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J Clin Periodontol 2013; 40: 296302 doi: 10.1111/jcpe.

12045

Aetiology, microbiology and


therapy of periapical lesions
around oral implants: a
retrospective analysis

David Lefever, Nele Van Assche,


Andy Temmerman, Wim Teughels
and Marc Quirynen
Department of Periodontology, School of
Dentistry, Oral Pathology & Maxillo-Facial
Surgery, Faculty of Medicine, Catholic
University Leuven, Leuven, Belgium

Lefever D, Van Assche N, Temmerman A, Teughels W, Quirynen M. Aetiology,


microbiology and therapy of periapical lesions around oral implants: a retrospective
analysis. J Clin Periodontol 2013; 40: 296302. doi: 10.1111/jcpe.12045.

Abstract
Objective: The aim of this study was: (i) to evaluate whether an endodontic
pathology on the extracted tooth or adjacent teeth of an implant site has an
influence on the emergence of a periapical lesion, (ii) to retrospectively analyse
the outcome of different treatment strategies, (iii) to determine which bacteria
were present in periapical lesions.
Methods: The endodontic status of the tooth at the implant site and the adjacent
teeth was explored and linked to the periapical status of the implant. For all the
lesions treated since 2000, their survival was assessed. Finally, microbial samples
(culturing) from the periapical lesions, were analysed.
Results: If an endodontic treatment or a periapical lesion at the apex of a tooth
is present, a periapical lesion around the implant can be detected in 8.2% up to
13.6% (OR 7.2). For periapical pathology at the adjacent teeth, the percentage
rises to 25% (OR 8.0). The best treatment option could not be found. Bacteria
were found in 9/21 lesions. The most prominent species was P. gingivalis.
Conclusions: When an endodontic pathology is present on the extracted or
neighbouring teeth, it is significantly more likely that a periapical lesion will
develop around a future implant.

A periapical lesion around a dental


implant, also called retrograde periimplantitis, is defined as a clinically
symptomatic lesion at the apex of
an implant that develops shortly
after fixture installation, while the
coronal portion of the implant
achieves a normal bone to implant
Conflict of interest and source of
funding
This article has been prepared without
any sources of institutional, private or
corporate financial support and there
are no potential conflicts of interest.

296

interface (Quirynen et al. 2003).


These clinical symptoms can include
pain, tenderness, swelling and/or
the presence of a fistula. An incidence of 0.26% up to 1.86% has
been reported in literature (Reiser
& Nevins 1995, Quirynen et al.
2005). In addition, the knowledge
on the incidence, aetiological factors and treatment of periapical
lesions around implants is scarce.
Different aetiological factors have
been suggested to play a role in the
emergence of retrograde peri-implantitis such as excessive heating of the
bone during the preparation of the

Key words: dental implant; implant failure;


microbiology; periapical lesion; retrograde
peri-implantitis
Accepted for publication 13 November 2012

osteotomy (McAllister et al. 1992,


Piattelli et al. 1998a), failed endodontic and/or apicoectomy procedures (Ayangco & Sheridan 2001),
placement of the implant in proximity of an existing infection (Reiser &
Nevins 1995, Shaffer et al. 1998),
excessive tightening of the implant
with compression of the bone during
implant placement (Piattelli et al.
1998b) and the presence of pre-existing microbial pathology (McAllister
et al. 1992, Sussman & Moss 1993,
el Askary et al. 1999). One case
report even mentions the occurrence
of a lesion after the implant was
2012 John Wiley & Sons A/S

