Blackwell Munksgaard

Karoussis et al. 2004, Peñarrocha et al.
2004, Wennström et al. 2004, Galindo-
Moreno et al. 2005, Nitzan et al. 2005,
Schwartz-Arad et al. 2005). No significant
difference in marginal bone loss
between smokers and non-smokers was
observed by Aalam & Nowzari (2005).
Additional studies which have
addressed risk indicators associated
with peri-implant disease report a sig-
nificant association of smoking with
peri-implant mucositis, marginal bone
loss and peri-implantitis (Roos-Jansåker
et al. 2006a, Fransson et al. 2008).
Chung et al. (2007) reported in a retro-
spective study of 69 patients, including
seven smokers followed between 3 and
24 years, significantly more bone loss in
smokers. Another long-term retrospec-
tive study (DeLuca & Zarb 2006)
showed that peri-implant bone loss was
associated with a positive smoking
history.
Alcohol consumption
The only study indicating alcohol as a
risk indicator for peri-implant infection
is a recent prospective study. Galindo-
Moreno et al. (2005) investigated the
influence of alcohol and tobacco habits
on peri-implant marginal bone loss.
One-hundred and eighty-five patients
who received 514 implants were fol-
lowed for 3 years. Multivariate analysis
showed that peri-implant marginal bone
loss was significantly related to a daily
consumption of 410 g of alcohol,
tobacco use and increased plaque levels
and gingival inflammation. It was of
note that alcohol use induced greater
marginal bone loss compared with
tobacco use.
Oral Hygiene
In a prospective clinical study, Lind-
quist et al. (1997) reported an associa-
tion between poor oral hygiene and
peri-implant bone loss at 10-year
follow-up. Poor oral hygiene had a
greater influence on marginal bone loss
in smokers than non-smokers. For
patients with poor oral hygiene, smokers
had nearly three times the amount of
bone loss than non-smokers.
In a study analysing risk variables in
a Brazilian population, presence of pla-
que and periodontal BOP at 430% of
sites were associated with increased risk
of peri-implant mucositis and peri-
implantitis. The association between
the full-mouth plaque score and peri-
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Journal compilation r 2008 Blackwell Munksgaard
implant disease was dose dependent.
Very poor oral hygiene (median full-
mouth plaque score X2) was highly
associated with peri-implantitis with an
OR 5 14.3; 95% CI 2.0–4.1 (Ferreira
et al. 2006).
Presence of keratinized mucosa
The role of keratinized mucosa in peri-
implant disease was studied by Roos-
Jansåker et al. (2006b) who examined
218 patients treated with titanium
implants. A multivariate analysis of
potential explanatory variables for
peri-implant mucositis and peri-implan-
titis was made. No association between
the absence of keratinized peri-implant
mucosa and peri-implant disease was
found.
Implant surface characteristics
Implant surface characteristics vary with
respect to topography, surface rough-
ness and chemical composition. The
majority of currently marketed implants
have moderately rough (Sa between 1.0
and 2.0 mm) surfaces, as they show
improved bone responses compared
with smoother or rougher surfaces
(Albrektsson & Wennerberg 2004a, b).
The evidence for the influence of
implant surface and design as a risk
indicator for peri-implant disease is
limited with conflicting results.
In some studies where both rough and
moderately rough implant surfaces were
used the marginal bone loss was
reported to be greater at rough implant
surfaces (Ellegaard et al. 1997a, b,
Baelum & Ellegaard 2004). Astrand
et al. (2004) reported a short-term fol-
low-up (3 years) of a randomized con-
trolled trial comparing implants with
different surface roughness. Twenty-
eight patients were provided with two
to four implants on each side of the
dentition and were randomly allocated
to implants with a turned surface or
implants with a rough surface. No sta-
tistically significant differences were
found between the implants studied,
except for the frequency of peri-implan-
titis, which was higher for the rough
surface implants. Peri-implantitis (infec-
tion including pus and bone loss) was
observed with seven rough surface
implants but with none of the turned
surface implants.
Wennström et al. (2004) in a prospec-
tive randomized controlled trial of 51
patients treated for periodontitis
Peri-implant diseases 301
reported similar bone level changes for
turned (Sa  0.5 mm) and moderately
rough surface implants.
Conclusions
Diagnosis
 Probing is essential for diagnosis of
peri-implant diseases.
 Probing using a light force (0.25 N)
does not damage the peri-implant
tissues.
 BOP indicates presence of inflam-
mation in the peri-implant mucosa.
 BOP may be used as a predictor for
loss of tissue support.
 An increase in probing depth over
time is associated with loss of
attachment and supporting bone.
 The probing depth (using a light
force, 0.25 N), the presence of
BOP, and suppuration should be
assessed regularly for the diagnosis
of peri-implant diseases.
 Radiographs are required to evaluate
supporting bone levels around
implants.
