ArticlePDF Available

A Radiographic Classification for Retrograde Peri-implantitis

Authors:
  • Bapuji Dental College & Hospital, Davangere, India.

Abstract and Figures

Background: Retrograde peri-implantitis (RPI) is an inflammatory disease that affects the apical part of an osseointegrated implant, while the coronal portion of the implant sustains a normal bone-to-implant interface. It is a diagnostic and therapeutic dilemma for implantologists. There is lack of a standard classification system and a definite treatment algorithm for the same. This article aims to introduce a classification system for RPI based on the radiographic amount of bone loss around an implant apex. Materials and methods: A search of PubMed database was conducted with the keywords "retrograde peri-implantitis" and "implant periapical lesion." Preoperative intraoral periapical (IOPA) radiographs of implants with RPI in case reports/case series were compiled. A total of 54 lOPAs from 36 articles were compiled and were assessed. Results: Three different classes were proposed. The amount of bone loss from the apex of the implant to the most coronal part of radiolucency was calculated as a percentage of the total implant length and classified into one of the three classes: Mild, moderate, and advanced. Treatment options and prognosis have been suggested for each class. Conclusion: The proposed classification may allow for an easy and reproducible radiographic assessment of the RPI lesion and may serve as a guideline to prognosis and treatment planning.
Content may be subject to copyright.
A Radiographic Classication for Retrograde Peri-implantitis
The Journal of Contemporary Dental Practice, April 2016;17(4):313-321 313
JCDP
ABSTRACT
Background: Retrograde peri-implantitis (RPI) is an inamma-
tory disease that affects the apical part of an osseointegrated
implant, while the coronal portion of the implant sustains a normal
bone-to-implant interface. It is a diagnostic and therapeutic
dilemma for implantologists. There is lack of a standard classica-
tion system and a denite treatment algorithm for the same. This
article aims to introduce a classication system for RPI based on
the radiographic amount of bone loss around an implant apex.
Materials and methods: A search of PubMed database was
conducted with the keywords “retrograde peri-implantitis” and
“implant periapical lesion.” Preoperative intraoral periapical
(IOPA) radiographs of implants with RPI in case reports/case
series were compiled. A total of 54 IOPAs from 36 articles were
compiled and were assessed.
Results: Three different classes were proposed. The amount
of bone loss from the apex of the implant to the most coronal
part of radiolucency was calculated as a percentage of the total
implant length and classied into one of the three classes: Mild,
moderate, and advanced. Treatment options and prognosis have
been suggested for each class.
Conclusion: The proposed classication may allow for an easy
and reproducible radiographic assessment of the RPI lesion and
may serve as a guideline to prognosis and treatment planning.
Keywords: Implant, Periapical implant bone loss, Periapical
infection.
How to cite this article: Shah R, Thomas R, Kumar ABT,
Mehta DS. A Radiographic Classication for Retrograde Peri-
implantitis. J Contemp Dent Pract 2016;17(4):313-321.
Source of support: Nil
Conict of interest: None
A Radiographic Classication for Retrograde
Peri-implantitis
1Rucha Shah, 2Raison Thomas, 3AB Tarun Kumar, 4Dhoom Singh Mehta
1-4Department of Periodontics, Bapuji Dental College and
Hospital, Davangere, Karnataka, India
Corresponding Author: Rucha Shah, Lecturer, Department
of Periodontics, Bapuji Dental College and Hospital, Davangere
Karnataka, India, Phone: +917676279879, e-mail: srucha2k@
yahoo.com
INTRODUCTION
Dental implants have revolutionized the field of dentistry.
Since the era of Brånemark, vast improvements have been
made in our understanding of dental implant physiology
and biology. Similar to natural teeth, implants are also
susceptible to plaque biofilm formation and subsequent
soft tissue and bone destruction. The most common inflam-
matory lesion of dental implant is peri-implantitis. The
term was first suggested by Mombelli et al1 and several
classifications for the same exist.2-4 Another separate entity
“retrograde peri-implantitis (RPI)” was first introduced by
McAllister et al in 1992.5 It was described as a “clinically
symptomatic periapical lesion that develops within the
first few months after implant insertion while the coronal
portion of the implant sustains a normal bone to implant
interface.” Retrograde peri-implantitis is a relatively rare
clinical entity and there is a paucity of scientific literature
on this topic.6,7 The etiology is not clear but most of the
cases show bacterial infection. The management of this
lesion is mainly empirical and may include open-flap
debridement, guided bone regeneration, implant apical
resection, or explantation.
Till date, there is no uniformly accepted definition or
classification of RPI. A previous classification has been pro-
posed by Reiser and Nevins,8 who classified RPI as either
inactive or infected lesions. Sussman9 classified RPI into
two types based on the origin of the lesion: Type 1 – implant
to tooth, which occurs during osteotomy preparation either
by direct trauma or through indirect damage, which causes
the adjacent pulp to undergo devitalization, and type 2 –
tooth to implant, which occurs shortly after the placement
of the implant when an adjacent tooth develops a periapi-
cal pathology, either by operative damage to the pulp or
through reactivation of a prior apical lesion. Peñarrocha-
Diago et al10 classified the RPI lesion according to the
stages in which it involves into acute nonsuppurated apical
peri-implantitis, acute suppurated apical peri-implantitis,
ORIGINAL RESEARCH
10.5005/jp-journals-10024-1847
Rucha Shah et al
314
or subacute or suppurated fistulized apical peri-implantitis.
They also suggested treatment guidelines for all the stages.
A periodontal, implant, separate, and traumatic (PIST)
classification has been proposed by Kadkhodazadeh and
Amid,11 which has combined peri-implant, periodontal,
and periapical lesions. The degree of bone loss around the
implant apex may influence the choice of treatment and
prognosis of RPI. None of the existing classifications clas-
sify RPI according to the severity of involvement. Also, no
guidelines are present regarding the prognosis for the same.
A reproducible quantitative classification is much
more objective and has several benefits. It aids in the
determination of relatively more accurate and standard-
ized diagnosis and prognosis. A quantitative classification
considering the degree of bone destruction around an
implant is not present. Such classifications already exist
for periodontitis and peri-implantitis.2,12 A standard case
definition enables the estimation of true prevalence of any
condition. While analyzing different treatment modali-
ties, a baseline standard classification system may give a
better guideline so as to assess which treatment modality
is more effective. It can be expected that the severity of
involvement is one of the main factors that can dictate
the type of treatment and prognosis of a case. Thus, this
classification was based on the severity of involvement.
The aim of this article is to introduce a classification for
RPI quantitatively based on the radiographic amount of
bone destruction seen for mild, moderate, and advanced
grades of RPI.
MATERIALS AND METHODS
Literature Search
An electronic literature search was done in the PubMed
database. The keywords used were “retrograde peri-
implantitis (RPI)” and “implant periapical lesion (IPL).”
The search was performed in December 2015 and all
results thus, obtained were included. The total number of
hits using RPI was 22 and using IPL was 76. After removal
of duplicates (n = 8), 89 results were obtained. The search
hits were then screened for clear relevance by an analysis
of the title and abstract by two reviewers. A total of
56 articles were considered.6-11,13-62 A total of 33 articles
were excluded as being not relevant.63-95 Those articles not
in the English language were excluded (n = 1).40 Full text
of rest of the articles was sought. Seven were not available
as full text, and hence were not included.9,27,28,32,46,59,62
Another article was excluded as it was an animal study
(n = 1).56 The process is demonstrated in Flow Chart 1.
From the articles for which full text was available, images
of high-quality intraoral periapical (IOPA) radiographs of
the implant having RPI immediately after diagnosis were
obtained. Twelve of the articles were excluded as they
had no IOPAs of the lesion.7,11,24,25,33,35,37-39,45,48,53 A total of
54 IOPAs from 36 articles were compiled. One periodon-
tist (SR) and one implantologist (TAB) independently
analyzed the IOPAs. The proposed classification was pre-
pared keeping in mind several requirements as previously
described.63 The requirements were for it to be comprehen-
sive enough to include all possible periapical lesions around
the dental implant, to be simple, logical, reasonable, and
reproducible. It should be acceptable, have ease of applica-
tion, should be scientifically based (by considering all the
recently published literature), and should be helpful to
determine the prognosis and treatment guidelines.11 After
several sessions of discussion, consensus regarding the
radiological classification was reached and the following
classification was proposed. Also, wherever the treatment
protocol was mentioned, it was recorded against the type
of treatment given in different class.
