JPOR-286; No.

of Pages 9

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Available online at www.sciencedirect.com

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journal homepage: www.elsevier.com/locate/jpor

Review

Soft tissue sealing around dental implants based

on histological interpretation

Ikiru Atsuta DDS, PhD*, Yasunori Ayukawa DDS, PhD,

Ryosuke Kondo DDS, PhD, Wakana Oshiro DDS, PhD,
Yuri Matsuura DDS, Akihiro Furuhashi DDS, PhD,
Yoshihiro Tsukiyama DDS, PhD, Kiyoshi Koyano DDS, PhD
Section of Implant and Rehabilitative Dentistry, Division of Oral Rehabilitation, Faculty of Dental Science, Kyushu
University, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan

article info abstract

Article history: Purpose: The aim of this study was to provide an overview on the biology and soft tissue
Received 19 March 2015 sealing around dental implants and teeth.
Received in revised form Study selection: This is a narrative review performed through scientific articles published
3 June 2015 between 1977 and 2014, indexed in MEDLINE and PubMed databases. The study selected
Accepted 3 July 2015 articles that focused on epithelial sealing around dental implant or teeth with cell biology
Available online xxx and histology of soft tissue.
Results: Implant therapy has been widely applied in dental rehabilitation for many years,
Keywords: with predictable long-term results. The longevity and functionality of dental implants is
Dental implant dependent on both osseointegration around the implant body and the establishment of a
Oral epithelial mucosa soft tissue barrier that protects the underlying hard tissue structures and the implant
Soft tissue sealing itself. The health and stability of the peri-implant mucosa also affects the esthetics of
the implant. The healing and maintenance of the epithelial and connective tissues
around implants are increasingly recognized as being fundamental to implant success.
However, there has been little research into the function or formation of the soft tissue
seal around dental implants, and the roles of this unique mucosal interface remain
unclear.
Conclusions: This narrative review explores the extent of the current knowledge of soft
tissue barriers around implants from both a basic and clinical perspective, and aims to
consolidate this knowledge and highlight the most pertinent questions relating to this area
of research.
# 2015 Japan Prosthodontic Society. Published by Elsevier Ireland. All rights reserved.

* Corresponding author at: Section of Implant and Rehabilitative Dentistry, Division of Oral Rehabilitation, Faculty of Dental Science,
Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Tel.: +81 92 642 6441; fax: +81 92 642 6380.
E-mail address: atyuta@dent.kyushu-u.ac.jp (I. Atsuta).
http://dx.doi.org/10.1016/j.jpor.2015.07.001
1883-1958/# 2015 Japan Prosthodontic Society. Published by Elsevier Ireland. All rights reserved.

Please cite this article in press as: Atsuta I, et al. Soft tissue sealing around dental implants based on histological interpretation. J Prosthodont Res
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Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
2. Compared with structure of soft-tissue around natural teeth and implants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
2.1. Epithelial tissue around natural tooth and implant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
2.1.1. Epithelial structure around natural tooth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
2.1.2. Epithelial structure around dental implant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
2.2. Interface structure between soft-tissue and tooth/implant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
2.2.1. Structure of the interface between the tooth and gingivae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
2.2.2. Structure of the interface between implant and oral epithelium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
2.2.3. Structure of the interface between the implant and connective tissue. . . . . . . . . . . . . . . . . . . . . . . . . 000
3. Maintenance of soft-tissue around the dental implant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
3.1. Structure of soft-tissue sealing around implant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
3.2. Maintenance of soft-tissue around implant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
4. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 000