Periapical implant lesions


placed, penetrating the nasal cavity
(Silva et al. 2010). All these factors
cause what can be called an active
lesion.
Besides these, there are also inactive lesions, when radiographic findings are not associated with clinical
symptoms. For example an asymptomatic radiolucency can be seen at
the radiography when the drilling
depth during the preparation of the
surgical site exceeded the length of
the implant that is placed or when
an implant is placed next to an
already existing radiolucency, caused
by scar tissue (McAllister et al. 1992,
Reiser & Nevins 1995).
At present, periapical lesions
around dental implants are considered to have a multifactorial aetiology, combining one or more of the
above. Therefore, there is no consensus regarding the therapy. While most
authors agree that the apex of the
implant should be surgically exposed,
there is less agreement about how the
therapy should be continued. Some
propose a curettage and detoxification of the implant surface using
different solutions (Balshi et al. 1994,
Bretz et al. 1997, Esposito et al.
1999), while others combine this with
a guided bone regeneration (GBR)
procedure using a bone substitute
material and a bioresorbable membrane (Quirynen et al. 2005). Even
more aggressive approaches have
been proposed such as an intra-oral
apicoectomy procedure (Balshi et al.
2007, Dahlin et al. 2009).
Even though most authors suggest that there is a microbiological
factor in the aetiology of periapical
lesions around dental implants, this
aspect has been hardly investigated.
In a recent review, it was reported
that in a total of 32 implants with
retrograde peri-implantitis that were
histologically evaluated, bacteria
were detected in only one case.
Three other studies showed aseptic
bone necrosis (Romanos et al. 2011).
Therefore, the aim of this study was
threefold. As a pre-existing microbial
pathology and the presence of an existing infection is suggested to play a role
in the aetiology of periapical lesions, the
first aim of this study was to evaluate
retrospectively whether an endodontic
pathology or apical radiolucency at the
tooth prior to extraction (at the implant
site) or at the adjacent teeth has an
influence on the emergence of a
2012 John Wiley & Sons A/S

periapical lesion around a dental


implant. Secondly, a retrospective analysis of the different treatments performed at our department was included
to evaluate their outcome. The last aim
of this study was to determine which
kind of bacteria were present in periapical lesion around implants.
Materials and Methods
Endodontic pathology

All single tooth implants, placed in


the upper and lower jaw at the
Department of Periodontology (University Hospital, Catholic University
Leuven) between January 2004 and
December 2009, were included in
this retrospective case-control study.
If a tooth showed a periapical lesion
at the moment of extraction, a
thorough curettage was standard
performed. Adjacent teeth, that not
needed to be extracted, were (re)treated endodontically. Implant placement was always delayed until full
healing of the future implant site.
The periapical status of the tooth
at the implant site and the adjacent
teeth prior to implant placement
were evaluated primarily on digital
intra-oral radiographs (Minray;
Soredex, Tuusula, Finland). If such
radiograph was not available, an
extra-oral panoramic radiograph was
used to judge the periapical condition (Cranex Tome; Soredex, Tuusula, Finland). No cone beam CTs
were evaluated. The analysis of
the periapical implant lesions was
performed by two calibrated, independent periodontologists. Results
were re-evaluated when there was an
inter-examiner difference. The periapical status of the tooth at the
implant site and the adjacent teeth
prior to extraction was explored and
identified as:
(a) no endodontic treatment and no
periapical lesion
(b) a periapical lesion at the root
combined with or without an
endodontic treatment, and
(c) an endodontic treatment without
clear signs of a periapical lesion.
For implants with a radiological
follow-up of at least 6 months after
implant placement, the implant itself
was evaluated for the presence of an
apical pathology visible via intra-oral

297

radiographs. All radiographs available in the patient files, taken after


implant installation until August
2010 were subjected to such evaluation. If no periapical radiological
information was available about the
tooth at the implant site, or the adjacent teeth the implant was excluded
from the analysis. A lesion was radiologically defined as a radiolucent area
at the apical part of the teeth or
implants.
Treatment and survival

All periapical lesions around dental


implants, observed and treated at our
department since January 2000, were
examined retrospectively. Included
were: implants placed for single tooth
replacement, partial and full fixed restorations, or as support for overdentures in both the upper and lower
jaw. For each implant, the kind of
treatment performed and the implant
survival (no disintegration, absence
of mobility, implant still in function
without signs of infection or pain),
were registered.
Microbiology

In 21 cases, whenever possible, a microbial sample of the periapical lesion was


taken at the moment of treatment.
These samples were analysed for
enterococcus species, Aggregatibacter
actinomycetemcomitans, Campylobacter
rectus,
Fusobacterium
nucleatum,
Prevotella intermedia and Porphyromonas gingivalis. Furthermore, also the
total count of aerobic and anaerobic
bacteria was explored.
The samples were taken with sterile paper points (Roeko; Roeko,
Langenau, Germany), which were
inserted into the area for 20 s during
the moment of treatment and were
dispersed in 2 ml of reduced transport fluid (RTF). Each sample was
homogenized by vortexing for 30 s
and processed within 12 h by culturing (for details, see Quirynen et al.
1999).
Results
Endodontic pathology

