Biol width on impl review

REVIEWS
Stomatologija, Baltic Dental and Maxillofacial Journal, 10:27-35, 2008

Biologic Width Around Implants. An Evidence-Based
Review
Tomas Linkevicius, Peteris Apse

SUMMARY

Purpose. The concept of biologic width forms a basis for successful peri-implant soft tissue inte-
gration around titanium implants. Therefore, the objectives of this review are to determine and critically
evaluate the present knowledge about biologic width around implants and to establish future research
trends.
Materials and Methods. The literature was selected through several electronic databases, as well
as a manual search in the major dental implant, prosthetic and periodontal journals. The reviewed data
was published in English from 1980 to December 2007. Questions for systematic review were formu-
lated. Abstracts, chapters from books, and unpublished materials were excluded, as they do not meet
criteria for evidence-based studies. Articles were prioritized according to the value of different study
types on the same issue. In vitro studies and literature reviews were excluded. The included publica-
tions were clinical, human histology and animal studies.
Results. In total, 75 articles were obtained. After two rounds of evaluation and criteria application
54 papers remained for final appraisal, namely 2 clinical papers, 8 human histology and 44 animal
studies were analysed. Twenty-one full-text articles were excluded.
Conclusions. Evidence analysis shows that the present knowledge about biologic width around im-
plants is mainly derived from animal studies and that clinical controlled human studies are insufficient.

Key words: biologic width, crestal bone loss, implant, abutment, peri-implant soft tissues.

INTRODUCTION

It has been well documented in literature that bone main reason for crestal bone level changes, but recent
supporting two-piece implants undergo crestal bone loss studies have questioned the role of loading in aetiology
after the connection of the abutment and delivery of of early crestal bone loss [13, 14, 15]. Microgap (the
prosthesis in single tooth replacements [1, 2], partially implant-abutment interface) has been shown to be a
edentate [3, 4] and completely edentulous patients [5, factor, if placed at bone level or subcrestally [9, 16], but
6]. Albrektsson et al in 1986 established success crite- such changes can be neutralized by positioning implant
ria for implant treatment that included 1.5 mm loss of about 2 mm supracrestally [17]. A polished implant col-
crestal bone in the first year of implant function [7]. lar may provoke crestal bone loss associated with
While the reasons for early crestal bone loss have “nonload” factor, but, similarly to microgap, bone loss
been extensively discussed in last decade, stability of can be avoided by leaving smooth implant neck above
crestal bone still remains a controversial issue. Over- the bone level [11]. One further factor that should be
load [8], microgap [9], polished implant neck [10, 11], considered may be biologic width, i.e. the distance be-
and infection [12] are some factors implicated in early tween the margin of peri-implant mucosa and underly-
peri-implant bone loss. ing bone crest [18], which has not been as extensively
For a long time overload was considered to be the studied as the other reasons for crestal bone loss.
The term biologic width was based on the work of
1
Vilnius Implantology Center, Vilnius, Lithuania Gargulio et al in 1961 who described the dimensions
2
Department of Prosthodontics, Riga Stradina University, Riga, and relationship of dentogingival junction in human ca-
Latvia
davers [19]. It has been hypothesised that a similar re-
Tomas Linkevicius1 – DDS, Dip. Pros. lationship of bone to overlying soft tissue exists around
Peteris Apse2 – D.D.S., prof., Dip. Pros., MSc (Toronto), Dr.
hab.med (Latvia) implants and changes in this relationship may be one of
the reasons for the early crest bone loss [20].
Address correspondence to Tomas Linkevicius, Vilnius Implantology There is a number of literature reviews published
Center, Kalvariju str. 121-2, LT-08221, Vilnius, Lithuania.
E-mail: linktomo@gmail.com on biologic width around implants, all of them following

