Review Article

Implant–abutment gap versus microbial colonization: Clinical

significance based on a literature review

€
Sheila Pestana Passos,1 Liliana Gressler May,2 Renata Faria,3 Mutlu Ozcan, 4
5
Marco Antonio Bottino
1
Department of Dentistry, University of Alberta, Edmonton, Canada
2
Departament of Restorative Dentistry, Federal University of Santa Maria, Brazil
3
~o Paulo, Brazil
Department of Prosthodontics, Paulista University, Sa
4
Department of Dentistry and Dental Hygiene, Clinical Dental Biomaterials, University of Groningen, Groningen, The
Netherlands
5
Department of Dental Materials and Prosthodontics, Sa ~o Paulo State University, Sa
~ o Jose
 dos Campos, Sa
~o Paulo, Brazil

Received 1 October 2012; revised 18 February 2013; accepted 25 February 2013

Published online 10 May 2013 in Wiley Online Library (wileyonlinelibrary.com). DOI: 10.1002/jbm.b.32945

Abstract: Microorganisms from the oral cavity may settle at
the implant–abutment interface (IAI). As a result, tissue
inflammation could occur around these structures. The data-
bases MEDLINE=PubMed and PubMed Central were used to
identify articles published from 1981 through 2012 related to
the microbial colonization in the implant–abutment gap and
its consequence in terms of crest bone loss and osseointe-
gration. The following considerations could be put forward,
More studies are necessary to clarify the relationship
between leakage at IAI and abutment connection designs; (c)
losses at the peri-implant bone crests cannot be related to
the IAI size, since few studies have shown no relationship.
Also, the microbial leakage at the IAI cannot be related to the
bone crest loss, since there are no articles reporting this rela-
tionship; remains controversial the influence of the IAI posi-
tion on the bone crest losses. V C 2013 Wiley Periodicals, Inc. J

with respect to the clinical importance of IAI: (a) the space Biomed Mater Res Part B: Appl Biomater 101B: 1321–1328, 2013.
present at the IAI seems to allow bacterial leakage to occur,
in spite of the size of this space; (b) bacterial leakage seems Key Words: implant–abutment gap, implant–abutment con-
to occur at the IAI, irrespective of the type of connection. nection, microbial leakage, bone loss, osseointegration

€
How to cite this article: Passos SP, GresslerMay L, Faria R, Ozcan M, Bottino MA. 2013. Implant–abutment gap versus micro-
bial colonization: Clinical significance based on a literature review. J Biomed Mater Res Part B 2013:101B:1321–1328.

INTRODUCTION of the screw to the implant,6 use of silicone to seal the

In spite of the excellent success rates in osseointegrated
implant rehabilitations, failures have been described in the
literature, and related to mechanical and microbiological
factors, frequently acting in association.1,2 In the long term,
the role of microorganisms must be considered in implant
survival. The following are among the factors that may favor
bacterial colonization: poor oral hygiene, pre-existent peri-
odontal disease, implant surface topography, implant design,
and space at the implant–abutment interface (IAI). Bacteria
and their byproducts may cause inflammatory reactions in
the peri-implant soft tissues.3,4
Inevitably, there is a microgap between the implant and
the prosthetic connector. However, artifices can be created
to make the clinical significance of this gap negligible. The
supracrestal position of the interface,5 the adaptation torque
interface,7 and the system design8–10 are the main findings
that can present clinical significance. The occurrence of bac-
terial leakage at the internal surface of implants, through
IAI, is one of the parameters for analyzing the degree of
quality in the fabrication of these connections.
Several studies have demonstrated the occurrence of
bacterial leakage in IAI.7,8,10–15 But to what extent can the
presence of bacteria in this region be related to events such
as loss of height at the bone crest and other undesirable
sequelae of treatment with implants? Are there prosthetic
connection designs that enable bacterial leakage to be
reduced or eliminated? The proposal of this review was to
verify and show what there is in the literature at present to
try to answer these questions. Therefore, a detailed search
was performed by means of relevant databases, such as

Correspondence to: S. P. Passos; e-mail: sheilapestana@hotmail.com

C 2013 WILEY PERIODICALS, INC.