Between January 2004 and December


2009, a total of 230 implants in the
upper jaw and 88 in the lower jaw
were placed in 291 patients for single

298

Lefever et al.

tooth replacement. Two hundred and


sixty-five patients received a single
implant, 25 patients 2 and 1 patient 3
implants. Of the 318 implants placed,
245 (77%) were Br
anemark TiUnite
implants (Nobel Biocare, Gothenburg, Sweden), 67 (21%) were OsseoSpeed (Astra Tech Dental, M
olndal,
Sweden), and 6 (2%) were SLActive
(Straumann, Basel, Switzerland).
For 70 of these implants, no information about periapical condition of
the extracted tooth could be retrieved.
For four implants no information
was available about the periapical
condition on the mesial and for eight
on the distal adjacent tooth. The
kappa-value for the inter-examiner
reliability was 0.9 (p < 0.001).
In total, 248 implants (182 upper
jaw / 66 lower jaw) placed in 232
patients were subjected to analysis [185
TiUnite (75%), 58 OsseoSpeed (23%),
and 5 SLActive implants (2%)]. For
124 and 38 of the implants in upper
and lower jaw, respectively, intra-oral
digital radiographs were available, the
others, (58 in upper, 28 in lower jaw)
were analysed on panoramic radiographs.
Most of the periapical lesions
were identified at a control visit
between implant insertion and abutment connection (thus during the
submerged healing, n = 36), at abutment connection (n = 11), or soon
afterwards (n = 5 within first year,
n = 7 afterwards).
The relationship of the endodontic
status of the tooth prior to extraction
and periapical pathology around
inserted implant is summarized in
Table 1. If the tooth showed no signs
Table 1. The presence of periapical lesions
at implants, in relation to the condition of
the previously extracted tooth (%)
Condition of
extracted
tooth

No periapical
pathology
Periapical
radiolucency
Endodontic
treatment
without
periapical
lesion
Total

Condition
of the implant
No
pathology

Periapical
radiolucency

97.9

2.1

86.4

13.6

91.8

8.2

92.3

7.7

Fig. 1. A lesion around tooth number 14 and around the subsequently placed
implant.

of a periapical lesion and had no endodontic treatment, the incidence of an


apical pathology was 2.1%. On the
other hand, if an endodontic treatment
or a periapical lesion at the apex of the
tooth was present at the moment of
extraction, a periapical lesion could be
found around the implant in 8.2%
and 13.6% of the cases respectively
(Table 1). The Odds ratio for an apical pathology around an implant was
7.2 (p < 0.001) for a tooth with an
endodontic history, compared with a
pathology free tooth. Figure 1 shows
the radiological findings of a tooth
prior to extraction and the periapical
status of the implant that was subsequently placed.
The influence of the adjacent
teeth, in case the extracted tooth
showed neither a pathology nor an
endodontic treatment, can be seen in
Table 2. If the neighbouring teeth,
either on the mesial or the distal side,
showed no signs of pathology or did
not receive endodontic treatment,
only 1.2% of the implants presented
with a periapcial lesion. When an
Table 2. Percentage distribution of periapical lesions along implants per condition of
neighbouring teeth, for sites where a tooth
had been extracted without endodontic
pathology or treatment
Condition of
neighbouring
tooth

Condition
of the implant
No
Periapical
pathology radiolucency

No periapical
pathology
Periapical
radiolucency
Endodontic
treatment
without
periapical lesion
Total

98.8

1.2

75.0

25.0

100

97.8

2.1

endodontic treatment was performed


in the past, but no signs of periapical
pathology could be detected, no periapical lesions around the implants
could be found. However, if there
were signs of periapical pathology at
the neighbouring teeth, 25% of the
implants also showed a periapical
lesion (OR 8.0, p = 0.01).
Treatment and survival