Radiographic Classication of RPI
To classify the RPI lesions, bone loss was measured in
an apico-coronal direction from the apex of the implant
to the most coronal point of extension of bone loss in
millimeters. The derived value was then calculated as a
percentage of the radiographic implant length (Fig. 1A).
The bone loss around the implant may or may not involve
both the implant surfaces (medial and distal) (Figs 1B to
1D). Depending on this percentage, the observed bone
loss was assigned into one of the three categories:
1. Mild lesion (class I) is characterized by radiographic
bone loss that extends to <25% of the implant length
from the implant apex (Fig. 2A).
2. Moderate lesion (class II) is characterized by radio-
graphic bone loss between 25 and 50% of the implant
length as measured from the implant apex (Fig. 2B).
3. Advanced lesion (class III) is characterized by
radiographic bone loss extending to > 50% of the
implant length from the implant apex (Fig. 2C).
Flow Chart 1: Process for selection of articles for
proposed classication
A Radiographic Classication for Retrograde Peri-implantitis
The Journal of Contemporary Dental Practice, April 2016;17(4):313-321 315
JCDP
Statistical Analysis
The statistical analysis was done using Statistical Package
for the Social Sciences (SPSS) software version 16.0. The
frequency of observation of each class was also calculated.
Interexaminer variation was assessed using Cohen K
values.
RESULTS
In the classification agreement of the evaluators, the K
value was found to be 0.67, which can be considered
as a good agreement. The distribution of the different
classes is demonstrated in Table 1. The most commonly
encountered classification is class II.
A
C
B
D
Figs 1A to D: The method to classify a retrograde peri-implantitis
lesion: (A) Measurement of bone loss (measure the length marked
in arrow and divide by the radiographic total length of implant),
(B and C) Both these lesions would be classied as class I (% bone
loss is < 25% in both scenario), and (D) Even though the apical
extension of lesion is same as in Figure B, this is class III lesion as
percentage of involved implant is more than 50%
A
B
C
Figs 2A to C: Figure demonstrating the various proposed classes
for retrograde peri-implantitis (RPI): (A) Class I mild RPI (bone loss
< 25% of implant length from implant apex), (B) class II moderate
RPI (bone loss 25–50% of implant length from implant apex), and
(C) Class III advanced RPI (bone loss > 50% of implant length from
implant apex)
Table 1: Proposed classication of retrograde periodontitis
Classication Stage Amount of bone loss
Class I Mild Extends <25% of the implant
length from implant apex
Class II Moderate 25–50% of the implant length
from implant apex
Class III Advanced >50% of the implant length from
implant apex.
DISCUSSION
Implant dentistry is becoming widely accepted as a
routine treatment modality. With the increase in the
number of implants being placed, cases of RPI are not as
rare as they were once. Retrograde peri-implantitis has
been attributed to a large number of etiologies including
bone overheating, poor bone quality, drilling beyond
implant length, contamination during insertion, bone
microfractures secondary to premature loading, and
implant insertion in a site with existing inflammation, such
as apical periodontitis. However, the current consensus is
that the etiology for RPI is primarily bacterial in nature
and other factors may act as secondary complicating
factors.30 The diagnosis of RPI is based on clinical signs
and symptoms and radiographic findings. The clinical
manifestations of RPI include pain, inflammation, fistula
formation, and swelling or in advanced cases implant
mobility.31 The clinical features may not clearly indicate/
Rucha Shah et al
316
corelate with the actual extent of the lesion. Radiographic
features include a radiolucency surrounding or including
the implant apex with relatively normal marginal bone.31
This article introduces a simple and descriptive
classification for RPI. The interprofessional commu-
nication can be benefited from such a classification
system, which clearly differentiates lesions based on
their severity. A well-accepted classification has the
advantages of facilitating communication, improved
understanding of the nature, and response of the treated
cases. The proposed classification takes into considera-
tion the radiographic extent of peri-implant bone loss.
The rationale of classification was to give a clear clinical
distinction of various stages, treatment suggestions,
and prognosis.
Unlike periodontitis and peri-implantitis, the RPI
lesion is not amenable to clinical examination like probing
and even may not show telltale clinical signs. The clinical
features are not definite or omnipresent and vary greatly.31
Sometimes, the lesion may be asymptomatic. Although
radiographic changes may not be present in the acute
initial stages, the late and symptomatic stages always
demonstrate the presence of an apical radiolucency.31
Hence, radiographic features were taken as the basis of
this classification.
A standardized periapical radiograph can give
accurate values of the amount of bone loss around the
implant apex; however, owing to the vast variety of
shapes and morphology of implants, absolute values
may be difficult to compare among different implants.
Hence, the present classification is proposed based on
the percentage bone loss relative to the length of the
implant. A standardized radiograph immediately after
implant placement may provide details about the baseline
relationship of bone-to-implant apex and facilitate
comparison with the later radiographs to assess the extent
of bone that has been lost during the given time period.
The previous classification by Reiser and Nevins8
proposed that the inactive form was actually an apical
scar which could have resulted from a residual bone
cavity created while placing an implant that was shorter
than the osteotomy. The active or infected form was
explained as occurring when an implant apex was placed
in close proximity to an existing infection or placement of
contaminated implant or that resulting from bone necrosis
caused by overheating during preparation. The authors
suggested that the inactive type of RPI should be observed
and monitored whereas the infected type required
surgical intervention, elimination of the infection, and
reception of apical part of implant or implant removal
depending on the extent of the infection and the stability
of the implant. This classification is based on the lesion
activity and does give treatment guidelines. However, it
does not differentiate between the treatment modalities
on the basis of extent of bone involvement.
The classification of RPI by Sussman9 describes two
types of RPI, i.e., Type 1: Implant to tooth caused due
to a direct or indirect trauma caused to the adjacent
tooth during osteotomy preparation. A type 2 lesion is
described as tooth to implant in which there is spread
of infection from an endodontically involved tooth
to adjacent implant. This classification gives an idea
about the etiology of the RPI lesion. It does not give any
information regarding the degree of bone destruction
around the implant. Also it does not provide any
overview of the prognosis or guidelines for the type of
treatment to be rendered in specific cases.
Peñarrocha-Diago et al classified the RPI lesion
according to the stages of involvement. The first stage
was the acute non-suppurated apical peri-implantitis
characterized by redness, swelling, and acute pain but
no radiographic features. The second stage was acute
suppurated apical peri-implantitis, which has similar
clinical features as the first stage along with a radiolucent
lesion at the implant apex. The next stage was subacute
or suppurated fistulized apical peri-implantitis, which is
characterized by dull pain and mild swelling and redness
along with defined periapical radiolucency, which may
continue as marginal bone loss. For the first two stages,
periapical surgery was suggested, whereas for the third
stage, surgery was suggested in the absence of implant
mobility. In this classification, treatment guidelines are
provided, but the extent of involvement of the lesion was
not considered.
The PIST classification has been proposed by
Kadkhodazadeh and Amid for peri-implant, periodontal,
and periapical lesions. It is an etiology-based classifica-
tion. The classes relating to apical peri-implantitis are
P-1, which is primary periodontitis in adjacent tooth
and secondary involvement of implant. In P-3 there is
primary periodontitis in adjacent tooth and marginal and
periapical implantitis. In class I-1 it is primarily apical
peri-implant lesion, which may involve the apical part
of adjacent tooth secondarily. In the S-1 lesion, apical
lesions are seen on both implant and adjacent tooth but
they occur independently of each other. In S-3 there are
apical and marginal lesions on both implant and natural
tooth, also occurring separately from each other. T-0 is an
asymptomatic periapical lesion involving implant and/or
adjacent tooth, whereas T-1 is a symptomatic periapical
lesion involving implant and/or adjacent tooth. This clas-
sification is comp rehensive; however, it does not provide
any treatment indications.