Stomatologija, Baltic Dental and Maxillofacial Journal, 2008, Vol. 10, No. 1 27

Tomas Linkevicius, Peteris Apse REVIEWS

the traditional narrative approach [21, 22, 23, 24]. The tological human studies (4th level), case series (3rd level),
traditional review is informative and can provide a gen- clinical studies (2nd level) and long term clinical studies
eral perspective of the topic, but it is susceptible to bias (1st level) [27].
in the selection of the publications to review [25]. It has In order to determine which studies would be in-
been suggested, that a systematic critical review is the cluded in the review, several criteria were used depend-
best method to extract the evidence from the literature ing on the type of the study. Evidence-based selection
[26]. However, there is a lack of critical review of the criteria have been published for clinical studies; however
literature about biologic width around implants. The ob- similar criteria are not available for animal studies [28, 29,
jective of this paper is twofold: (1) to evaluate up-to- 30]. In default of standard criteria, the following inclu-
date evidence from different type of studies of biologic sion/exclusion criteria were formulated for animal stud-
width around implants; and (2) to establish future re- ies: (1) the number, type, age of tested animals should be
search trends. clearly mentioned in the study; (2) the number of implants
tested should not be fewer than four per animal [31]; (3)
MATERIAL AND METHODS the study should include trials with titanium or titanium
alloy endosseous implants used in oral cavity.
Literature was selected through a search of Human histological studies were reviewed for the
PubMed, Embase and Cochrane Central Register of presence of (1) a clear outcome, and (2) examination of
Controlled Trials electronic databases. The keywords titanium implants. Clinical studies were included if they
used for search were biologic width, peri-implant soft reported (1) a clear outcome of the study,(2) had a con-
tissues, crestal bone loss, microgap, peri-implant trol group of titanium abutments or one-piece implants,
seal, implant and abutment. The search was restricted and (3) the study included at least a 12-month follow-up
to English language articles, published from 1980 to analysis.
December 2007.
Additionally, a manual search in the major dental RESULTS
implant, prosthetic and periodontal journals and books was
performed. The issues from 1990 were searched in fol- The search identified 75 full-text articles, related to
lowing journals: Clinical Oral Implant Research, Jour- biologic width around implants. Unpublished materials
nal of Clinical Periodontology, International Jour- (congress, workshop materials and personal communi-
nal of Oral and Maxillofacial Implants, International cation) were excluded since they do not meet the crite-
Journal of Periodontics and Restorative Dentistry, In- ria for evidence-based studies. Standard reviews and
ternational Journal Of Prosthodontics Journal of hypothetic articles were excluded due to possible bias.
Periodontology, Journal of Prosthetic Dentistry, In vitro studies were excluded as they have low clinical
Periodontolgy 2000, Implant Dentistry, Journal of relevance [32, 33].
Oral Implantology, Journal of Periodontal Research Therefore, (1) animal; (2) human histology and (3)
and Clinical Implant Dentistry Related Research. clinical studies were included in this critical analysis.
In order to be precise in data collection and to ob- After the application of the inclusion/exclusion cri-
tain all available information, references to all articles teria, 54 articles were reviewed:
on biologic width were examined. In addition, con- • 2 clinical studies;
gresses, courses and workshop materials were also as- • 8 human histological studies;
sessed. Within the context of the aim of this review, • 44 animal histological studies.
following questions were formulated:
• What is the structure of biologic width around What is the structure of biologic width around
implants? implants?
• What is the function of biologic width? The included studies can be found in the Table 1.
• What is the influence of mucosal thickness on Animal studies
biologic width formation? Biologic width around titanium implants is well in-
• Does abutment connection/disconnection have vestigated in animal studies. Experiments in dogs focused
influence on biologic width? on examining vertical extension and composition of tis-
Full-text papers were sorted according to the na- sues that form the biologic width. Included literature con-
ture of publication – experimental publications, reviews, sisted of studies with teeth as a control [34], uncontrolled
hypothetical articles, technical notes, etc. descriptive study [35], comparative studies between sub-
Experimental publications were prioritized according merged and non-submerged implants [36, 37, 38, 39, 40],
to the value of different study types on the same issue – comparison between one- and two-piece implants [40].
in vitro studies (6th level), animal studies (5th level), his- Another series of studies tested the influence of loading