induce pathological changes at the interface between the

1. Introduction
Implant therapy is a superb treatment option for completely
and partially edentulous patients and has become astonish-
ingly widespread. The dental implant is based on the concept
of ‘‘osseointegration’’, a direct and tight binding of the implant
to the bone surface without any interposed tissue, which has
been dramatically improved since Brånemark coined the term
in the late 1960s to describe the fixation of a titanium implant
into bone [1]. Direct contact between the bone and the implant
became a critical factor in implant therapy, and a number of
research have been performed in modifying materials to
achieve better osseointegration [2,3]. Actually, more than
30,000 papers can be retrieved from PubMed when we use
‘‘bone’’ and ‘‘implant’’ as searching phrases (National Center for
Biotechnology Information. PubMed [online] available at: http://
www.ncbi.nlm.nih.gov/pubmed (accessed December 10–11,
2014)) [4]. These studies are mainly aiming at the acceleration
of osseointegration for the reduced treatment period.
However, in long-term clinical studies, the failure rate of
implants was increasing with time [5,6]. It is well known that a
major reason for implant loss is peri-implantitis, a condition
bearing great similarity to periodontal disease [7]. We know
that mechanical stress, including occlusal force [8], is one of
the most famous factors to promote the peri-implantitis, but
the elimination of the suitable stress is too difficult. That is
why recent dental implant research has also focused on the
interface between titanium implants and the surrounding soft
tissues [9,10]. The oral mucosa provides protection to the
periodontal tissue, including alveolar bone, against bacteria
and other deleterious stimuli, but when breached by implant
placement, the continuity of this barrier is disrupted. Namely,
peri-implantitis may caused by the oral epithelium having
only a lower capacity to seal tightly around the implant than it
does around a natural tooth [11], despite there being minimal
morphological differences between the peri-implant and
gingival soft tissues [12,13]. Although it may be that immune
system of peri-implant tissue is inferior in local defense to one
of periodontal tissue [14,15], the difference has not been
clarified still now. This advanced inflammation was shown to
implant and surrounding tissue [16], and such inflammation is
well known to induce resorption of the alveolar bone in which
the implant is anchored [17]. The needs of patients are diverse,
and esthetics is an increasingly important demand; implant
treatment must thus not only address occlusal function, but
must do so with satisfactory esthetic results to be counted as a
true success. Management of the soft tissues to achieve these
esthetic results is an issue that cannot be neglected by a
dentist, but there is a deficit in our understanding of the
biology and mechanisms of soft tissue sealing around
implants that limits our ability to guarantee high implant
stability and esthetics under oral conditions for a long term.
In vivo and in vitro investigations can help to understand the
structural, functional and molecular properties of the biologi-
cal seal and the defence mechanisms acting at the interface
between the peri-implant mucosa and dental implants [18,19].
Histological analysis of in vivo animal models is a standard
method for investigating the mechanisms that govern the
implant-soft tissue interface [20–22]. However, data on peri-
implant tissues derived from human subjects are scarce
because of the limited opportunity and ethical issues
associated with collecting these tissues [18,23,24]. This review
collects the evidence from human clinical studies and recent
animal studies to define the morphological and functional
features of the soft tissue surrounding dental implants, with
emphasis on the interface between the implant and the peri-
implant mucosal epithelium, to clarify the relevance of this
interface to the successful day-to-day clinical application of
titanium implants.
2. Compared with structure of soft-tissue
around natural teeth and implants
2.1. Epithelial tissue around natural tooth and implant
2.1.1. Epithelial structure around natural tooth
The gingival epithelium is composed of three types of
epithelium: junctional epithelium (JE), oral sulcular epithelum
(OSE), and oral epithelium (OE) [25] (Fig. 1). The JE around a

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Fig. 1 – Landmarks of peri-implant and periodontal tissue. Diagram shows the key landmarks of the soft tissue attachment
to natural tooth tissue (left panel) and their functional equivalents in the soft tissue attachment to an implant surface (right
panel). (JE: junctional epithelium, OSE: oral sulcular epithelium, OE: oral epithelium, PIE: peri-implant epithelium, PISE:
peri-implant sulcular epithelium).