In the current classifications, no quantification of bone
loss, prognosis, or case-specific treatment indications are
outlined clearly. Some cases can occur as an overlap in
A Radiographic Classication for Retrograde Peri-implantitis
The Journal of Contemporary Dental Practice, April 2016;17(4):313-321 317
JCDP
two stages. To overcome the shortcomings of the present
classifications, this classification is being proposed.
The chances of overlap are minimum and the degree
of bone loss can be clearly assessed. When assessed for
interobserver agreement, the scores were interpreted as
good. Hence, it can be said that it is easy and reproducible
and has good interexaminer reliability. To the best of our
knowledge, this is the first attempt at classifying RPI
quantitatively according to the radiographic amount of
bone destruction seen.
On performing literature search, the authors found
56 published reports on RPI. This demonstrates the
relatively low frequency of occurrence of these lesions.
The incidence of this lesion may range from 1.6%
in the maxilla to 2.7% in the mandible.6 To create a
classification, sufficient data should be assessed for it to
be comprehensive and universally applicable. Hence, the
authors collected all available high-quality IOPA from the
published literature on which the proposed classification
was based.
Majority of the IOPAs examined by the authors fell
in class II as per the proposed classification. This can
be attributed to the fact that an unchecked lesion
progresses from class I to III over a period of time. A
class I lesion is an early mild lesion and may not be
often diagnosed. A class III lesion is too advanced, may
frequently be associated with implant mobility, and hence
may be explanted. Such cases may not be reported as
frequently as their successfully managed counterparts.
A class II lesion is more successfully managed when
detected.
Chan et al15 have proposed a decision tree for the
management of RPI. According to them, a mobile implant
must be explanted; symptomatic immobile implant
should be managed by surgical intervention. For lesions
associated with endodontically involved teeth, the
first line of management is to treat the tooth and wait,
and if lesion does not resolve, surgical intervention is
indicated. However, there is no differentiation between
lines of treatment depending on the size of the lesion at
the time of diagnosis. A class III or II lesion may require
comparatively aggressive and extensive management as
compared with a class I lesion. Another excellent decision
tree has been proposed by Park et al55 for the management
of RPI. They have considered bone loss less than half
the length of implant as adequate osseointegration.
For such cases they suggested surgical management
of nonendodontically compromised cases. When the
bone loss involved more than half the length of implant,
osseointegration is considered inadequate and implant
is suggested to be removed and new wider implant
placement is recommended. They have also classified
the bone defect of less than 5 mm to be managed by
membrane placement only, whereas more than 5 mm to be
managed by bone grafting in conjunction with membrane
placement. Though the basic distinction is presented for
the extent of lesion, the distinction between adequate
and inadequate osseointegration is too sudden. This may
lead to improper management of borderline cases, and
some cases that could be managed surgically can go for
explantation.
From the selected articles, the type of treatment done
was also recorded. When reviewed in the cases selected,
class I and II lesions are most commonly managed with
open-flap debridement. This may or may not be followed
by placement of bone graft and/or barrier mem-
brane.19,21 Also, most of the lesions in these classes tend
to show complete resolution. Some of the reports also
advocate the apical resection of implant,7 but increas-
ing evidence indicates that guided bone regeneration
is successful in the management of these cases. When
the lesions belonged to class III at the time of diagnosis,
the management is frequently more aggressive includ-
ing open-flap debridement, bone graft, and barrier
membrane placement and/or resection of the apical
part of the implant.7,13,14,18,51 If the lesion does not
resolve or the implant is clinically mobile, the implant
has to be explanted.36,42,54,55 There are also reports of
successful implant placement after explantation at the
same site.54
The pathogenesis of an endodontic lesion is remark-
ably similar to periodontitis and peri-implantitis in
terms of involved chemical mediators and responses at
the host cellular level.96 However, the healing potential
of an endodontic lesion is quite high as compared with
a periodontitis or conventional peri-implantitis. It has
been observed that following the treatment, resolution of
the apical radiolucency is observed in most of the cases.
This has been attributed to the fact that after completion
of the therapy, a closed environment is obtained and
healing occurs relatively undisturbed.96 Similarly, RPI is
a closed lesion. Once the nidus of infection is removed by
open-flap debridement, a completely closed environment
is achieved. The healing potential of such lesions after
intervention may be similarly higher than in conven-
tional peri-implantitis, where the crestal bone is involved.
This justifies the finding in the literature that even after
advanced bone involvement such as in proposed class III
there are chances of complete resolution of the lesion.19
Based on the above observations and two previously
published treatment algorithms, a modified decision tree
has been proposed. Apart from the etiology, it also consid-
ers the extent of the lesion and gives treatment sugges-
tions based on it (Flow Chart 2). Once the diagnosis of RPI
is established, the clinician must differentiate it as either a
primary implant lesion or a lesion arising endodontically
Rucha Shah et al
318
in adjacent tooth and involving implant secondarily. If
the lesion is primary, it should be classified into class I,
II, or III. A class I lesion can be managed by open-flap
debridement and it can be followed by implant surface
decontamination. A class II lesion has to be assessed for
accessibility. Open-flap debridement followed by guided
bone regeneration using barrier membranes and/or bone
graft is suggested when accessibility to the lesion is good.
In case of poor accessibility, open-flap debridement fol-
lowed by resection of apical part of implant, followed by
guided bone regeneration using barrier membranes and/
or bone graft, is suggested. A class III lesion demonstrates
advanced bone loss, and hence, the implant mobility must
be assessed. If mobility is absent, the treatment should
be done similar to a class II lesion; however, if implant
mobility is seen, explantation should be performed. After
explantation, if sufficient bone remains to achieve good
implant stability and the decontamination of the site is
thorough, immediate wide diameter implant placement
can be done. However, if sufficient bone is not present,
guided bone regeneration followed by delayed implant
placement has to be followed.
If the lesion is secondary to primary endodontic lesion
from an adjacent tooth, endodontic management of the
offending tooth should be performed. This should be
followed up for up to 1 to 3 months. Closed endodontic
lesions have high healing potential and demonstrate com-
plete resolution of periapical lesion.96 If resolution occurs,
the patient should be kept under monitoring. If the lesion
shows no sign of resolution or shows signs of progressing,
it should now be managed as a primary implant lesion.
Also, from the reviewed articles it was noted that most of
the lesions in classes I and II tend to show complete reso-
lution.13,14,18,19,21 The prognosis can be considered fair to
good. The resolution frequency of class III lesions is lower
than that of class I and II lesions. The prognosis can be from
fair to poor (in case of mobility).36,42,54,55 To the best of our
knowledge, this is the first classification that comments
on the prognosis based on the extent of the lesion of RPI.
This classification can be used in the formulation of
sophisticated standardized treatment algorithms. Such
algorithms guide clinicians, so as to decide which treat-
ment modality to follow when faced by a particular clinical
scenario. It may be helpful to clinicians managing cases of
RPI, the treatment of which still remains highly empirical.
As our knowledge about the pathogenesis of RPI increases,
modifications of this classification may be suggested.
CONCLUSION
This classification quantifies and describes peri-implant
apical bone loss in an objective and reproducible
manner. The proposed classification can be applied for
standardization purposes in research methodologies so
as to have a reliable comparison of the initial lesion and
compare the treatment outcomes in different studies with
similar aims. Further research is required to analyze the
validity of this proposed classification.
REFERENCES
1. Mombelli A, Van Oosten MA, Schurch E Jr, Land NP. The micro-
biota associated with successful or failing osseointegrated tita-
nium implants. Oral Microbiol Immunol 1987 Dec;2(4):145-151.
Flow Chart 2: Decision tree and prognosis for mild, moderate, and advanced classes of RPI15,55
A Radiographic Classication for Retrograde Peri-implantitis
The Journal of Contemporary Dental Practice, April 2016;17(4):313-321 319
JCDP
2. Froum SJ, Rosen PS. A proposed classification for peri-
implantitis. Int J Periodont Restor Dent 2012 Oct;32(5):533-540.