28 Stomatologija, Baltic Dental and Maxillofacial Journal, 2008, Vol. 10, No. 1

REVIEWS Tomas Linkevicius, Peteris Apse

time on parameters of peri-implant seal [41, 42, 43]. One sue contact to implant surface was characterised by the
study looked at the influence of location of microgap to absence of blood vessels and the abundance of fibro-
bone crest on extension of BW around implants [44]. blasts interposed between collagen fibers. More lateral
Ten studies showed that biologic width around im- to this area there was a zone of fewer fibroblasts, more
plants consists of sulcular and junctional epithelium and and larger collagen fibers and numerous blood vessels.
an underlying connective tissue zone [34, 35, 36, 37, 38, Circular collagen fiber network in horizontal sec-
39, 40, 41, 42, 43, 44]. Morphological structure of the tions around implant neck was found in the study by
epithelial part was investigated by Kawahara et al [45] in Ruggeri et al with 4 monkeys and 32 implants [48].
the study with 3 monkeys and 6 titanium blade implants Human histological studies
and by Abrahamsson et al [36] in the study with 5 dogs The search identified 4 histological human studies,
and 30 titanium screw-type implants. They showed that describing the structure of biologic width around im-
the apical part of the epithelium is very thin and attaches plants. The most informative is a recent publication by
to implant surface with hemidesmosome-like structures. Glauser et al. Five patients received a total of 12 experi-
Other studies elaborated on the connective tissue zone. mental one-piece mini-implants – equal number of an
The connective tissue appeared to be similar to scar-like oxidized and acid-etched or a machined surface. The
tissue and had direct contact with implant surface, but total height of peri-implant tissues was calculated to be
without any attachment [46, 47]. Direct connective tis- from 4 to 4.5 mm. The peri-implant sulcus varied from

Table 1. Included studies describing the structure of biologic width around implants

Publication Study Sample size and Follow-up Results
species
Berglundh et al [34] Animal controlled 5 dogs, 9 months BW extension – 3.80 mm around implants
histology 5 implants and teeth and 3.17 mm around teeth.
Tenenbaum et al [35] Animal histology 6 dogs, 9 months Total extension of BW was 4.00 mm on
12 implants buccal and 4.92 mm on lingual sites
Abrahamsson et al [36] Animal histology 5 dogs 9 months Non-submerged implants BW – 3.50 mm,
30 implants submerged - 3.11 to 3.42 mm
Weber et al [37] Animal histology 6 dogs 4.5 months No statistical difference between submerged
38 implants and non-submerged implants
Ericsson et al [38] Animal histology 5 dogs 6 months No statistical difference between submerged
30 implants and non-submerged implants
Abrahamsson et al [39] Animal histology 6 dogs 9 months Submerged 3.00 mm, non-submerged 3.15
18 implants mm. No statistical difference
Hermann et al [40] Animal histology 5 dogs 6 months No difference between one- and two-piece
59 implants implants
Hermann et al [41] Animal histology 6 dogs 3 – 12 Unloaded group – 3.01 mm, loaded – 2.94 to
69 implants months 3.08 mm. No statistical difference.
Cochran et al [42] Animal histology 6 dogs 3 – 12 No statistical difference between loaded and
69 implants months unloaded groups
Siar et al [43] Animal histology 6 monkeys 3 months of Immediate loading group – 3.9 mm, delayed
18 implants loading loading – 3.78 mm. No statistical difference.
Todescan et al [44] Animal histology 4 dogs 6 months Longer BW in deeper placed implants
24 implants
Kawahara et al [45] Animal histology 3 monkeys 9 months Morphometric evaluation of JE attachment
6 blade implants zone.
Buser et al [46] Animal histology 6 dogs 3 months Similar composition of CT around implants
24 implants with different surface roughness.
Moon et al [47] Animal histology 6 dogs 9 months CT divided into 2 zones: central, 40µm wide
36 implants and lateral zone - 160µm. Scar-like tissue.
Ruggeri et al [48] Animal histology 4 monkeys 14 months Circular fiber network around implant neck
32 implants in horizontal sections.
Glauser et al [49] Human histology 5 patients, 12 2 months BW was found to be 4.0 – 4.5 mm. SD 0.2 –
implants 0.5 mm, JE 1.4 - 2.9 mm, CT 0.7 – 2.6 mm.
Arvidson et al [50] Human histology 10 patients At least 36 JE attachment to implant via
10 implants months hemidesmosome-like structures
Scierano et al [51] Human histology 7 patients At least 12 Horizontal and vertical alignment of CT
9 abutments months fibers around implant abutments.
Liljenberg et al [52] Human histology 9 patients 12 months Inflammatory cells found in peri-implant
18 implants mucosa.
Kan et al [53] Clinical study 45 patients Mean 32 Facial extension was 3.63 mm, medial – 6.17
45 implants with months mm and distal – 5.93 mm.
crowns