V 1321
MEDLINE=PubMed and PubMed Central. The relevant peer
reviewed studies were searched between 1981 and 2012.
This present review is organized into four parts: bacterial
leakage at the IAI, relationship between leakage at IAI and
abutment connection designs, presence of IAI and losses at
the bone crest, and bacterial leakage 3 osseointegration.
Bacterial leakage at the IAI
In spite of all the efforts as regards technical–scientific de-
velopment of dental implant systems in search of success,
one of the factors causing most concern is IAI. If the inter-
face of the implant with its respective prosthetic connection
is not precise and does not fit adequately, it can have a neg-
ative influence, not only on the prosthesis=implant system
but also on the conditions of the periodontal tissues, pro-
ducing alteration in the clinical and microbiological parame-
ters, because bacterial growth may occur in this area,3,7,16–
20
and compromise the adjacent periodontal tissues.20–26
According to Broggini et al.,27 the precision of the space
in the IAI at the level of the bone crest is associated with
reduction in the accumulation of inflammatory peri-implant
cells and minimum bone loss. Rangert et al.,28 McCartney
et al.,29 and May et al.30 also affirmed that the accurate as-
sembly of implant components and the precision of fit of
the prosthesis to the implant is absolutely essential for the
long-term survival of dental implants and the preservation
of the supporting bone.
The presence of bacteria contaminating the internal por-
tion of osseointegrated implants may result in contamina-
tion of the implant or pillar during the first or second stage
surgery. Contamination may also occur by transmission of
microorganisms from the oral medium after the prosthetic
pillar placement by means of the gap at the IAI.31 Nakazato
et al.32 verified that in 4 h of exposure to the oral medium,
there was bacterial colony formation at the surface of the
prosthetic connecters; therefore there was a possibility of
this occurring at the IAI. Koka et al.33 evidenced subgingival
secondary bacterial colonization 14 days after coupling the
prosthetic connector to the implant.
Both in vitro and in vivo4,7,13,19 studies have demon-
strated contamination of the internal portion of osseointe-
gratable implants by bacteria. Inadequate fit between the
implant and prosthetic pillar may be considered a risk fac-
tor similar to that in poorly adapted dental restorations,
capable of leading to clinical and microbiological alterations
in the peri-implant tissues. Furthermore, because of allow-
ing micromovements of the prosthetic pillar, a lack of fit
between it and the implant presents a biomechanical risk,
since it enables the set to be submitted to undesirable
loads, capable of resulting in loosening or fracturing the
prosthetic screw, or fracturing the implant body.
Callan et al.,34 analyzing the size of the IAI interface,
found mean values between 30 mm and 135 mm; Dellow
et al.35 between 0 and 7.15 mm; and Jansen et al.7 between
1 mm and 10 mm. Due to the existence of the interface, the
possibility of fluid and microorganism exchanges is very evi-
dent. For Jansen et al.,7 the presence of these spaces at the
IAI located at the bone crest level is inevitable, and implant
1322 PASSOS ET AL.
systems are not capable of preventing a possible microbial
colonization of this interface. In histologic studies, van Win-
kelhoff et al.36 and Quirynen et al.37 verified that there is an
inflammatory cell infiltrate at the IAI junction, even in
implants with adequate biofilm control and clinically
healthy soft tissue.
The IAI can allow the passage of fluids and bacteria,
irrespective of the implant system (with tapered or flat con-
nections). Even well fitting interfaces (smaller than 5 mm)
were incapable of preventing bacterial leakage and coloniza-
tion of internal implant surfaces. A large variety of microor-
ganisms appears to have the ability to penetrate at the IAI
and reach the inside of implants, ranging from Gram-posi-
tive coccus to Gram-negative rods. Streptoccocus sanguis
presents a mean size ranging between 0.8 mm and 1 mm
and Escherichia coli presents a mean size ranging between
1.1 mm and 1.5 mm in diameter and 2 mm and 6 mm in
length, being considered of medium size in comparison with
the oral microflora. These characteristics enable bacterial
leakage at interfaces with maladaptations within the values
described in the literature.7
Quirynen and van Steenberghe17 in an in vivo study,
proved bacterial leakage in the internal components of the
Brånemark system. When examining the most apical part of
prosthetic connector screws submitted to microbiological
analysis after 3 months, in nine patients, the author verified
the presence of bacteria in all the samples, with 86.2%
being coccus; 12.3%, nonmobile rods and 1.5%, spirochetes
and others. To these authors, microleakage at the IAI was
the most probable origin of this contamination.
Various authors have studied measurement of the IAI
gap, in an endeavor to correlate the increase in space with
the possibility of grater bacterial leakage. Jansen et al.7 com-
pared the size of the spaces and proportion of contamina-
tion. They found no statistically significant correlation
between the size of these spaces (means), determined by
scanning electronic microscopy, and the proportion of leak-
age, by means of the microbiologic test. Some implants
were in accordance with this trend, while others that had
low maladaptation means obtained a high contamination
index, when the tapered prosthetic connection was used.
Guindy et al.3 determined bacterial leakage with Strepto-
R
coccus aureus between Ha-TiV implants and prefabricated
crowns in the region of the marginal gap and the screw.
The experiments were performed under two conditions:
with the crown-implant set either completely or partially
immersed (up to the IAI) in a medium. Bacterial leakage
was observed in 48 h, when the specimens were completely
immersed, and in 120 h when partially immersed. The
transversal screw allowed faster leakage, but in 120 h (5
days) all the systems presented leakage. For other authors,
this delay in marginal leakage that occurred, in comparison
with leakage through the screw cannot be considered clini-
cally relevant.
The gap in IAI is found in all the implant systems stud-
ied in the literature. Its clinical significance is frequently
ignored by professionals that use the connectors without
applying the due torque indicated by the manufacturer. The
IMPLANT–ABUTMENT GAP VERSUS MICROBIAL COLONIZATION

