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Clinical and morphological aspects of the implant/soft tissue interface
Rodrigo F. Neiva, DDS,a Kathleen G. Neiva, DDS,b Tae-Ju Oh, DDS, MS,a and
Hom-Lay Wang, DDS, MSDaa

Department of Periodontics/Prevention/Geriatrics, and bDepartment of Cariology/
Restorative Science/Endodontics, School of Dentistry, University of Michigan,
Ann Arbor, MI, USA
Purpose: This paper is aimed to describe clinical and morphological aspects of the soft tissue implant/soft
tissue interface and to provide guidelines for assessment of peri-implant mucosal health.
Materials and Methods: Critical appraisal of the current literature regarding the interface between dental
implants and the peri-implant mucosa is performed.
Results: The articles reviewed agree that smooth titanium surfaces are highly compatible with oral soft
tissues. The biological seal that is formed by the mucosa surrounding dental implants is established toprovide protection against microbial invasion. Implant design may influence the location of the biologicalseal, but not the formation of the seal. Non-keratinized peri-implant mucosa does not seem to predisposeperi-implant disease. Keartinized mucosa seems to be desirable for hygiene procedures and esthetics, but
not necessary for implant success.

Assessment of peri-implant mucosal health has shown to be a

predictable indicator of peri-implant disease.
Conclusion: Studies have consistently shown that biologic seal is formed between the oral cavity and theunderlying tissues after implant placement, providing protection against the microbial challenge. However,
future studies are needed in order to clarify the importance of the biological seal for implant success.
(Int Chin J Dent 2002; 2: 151-161.)
Clinical Significance: Since dental implant penetrate into the oral cavity, the interface between dental
implants and oral soft tissues allows the formation of a biologic seal. This biologic seal has the ability toprotect the underneath structures by closing the pathway of communication between the oral environment
and the alveolar bone. Assessment of the integrity of this interface aids in early detection of peri-implant
pathologies, and may prevent future implant bone loss. In addition, the implant/soft tissue interface may
provide esthetics that implant supported restoration needs.
Key words: biological width, dental implants, mucositis, peri-implant mucosa.

INTRODUCTION
The replacement of missing teeth by means of endosseous dental implants has become an important partof dentistry. Over the last two decades, research has validated the success of osseointegrated implants as a

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viable replacement for partial and complete edentulism. Although techniques and materials have beendeveloped which are capable of a high degree of clinical success, the ultimate long-term success of
implants is dependent upon the efforts of both the patient and dentist in maintaining the health of theperi-implant tissues.
Dental implants have two distinct interfaces with oral tissues. First, there is the peri-mucosal interface
where soft tissue meets the implant, creating a biological seal. Secondly, the endosseous interface exists
where alveolar bone is in close proximity with the titanium surface, providing stability and rigidity to theimplant. Since the soft tissues reform around dental implants as a result of a healing process following
implant placement, they are called peri-implant mucosa, not gingiva.
The aim of this paper is to review the literature regarding the interface between the implant andperi-implant mucosa, which is divided into epithelium and connective tissue.

EPITHELIUM
Epithelial tissues have the capacity to proliferate and to move on surfaces. Following implant/abutment
placement, epithelial migration from adjacent soft tissues begins. The epithelium moves in apico-coronal
direction as soon as it reaches the implant surface, giving rise to a junctional epithelium about 2 mm
long.1-3 The formation of a junctional epithelium in the implant/mucosal interface can be considered thefirst barrier of defense against oral microflora. Figs. 1a and 1b illustrate the relationship between implantand surrounding soft tissue.

JE
oCT

MM
cJE
oCT

iCT
aJE
iCT
a
b
Fig. 1. a. Diagram illustrates the relationship between implant and surrounding soft tissue
interface. b. Histological sections of the implant/peri-implant mucosal interface.
JE: Junctional epithelium; oCT: Outer connective tissue; iCT: Inner connective tissue; MM: Mucosal margin; cJE: Coronaljunctional epithelium; aJE: Apical juctional epithelium; iCT: Inner connective tissue.