0.2 – 0.5 mm, junctional epithelium was limited to 1.4 – the abutment [51]. Liljenberg et al measured the thick-
2.9 mm and connective tissue had apical extension from ness of peri-implant soft tissues biopsies from 9 partially
0.7 – 2.6 mm [49]. edentulous patients. The mean mucosa thickness was
Arvidson et al evaluated the peri-implant seal of calculated to be 1.87 mm [52]. There seems to be clear
Brånemark titanium implants in 10 patients by taking evidence that the soft tissues histologically are capable
soft tissue biopsies. The attachment of junctional epi- of creating a seal around the implant neck.
thelium to implant surface via hemidesmosome-like struc- Clinical studies
tures was noted [50]. The vertical extension of soft peri-implant tissues
Schierano et al investigated the direction of col- was examined by Kan et al in a study of single anterior
lagen fibers from 9 retrieved abutments with adjacent implants in 45 humans. In each patient implant soft tis-
peri-implant mucosa in 7 patients. They reported that sues were probed to the bone on mesial, mid-facial and
fibers align themselves circularly and horizontally around distal aspects. The mean dimension of biologic width

Table 2. Included studies describing the function of biologic width around implants

Publication Study Sample size Follow-up Results
and species
Kawahara et al [45] Animal histology 3 monkeys 9 months Migration of leukocytes through junctional
6 blade implants epthelium
Bergludh et al [54] Animal histology 5 dogs 3 weeks of No bone loss, increased rate of leukocytes
15 impla nts plague migration (1.9% vs. 0. 9%).
5 teeth
Lindhe et al [55] Animal histology 5 dogs 4 months Mean 3.0 mm of crestal bone loss
15 impla nts
Marinello et al [56] Animal histology 5 dogs 1-1.5 25% of original bone height was lost
20 impla nts months
Zitzmann et al [57] Animal histology 5 dogs 2 months Mean bone loss was 4.10 mm
22 impla nts
Ericsson et al [58] Animal histology 5 dogs 1. 5 - 2 20% of implant length bone loss
30 impla nts months
Zechner et al [59] Animal histology 8 dogs 8 months Bone loss and increased gingival probing
48 impla nts depths around all ligatured implants.
Shibli et al [60] Animal histology 6 dogs 0 –2 Bone loss from 1.62 mm to 2. 09 mm around
36 impla nts months implants with different surfaces.
Hayek et al [61] Animal histology 9 dogs 8 months All ligatur ed implants developed peri-
18 impla nts implantitis.
Gotfredsen et al [62] Animal histology 5 dogs 4 months Approximately 40% of initial bone support
30 impla nts was lost.
Warrer et al [63] Animal histology 5 monkeys 9 months All implants had attachment loss. BIC varied
30 impla nts from 54% – 65% of total implant length.
Shou et al [64] Animal histology 8 monkeys 0-7 we eks Increase of probing depth, gingival with
32 cylindric bleeding score and bone loss around
implants ligatured implants.
Shou et al [65] Animal histology 8 monkeys 9-18 months Bone loss of 4-6 mm around all implants.
64 impla nts
Shou et al [66] Animal histology 8 monkeys 8 months Bone loss of 2-4 mm prevailed within peri-
32 impla nts implantitis group.
Ericsson et al [67] Animal histology 5 dogs 3 months Spread of infiltrate (ICT) was 1.3 mm at
15 impla nts implants and 0. 9 mm at teeth. No bone loss,
15 teeth inflammation.
Abrahamsson et al [68] Animal histology 5 dogs 5 months Clinical signs of inflammation, ICT size
30 impla nts about 1.6-2. 0 mm, bone loss 0.64 mm.
Ericsson et al [69] Animal histology 5 dogs 9 months Inflammation, ICT – 1.8 mm, bone loss – 1.4
15 impla nts mm.
Watzak et al [70] Animal histology 9 implants 1. 5 yea rs Inflammation, bone loss 0.6-0.9 mm.
54 impla nts
Sanz et al [71] Human histology 12 pa tients 9 months Significantly higher migration of
12 impla nts inflammatory cells to JE.
Zitzmann et al [72] Human histology 12 pa tients 3 weeks Increase of inflammation markers in JE –
24 impla nts 5.0% infected sites vs. 3.5 % healthy sites.