importance of the ideal torque used on the screw that
retains the prosthetic connector must be taken into consid-
eration, since it could interfere in the size of the microspace
of the IAI.6,38,39 According to Weiss et al.,39 the repeated re-
moval and placement of the connectors while the prosthesis
is being made could alter the surface of the screw threads
and the internal parts of the implant, causing progressive
loss of the recommended torque, favoring an increase in IAI.
Goheen et al.38 observed that the manual torque was three
times lower than the mechanical torque, and could favor an
increase in IAI, allowing a two-directional exchange of fluids
and bacteria between the implant and peri-implant tissues.
In a leakage study using dye at the IAI of five implants
available on the market and varying the torque (10 Ncm
and 20 Ncm), Gross et al.6 observed a gradual increase in
microleakage with the passage of time for all implant sys-
tems. Microleakage diminished significantly with an increase
in torque in all the systems. The results indicated that fluids
and molecules are capable of passing through the interface
of all the implant=prosthetic pillar sets studied. The authors
suggested the bacterial by-products and nutrients required
for bacterial growth could equally pass through this space,
contributing to the malodor and peri-implantitis observed
clinically.
Relationship between leakage at IAI and abutment
connection designs
In rehabilitations with implants, external prosthetic connec-
tions of the external hexagon type, and internal connections,
such as hexagonal, tapered (Morse Cone), or both in combi-
nation are basically used. Tapered connections appear to
have superior stability when compared with the external
hexagon type.39,40 According to Dibart et al.,9 the frictional
connection of a tapered pillar consists of a cold, metal-to-
metal solder, creating sealing, making the IAI very narrow
for the passage of bacteria.
Prosthetic connections with better capacity to seal the
IAI have been investigated in order to eliminate bacterial
leakage. Cemented pillars,1 varnish containing 1% chlorexi-
dine,12,41 silicon sealant,41 and the silicone ring7 have been
assessed. The authors verified that cement-retained
implant–abutments offer better results relating to fluid and
bacterial permeability compared with screw-retained
implant–abutments.1 Besimo et al.12 observed no contami-
nation until 11 weeks at the internal surface of implants
when chlorexidine varnish was applied at the IAI, in internal
hexagonal connection; however, Duarte et al.41 when assess-
ing varnish containing 1% chlorexidine and a silicone seal-
ant, verified that these materials were incapable of
preventing bacterial leakage.
Jansen et al.7 assessed microbial penetration at the IAI
in thirteen different prosthetic implant-pillar combinations
(Table I). In the majority of cases, leakage was observed in
the first 2 days. At the end of the assessment period, from
16 (for Frialit-2, with silicone ring application) to 100% (for
calcitek and Ha-Ti with “crown” base) of the samples had
allowed E. coli to go out to the culture medium through the
IAI. Ankylus (tapered connection) presented 50% of the
JOURNAL OF BIOMEDICAL MATERIALS RESEARCH B: APPLIED BIOMATERIALS
REVIEW ARTICLE
samples with microleakage. There was no significant corre-
lation (r2 5 0.44) between the gap size and the proportion