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Donley et al. suggested that junctional epithelium cells adjacent to a titanium implant to form ahemidesmosomal type of attachment to the implant surface similar to that of a natural tooth.4 On the other
hand, Meffert et al. suggested that the junctional hemidesmosomal arrangement may not be predictable in a
metallic system.5 Research has shown that once epithelial cells have reached the implant surface, their
attachment occurs directly via a basal lamina (<200 nm) and hemidesmosomes.6-8

Kawahara et al.

hypothesized another form of attachment, where a glycoprotein layer of approximately 200 nm forms
between the cell wall, without direct epithelium/implant contact.9,10 Lekholm and Adell, however, havediscussed the fact that the seal is probably viable and adequate in function based on the fact that there wereminimal histologic inflammatory reactions in the underlying connective tissues.11,12

The surface

topography has also shown to play a role in the soft tissue attachment to titanium surfaces, since polishedsurfaces have shown higher compatibility to fibroblasts when compared to rough surfaces.13-18
A prerequisite to a successful dental implant should be obtaining a peri-implant mucosal seal to theimplant surface.19,20 Failure to achieve or maintain this seal results in the apical migration of the epithelium
into the bone/implant interface and possibly caused partially or completely encapsulation of the endosseous
implant.21,22 In a natural dentition, the junctional epithelium provides a seal at the base of the sulcus against
the penetration of chemical and bacterial substances. If the seal is disrupted and/or the fibers apical to theepithelium are destroyed, the epithelium migrates apically, forming a periodontal pocket after cleavage ofthe soft tissue from the radicular surface. The importance of the biologic seal should be emphasized due tothe absence of cementum and fiber insertion into the implant surface which may cause formation of a"peri-implant pocket" extending into the osseous structures. The characteristics of the soft tissues adjacent
to teeth and implants were listed in Table 1.
Table 1. Soft tissues adjacent to teeth and implants.

Teeth

Attachment

Orientation of collagen fibers

Basal lamina

Perpendicular

Source of blood supply

Biological width/Seal

Periosteum, PDL

JE: 0.97 mm70
CT: 1.07 mm70

and hemidesmosomes
Implants

Basal lamina

Parallel

Periosteum

JE: 1.88 mm1
CT: 1.05 mm1and hemidesmosomes

PDL: Periodontal ligament; JE: Junctional epithelium; CT: Connective tissue.

CONNECTIVE TISSUE
For the connective tissue attachment to the implant, collagen fibers form a tight cuff around the implant
abutment. The length of the connective tissue attachment ranges from 1.3 to 1.8 mm,1,23 and is also
dependent on the design of the implant (one- or two-part implant). There have been reports in the literaturethat the use of a plasma spray surface promotes connective tissue adherence with fibers inserted

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functionally at 90° into the plasma sprayed surface of the implant.15,24 However, most reports have shownthat connective tissue fibers are not inserted into the implant surface. Dense bundles of thick collagenfibers are oriented only longitudinally due to a lack of fiber insertion.25,26
The connective tissue of the peri-implant mucosa can be subdivided into two distinct zones. The outerzone located under the junctional epithelium, composed of collagen Types I and III, is responsible for thetransformation of collagen. The inner supracrestal connective tissue zone, composed mainly of Type I
collagen, is responsible for mechanical resistance and stability of the peri-implant mucosa.25,27
The connective tissue surrounding dental implants possess fewer capillaries as compared to theconnective tissue surrounding natural teeth.28 The blood supply of the peri-implant mucosa is composed ofterminal branches of larger vessels originating from the periosteum of the alveolar bone, while thevasculature of the gingiva and the supracrestal connective tissue at teeth is derived from the supraperiosteal
vessels lateral of the alveolar process and the vessels of the periodontal ligament.28 The peri-implantmucosa has also shown to exhibit an inflammatory response, similar to gingival tissues, characterized byincreased proportions of T- and B-cells in the inner connective tissue. However, the host response is lesspronounced than in gingival tissues.29-31

BIOLOGICAL WIDTH/SEAL
Animal and human studies have shown that an adequate biological width/seal can only be achieved if
there is a supracrestal smooth titanium surface of at least 3 mm long in the apico-coronal direction.1,21,32-35
The junctional epithelium occupies approximately 2 mm of this surface, while the rest of it is occupied by
the connective tissue. Berglundh and Lindhe observed that the values for two-part implants were 2.0 mm
for JE, and 1.3 to 1.8 mm for CT.23 Cochran et al. observed the values for a biological width/seal around
one-part implants before and after loading period of 12 months. Mean values for 3-month unloaded
implants were 0.49 mm for sulcus depth (SD), 1.16 mm for the junctional epithelium attachment (JE), and1.36 mm for the connective tissue attachment (CT). These dimensions differed from the 3-month loaded
implants that showed 0.50 mm for SD, 1.44 mm for JE, and 1.01 mm for CT. After the 12-month loading
period, these values were 0.16 mm for SD, 1.88 mm for JE, and 1.05 mm for CT.1 It can be speculated thatthe biological width/seal increases approximately 1 mm after implant loading, possibly due to crestal bone
resorption.