natural tooth is characterized by a wide intercellular space,
because JE is a non-keratinized epithelium that has only weak
cell-to-cell contacts and is affected by exogenous factors.
Therefore, JE has several unique and original defence
structures: (1) endocytosis and decomposition of exogenous
factors by neutrophils with chemotactic activity in the JE;
(2) self-cleansing and anti-bacterial action of the gingival
crevicular fluid; (3) exfoliation of the JE cell layer; and
(4) endocytosis and decomposition of exogenous factors by
the JE itself [26,27].
The oral cavity is constantly exposed to attack from
physical, chemical and bacterial insults. OE is a thick mucosal
epithelium that protects hard- and soft tissues from exoge-
nous stimulation. However, penetration of the teeth through
the OE into the oral cavity compromises this barrier, so the
gingiva must form a strong impenetrable bond with the tooth
surface in order to maintain the protection of the submucosal
tissue. This seal around the tooth extends from the bottom of
the OSE to the top of the alveolar bone and comprises both
epithelial and connective tissue components (Fig. 1). The
attachment structure is usually 2 mm in width and is termed
the ‘‘biologic width’’. Approximately 0.5–1 mm of this width
is JE, a stratified squamous epithelium that attaches to the
cervical enamel layer in younger generations, and moves
progressively to the cementum layer around the tooth root as
patients age [28]. Chronic inflammation of the periodontal
tissue destroys these adhesion structures, allowing disease to
spread easily to the periodontal tissue.
2.1.2. Epithelial structure around dental implant
The mucosa surrounding implants also forms a seal that is
comparable to the JE. This peri-implant junction is composed
of three types of epithelium: peri-implant epithelium (PIE),
peri-implant sulcular epithelium (PISE), and oral epithelium
(OE) [28–30] (Fig. 1). In addition, there is a biologic width of 3–
4 mm around implant, slightly longer than that around natural
tooth [21]. The PIE performs a similar epithelial attachment
function to the JE, and forms from the OE within 2–3 weeks after
implantation. Morphologically, PIE is composed of a thin layer of
3–4 cells, and has immunoglobulins, neutrophils, lymphocytes
and plasma cells, in a wide intercellular space, which together
protect the underlying tissue from deleterious exogenous
factors [13]. However, despite oral mucosa contacting both
the implant abutment and implant body immediately after
placement, the PIE often ultimately contacts only the implant
body because of on-going bone resorption around the implant
as the implant-abutment interface becomes a cause of
inflammation [21,31] (Fig. 3). Because of the shifting nature of
this bone level, it is challenging to predict the condition of the
gingiva after implant surgery. Furthermore, the PIE has a much
lower functional sealing capacity than JE, despite having very
similar epithelial structures (Fig. 2; middle panels) [11,12,32,33].
The lower adhesion of the OE to titanium seems to be caused by
the electrostatic characteristics of the implant and ion elution
(Fig. 2; right line) [34–36], but the precise reason remains unclear.
2.2. Interface structure between soft-tissue and tooth/
implant
2.2.1. Structure of the interface between the tooth and
gingivae
The JE, which seals the periodontal tissue from the oral cavity,
is surrounded on a basement membrane (BM) comprising two
layers (internal and external basement laminae (IBL and EBL,
respectively)), which are divided into electron-lucent and
electron-dense laminae (the lamina lucida (LL) and lamina
densa (LD), respectively), through which the epithelial cells of
the JE attaches to tooth surface [37,38]. On the enamel side, the
LL connects to the JE cells, an interaction that is reinforced by
hemidesmosomes, epithelial adhesion plaques that tack the
plasma membrane of the epithelial cells to the adjacent LL.
The LD is connected to the enamel [37,38]. The BM forms an
interface between the epithelial and connective tissue [39,40].
At the dento–JE interface, it is visible on an electron micrograph
as a 60–150 nm-wide band of low (LL) and high (LD) electron
density. The BM is composed of structural proteins such as type
IV collagen, fibronectin and laminin [41,42].
The gingival JE is slightly different from the other epithelium,
in that it also has an EBL, which consists of a LL, LD and a
lamina fibroreticularis (sublamina densa). The LL connects to
the basal cells of the JE, reinforced by hemidesmosomes, while
the LD connects to the lamina fibroreticularis [43,44].

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Fig. 2 – Epithelial-sealing structure of peri-implant and periodontal tissue. Middle panels showed that peri-impalnt
epithelium (PIE) (Lower panel) had a structure similar to junctional epithelium (JE) around natural tooth (Upper panel). Both
peri-implant and periodontal tissue were stained by anti-rat Laminin-322 (Ln) g2 chain antibody, and counterstained
lightly with hematoxylin. Ln was scarcely expressed along the upper portion of the implant-PIE interface in light
micrographs. Bar = 20 mm. Electron microscopy was used to show the middle region of the PIE in more detail (Right panels).
Peri-implant tissues were stained for Ln and compared with expression patterns in the JE surrounding a natural tooth.
Bar = 150 nm. Arrows indicate the normal appearance with a dual layer of Ln staining representing the lamina densa and
lamina lucida. Black arrowheads denote regions where this dual layer is not apparent, while white arrowheads indicate
hemi-desmosome-like structures. (JE: junctional epithelium, OSE: oral sulcular epithelium, OE: oral epithelium, PIE: peri-
implant epithelium, PISE: peri-implant sulcular epithelium).