3. Jovanovic SA. Diagnosis and treatment of peri-implant
disease. Curr Opin Periodontol 1994;2:194-204.
4. Spiekerman, H. Atlas de Implantología. Barcelona: Editorial
Masson; 1995.
5. McAllister BS, Masters D, Meffert RM. Treatment of implants
demonstrating periapical radiolucencies. Pract Periodontics
Aesthet Dent 1992 Nov-Dec;4(9):37-41.
6. Quirynen M, Vogels R, Alsaadi G, Naert I, Jacobs R, van
Steenberghe D. Predisposing conditions for retrograde peri-
implantitis, and treatment suggestions. Clin Oral Implants
Res 2005 Oct;16(5):599-608.
7. Balshi SF, Wolfinger GJ, Balshi TJ. A retrospective evaluation
of a treatment protocol for dental implant periapical lesions:
long-term results of 39 implant apicoectomies. Int J Oral
Maxillofac Implants 2007 Mar-Apr;22(2):267-272.
8. Reiser GM, Nevins M. The implant periapical lesion: etiology,
prevention, and treatment. Compend Contin Educ Dent 1995
Aug;16(8):768, 770, 772.
9. Sussman HI. Periapical implant pathology. J Oral Implantol
1998;24(3):133-138.
10. Peñarrocha-Diago M, Maestre-Ferrín L, Cervera-Ballester J,
Peñarrocha-Oltra D. Implant periapical lesion: diagnosis and
treatment. Med Oral Patol Oral Cir Bucal 2012 Nov 1;17(6):
e1023-e1027.
11. Kadkhodazadeh M, Amid R. A new classification for the
relationship between periodontal, periapical, and peri-implant
complications. Iran Endod J 2013 Summer;8(3):103-108.
12. Armitage GC. Periodontal diseases: diagnosis. Ann
Periodontol 1996 Nov;1(1):37-215.
13. Quaranta A, Andreana S, Pompa G, Procaccini M. Active
implant peri-apical lesion: a case report treated via guided
bone regeneration with a 5-year clinical and radiographic
follow-up. J Oral Implantol 2014 Jun;40(3):313-319.
14. Mohamed JB, Alam MN, Singh G, Chandrasekaran SC. The
management of retrograde peri-implantitis: a case report.
J Clin Diagn Res 2012 Nov;6(9):1600-1602.
15. Chan HL, Wang HL, Bashutski JD, Edwards PC, Fu JH, Oh
TJ. Retrograde peri-implantitis: a case report introducing an
approach to its management. J Periodontol 2011 Jul;82(7):
1080-1088.
16. Mohamed JB, Shivakumar B, Sudarsan S, Arun KV, Kumar
TS. Retrograde peri-implantitis. J Indian Soc Periodontol 2010
Jan;14(1):57-65.
17. Waasdorp J, Reynolds M. Nonsurgical treatment of retrograde
peri-implantitis: a case report. Int J Oral Maxillofac Implants
2010 Jul-Aug;25(4):831-833.
18. Dahlin C, Nikfarid H, Alsén B, Kashani H. Apical peri-
implantitis: possible predisposing factors, case reports, and
surgical treatment suggestions. Clin Implant Dent Relat Res
2009 Sep;11(3):222-227.
19. Ataullah K, Chee LF, Peng LL, Lung HH. Management of
retrograde peri-implantitis: a clinical case report. J Oral
Implantol 2006;32(6):308-312.
20. Tözüm TF, Sençimen M, Ortakoğlu K, Ozdemir A, Aydin
OC, Keleğ M. Diagnosis and treatment of a large periapical
implant lesion associated with adjacent natural tooth: a case
report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
2006 Jun;101(6):e132-e138.
21. Flanagan D. Apical (retrograde) peri-implantitis: a case report
of an active lesion. J Oral Implantol 2002;28(2):92-96.
22. Ayangco L, Sheridan PJ. Development and treatment
of retrograde peri-implantitis involving a site with a
history of failed endodontic and apicoectomy procedures:
a series of reports. Int J Oral Maxillofac Implants 2001
May-Jun;16(3):412-417.
23. Bretz WA, Matuck AN, de Oliveira G, Moretti AJ, Bretz WA.
Treatment of retrograde peri-implantitis: clinical report.
Implant Dent 1997 Winter;6(4):287-290.
24. Truninger TC, Philipp AO, Siegenthaler DW, Roos M,
Hämmerle CH, Jung RE. A prospective, controlled clinical
trial evaluating the clinical and radiological outcome after
3 years of immediately placed implants in sockets exhibiting
periapical pathology. Clin Oral Implants Res 2011 Jan;22(1):
20-27.
25 . Nguyen-Hieu T, Borghetti A, Aboudharam G. Peri-implantitis:
from diagnosis to therapeutics. J Investig Clin Dent 2012
May;3(2):79-94.
26. Zhou W, Han C, Li D, Li Y, Song Y, Zhao Y. Endodontic
treatment of teeth induces retrograde peri-implantitis. Clin
Oral Implants Res 2009 Dec;20(12):1326-1332.
27. Meffert RM. Maintenance and treatment of the ailing and
failing implant. J Indiana Dent Assoc 1994 Fall;73(3):22-24.
28. Meffert RM. Treatment of failing dental implants. Curr Opin
Dent 1992 Mar;2:109-114.
29. Kahler B. Healing of a cyst-like lesion involving an implant
with nonsurgical management. J Endod 2015 May;41(5):
749-752.
30. Feller L, Jadwat Y, Chandran R, Lager I, Altini M, Lemmer J.
Radiolucent inflammatory implant periapical lesions: a review
of the literature. Implant Dent 2014 Dec;23(6):745-752.
31. Temmerman A, Lefever D, Teughels W, Balshi TJ, Balshi SF,
Quirynen M. Etiology and treatment of periapical lesions
around dental implants. Periodontol 2000 2014 Oct;66(1):
247-254.
32. Kutlu HB, Genc T, Tozum TF. Treatment of refractory
apical peri-implantitis: a case report. J Oral Implantol 2016
Feb;42(1):104-109.
33. Buhara O, Uyanık LO, Ayalı A, Aydın M. Active implant
periapical lesions leading to implant failure: two case reports.
J Oral Implantol 2014 Jun;40(3):325-329.
34. Qu C, Meng H, Han J. Implant periapical lesion – a review and
a case report with histological evaluation. Clin Oral Implants
Res 2014 Sep;25(9):1099-1104.
35. Peñarrocha-Diago M, Maestre-Ferrín L, Penarrocha-Oltra D,
Canullo L, Piattelli A, Peñarrocha-Diago M. Inflammatory
implant periapical lesion prior to osseointegration: a case
series study. Int J Oral Maxillofac Implants 2013 Jan-Feb;28(1):
158-162.
36. Lefever D, Van Assche N, Temmerman A, Teughels W,
Quirynen M. Etiology, microbiology and therapy of periapical
lesions around oral implants: a retrospective analysis. J Clin
Periodontol 2013 Mar;40(3):296-302.
37. Esfahrood ZR, Kadkhodazadeh M, Amid R, Rokn A. Is the
periapical lesion a risk for periimplantitis? (A review). J Dent
2012 Spring;9(2):162-173.
38. Fugazzotto P. A retrospective analysis of immediately placed
implants in 418 sites exhibiting periapical pathology: results
and clinical considerations. Int J Oral Maxillofac Implants
2012 Jan-Feb;27(1):194-202.
39. Zhou Y, Cheng Z, Wu M, Hong Z, Gu Z. Trepanation and
curettage treatment for acute implant periapical lesions. Int J
Oral Maxillofac Surg 2012 Feb;41(2):171-175.
Rucha Shah et al
320
40. Beitlitum L, Artzi Z, Tsesis I, Nemcovsky CE. Clinical
dilemmas concerning immediate implants in the esthetic
zone. Refuat Hapeh Vehashinayim (1993) 2011 Jan;28(1):
20-30,77.