Bullon et al [73] Human histology 5 patients No Increase of T lymphocytes
5 implants
Chavier and Coubles [74] Human histology 8 patients 2 years Type I collagen was dominant in CT
32 impla nts biopsies.



was recorded to be 6.17 mm at mesial, 3.63 mm at mid- Human histological studies
facial and 5.93 mm at distal sites of implants [53]. The function of junctional epithelium was investi-
gated by Sanz et al. Comparative histological study of
What is the function of biologic width around healthy and infected implant sites in 12 patients revealed
implants? that biopsies from implant infection group showed sig-
It has been suggested that soft tissue around im- nificant higher transmigration of inflammatory cells in
plants form biological structures similar to BW around sulcural epithelium [71]. Zitzmann et al investigated the
teeth and may serve as a protective mechanism for reaction of peri-implant mucosa to plaque accumulation
underlying bone. Included studies can be found in the for three weeks in 12 partially edentulous patients. In
Table 2. each patient two implants sites were selected and soft
Animal studies tissue biopsies obtained. There was significant increase
Migration of leukocytes through junctional epithe- in density of PMN elastase+ -cells (inflammation mark-
lium towards bacterial plaque was reported in an animal ers) within the junctional epithelium after 21s day of
experiment with monkeys [45]. Accumulation of these plague accumulation – 5.0% in comparison to 3.5% in
cells in the presence of infection may demonstrate the healthy implant soft tissues [72]. A case-controlled study
possible defence mechanism of biologic width. In a dog showed significant increase of T lymphocytes in sulcular
experiment soft tissues around implants after uninter- epithelium in peri-implantitis biopsies, compared with
rupted plague accumulation were characterized by an healthy peri-implant tissue [73].
increased rate of migration of leukocytes through the Chavier and Couble focused their study on con-
junctional epithelium, as compared to not infected connective tissues around implants. The biopsies were ob-
trol implants (1.9% vs 0.9%) [54]. tained from healthy keratinized soft peri-implant tissues
The evidence of the protective peri-implant seal abili- of 32 implants in 8 patients and analysed for structure
ties may be found in animal studies, which use induced and function of the connective tissue. Type I collagen
peri-implantitis model. Lindhe and co-workers in an ex- was found to be the dominant fiber [74].
periment with 5 dogs (15 implants), induced peri- No clinical trial articles on the issue were found.
implantitis using ligatures and within 4 months, had about
3 mm of bone height loss around the implants [55]. Seven What is the influence of mucosa thickness on
subsequent experiments with dogs [56, 57, 58, 59, 60, biologic width around implant formation?
61, 62] and four with monkeys [63, 64, 65, 66] con- It has been hypothesized that a certain width of the
firmed that the combination of plaque accumulation and peri-implant mucosa is required to enable a proper epi-
biologic width injury can result in crestal bone loss around thelial – connective tissue attachment and, if this soft
implants. tissue dimension is not satisfied, bone resorption may
In contrast, a number of studies in which implants occur to ensure the establishment of attachment with
were exposed to undisturbed plaque formation without an appropriate biologic width [75]. Included studies can
ligature placement for different periods of time, ranging be found in the Table 3.
from 3 weeks to 1.5 years [54, 67, 68, 69, 70], reported Animal studies
no or only minimal bone loss in the presence of soft Berglundh and Lindhe in a controlled experiment with
tissue inflammation. It would seem that the ligature may 5 dogs (30 implants) tested the influence of mucosa thick-
disrupt the epithelial attachment causing the bone loss. ness on biologic width formation around implants [18]. At