of contaminated implants. Silicone ring application in the
Frialit-2 system enabled a reduction in microleakage.
Dibart et al.9 tested the sealing capacity of the locking
R
taper connection of the BiconV System. Both in the scanning
electronic microscopy test and in the assessment of bacte-
rial growth in agar nutrient, the locking taper system dem-
onstrated sealing and absence of bacteria at the IAI junction
which, according to the authors, was due to the reduced
size of the gap at the IAI, which presented a height of <0.5
mm. According to these authors, the locking of the tapered
type prosthetic pillar was shown to be hermetic to bacterial
invasion at the IAI.
Possible prosthetic connections on implants that attest
to elimination or diminishment of the microgap could col-
laborate and prevent the accumulation of pathogens in the
peri-implant chamber and contact surface at the IAI.7,9,42,43
Pautke et al.43 developed a new design of abutments dem-
onstrating that dental implants fabricated with gap-free
abutments using a shape memory alloy showed significantly
reduced bacterial leakage versus conventional implants.
Bacterial colonization in the internal portion of osseoin-
tegrated implants, due to leakage, was demonstrated in vari-
ous systems,1,3,4,7,8,10,11,17,44–46 except few studies, in which
conic locking,9 internal conical connection,47 cemented con-
nection47 and internal hex with chlorhexidine varnish12
were shown to be hermetic with regard to bacterial inva-
sion in vitro.
Presence of IAI and losses at the bone crest
Bone loss around implants is expected in the first year of
function. Jung et al.48 observed alveolar bone loss during
the first year after adapting the prosthetic connector to the
implant. Bone loss was measured by means of periapical ra-
diographs and changes in bone density by the digital sub-
traction method. The largest quantity of bone lone around
implants occurred in the first 3 months, stabilizing at the
level of the first thread. Adell et al.49 followed up two-stage
implants for 15 years and related a mean marginal bone
loss of 1.2 mm as from the period of cicatrization to the
end of the first year in function. Nonsubmersed implants
also demonstrated bone loss in the crest region, with
greater loss in the maxilla than in the mandible.50 Some
possible etiologies for this bone loss around implants have
been suggested, such as surgical trauma, occlusal overload,
peri-implantitis, reformulation of the biologic space and
presence of gap at the IAI interface.51 Another factor that
can influence bone reabsorption around implants is
repeated connections and disconnections of prosthetic pil-
lars that may also lead to marginal recession.52
According to Quirynen et al.,2 the bone crest loss associ-
ated with dental implants is directly related to the existence
of IAI at the alveolar crest, which could favor the mainte-
nance of a chronic inflammatory process in the area, due to
the accumulation of bacteria.
Peri-implant bone loss may lead to proportional gingival
recession,27,53 such as occurs in natural dentition.54
| OCT 2013 VOL 101B, ISSUE 7 1323
TABLE I. Microbial Leakage Trough the Implant–Abutment Interface (IAI) in Different Connection Designs
Percentage of
Microorganism Microleakage in the
Implant–Abutment Connection Used in the IAI (Total Number Time of
Authors (Year) Implant System Design IAI Widtha Research of Assemblies) Incubation