2.2.2. Structure of the interface between implant and oral
epithelium
Previous reports indicate that hemidesmosomes and the IBL
(consisting of the LL, LD, and sublamina lucida) are formed on
apatite, polystyrene, and ceramic substrates [45,46]. However,
few studies have investigated the attachment structures at the
PIE–implant interface. Gould et al. [29] reported that PIE cells
connect to titanium in a similar manner to that JE cells connect
to natural teeth, via the IBL and hemidesmosomes. Donley and
Gillette [47] suggested that the hemidesmosomal attachment
seen between epithelial cells and natural teeth is produced by
epithelial cells close to the implant surface. We have
confirmed this using both light and electron microscopy in
an animal model [11,48]. This in vivo model uses a 4-week
implantation system, where an extracted maxillary first molar
is immediately replaced with a screw-type pure titanium
implant (4 mm in length, 2 mm in diameter). Samples are
collected 4 weeks after placement and analyzed. This model
allows preservation of the implant-soft tissue interface
such that it can be examined at the ultrastructural level
for various cellular features (e.g., microvilli, cytoplasmic
processes, cytoplasmic organelles of epithelial cells, nerve
fibers and terminals, blood vessel components, immune cells)
and epithelial attachment characteristics (basal lamina and
hemidesmosomes) (Fig. 2). The PIE was found not to be
morphologically different when the implant body was placed
immediately after tooth extraction, in comparison to when
placement was delayed by 2 weeks. Furthermore, immuno-
histochemical analysis showed that the process of PIE
formation after implantation was very similar to the processes
seen during oral mucosa healing after tooth extraction [32].
These results suggest that the OE is the origin of the PIE.
Previous papers have also reported that hemidesmosomes
and the IBL (LL and LD) were formed only in the lower region of

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Fig. 3 – Effect of micro-gaps in the peri-implant epithelium on bone formation and resorption. Bone is protected by both
epithelial and connective tissue. After maxillary bone resorption, an epithelial and connective tissue seal is formed on the
bone around the implant, which determines the biological width. (a) Placement of implant to the same level as the
surrounding alveolar bone. (b) Bone resorption, near the micro-gap (which may be a source of infection) creates space for
the peri-implant epithelium to form and bind to the implant surface. (c) On the view of infection prevention, bone around
implant wholly reduced lower than peri-implant epithelium.

Fig. 4 – Locus of collagen fibers and blood vessels in gingivae. (a) Natural tooth has collagen fibers perpendicular to the
cementum surface, whereas around implants, these fibers extend from the bone and run parallel to the implant surface.
(b) Normal periodontal soft tissue is supplied by blood from vessels running both outside the alveolar bone and through the
periodontal ligament; in contrast, the peri-implant tissue has a reduced blood supply as the periodontal ligament source is
not present.

the PIE–titanium interface, in contrast to natural teeth where
the hemidesmosomes and IBL are evident throughout the
JE-tooth interface [13], suggesting the inferior PIE adhesion to
titanium (Fig. 2; right panels). Ericsson and Linde [49] reported
that the resistance to probing offered by PIE was weaker than
that of gingivae around natural teeth, demonstrating that the
PIE-implant connection is much weaker than the JE-enamel
connection. However, in summary, no basic research has
presented any evidences regarding this clinical issue, except
for estimating the amount of adhesion structures by immuno-
staining of adhesion proteins [12].
2.2.3. Structure of the interface between the implant and
connective tissue
In case of natural teeth, the connective tissue attachment is
apical to the JE and resists the physical invasion of bacteria by
providing strong adhesion between the special fibers as
periodontal ligament and cementum, and through compact
type III collagenous fibers. However, around an implant there
are many type V collagenous fibers with resistance to collage-
nase, so peri-implant connective tissue is generally a chronic
inflammatory condition rather than intercept or defence
structure. In addition, the fiber orientation and attachment
patterns of the epithelium to the implant and tooth are
fundamentally different because of the absence of cementum
and periodontal ligament around the implant [30]. In short,
while the fiber orientation in the connective tissue around
natural teeth is perpendicular to the root surface, it runs parallel
to the surface around dental implants [50] (Fig. 4). This weak,
poorly-sealing connective tissue around the implant may
accelerate horizontal recession.
The role of connective tissue around both implant and tooth
is not only for the protection from the extra stimulation as oral
bacteria, but also for the supply of nutrients from the blood
vessel. However, the PIE is also disadvantaged in comparison
with the JE by its limited supply of nutrients. While the
periodontal tissue has ample blood flow from the periodontal
ligament, periosteum, and connective tissue, the blood supply
to peri-implant soft tissue is mainly from the connective tissue
[51] (Fig. 4). In addition, the soft tissue around the implant is
dependent upon the alveolar bone for its blood supply in the
absence of other supporting periodontal tissues [52].
In summary, high quality management of the peri-implant
soft tissues such that they act as a healthy periodontal tissue
is as indispensable as the maintenance of those around a
natural tooth.