41. Chang LC, Hsu CS, Lee YL. Successful medical treatment of
an implant periapical lesion: a case report. Chang Gung Med
J 2011 Jan-Feb;34(1):109-114.
42. Silva GC, Oliveira DR, Vieira TC, Magalhães CS, Moreira AN.
Unusual presentation of active implant periapical lesions: a
report of two cases. J Oral Sci 2010 Sep;52(3):491-494.
43. Romanos GE, Froum S, Costa-Martins S, Meitner S, Tarnow
DP. Implant periapical lesions: etiology and treatment options.
J Oral Implantol 2011;37(1):53-63.
44. Merheb J, Coucke W, Jacobs R, Naert I, Quirynen M. Influence
of bony defects on implant stability. Clin Oral Implants Res
2010 Sep;21(9):919-923.
45. Naves MM, Horbylon BZ, Gomes CF, Menezes HH, Bataglion
C, Magalhães DD. Immediate implants placed into infected
sockets: a case report with 3-year follow-up. Braz Dent J
2009;20(3):254-258.
46 . Rosendahl K, Dahlberg G, Kisch J, Nilner K. Implant periapical
lesion. A case series report. Swed Dent J 2009;33(2):49-58.
47. Favia G, Piattelli A, Sportelli P, Capodiferro S, Iezzi G.
Osteonecrosis of the posterior mandible after implant
insertion: a clinical and histological case report. Clin Implant
Dent Relat Res 2011 Mar;13(1):58-63.
48. Peñarrocha-Diago M, Boronat-Lopez A, García-Mira B.
Inflammatory implant periapical lesion: etiology, diagnosis,
and treatment – presentation of 7 cases. J Oral Maxillofac Surg
2009 Jan;67(1):168-173.
49. Rokadiya S, Malden NJ. An implant periapical lesion leading
to acute osteomyelitis with isolation of Staphylococcus aureus.
Br Dent J 2008 Nov;205(9):489-491.
50. Steiner DR. The resolution of a periradicular lesion involving
an implant. J Endod 2008 Mar;34(3):330-335.
51. Nedir R, Bischof M, Pujol O, Houriet R, Samson J,
Lombardi T. Starch-induced implant periapical lesion: a case
report. Int J Oral Maxillofac Implants 2007 Nov-Dec;22(6):
1001-1006.
52. Lin S, Mayer Y. Treatment of a large periradicular lesion of
endodontic origin around a dental implant with enamel matrix
protein derivative. J Periodontol 2007 Dec;78(12):2385-2388.
53. Casap N, Zeltser C, Wexler A, Tarazi E, Zeltser R. Immediate
placement of dental implants into debrided infected dento-
alveolar sockets. J Oral Maxillofac Surg 2007 Mar;65(3):384-392.
54. Tseng CC, Chen YH, Pang IC, Weber HP. Peri-implant
pathology caused by periapical lesion of an adjacent natural
tooth: a case report. Int J Oral Maxillofac Implants 2005
Jul-Aug;20(4):632-635.
55. Park SH, Sorensen WP, Wang HL. Management and
prevention of retrograde peri-implant infection from retained
root tips: two case reports. Int J Periodont Restor Dent 2004
Oct;24(5):422-433.
56. Shabahang S, Bohsali K, Boyne PJ, Caplanis N, Lozada J,
Torabinejad M. Effect of teeth with periradicular lesions on
adjacent dental implants. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 2003 Sep;96(3):321-326.
57. Oh TJ, Yoon J, Wang HL. Management of the implant
periapical lesion: a case report. Implant Dent 2003;12(1):41-46.
58. Scarano A, Di Domizio P, Petrone G, Iezzi G, Piattelli A.
Implant periapical lesion: a clinical and histologic case report.
J Oral Implantol 2000;26(2):109-113.
59. Jalbout ZN, Tarnow DP. The implant periapical lesion: four
case reports and review of the literature. Pract Proced Aesthet
Dent 2001 Mar;13(2):107-112.
60. Piattelli A, Scarano A, Balleri P, Favero GA. Clinical and
histologic evaluation of an active “implant periapical
lesion”: a case report. Int J Oral Maxillofac Implants 1998
Sep-Oct;13(5):713-716.
61. Piattelli A, Scarano A, Piattelli M, Podda G. Implant periapical
lesions: clinical, histologic, and histochemical aspects. A case
report. Int J Periodont Restor Dent 1998 Apr;18(2):181-187.
6 2. Sussman HI. Endodontic pathology leading to implant failure –
a case report. J Oral Implantol 1997;23(3):112-115.
63. Flanagan D. Implant placement in failed endodontic sites: a
review. J Oral Implantol 2016 Apr;42(2):224-230.
64. Langer L, Langer B, Salem D. Unintentional root fragment
retention in proximity to dental implants: a series of six
human case reports. Int J Periodont Restor Dent 2015
May-Jun;35(3):305-313.
65. Verdugo F, Castillo A, Simonian K, Castillo F, Farez-Vidal
E, D’Addona A. Periodontopathogen and Epstein-Barr
virus-associated periapical periodontitis maybe the source
of retrograde infectious peri-implantitis. Clin Implant Dent
Relat Res 2015 Feb;17(1):199-207.
66. Martins JN, Freitas F, Andre S, Moreira A, Carames J. Very
large inflammatory odontogenic cyst with origin on a single
long time traumatized lower incisor. J Clin Diagn Res 2015
Jul;9(7):ZD07-ZD10.
67. Hegde R, Krishna Prasad D, Shetty DV, Shetty M. Immediate
placement and restoration of implant in periapical infected
site in the maxillary esthetic zone: a case report. J Indian
Prosthodont Soc 2014 Dec;14(Suppl 1):299-302.
68. Bassi F, Poli PP, Rancitelli D, Signorino F, Maiorana C. Surgical
treatment of peri-implantitis: a 17-year follow-up clinical case
report. Case Rep Dent 2015;2015:574676.
69. Wolgin M, Tschoppe P, Kielbassa AM. Conservative, surgical,
and prosthetic treatment of a patient with a periapical lesion
associated with an atypical intraoral sinus tract. Case Rep
Dent 2015;2015:495206.
70. Lee CT, Chuang SK, Stoupel J. Survival analysis and other
clinical outcomes of immediate implant placement in sites
with periapical lesions: systematic review. Int J Oral Maxillofac
Implants 2015 Mar-Apr;30(2):268-278.
71. Rosa AC, Francischone CE, Cardoso Mde A, Alonso AC,
Filho LC, da Rosa JC. Post-traumatic treatment of maxillary
incisors by immediate dentoalveolar restoration with long-term
follow-up. Compend Contin Educ Dent 2015 Feb;36(2):130-134.
72. Borgonovo AE, Rigaldo F, Battaglia D, Re D, Giannì AB.
Digital device in postextraction implantology: a clinical case
presentation. Case Rep Dent 2014;2014:327368.
73. Sübay RK, Sübay MO, Balkaya CM. Intentional replantation
of a mandibular canine with multiple iatrogenic endodontic
complications. Oral Health Dent Manag 2014 Sep;13(3):811-814.
74. Peñarrocha-Diago MA, Aloy-Prósper A, Peñarrocha-Oltra
D, Peñarrocha-Diago M. Replantation of a maxillary second
molar after removal of a third molar with a dentigerous cyst:
case report and 12-month follow-up. J Clin Exp Dent 2014
Apr 1;6(2):e185-e188.
75. Asgary S, Nosrat A. Concurrent intentional replantation of
maxillary molars using a novel root-end filling. Gen Dent
2014 May-Jun;62(3):30-33.
76. Montoya-Salazar V, Castillo-Oyagüe R, Torres-Sánchez C,
Lynch CD, Gutiérrez-Pérez JL, Torres-Lagares D. Outcome of
A Radiographic Classication for Retrograde Peri-implantitis
The Journal of Contemporary Dental Practice, April 2016;17(4):313-321 321
JCDP
single immediate implants placed in post-extraction infected
and non-infected sites, restored with cemented crowns: a
3-year prospective study. J Dent 2014 Jun;42(6):645-652.