 Analysis of PICF is not a clinically
useful diagnostic parameter for peri-
implant disease.
Risk indicators for peri-implant diseases
There is substantial evidence that the
following factors are associated with
peri-implant diseases:
1. Poor oral hygiene: Ferreira et al.
(2006) OR 14.3 (95% CI: 2.0–4.1),
Lindquist et al. (1997).
2. History of periodontitis: Four sys-
tematic reviews; Van der Weijden
et al. (2005), Schou et al. (2006),
Karoussis et al. (2007) and Quirynen
et al. (2007). Ten of 11 studies
(comparing patients with a history
of periodontitis with non-perio-
dontitis patients) show an increased
risk for peri-implant disease.
3. Cigarette smoking: A systematic
review by Strietzel et al. (2007)
reported five retrospective and one
prospective studies showing an asso-
ciation between smoking and peri-
implantitis. Twelve of 13 studies
showed a significant increase in mar-
ginal bone loss in smokers compared
with non-smokers.
302 Heitz-Mayfield
There is limited evidence that the
following factors are associated with
peri-implant diseases:
1. Diabetes – poor metabolic control –
one study Ferreira et al. (2006).
2. Alcohol consumption 410 mg/day –
one study Galindo-Moreno et al.
(2005).
There is conflicting and limited evi-
dence for an association with peri-
implant diseases and:
1. Genetic traits
(1) Study Laine et al. (2006) showed a
significant association with peri-
implantitis.
(2) Studies showed no association (Wilson
& Nunn 1999, Lachmann et al.
2007).
(3) Studies showed evidence for a
synergism between genetic traits
and smoking (Feloutzis et al. 2003,
Gruica et al. 2004, Jansson et al.
2005).
2. Implant surface
(1) Studies with implants with different
surfaces within the same patient.
 Astrand et al. (2004) found a rough
surface was worse than a smooth
surface.
 Wennström et al. (2004) found a
moderately rough surface similar to
a smooth surface.
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tions between clinical parameters and inter-
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from totally edentulous patients with peri-
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543–550.
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Salum, O. & Fischer, K. (2004) Correlation
of peri-implant health and myeloperoxidase
levels: a cross-sectional clinical study. Clin-
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(2007) Osseointegrated implants in subjects
treated for generalized aggressive perio-
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aggressive and chronic periodontitis: a 3-year
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(2006) Digital volume tomography in the
diagnosis of peri-implant defects: an in vitro
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noline and interleukin-1beta in peri-implant
crevicular fluid of patients with peri-implan-
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on marginal bone loss. The International
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Stilio, M., Contento, A. & Spoto, G. (2000)
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study of marginal bone loss around 108
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(2002) Elastase, alpha2-macroglobulin and
alkaline phosphatase in crevicular fluid from
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Impact of supportive periodontal therapy and
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aspartate aminotransferase in the crevicular
fluid of implants with bone loss and signs of
Clinical Relevance
Scientific rationale for the study:
This review addressed firstly the evi-
dence for diagnostic criteria and sec-
ondly the potential risk factors for
peri-diseases (peri-implant mucositis
and peri-implantitis).
progressive disease. The International Jour-
nal of Oral and Maxillofacial Implants 14,
428–435.
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(1997) The clinical, microbial, and host
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observations in cynomolgus monkeys (Maca-
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(2002) Probing around implants and teeth
with healthy or inflamed peri-implant muco-
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Principal findings: Probing using a
light force (0.25N) does not damage
the peri-implant tissues and is a use-
ful diagnostic tool to detect signs of
inflammation. Radiographs are
required to diagnose loss of support-
ing bone around implants. Risk indi-
cators for peri-implant disease
Journal compilation r 2008 Blackwell Munksgaard
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rehabilitation with implant-supported
fixed partial dentures in periodontitis-suscep-
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724.
Weyant, R. (1994) Characteristics associated
with the loss and peri-implant tissue health
of endosseous dental implants. The Interna-
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Implants 9, 95–102.
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between the interleukin-1 periodontal geno-
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Yalçn, S., Baseğmez, C., Mijiritsky, E., Yalçn,
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fixed prostheses for the rehabilitation of
periodontally compromised dentitions: a 3-
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Zitzmann, N. U. & Berglundh, T. (2008)
Definition and prevalence of peri-implant
disease. Journal of Clinical Periodontology
35 (Suppl. 8), 286–291.
Address:
Lisa J. A. Heitz-Mayfield
Centre for Rural and Remote Oral Health
The University of Western Australia
35 Stirling Highway
Crawley, WA 6009
Australia
E-mail: heitz.mayfield@iinet.net.au
include poor oral hygience, smoking
and history of periodontitis.
Practical implications: Probing
around implants should be performed
regularly to diagnose signs of peri-
implant disease. Patients who are at
risk for peri-implant disease should
be informed and monitored carefully.
r 2008 The Author