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Fig. 5 – Clinical landmarks of the gingivae. Free gingiva is composed of epithelial tissue with an attaching structure. Below
this is the attached gingiva. The diagrams show (a) the front picture of typical healthy gingiva (bar = 1 mm) (b) the cross
section of gingiva penetrated by tooth (c) the clinical front view.

In the normal periodontium, epithelial and connective

3. Maintenance of soft-tissue around the
dental implant
3.1. Structure of soft-tissue sealing around implant
The goal of management for peri-implant tissue depends on
many clinical factors, including the location of implant
placement, the form of the implant abutment, and the clinical
type of gingiva. For example, in a posterior tooth, the
acquisition of attached gingiva is important because effective
cleaning is a high priority and the peri-implant soft tissue
must be able to withstand it. In anterior teeth, esthetics is a
higher priority, so natural gingival form and a healthy color are
the prerequisite properties.
Physiologically, the attached gingiva is a firmly
anchored with oral mucosa that has less mobility, being
tethered to the underlying periosteum by epithelial and
connective tissue attachments (JE and periosto-gingival
fibers, respectively) (Fig. 5). The width of this attached
gingiva varies, even in the same oral cavity; upper and
anterior sites have wider attached gingivae than lower
and posterior sites. It is desirable that the attached
gingiva is clinically at least 3 mm, giving careful consider-
ation to the acquisition of biological width and easy
cleaning [53–55].
tissue attachments with more than 2 mm width are required
above the alveolar bone crest to maintain biologic width,
sulcus depth (0.5–2.0 mm), epithelial attachment (0.5–1.5 mm),
and connective tissue attachment (0.75–2.5 mm) [56]. Peri-
implant tissue has a defence structure that substitutes for
biological width, but this structure is not stable. Clinically,
there is often resorption of the surrounding bone in the
mesiodistal and buccolingual areas around the first thread of
the implant [21,31]. Furthermore, the adhesion structures that
anchor the soft tissue to the implant surface move apically
following bone resorption. Several papers have reported
immediate buccal bone resorption after setting an implant
abutment [57], and that buccal gingival recession of 0.6 mm in
the first year after superstructure placement was common-
place [58]. Therefore, there are a few differences of structure
around between peri-implant and periodontal tissue. For
example, the implant has slightly longer biologic width and
thicker surounding mucosa than the natural tooth [21].
In the case of implants in the anterior sectors, the esthetics
of the implant prosthesis becomes critical to the acceptance of
the implant treatment, a consideration to which soft tissue
control is absolutely fundamental. Indeed, differences in
gingival biotype have a considerable influence on soft tissue
management in implant treatment. Thin gingivae often result
in recession at the mid-buccal surface after superstructure