Jansen et al. Ankylus, Degussa, Frankfort, Germany Conical About 4 mmb Escherichia coli 50 (16) 14 days
(1997)7
Jansen et al. Astra, Astra tech, Mo
€ ndal, Sweden Conical <1 mmb Escherichia coli 69 (16) 14 days
(1997)7
Jansen et al. ITI Bonefit, Straumann, Waldenburg, Conical <1 mmb Escherichia coli 96 (23) 14 days
(1997)7 Switzerland
Jansen et al. ITI Bonefit, Straumann, Waldenburg, Octa abutment, flat (slightly About 5 mmb Escherichia coli 75 (16) 14 days
(1997)7 Switzerland angulated) interface
Jansen et al. Branemark, Nobel Biocare, Go€ teborg, Sweden External hex flat About 5 mmb Escherichia coli 82 (17) 14 days
(1997)7
Jansen et al. Integral Omniloc, Calcitek, Carlsbad, EUA External hex flat About 4 mmb Escherichia coli 100 (17) 14 days
(1997)7
Jansen et al. Frialit-2, Friatec, Mannheim, Germany Flat with silicon washer About 1 mmb Escherichia coli 16 (19) 14 days
(1997)7
Jansen et al. Frialit-2, Friatec, Mannheim, Germany Flat without silicon washer About 2 mmb Escherichia coli 72 (18) 14 days
(1997)7 (standard)
Jansen et al. Ha-Ti crown base, Mathys, Bettlach, Flat 1 conical at the inside About 5 mmb Escherichia coli 100 (17) 14 days
(1997)7 Switzerland
Jansen et al. Ha-Ti telescopic post, Mathys, Bettlach, Flat About 5 mmb Escherichia coli 88 (17) 14 days
(1997)7 Switzerland
Jansen et al. IMZ with TIE, Interpore International, Irvine, Flat About 5 mmb Escherichia coli 68 (19) 14 days
(1997)7 EUA
Jansen et al. IMZ with IMC insert, Interpore International, Flat About 2 mmb Escherichia coli 38 (21) 14 days
(1997)7 Irvine, EUA
Jansen et al. Semados, Bego Semados, Bremen, Germany Flat (slightly angulated) About 2 mmb Escherichia coli 42 (19) 14 days
(1997)7
Guindy et al Ha-Ti, Mathys, Bettlach, Switzerland Internal hex – Staphylococcus aureus 100 (30) 120 h
(1998)3
Besimo et al. Ha-Ti, Mathys Corporation, Bettlach, Internal hex with chlorhexidine – Staphylococcus aureus 0 (30) 3–11 weeks
(1999)12 Switzerland varnish
Dibart et al. Bicon, Bicon, Boston, EUA Locking taper (1.5 tapered) <0.5 mm Actinobacillus 0 (9) 24–72 h
(2005)9 actinomycetemcomi-
tans, Streptococcus
oralis and Fusobacte-
rium nucleatum
mixture
Steinebrunner Branemark, Nobel Biocare, Go
€ teborg, Sweden External hex – Escherichia coli 100 (8) 12,00,000 cycles
et al. (2005)8
Steinebrunner Frialit-2, Friatec, Mannheim, Germany Guide rod with integrated hex – Escherichia coli 100 (7) 12,00,000 cycles
et al. (2005)8 and silicon washer
Camlog, Wurmberg, Germany – Escherichia coli 100 ((8) 12,00,000 cycles
TABLE 1. Continued
Percentage of
Microorganism Microleakage in the
Implant–Abutment Connection Used in the IAI (Total Number Time of
Authors (Year) Implant System Design IAI Widtha Research of Assemblies) Incubation