77. Yamazaki S, Arakawa H, Maekawa K, Noda K, Hara
ES, Minakuchi H, Sonoyama W, Matsuka Y, Kuboki T.
A retrospective comparative 8-year study of cumulative
complications in teeth adjacent to both natural and implant-
supported fixed partial dentures. Int J Prosthodont 2013
May-Jun;26(3):260-264.
78. Kim JE, Shim JS, Huh JB, Rim JS, Lee JY, Shin SW. Altered
sensation caused by peri-implantitis: a case report. Oral Surg
Oral Med Oral Pathol Oral Radiol 2013 Jul;116(1):e9-e13.
79. Sun CX, Henkin JM, Ririe C, Javadi E. Implant failure
associated with actinomycosis in a medically compromised
patient. J Oral Implantol 2013 Apr;39(2):206-209.
80. Chou YH, Du JK, Chou ST, Hu KF, Tsai CC, Ho KY, Wu YM,
Ho YP. An interdisciplinary treatment approach combining
orthodontic forced eruption with immediate implant
placement to achieve a satisfactory treatment outcome: a case
report. Clin Implant Dent Relat Res 2013 Feb;15(1):113-120.
81 . Krithika C, Kota S, Gopal KS, Koteeswaran D. Mixed periapical
lesion: differential diagnosis of a case. Dentomaxillofac Radiol
2011 Mar;40(3):191-194.
82. Park JB. Healing of extraction socket grafted with deproteinized
bovine bone and acellular dermal matrix: histomorphometric
evaluation. Implant Dent 2010 Aug;19(4):307-313.
83. Bornstein MM, Wiest R, Balsiger R, Reichart PA. Anterior
Stafne’s bone cavity mimicking a periapical lesion of endodontic
origin: report of two cases. J Endod 2009 Nov;35(11):1598-1602.
84. Tyndall DA, Rathore S. Cone-beam CT diagnostic applica-
tions: caries, periodontal bone assessment, and endodontic
applications. Dent Clin North Am 2008 Oct;52(4):825-841.
85. Casado PL, Donner M, Pascarelli B, Derocy C, Duarte ME,
Barboza EP. Immediate dental implant failure associated with
nasopalatine duct cyst. Implant Dent 2008 Jun;17(2):169-175.
86. Schwartz-Arad D, Levin L. Post-traumatic use of dental
implants to rehabilitate anterior maxillary teeth. Dent
Traumatol 2004 Dec;20(6):344-347.
87. Eratalay K, Demiralp B, Akincibay H, Tözüm TF. Localized
edentulous ridge augmentation with upside down osteo-
tomy prior to implant placement. Dent Traumatol 2004
Oct;20(5):300-304.
88. Reiser GM, Manwaring JD, Damoulis PD. Clinical significance
of the structural integrity of the superior aspect of the
mandibular canal. J Periodontol 2004 Oct;75(2):322-326.
89. Bencharit S, Schardt-Sacco D, Zuniga JR, Minsley GE. Surgical
and prosthodontic rehabilitation for a patient with aggressive
florid cemento-osseous dysplasia: a clinical report. J Prosthet
Dent 2003 Sep;90(3):220-224.
90. Hosny M, Duyck J, van Steenberghe D, Naert I. Within-subject
comparison between connected and nonconnected tooth-
to-implant fixed partial prostheses: up to 14-year follow-up
study. Int J Prosthodont 2000 Jul-Aug;13(4):340-346.
91. Horton RA, Ludlow JB, Webber RL, Gates W, Nason RH Jr,
Reboussin D. Detection of peri-implant bone changes with
axial tomosynthesis. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 1996 Jan;81(1):124-129.
92. Kenney EB, Lekovic V, Han T, Carranza FA Jr, Dimitrijevic B.
The use of a porous hydroxylapatite implant in periodontal
defects. I. Clinical results after six months. J Periodontol 1985
Feb;56(2):82-88.
93. Kwon EY, Cho Y, Lee JY, Kim SJ, Choi J. Endodontic treat-
ment enhances the regenerative potential of teeth with
advanced periodontal disease with secondary endodontic
involvement. J Periodontal Implant Sci 2013 Jun;43(3):
136-140.
94. Tözüm TF, Sençimen M, Ortakoğlu K, Ozdemir A, Aydin
OC, Keleğ M. Diagnosis and treatment of a large periapical
implant lesion associated with adjacentnatural tooth: a case
report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
2006 Jun;101(6):e132-e138.
95. Jung RE, Zaugg B, Philipp AO, Truninger TC, Siegenthaler
DW, Hämmerle CH. A prospective, controlled clinical trial
evaluating the clinical radiological and aesthetic outcome after
5 years of immediately placed implants in sockets exhibit-
ing periapical pathology. Clin Oral Implants Res 2013 Aug;
24(8):839-846.
96. Nair PN. Pathogenesis of apical periodontitis and the causes
of endodontic failures. Crit Rev Oral Biol Med 2004 Nov 1;
15(6):348-381.
... Different systems for classification of retrograde periimplantitis were proposed. The classification could be based on: radiographic findings [2,3]; etiology [4]; nature of the lesion [5] or its evolution [6]. According to the radiographic findings, the retrograde peri-implantitis is classified into three classes, depending on the amount of bone resorption in the apical portion of an implant, visible on radiography. ...
... According to the radiographic findings, the retrograde peri-implantitis is classified into three classes, depending on the amount of bone resorption in the apical portion of an implant, visible on radiography. The bone loss was presented as a percentage of the entire length of the implant, according to which the lesion is classified into one of the following classes [2]:  mild  moderate  advanced Shah et al. [3] concluded, that this classification is reliable and useful, providing options for a treatment plan and for prognosis. ...
... All of the proposed classification models [2,4,5,6] differed significantly from one another. In the majority of the studies similar symptoms were reported, including pain, apical radiolucency [ 7,8,9,10,11] and fistula formation [12,13,14]. ...
Article
Full-text available
Introduction: The retrograde peri-implantitis is a condition, that is not very common, but threatens seriously the implant survival. Aim: The aim of this review was to summarize the basic data about the retrograde peri-implantitis and clarify the causes and treatment options for the condition. Material and Methods: The review includes articles in English language, which were published in the period of 1992 to 2019. Articles, which were directly related to the topic were selected, as the search was conducted using the following combinations of keywords: "retrograde peri-implantitis", "implant periapical lesion", "apical peri-implantitis". Results: In the different articles the condition was termed three different ways: retrograde peri-implantitis, implant periapical lesion and apical peri-implantitis. The selected articles described different classification systems, etiological factors and treatment options. Conclusion: Unified classification system for retrograde peri-implantitis combining all the available classification models should be considered. Various factors could lead to development of implant periapical lesion, as the most important remains the infectious component. The treatment plan in the cases of retrograde peri-implantitis depends on the evolution stage of the disease, considering the clinical and radiological findings.
... In these cases, if the periapical radiolucency is less than 50% of the implant length, the clinician must ensure that the stability of the implant has not been compromised. 20 The most studied treatment of implant periapical lesions with no associated implant mobility is implant apical surgery. 33 pathways and destroys bone around the implant apex; once the drainage pathways are created a subacute or chronic apical periimplantitis is established. ...
... Depending on the progress of the process the implant may be mobile, and a peri-implant bone destruction along the body of the implant may be seen in the radiograph and should be classified in regard to the implant length. The author suggests classifying the amount of peri-implant bone loss in correlation to the implant length according to Shah et al. 20 The clinician must be careful when making this assessment because 2-dimensional (2D) periapical radiographs do not always show the actual size of an intrabony defect. These kinds of defects can be identified only when the junctional area is involved. ...
... If the lesion shows no sign of resolution or shows signs of progressing, it should at this point be managed as a primary apical implant lesion. 20 Resection of the implant allows for the complete removal of the lesion and the contaminated implant surface while leaving enough integrated implant length to support the restoration and the stability of the implant. It is crucial to treat the implant before the lesion spreads coronally. ...