Table 3. Included studies describing influence of mucosa Table 4. Included studies describing influence of abutment
thickness manipulation

Publication Study Sample Follow- Results Publicatio Study Sample size Follo Results
size and up n and species w-up
species Abrahams- Animal 5 dogs 9 Bone loss in
Berglundh Animal 5 dogs 9 Bone resorption son et al histology 10 implants monthtest group –
and Lindhe histology 30 imp- months and angular [77] s 1.49 mm and
[18] lants defects around 0.78 mm in
implants with control group.
<2 mm mucosa Abrahams- Animal 6 dogs 12 Bone loss at test
thickness. son et al histology 36 implants month group – 0.7 mm
Bergludh et Animal 20 dogs 0-12 BW formation [78] s and in control
al [76] histology 80 weeks included crestal group – 1.1mm.
implants bone loss, how- Watson et Clinical 117 patients 3 Mean levels of
ever no precise al [79] retrospective 430 years marginal bone
measurements. study abutments were not higher.



the second stage surgery in test implants, peri-implant the light of evidence-based dentistry, the place of ani-
mucosa was thinned to about 2 mm, while control im- mal study is not clear. The similarity of physiology be-
plants had healing abutment connected without tissue tween animals and humans forms the reason for animal
thickness alteration. The histology showed that in the test studies, and the results obtained may have a high de-
implants bone resorption was consistently observed after gree of relevance for humans, although they can not be
soft tissue healing, while the total biologic width was not directly transferred to clinical situations. On the other
statistically significant between the test and control im- hand, some researchers have postulated that animal stud-
plants. The process of biologic width formation around ies are of low clinical relevance and even a simple case
implants was described by Berglundh et al in a dog study. report may have more clinical validity than well con-
The authors observed that the morphogenesis of peri- trolled and randomised animal experiment [81]. How-
implant mucosa involved loss of marginal bone [76]. ever, not all experiments on biologic width can be re-
No human histology or clinical studies about for- peated in humans, due to ethical reasons, leaving clini-
mation of biologic width or influence of mucosal thick- cians to rely on data from animal studies. It is agreed
ness on bone resorption could be found. that animal experiments are more significant than in vitro
studies; however, they provide a lower rank of evidence
Does abutment disconnection/connection as compared to human histological or clinical trials [27].
(prosthetic manipulation) have influence on the In summary, it can be said that histological animal
stability of biologic width? studies provide sufficient information to state that struc-
Included studies can be found in the Table 4. ture of biologic width around implants is composed of
Animal studies peri-implant sulcus, junctional epithelium and connec-
Abrahamsson et al [77] in a controlled histological tive tissue zone. Human histology studies are in agree-
study with 5 dogs (10 implants) proved that disconnec- ment with the outcome of animal experiments, listing
tion of healing abutment five times may cause crestal the same component parts of the biological dimension
bone loss. Test implants showed significantly higher [49, 50, 51, 52]. The results of dog studies indicate that
reduction of bone height than control implants - 1.49 the parameters of biologic width are very similar around
mm and 0.78 mm. Clinically, the bleeding and ulceration one-piece and two-piece implants. Submerged and non-
of soft peri-implant tissues after the disconnection of submerged implants, as studied by Weber et al [37],
the abutment was observed. In a later study in 6 dogs Ericsson et al [38], Abrahammson et al [39] and