Since 2000, 59 implants (41 upper / 18


lower jaw) treated at our department
for a periapical lesion could be
retrieved. Different treatment options
had been chosen: explantation of the
affected implant (17/59), curettage of
the defect and application of a
bone substitute (Bio-Oss, Geistlich,
Schlieren, Switzerland) in the defect
(14/59), curettage and administration
of systemic antibiotics (10/59), simply
curettage (11/59), no treatment
(2/59), only systemic antibiotics without curettage (2/59), curettage with
the usage of a barrier membrane
without application of a bone substitute (2/59), and curettage and application of autogenous bone chips
(1/59). All curettages were conducted
via an explorative flap. Of the 42
non-explanted implants, 9 implants
were lost during follow-up, all during
the first 4 years of loading. The
cumulative survival rate for an
implant showing a periapical lesion is
46.0% (Table 3). When the explanted
implants were excluded, the cumulative survival rate reached 73.2% after
10 years. The decision whether to
remove an affected implant or to treat
it, was mainly based on the extent of
the lesion and the part of osseointegration that was left at the moment of
treatment. Whenever an implant
showed very few bone to implant contact (mostly only two or three threats
coronally remaining), meaning that a
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Periapical implant lesions


Table 3. Cumulative survival rate (%) of
an implant showing a periapical lesion, with
a maximum follow-up time of 126 months
Month

06
612
1218
1824
2430
3036
3642
4248
4854
5460
6066
6672
7278
7884
8490
9096
96102
102108
108114
114120
120126

Implants Failed
Failure CSR
at start implants rate for
period
59
45
40
37
30
27
23
22
19
17
14
13
11
9
8
7
6
4
3
2
2

14
4
2
2
1
1
0
1
1
0
0
0
0
0
1
0
0
0
0
0
0

23.7
8.9
5.0
5.4
3.3
3.7
0.0
4.5
5.3
0.0
0.0
0.0
0.0
0.0
12.5
0.0
0.0
0.0
0.0
0.0
0.0

76.3
69.5
66.0
62.5
60.4
58.1
58.1
55.5
52.6
52.6
52.6
52.6
52.6
52.6
46.0
46.0
46.0
46.0
46.0
46.0
46.0

very large lesion was present, it was


decided to remove this implant. Other
cases were treated. Figure 2 shows an
implant before and after treatment
with a bone substitute. A clearcut
selection of best treatment strategy
could not be found. The marginal
bone level changes along the surviving implants remained stable (26/33
implants coronal to 2nd thread, 7/33
implants coronal to third thread).
Microbiology

A total of 21 lesions were sampled.


Bacteria were found in nearly all

sites, but only in 9/21 in concentrations  log 4. The proportion of


anaerobic species was always higher
when compared with aerobic species.
P. gingivalis and P. intermedia were
detected in reasonable concentrations at six and four sites respectively. The other specific species
tested (A. actinomycetemcomitans,
C. rectus and F. nucleatum, Enterococci) never reached the threshold
level for identification (see Table 4).
Discussion

A route for implant surface contamination at insertion can be the site into
which the implant is placed. An endodontic infection of an adjacent tooth
is frequently mentioned in the literature to be a causal factor in the process of developing a periapical lesion
(Shaffer et al. 1998, Sussman 1998).
Our observations are in agreement
with these findings. If an active endodontic lesion is present on an adjacent tooth, which can be verified true
conventional radiographs, indeed a
much higher frequency of affected
implants was observed. When the
adjacent teeth did not suffer from
endodontic pathology or when there
was an endodontic treatment present,
but without any signs of periapical
pathology, only in 1% of the cases
the implant showed a periapical
lesion. This percentage is much higher
(25%, OR 8.0), when an adjacent
tooth showed clear signs of endodontic pathology, meaning that an infection from a neighbouring tooth can
spread to the apex of an implant, and
thus can be the cause of an infection
in this area. This observation can be

299

of great importance in the treatment


protocol of the implant patient. Teeth
showing an endodontic pathology
should therefore be treated prior to
implant placement and the latter
should best be postponed until the
radiological sign of a periapical lesion
at the adjacent teeth disappeared.
In this study, two dimensional
radiographs were used for the analysis. This type of radiographs does
not always show the correct size of
an intra-bony defect. Only when the
junctional area is involved, these
kinds of defects can be identified.
Therefore, it might be possible that
some periapical pathologies are not
recognized on two dimensional
radiographs, which is a limiting factor in the diagnosis. A cone beam
CT can be used to overcome this
limitation (Van Assche et al. 2009).
A residual lesion of the extracted
tooth might be another explanation
of the contamination of the implant
surface. This can include granulomas, residual apical cysts, root remnants, (McAllister et al. 1992,
Ayangco & Sheridan 2001, Jalbout
& Tarnow 2001). This study clearly
indicates that the dental history of
the implant site is of remarkable
importance. At sites where a tooth
with a periapical lesion had been
extracted, the odds ratio for an apical lesion along the inserted implant
is very high (7.23) Even if no periapical lesion is present (i.e. visible on
conventional radiographs) at the
moment of extraction, but there is an
endodontic treatment, the risk of
implant pathology is higher. In a
cadaver study, Green et al. (1997) reported that even though endodontically