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journal of prosthodontic research xxx (2015) xxx–xxx
Fig. 6 – Effects of periodontal probing on peri-implant tissue. The periodontal probe can puncture the implant:PIE interface,
causing several disadvantageous effects, as shown.
setting [59,60], and a thin-scalloped gingiva is less likely than a
thick-flat type to achieve normal mucosal height and appear-
ance [61]. As stated above, because peri-implant tissue has no
blood supply from the periodontal ligament, the nutrient
depends heavily on the peri-osteum and the surrounding
connective tissue [52]. Additionally, the thinner surrounding
tissue has the smaller number of blood vessel, and blood flow
is not enough to maintain the gingival formation. Therefore, in
the case of maxillary anterior teeth, which are generally
surrounded by the gingiva with thin biotype that readily
causes bone resorption, it is desirable the amount of mucosal
recession to be predictable, and that the mid-buccal margin to
be located more than 2 mm above the implant superstructure.
Clinical cases exhibiting Maynard’s type IV recession (thin
alveolar bone and attached gingiva [61]) is improved to type II
or III by bone or connective tissue grafts that protect against
gingival recession after placement of the final prosthesis.
Namely, this operation aim that the blood volume is
maintained by increasing the surface area of periosteum
and the amount of connective tissue including the blood
vessel. However, the use of guided bone regeneration for
reconstruction around the implant is controversial because
the protective membrane often placed over these surgical sites
to aid healing may block the blood supply to the soft tissue,
resulting in a decrease in gingival thickness in clinical feeling.
3.2. Maintenance of soft-tissue around implant
As mentioned above, the changing nature of the periodontal
tissue around a recently placed implant could undermine the
prosthesis and its associated soft tissue, frustrating attempts
to maintain its functionality and esthetics in the long term.
Thus, detection and early resolution of mucosal inflammation
is critical in maintaining the implant in its optimal condition.
Routine indices, such as probing depth and gingival bleeding,
are universal techniques for objectively assessing gingival
health around teeth. However, these methods are less reliable
when exploring around implants because of the labile seal at
the interface between the implant and epithelium. A report
comparing the probing resistance of gingivae around natural
teeth and implants found that the measuring probe was
inserted more easily and deeper into the peri-implant sulcus
than into the gingival sulcus [62]. This is readily explained by
the weak attachment between the PIE and the titanium
implant surface, which is easily breached by light pressure on
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7
the probe in a way that the normal gingival sulcus, with the
strong epithelial sealing, is not (Fig. 6). This fragility of the
seal means that probing often induces bleeding and permits
the ingress of bacteria deep into the peri-implant tissues,
accelerating the physical destruction of the epithelial
and connective tissue. Therefore, probing around dental
implants appears to be of limited benefit (and often frankly
counter-productive), so visual inspection of the soft tissue
color, tone, elasticity, and crevicular fluid flow are frequently
the only available parameters that can be empirically
analyzed [63,64].
Dental plaque can, in the absence of good oral hygiene,
accumulate around teeth and implants, triggering a broad
inflammation of the oral mucosa [65], despite the protection of
epithelium-hard tissue interfaces that provide both mechani-
cal and biological defence elements [12]. Inflammation of both
the periodontal and peri-implant tissue occurs in as little as
three weeks after plaque deposition and appears to be caused
by very similar bacteria [66]. Interestingly, it has been reported
that bacterial accumulation, and the rate and extent of the
destruction it causes, is greater around implants than around
natural teeth [67]. Thus, pocket formation and bone resorption
around the implant seems almost inevitable [11]. The pockets
that form around the implant are the result of epithelial down-
growth at the soft tissue-implant interface [68], and produce
an area where anaerobic bacteria can accumulate and be
sheltered from mechanical cleaning, thus causing inflamma-
tion. Therefore, it is important that we recognize the inferior
sealing capability of peri-implant tissue and the need to
provide patients with regular monitoring of their dental health
after implantation, and that the concentration of research and
development into establish novel implant and abutment that
form better soft tissue seals and are easier to clean.
4. Conclusion
Recent study has been focused on improving the resistance to
peri-implantitis and achieving appropriate soft tissue man-
agement following implant placement. The fragile seal
between the implant surface and peri-implant tissue is
increasingly seen as a problem because this weakness
translates to an increased risk of inflammation. In the near
future, it is to be hoped that the epithelial seal around dental
implants will be at least equal to or higher than that around
JPOR-286; No. of Pages 9
8 journal of prosthodontic research xxx (2015) xxx–xxx
the natural tooth, with an attendant decrease in the clinical
occurrence of gingival recession or inflammation.
Conflict of interest statement
The authors have declared that no competing interests exist.
Acknowledgments
This work was supported by JSPS KAKENHI grant Scientific
Research (C) No. 23592888 (to I. Atsuta.) from the Ministry
of Education, Science, Sports, Culture, and Technology of
Japan.
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