Steinebrunner “Tube in tube” with cam slot

et al. (2005)8 fixation
Steinebrunner Replace Select, Nobel Biocare, Go
€ teborg, “Tube in tube” with cam slot – Escherichia coli 100 (8) 12,00,000 cycles
et al. (2005)8 Sweden fixation
Steinebrunner Screw-Vent, Zimmer Dental, Carlsbad, EUA Internal hex with friction – Escherichia coli 100 (8) 12,00,000 cycles
et al. (2005)8 fit=tapered
Duarte et al. Master Screw (Conexa ~ o, Brazil; Titamax (Neo- External hexagonal 8.19–9.30 mm Enterococcus faecalis 100 (5) 63 days
(2006)41 dent Brazil); EX (Serson, Brazil); Titanium Fix
(ASTechnology, Brazil)
D’Ercole et al. Cone Morse, Dentoflex, Sa ~o Paulo, Brazil Tapered – Pseudomonas 60 (5) 28 days
(2011)11 aeruginosa
D’Ercole et al. Cone Morse, Dentoflex, Sa
~o Paulo, Brazil Tapered – Aggregatibacter
(2011)11
actinomycetemcomitans 40 (5) 28 days
D’Ercole et al. Internal hex, Dentoflex, Sa
~ o Paulo, Brazil Internal hex – Pseudomonas 80 (5) 28 days
(2011)11 aeruginosa
D’Ercole et al. Internal hex, Dentoflex, Sa
~ o Paulo, Brazil Internal hex – Aggregatibacter
(2011)11
actinomycetemcomitans 80 (5) 28 days
Koutouzis et al. ANKYLOS Fixtures, DENTSPLY Friadent, Internal Morse-taper – Escherichia coli 7 (14) 5,00,000 cycles
(2011)10 Mannheim, Germany connection
Koutouzis et al. Straumann, Basel, Switzerland Four-groove conical internal – Escherichia coli 86 (14) 5,00,000 cycles
(2011)10 connection
Assenza et al. Nobel Biocare, Gothenburg, Sweden Screwed trilobed connection – Pseudomonas 80 (5) 28 days
(2012)47 aeruginosa
Assenza et al. Bone System, Milan, Italy Cemented connection – Pseudomonas 0 (5) 28 days
(2012)47 aeruginosa
Assenza et al. ANKYLOS plus, DENTSPLY Friadent, Mann- Internal conical connection – Pseudomonas 20 (5) 28 days
(2012)47 heim, Germany. aeruginosa
Assenza et al. Nobel Biocare, Gothenburg, Sweden Screwed trilobed connection – Aggregatibacter
(2012)47
actinomycetemcomitans 40 (5) 28 days
Assenza et al. Bone System, Milan, Italy Cemented connection – Aggregatibacter
(2012)47
actinomycetemcomitans 0 (5) 28 days
Assenza et al. ANKYLOS plus, DENTSPLY Friadent, Mann- Internal conical connection – Aggregatibacter
(2012)47 heim, Germany
actinomycetemcomitans 0 (5) 28 days
a
Interface implant–abutment.
b
Values of IAI gap were just presented in a graphic. The exact values could not be seen.
Marginal bone stability is an important factor for the lon-
gevity of implants. Horizontal and vertical bone loss is gen-
erally associated with the presence of space at the IAI and
peri-implant bacterial infection. However, it is very impor-
tant to know about other factors, as well as their etiologies
in determining bone loss.55 Hermann et al.56 concluded that
radiographic and histologic analyses indicated that altera-
tions at the bone crest depend on the characteristics of the
implant surface, presence, absence and location of gap.
Broggini et al.,27 by means of histomorphometric eviden-
ces, showed that an infiltrate of inflammatory cells develops
around implants and could vary according to their design.
In their study, an intense inflammatory cell infiltrate (pre-
dominantly neutrophils) and significant bone loss were
associated with the presence of microgap at the bone crest.
Hermann et al.,19 in a study with dogs, performed histo-
logical and histometric analyses of the bone around
implants with soldered prosthetic pillars or two-stage
implants, with varying microgap sizes (10 mm, 50 mm, and
100 mm). They observed that the changes in the bone crest
were significantly influenced by the possible movements
between the pillars and implants, but not by the size of the
IAI poor adaptation.
King et al.44 conducted a longitudinal study that
assessed the effect of the size of the microgap between the
prosthetic pillar and implant at the bone crest. All implants
remained stable throughout the study. The effects of micro-