Article
Full-text available
Retrograde peri-implantitis (RPI) is a primary microbial inflammatory condition that affects only the apical portion of an osseointegrated implant, which retains normal bone-to-implant contact in its coronal portion. Currently, no uniformly accepted definition or classification exists for RPI. This article reviews the etiopathological mechanisms, diagnostic pattern, and current treatment modalities for this type of periapical implant bone loss. The prevalence of RPI is reported to be relatively low, and along with a lack of an accepted classification system there is no widely accepted treatment algorithm. Therapeutic options include antibiotics, open-flap implant debridement, and apical resection eventually including apicoectomy of endodontically affected adjacent teeth, with or without bone grafting or removal of the affected implant. Implants with RPI usually remain osseointegrated. A diagnostic approach is proposed.
... Shah et al. classified retrograde implantitis into 3 classes. 43 It is defined as a clinically symptomatic periapical lesion that develops within the first few after implant insertion while the coronal portion of the implant sustains a normal bone to the implant interface. ...
... 51 Shah et al. in 2016 gave a simpler classification of retrograde peri-implantitis. 43 Vanden Bogaerde described the bone defects as closed and open. 31 It is the simplest classification but it lacks important information due to its broad approach. ...
Article
Full-text available
The cases of peri-implantitis are soaring rapidly in the current scenario. It is very important to have adequate knowledge about the etiology, pathogenesis, clinical features, radiological features, and treatment of peri-implantitis. In this context, the classification of the disease is of utmost importance for planning and execution of the treatment. Various classifications have been proposed over the years and with each classification, more information is being added and there is a lack of universal acceptance of a single classification. Clinical errors may be anticipated due to miscommunication and misguidance. Thus, it is important to sensitize the clinicians about different classification systems. This review attempts to compile and critically analyze existing classification systems of peri-implant diseases. Keywords: Dental implants; diagnosis; peri-implantitis.
... The "symptomatic T-1 lesion" is Sussman's "type I infection pattern." The PRI classification system was used in treatment planning and determination of prognosis in IPL based on the "bone loss/implant length" (in percentage) on periapical radiographs, which includes the following classes: mild-Class I (bone loss < 25%), moderate-Class II (bone loss 25% to 50%), and advanced-Class III (bone loss > 50%) [25,55]. Classes I and II lesions resolve completely; however, the prognosis of Class III lesions can range from fair to poor because the >50% bone loss may cause inadequate osseointegration [17,25]. ...
... A surgical approach is chosen based on implant stability and the extension of IPL [1,17,47,55]. Surgical debridement alone or combined with regenerative treatment has been suggested for bone loss <50% of implant length [47]. Resection of the implant apex may be needed in cases with >50% bone loss and with difficulty in accessing the IPL [17,52,65]. ...
Article
Full-text available
Implant periapical lesion (IPL) is an infectious-inflammatory alteration surrounding an implant apex. It is a multifactorial disease that may ultimately cause implant failure. The diagnosis of IPL is based on examination of clinical manifestations and apical radiolucency. Many etiologies have been attributed to IPL, including preexisting microbial pathology and surgical trauma. Moreover, many systems have been used to classify IPL based on different parameters. To date, non-surgical and surgical treatment, as well as removal of failed implants, have been considered to successfully manage IPL. However, prevention of IPL surpasses all modes of treatment. An increased number of IPL cases are expected as implants have become standard for tooth replacement in dentate arches. Therefore, it is necessary to understand IPL more comprehensively. Herein, an introduction to IPL, including its etiology, diagnosis, classification, treatment, and prevention, has been undertaken.
... A clinically symptomatic periapical lesion that develops with in the first few after implant insertion while the coronal portion of the implant sustains a normal bone to the implant interface. 11 Class I -Mild -Extends < 25% of the implant length fron implant apex. ...
Article
Full-text available
The term peri-implantitis is used to describe a destructive inflammatory process affecting the soft and hard tissues around osseo integrated implants, leads to the formation of a peri-implant pocket and loss of supporting bone. Predisposing factors are Poor Plaque Control, inflammation, infection, Smoking, Diabetes and Occlusal Overload. It is diagnosed on the basis of clinical and radiographic interpretation and still no definite criteria have been proposed for the diagnosis and treatment of peri-implantitis. However treatment can be both conservative and surgical. The cumulative interceptive supportive therapy protocol serves as good guide for the treatment of the peri-implantitis. There is lack of a standard classification system to differentiate the various degrees of peri-implantitis, which produces dilemma in evaluating the stages clinical and radiological status, treatment and its outcome. Many classification has been proposed in medical literature with their pros and cons but still there is lack of standard classification system of implant defects and definite treatment protocol according to the same. The classification should be easy to use, clearly understandable and help in communication by clinicians of different speciality. This review aimed to introduce a classification system based on added clinical, and detailed radiological parameters with prognosis and staged treatment algorithms.
Article
Dental implant therapy has become the prosthetic standard of care in modern comprehensive dental care. With increase in placement of dental implants, increase in prevalence of peri-implant diseases have also been reported. Two entities are described within the concept of peri-implant diseases; peri-implant mucositis and peri-implantitis. Various etiological factors are responsible for the occurrence of peri-implantitis with bacterial biofilm playing the major role. Appropriate diagnosis and timely management of peri-implant mucositis and peri-implantitis is essential to prevent the implant loss. Variety of treatment modalities are available for management of peri-implantitis which can eliminate the disease progression and enable the restoration of optimal implant function. This narrative review provides insight of the prevalence, etiology, pathogenesis, diagnosis and management of peri-implantitis with emphasis on current evidence.
Chapter
Dental implants have transformed the treatment of partially and completely edentulous patients. Despite their success, dental implants have the potential for biological and mechanical complications. This chapter focuses on the biological aspect of peri-implant disease in both soft and hard tissues. A review of the types of peri-implant diseases, including mucositis, peri-implantitis, and retrograde peri-implantitis, is presented. Their possible etiologies and predisposing factors are reviewed. Also, non-surgical therapeutic clinical treatment modalities, including cleaning and scaling, antiseptics, and the use of antibiotics locally and systemically, are discussed. Surgical resection and regenerative treatment modalities for advanced disease are presented based on the literature’s most recent evidence.
Article
Background: Retrograde periimplantitis (RPI) is the inflammatory disease that affects the apical part of an osseointegrated implant while the coronal portion of the implant sustains a normal bone-to-implant interface. The aim of the current study was to assess the intraexaminer and interexaminer reliability of a proposed new classification system for RPI. Materials and methods: After thorough electronic literature search, 56 intraoral periapical radiographs (IOPA) of implants with RPI were collected and were classified by 2 independent reviewers as per the new classification system into one of the 3-mild, moderate, and advanced-classes based on the amount of bone loss from the apex of the implant to the most coronal part as a percentage of the total implant length. The IOPAs were assessed twice by the same examiners and both were blinded to each other's observations. Results: The intraobserver agreement ranged from 0.85 to 0.91, which falls under the category of almost perfect agreement. The interexaminer agreement was found to be 0.83, also considered as almost perfect agreement. Conclusion: The proposed classification shows good intraexaminer and interexaminer reliability and can be used for treatment planning and prognosis in cases of RPI.
Article
Full-text available
Dental implants may fail to osseointegrate in sites of endodontic failure. This may occur as a result colonization by various anaerobic and facultative bacterial species. If an implant is placed in a site where vegetative bacteria are residing, the implant may fail to integrate if a bacterial colonization proceeds coronally. If the implant apical cortical bone is thin or if there is an apical fenestration the colonization may proceed through the thin or non-existent bone through the covering mucosa relieving inflammatory pressure to create an apical (retrograde) peri-implantitis. Enterococcus faecalis may be a prime culprit in these implant failures. After thorough debridement, the implant may be immediately placed after extraction of an endodontically failed tooth and the patient treated with an appropriate antibiotic. Alternatively waiting for post-extraction healing and subsequent implant placement can be done. Nevertheless either way may allow the formation of bacterial vegetative forms or biofilms. The implant surface may be colonized when the surface is exposed to the bacteria. Thorough debridement is crucial. Nevertheless organisms may persist. Randomized controlled trials are needed to elucidate this issue.