Fig. 2. The implant on position 23 shows an active periapical implant lesion. During surgery the defect was visualized and a thorough curettage was performed. Hereafter, a bone substitute was used to fill the defect. After 6 months of healing, there was no
recurrence of the lesion.
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300

Lefever et al.

Table 4. Microbiological data from 21 sampled periapical lesions

1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21

CFU/ml
Aerobic

CFU/ml
Anaerobic

0
0
0.006
22.8
0.7
0
0.002
0.038
0.016
0.008
0.004
0.042
2.02
1.3
0.014
0.034
0
0.006
0.048
0.004
0.178

0.096
0.012
0.018
24.0
12.0
0.002
0.01
0.078
0.118
13.0
0.07
0.086
19.2
15.4
0.242
0.058
0.1
0.9
264.0
0.006
1.02

9 104
9 104
9 104
9
9
9
9
9
9
9
9
9
9

104
104
104
104
104
104
104
104
104
104

9
9
9
9

104
104
104
104

9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9

104
104
104
104
104
104
104
104
104
104
104
104
104
104
104
104
104
104
104
104
104

P.g.

P.i.

F.n.

0
0
0
0
0
0
0
0
0
0
0
0.01 9 104
0.12 9 104
0.88 9 104
0.154 9 104
0
0
0.28 9 104
1820 9 104
0
0

0
0
0
0
0.02 9 104
0
0
0
0
0.002 9 104
0
0
0.04 9 104
0
0
0
0
0
0
0
0.098 9 104

0
0
0
0
0.02 9 104
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0

A. Actinomycetemcomitans, C. rectus and Enterococci have never been detected.

treated teeth may be clinically classified as successful on the basis of conventional radiographs, up to 26%
still exhibits histological signs of
inflammation. Therefore, a thorough
curettage of the future implant site,
even with bur, should be recommended at the moment of extraction.
In the past, we always tried to hermetically close the wound after tooth
extraction. Perhaps this approach
facilitated the encapsulation of
remaining pathology. As we changed
this approach, in combination with a
thorough curettage including the use
of burs, the incidence of periapical
lesions around implants reduced
dramatically.
Today, there is no consensus on
which kind of therapy is superior to
another for the treatment of periapical lesions around oral implants.
Already in 1992, McAllister and
co-workers introduced the concept
of a surgical flap approach with
curettage of the bony defect and
granulation tissue, detoxification of
the exposed implant surface and possibly a GBR procedure, but longterm outcome data are lacking. In
this study, 15 implants were treated
using a GBR procedure. After
36 months, 11 were still in function
without clinical or radiological signs
of inflammation, thus 26.7% of the
implants was lost during follow-up.

Another group suggested an apicoectomy on the affected implants


(Balshi et al. 2007). They treated 39
implants in 35 patients with this
intra-oral apicoectomy procedure.
Thirty-eight of the 39 implants
(97.4%) remained stable and continued in function with no further complication up to 5 years.
This could suggest that an apicoectomy procedure should be preferred above a GBR procedure. The
latter is in agreement with other
small case series (Bretz et al. 1997,
Ayangco & Sheridan 2001, Quirynen
et al. 2003, Bousdras et al. 2006,
Dahlin et al. 2009, Rosendahl et al.
2009).
Another group, however, published a case series where they did
not remove the apex of the implant,
but combined a thorough curettage
with saline and chlorhexidine rinsing,
followed by defect fill, using a tetracycline paste, and wound closure. A
follow-up time up to 36 months
showed no adverse events and a
good clinical and radiological healing (Zhou et al. 2012).
Another recent case report
described a treatment without a surgical intervention (Chang et al. 2011).
A patient showing periapical lesions
around two implants was first treated
with systemic antibiotics (amoxicillin)
and paracetamol. When the symp-