gap (varying from 10 mm to 100 mm) and assessment time
were not significant. The authors suggest that the stability
of the implant=prosthetic pillar set determined an important
role at the bone crest level.
The position of implant placement in relation to the al-
veolar crest could play an important role in peri-implant
bone reabsorption.5 A very relevant factor is the location of
IAI in relation to the alveolar crest. King et al.44 showed
that a more apical or coronal position of microgap can
determine an increase or decrease in bone loss. Hanggi
et al.57 demonstrated that the peri-implant bone edge and
the subjacent soft tissues are directly influenced by the api-
cal-coronal position of the implant shoulder, where the
microgaps in IAI are located. Callan et al.34 affirmed that
the location of IAI is of fundamental importance in analyz-
ing the causes of bone crest loss. Hermann et al.,56 Hermann
et al.,19 and Piattelli et al.5 affirmed that if the interface is
positioned on or below the level of the bone crest, one
could expect increased reabsorption in the crest. However,
Todescan et al.,58 observed that the placement of the IAI
below the bone crest did not increase bone reabsorption.
Heydenrijk et al.59,60 also found that the microgap did not
appear to influence the establishment of microflora or bone
loss.
Bacterial leakage X Osseointegration
Tonetti and Schimid61 conducted a literature review with
regard to pathogenic processes that lead to osseointegration
failures. The late failures that occurred after osseointegra-
tion was established were classified into disturbances of
biomechanical equilibrium (overload) and alterations in the
1326 PASSOS ET AL.
host–parasite equilibrium (infection). The stability of
osseointegration depends on a dynamic equilibrium in bio-
mechanical terms, and on interaction between the host–
parasite.
Covani et al.13 demonstrated intense bacterial coloniza-
tion at the IAI of implants that failed and were removed
several years after they had been placed. The majority of
these bacteria were cocci and filaments, which were
adhered to the implant surface in a perpendicular orienta-
tion to their long axes. Numerous microorganisms were
found in the peri-implant tissues; in these areas there were
filaments, rods and spirochetes.
According to Ceruti et al.,62 to reduce the effects of this
gap on peri-implant soft tissue stability, several options are
available: supracresta fixture positioning, reduction of the
fixture–abutment gap, and minimizing the prosthetic steps.
CONCLUSION
Based on the scientific literature produced up to the present
time, the following considerations could be established with
respect to the clinical significance of bacterial leakage at the
IAI:
 the space present at the IAI seems to allow bacterial leak-
age to occur, in spite of the size of this space;
 bacterial leakage seems to occur at the IAI, irrespective
of the type of connection. However, three in vitro studies
with tapered connection,33 internal hexagonal connection
treated with a chlorhexidine varnish35 and cemented con-
nection47 related to the absence of bacterial leakage at
this interface. More studies are necessary to clarify the
relationship between leakage at IAI and abutment con-
nection designs;
 losses at the peri-implant bone crests cannot be related
to the IAI size, since few studies have shown no relation-
ship. Also, the microbial leakage at the IAI cannot be
related to the bone crest loss, since there are no articles
reporting this relationship; remains controversial the
influence of the IAI position on the bone crest losses.
 although there are supposition of the relationship
between IAI gaps to microbial leakage and plaque accu-
mulation, crest bone loss and loss of osseointegration,
there are no evidences to prove these ideas.
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