Article
Full-text available
One of the consequences of traumatic injuries is the chance of aseptic pulp necrosis to occur which in time may became infected and give origin to periapical pathosis. Although the apical granulomas and cysts are a common condition, there appearance as an extremely large radiolucent image is a rare finding. Differential diagnosis with other radiographic-like pathologies, such as keratocystic odontogenic tumour or unicystic ameloblastoma, is mandatory. The purpose of this paper is to report a very large radicular cyst caused by a single mandibular incisor traumatized long back, in a 60-year-old male. Medical and clinical histories were obtained, radiographic and cone beam CT examinations performed and an initial incisional biopsy was done. The final decision was to perform a surgical enucleation of a lesion, 51.4 mm in length. The enucleated tissue biopsy analysis was able to render the diagnosis as an inflammatory odontogenic cyst. A 2 year follow-up showed complete bone recovery.
Article
Full-text available
Replacing both missing maxillary anterior teeth is particularly challenging, especially in compromised sockets. This case report describes the management of an 18-year-old female patient, who suffered avulsion of both maxillary central incisors at 7 years of age. This multidisciplinary implant technique, called Immediate Dentoalveolar Restoration (IDR), included extraction of the injured teeth and a single procedure for immediate implant placement and restoration of the compromised sockets after root fracture and periapical lesion development were detected during orthodontic treatment. Successful esthetic and functional outcomes and reestablishment of the alveolar process after bone reconstruction were observed during the 3-year follow-up period. The predictable esthetic outcomes and soft- and hard-tissue stability that can be achieved following IDR are demonstrated.
Article
Full-text available
This report describes a clinical case with an atypical intraoral sinus tract formation from diagnosis and treatment to short-term outcome and definitive prosthetic rehabilitation. In detail, the patient underwent conservative nonsurgical root canal treatment followed by guided bone augmentation of the regions involved in periapical inflammation and sinus tract formation. The removal of the inflammatory source of the lesion as well as the affected tissue clearly led to a healing of the surrounding bone tissues. Subsequently, the tooth was reconstructed using a fibreglass post and a metal-ceramic crown; an implant was successfully placed in the previously inflamed bone region. http://www.ncbi.nlm.nih.gov/pubmed/26064699#
Article
Full-text available
The purpose of the present case report was to describe the surgical treatment of a peri-implantitis lesion associated with a regenerative approach. A 48-year-old patient came to authors’ attention 36 months after the placement of a dental implant (ITI-Bonefit Straumann, Waldenburg, Switzerland) in position 46. A swelling of the peri-implant soft tissues was observed, associated with bleeding on probing and probing depth > 10 mm. A significant peri-implant bone loss was clearly visible on the periapical radiograph. A nonsurgical periodontal supportive therapy was firstly conducted to reduce the inflammation, followed by the surgical treatment of the defect. After mechanical and chemical decontamination with tetracycline solution, a regenerative approach consisting in the application of deproteinized bovine bone mineral (Bio-Oss, Geistlich Pharma AG, Wolhusen, Switzerland) and a collagen membrane (Bio-Gide, Geistlich Pharma AG, Wolhusen, Switzerland) was performed. An antibiotic therapy was associated with the treatment. The 17-year follow-up showed a physiological probing depth with no clinical signs of peri-implant inflammation and bleeding on probing. No further radiographic bone loss was observed. The treatment described in the present case report seemed to show improved clinical results up to a relevant follow-up period.
Article
There has been renewed interest in intentionally placing dental implants in proximity to or in contact with tooth root fragments. In clinical practice, human teeth are usually extracted due to nonrestorable caries, vertical or horizontal root fractures, periodontal disease, or endodontic failure, which is commonly accompanied by inflammation and bacterial contamination. The aim of this case series is to present the adverse effects in humans of clinically undetected root-to-implant contact (CURIC), where implants were unintentionally placed in proximity to undetected retained root fragments. The adverse effects of small (3 to 5 mm) root fragments were detectible 6 to 48 months post implant placement. Three out of seven implants in six patients were removed due to severe coronal bone loss. This differs from retrograde peri-implantitis, where only the apical area of the implant is affected and the coronal portion remains integrated. The detrimental effect of root fragment-to-implant contact is described along with its clinical management. Based on the review of currently relevant data, mixed results have been documented regarding the success of dental implants in proximity to tooth-root fragments. Careful evaluation of long-term, postloading results in humans where hopeless teeth have been extracted due to infection and significant bone loss are required before intentional root fragment retention is considered a safe and reliable clinical option for implant placement.
Article
Immediate implantation has become one of the therapeutic options for replacement of a hopeless tooth. In the case of a tooth with a periapical lesion, this approach remains controversial. The aims of this article were to systematically review the evidence on immediate implants in sites with periapical lesions with reference to: (1) survival rates, (2) changes in crestal bone levels and marginal tissues, (3) complication rates, and (4) comparison of clinical outcomes with other implant treatments. An electronic search was conducted in MEDLINE (PubMed), Cochrane Central Register of Controlled Trials (CENTRAL), and EMBASE for articles published between January 1990 and August 2013. Publications were screened, and data extraction and quality assessment were performed. Implant survival rates were calculated using predicted Kaplan-Meier survival analysis. Crestal bone level changes, soft tissue outcomes, complications, and procedure characteristics were analyzed descriptively. Initially, 301 articles were identified. Three prospective controlled trials of immediate implant placement in sites with periapical lesions with a follow-up period of at least 1 year were selected for the survival analysis. The predicted cumulative 5-year survival rate of immediate implants in sites with periapical lesions was 96.23%. Bone and gingival level changes were comparable to those of implants placed in sites without periapical pathology. The complication rates, reported in only one study, were 15.4% (2/13) in sites with periapical lesions and 6.7% (1/15) in healthy sites. Limited evidence suggests that immediate implant placement in sites with periapical lesions leads to clinical outcomes comparable to those of immediate implants in healthy sites. Additional prospective controlled trials with large sample sizes and long-term follow-up are needed to further investigate these results.
Article
Numerous reports primarily in the implant literature outline the loss of an implant claimed to be as a consequence of endodontic pathosis from an adjacent tooth. This case report outlines the resolution of a large cyst-like periapical lesion that resolved with nonsurgical management when the canal was dressed with calcium hydroxide on 4 occasions because of persistent intracanal exudate. A favorable healing outcome was achieved for the affected tooth and the implant. This report adds to a growing body of evidence to suggest that implant retained crowns are not vulnerable when an endodontic infection occurs in an adjacent tooth. Copyright © 2015 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.
Article
Immediate placement and restoration of the implant is a widely used protocol, but loading of implants in the site which is periapically infected is still not very popular. Very few studies have been conducted and its still in debate. The conventional protocol of placing implant and waiting for it to osseointegrate is time consuming and compromises patients esthetics and psychological comfort. This report presents a case of immediate placement and restoration of implant in the region with periapical infection.
Article
Twenty-five patients with advanced periodontal destruction were used in the study. Following initial therapy, two angular interproximal defects were selected in each patient. During flap surgery a porous hydroxylapatite implant shaped to fit the periodontal defect was placed in one defect, the other defect was used as nonimplanted control. The material used for implantation was a hydroxylapatite replicate of coral from the genus Porites, with a pore size of 190 to 220 μm. Clinical parameters were measured prior to flap surgery for each of the defects. An occlusal acrylic Stent was used to give a stable reference point for pocket depth, attachment level and gingival margin height measurements. Also gingival fluid, gingival inflammation, plaque index and tooth mobility were recorded. Periapical radiographs using a standardized positioning device were also taken. At the time of surgery, the depth of the osseous defect and the height of the alveolar crest were recorded. After 6 months the clinical measurements were repeated and a re-entry surgery was carried out in 15 selected sites. Results showed that the porous implant produced statistically significant reduction in pocket depth, in the depth of osseous lesion, and a statistically significant gain in attachment level, as compared to control areas.