THE INFLUENCE OF IMPLANT DESIGN
Since a biological seal is formed by epithelial and connective tissue attachments to the implant surface,
the length of titanium surface interfaced with the peri-implant mucosa may influence the location of thebiological seal. One-part implants seem to provide a more predictable surface for soft tissue attachment,
since the length of the smooth titanium surface is stable, and the implant/abutment connection is positioned
more coronally.36

Soft tissue attachment in two-part implants are dependent on the location of therestorative margin that must respect the dimensions necessary for the formation of a biological seal/width.

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If the required dimensions are not respected, an apical migration of the biological seal/width can be
expected with subsequent exposure of the rough implant surface to the implant/mucosal interface.
In two-part implant, the microgap present at the implant/abutment interface may result in an
inflammatory infiltrate due to presence of microorganisms that can populate the implant/abutment
junction.22

The inflammatory infiltrate is a protective host defense mechanism that limits microbial

invasion, preventing further deterioration of implant supporting tissues. Ericsson et al. showed that an
apical migration of the junctional epithelium occurs after abutment connection in two-part implant,
allowing a biological seal to be formed.34 Weber et al. compared the formation of the biological sealaround one- and two-part implants and demonstrated that a biological seal is formed irrespective of theimplant design. However, two-part implants resulted in a longer junctional epithelium attachment, which
was located more apically. The distance from the crestal bone was also shorter in comparison to one-part
implants. No differences were found in the length of connective tissue attachment.37 Similar findings was
also reported by Hermann et al.38

KERATINIZED VS. NON-KERATINIZED PERI-IMPLANT MUCOSAThe need of the keratinized mucosa surrounding dental implants in order to maintain peri-implantmucosal health is controversial, since healthy tissues can be noted not only on the presence but also on theabsence of keratinized peri-implant mucosa. Becker et al. speculated that keratinized peri-implant mucosa
is not a necessary prerequisite for peri-implant health and that movable mucosa around the trans-epithelial
extension of an endosseous implant is not necessarily a vulnerable situation.39 However, Warrer et al. used
an animal model and demonstrated that implants surrounded by non-keratinized mucosa may exhibit more
crestal bone loss and mucosal recession, when compared to implants surrounded by a keratinized mucosa,
under similar levels of plaque accumulation.40 Similar observation was also demonstrated by Strub et al.41
Adell et al. reported based on 15-year results of 2,768 implants placed in 371 subjects, that even when amovable mucosa was found surrounding implants, a clinically healthy mucosa was noted.42 Wennstromand Lindhe evaluated the prospective and retrospective studies of Branemark to associate implant failure
with nonkeratinized peri-implant mucosa. An overall 90% success rate in terms of fixture survival and inwhich the marginal tissue was keratinized gingiva in only 67% and 51% of the facial and lingual surfaces
respectively demonstrated that the absence of a keratinized peri-implant mucosa does not predispose
implant failure.3,43 On the other hand, Kirsch and Ackermann published 10-year clinical results of 2,284
implants, with a failure rate of 2.2%. The study suggested that the main cause of failure was insufficient
width of keratinized peri-implant mucosa.44 The difference in the two studies may be attributed to thedifference that the retrospective and prospective studies of Branemark were in fully edentulous cases, while
the majority of the implants in Kirsch's study were in partially edentulous mouths.
Although the absence of a keratinized mucosa does not seem to predispose implant failure, keratinizedtissue may facilitate personal home care and maintenance procedures. Connective tissue grafts, freegingival grafts, and other techniques, have been described and have achieved predictable results for

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augmentation of keratinized mucosa around dental implants.45-52

ASSESSMENT OF SOFT TISSUE HEALTH
Experimental evidence during the last decade supported the concept of a host-parasite imbalance being
the major responsible reason for implant failures after loading53,54. As in the case of teeth, the imbalance inthe host-parasite equilibrium can manifest itself in a series of inflammatory changes, which lead to two
distinct clinical syndromes: 1) Mucositis is a reversible inflammatory lesion confined to the superficial
peri-implant mucosal tissues, and 2) Peri-implantitis is a lesion involving the peri-implant soft tissues aswell as the marginal portion of the bone-implant interface.
As is true for gingivitis and periodontitis, the relationship between peri-implant mucositis andperi-implantitis is not known with respect to the natural history, evolution and progression.55 Endosseous
dental implants rarely fail beyond the first year after restoration.56,57 However, it has been suggested thatconventional periodontal therapy should be instituted if inflammation develops around an implant.58,59
Problems limited to the peri-implant mucosa and not involving the supporting bone have been defined as"ailing implants" and, more recently, as biological complications.36,54
Probing studies in dental implants are dependent on the emergence profile of the final restoration.
Assessment of probing depth around overcontoured crowns is largely irrelevant unless the superstructure isremoved, allowing probing parallel to the long axis of the fixture. Peri-implant probing depth, mucosal
recession, bleeding upon probing, and peri-implant exudation have been suggested as useful diagnostic
tools for biological complications.60-62