toms did not improve, the medications were changed to prednisolone,


augmentin and mefenamic acid. After
a follow-up period of 2 years, there
were no signs of recurrence. Another
case report also mentioned a non-surgical approach, using systemic antibiotics. The lesion slowly resolved after
9 months (Waasdrop & Reynolds
2010). In this study, two cases were
treated with only systemic antibiotics.
In both cases amoxicillin was the
medication of choice. After 3 years,
both implants were still in function
without signs of recurrence. These
data, with low number of cases, are,
however, not enough to conclude that
a treatment with systemic antibiotics,
without surgical intervention, should
be preferred.
Another treatment method for
these kind of lesions could be the
use of laser therapy, such as Er:
YAG laser or CO2 laser (Schwarz
et al. 2006, Romanos & Nentwig
2008), or the use of photodynamic
therapy (Takasaki et al. 2009). However, there are no scientific data
available for the use of these methods in the treatment of peri-apical
implant lesions, only in the treatment of peri-implant disease.
Most authors agree that there is
a role of bacteria in the development
of the periapical lesion.Rokadiya &
Malden (2008) described a case were
a mandibular implant showed swelling and pain 5 weeks after the installation due to a periapical lesion.
After removal of the implant, a
microbial analysis of the apical tissue
was performed showing the presence
of Staphylococcus aureus. A more
recent case report found actinomycotic colonies in the granulation tissue surrounding a periapical lesion
around an implant (Sun et al. 2012).
In this study, most lesions were
found to be colonized by bacteria
with higher counts of anaerobic bacteria, compared with aerobic bacteria. This is logical as the lesions are
located inside the bone, were anaerobic bacteria can survive more easy.
The most prominent species (from
the group of periodontal pathogens)
was P. gingivalis. The latter might be
taken into consideration when antibiotics have to be selected.
In this study, the microbial samples are all from rough surfaced
implants. One can however question
if the type of implant surface is an
2012 John Wiley & Sons A/S

Periapical implant lesions


important factor in bacterial adhesion and thus if these findings could
be compared with machined implant
surfaces. A recent literature review
addressed this question (Renvert
et al. 2011). The review revealed that
very little data are provided on how
implant surfaces influence periimplant disease. They concluded that
there is no evidence that implant surface characteristics can have a significant effect on peri-implant disease.
It is important to note however, that
this study has very few to no data
specific for periapical lesions.
Conclusion

Different aetiological factors have


been suggested to play a role in the
occurrence of a periapical lesion
around a dental implant: excessive
heating of the bone during the osteotomy, failed endodontic and/or apicoectomy procedures, placement of the
implant in proximity of an existing
infection, excessive tightening of the
implant with compression of the bone
during implant placement, and the
presence of pre-existing microbial
pathology. From this study one can
conclude that the endodontic status
of the extracted tooth has a major
influence on the occurrence of periapical lesions. When an endodontic
pathology is present at the moment of
extraction, it is approximately seven
times more likely that a lesion will
develop around the implant. Also, if
periapical pathology is present at the
adjacent teeth, the risk of developing a
lesion at the apex of the implant is
increased. A thorough curettage at the
time of tooth extraction seems crucial.
There are different treatment
approaches, with explantation as the
most aggressive one, but an effective
one to resolve the pathology. Furthermore, curettage of the defect in combination with a bone substitute shows
to be an effective but not impeccable
technique, an apicoectomy procedure
seems more favourable. The microbiological part of this study indicates
that bacteria are present in these periapical lesions, even though their
active role is still unclear.
References
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Address:
David Lefever
Kapucijnenvoer 33
B-3000 Leuven
Belgium
E-mail: david_lefever@hotmail.com

302

Lefever et al.

Clinical Relevance

Scientific rationale for the study:


Periapical lesions around oral
implants have an incidence of
almost 2%. There is not much
known about the aetiological factors, the treatment and the microbiology of these lesions.

Principal findings: the presence of


endodontic
pathology
on
the
extracted tooth at the implant site or
the adjacent teeth will increase the
risk of developing a periapical
lesions around a future implant. The
role of bacteria is still unclear. Of
the treatments evaluated, there was

not one that showed clear superiority over the others.


Practical implications: the history
of the tooth at implant sites is crucial and a thorough curettage is
necessary at the moment of extraction. Concerning the treatment,
there is still more research needed.

2012 John Wiley & Sons A/S

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