Probing studies in dental implants are also dependent on thepresence or absence of inflammation since it has been shown that a probe is able to penetrate into theconnective tissue and reaching close proximity to the alveolar bone even in presence of mild to moderatemucositis.63 Successful implants usually allow approximately 3 mm of probe penetration, while deeper
probing depths are often associated with a marked difference in the composition of the peri-implantmicroflora.1, 62
While the overall prevalence of peri-implantitis ranges from 5-10%, the prevalence of peri-implantmucositis seems to be higher. Smedberg et al. reported that radiological diagnosed marginal bone defects
in 6% of implants after 2 years in function; 28% of the patients were diagnosed as having peri-implantmucositis.64

However, the classic study of Adell and coworkers reported that the mean values of

peri-implant mucositis and plaque were 7.6 and 13.7% respectively.42
The microbiological findings related to healthy and failing implants are similar as those for healthy andperiodontally compromised teeth.60,62

Increased levels of subgingival Porphyromonas gingivalis,

Prevotella intermedia, and Fusobacterium nucleatum may lead dental implants to fail. On the other hand,failing implants with a traumatic etiology may have a microflora comprised predominantly of streptococci
which is consistent with periodontal health.65 The microbiota present in the oral cavity can influencebacterial colonization around implants since implants placed in partially edentulous periodontal patients
had the same microflora found in their periodontal pockets.66,67 Salcetti et al. found increased levels of156

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PGE2, IL-1ß, and PDGF in failing implant sites demonstrating that not only the microbiota but also the host
response is similar to those of periodontally diseased teeth.68
Sbordone et al. evaluated implants placed in partially edentulous patients with previous history ofmoderate to severe chronic periodontitis. They found that the treated periodontal sites were stable at 3
years, with nearly 90% of the sites demonstrating CAL<1 mm. Despite the similarity of the microbiota of
the samples from implant and natural tooth sites, no evidence of recurrent periodontal attachment loss or
implant failure was noted.69 These findings support the recommendation that patients with implants shouldbe evaluated at regular visits for periodontal maintenance procedures, and any clinical signs and symptoms
of peri-implant mucositis or peri-implantitis should be recorded and treated.

CONCLUSIONSThe use of dental implants in the treatment of partially or fully edentulous patients has become an
important addition in oral/dental rehabilitation. The literature to date concurs that coated, non-coated, or
plasma-sprayed implants all have the capacity to achieve osseointegration, if appropriate surgical
techniques are involved.
The fact that implants penetrate the oral mucosa and the mucosa is able to seal around the implant, leads
to the assumption that the peri-implant mucosa fulfills the function of acting as a barrier to protect theanchorage to the alveolar bone. The biological seal has shown to be present irrespective of the implantdesign, but a smooth titanium surface is preferable for soft tissue attachment.
Research has shown that insufficient plaque removal may lead to peri-implant disease with or withoutbone loss. However, it is unclear how important this cause is as a cause of implant failure, compared withother factors, such as inadequate bone healing, unfavorable quantity and quality of bone, or (bio)mechanical and functional problems. It is also not understood if the presence or absence of keratinizedperi-implant mucosa is needed to slow down or prevent tissue breakdown. The current knowledge has
shown that the keratinized mucosa maybe desirable, but not necessary.
Future studies in these areas are necessary and will certainly provide a better understanding in this field.

ACKNOWLEDGMENT
This work was partially supported by the University of Michigan Periodontal Graduate Student Research
Fund.

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Reprint request to:
Dr. Hom-Lay Wang
Graduate Periodontics, University of Michigan School of Dentistry1011 N, University Avenue, Ann Arbor, Michigan 48109-1078, USA
FAX: +1-734-763-5503
E-mail: homlay@umich.edu
Received on November 18, 2002. Revised on December 12, 2002. Accepted on December 21, 2002.
Copyright ©2002 by the Editorial Council of the International Chinese Journal of Dentistry.

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