and 36 implants, Abrahammson et al [78] found that Hermann et al [40], had a very similar soft tissue length;
single disconnection of healing abutment to prosthetic therefore, it can be concluded that surgical techniques
abutment did not cause any additional bone loss. do not influence formation, composition or extension of
Clinical studies biologic width. It seems that conventional or immediate
Watson et al [79] in retrospective clinical study evalu- loading of implants does not influence the parameters
ated soft tissue condition and crestal bone loss around of peri-implant seal, as it was observed in comparative
implants which had earlier healing abutments placed af- studies with unloaded implants [43]. Only the position
ter second stage surgery. After a 3-year follow-up, it was of implant/abutment interface (microgap) to bone level
concluded that there was no evidence to suggest that proved to affect the vertical extension of biologic width –
abutment exchange adversely affects the outcome of the deeper implant is placed, the longer biological di-
implant treatment. The shift from healing abutment to mension is formed [44]. However, it must be noted that
prosthetic analogue neither affected the survival rates of the majority of histological experiments were performed
implants nor increased the marginal bone loss. on dogs, although non-human primates are considered
to better resemble human oral anatomy and histology
DISCUSSION than any other animal [82]. The literature search identi-
fied only two studies performed on monkeys, which in-
The first unexpected finding was the insufficiency vestigated the structure of biologic width [43, 45].
of clinical studies on biologic width around implants, as In a human histological study the length of the peri-
only 2 papers were identified. The requirements for sys- implant seal was found to be about 4-4.5 mm [49]. In
tematic reviews state that randomised controlled trials contrast, Liljenberg et al [53] reported the same mea-
are preferred because they provide the highest level of surement to be 1.57 mm. However, the authors of the
evidence [80]. However, in the absence of available latter experiment admitted that such results may have
randomised controlled clinical trials evidence is sought occurred due to improper biopsy harvesting. The mean
at less reliable levels. extension of biologic width around implants in primate
The major part of the information about biologic studies was recorded to be 3.84 mm. In histological dog
width around implants is derived from animal studies. In studies this distance was calculated to be around 4 mm.



As compared to biologic width around teeth, the same The hypothesis that tissue thickness and biologic
parameter around implants was longer nearly by the width formation may influence crestal bone loss is sup-
factor of 1.5 mm. Gargulio et al [19] found the dimen- ported by animal studies [75, 76]. A similar conclusion
sion of biologic width around cadaver teeth to be 2.73 was made by Oakley et al in the study on the formation
mm and Vacek et al – 3.25 mm respectively [83]. It is of biologic width around teeth after crown lengthening
evident that the peri-implant seal around implants tends in primates [86]. After 3 months, a mean crestal bone
to be longer, than around teeth. However, the clinical loss of 0.6 mm was registered as the biologic width was
importance of this difference is unknown. Clinical study regaining its dimension. In addition, Albrektsson et al
by Kan et al recorded most extension of biologic width noticed that implant sites with thin tissues were prone to
around implants – 6.17 mm at medial and 5.93 mm at form angular defects around fixtures after healing [87].
distal sites of implants. These results were obtained by Clinically, thin tissues can be expected if thin gingival
probing to bone level and may have been influenced by biotype is present [88], and crestal bone loss may be
the emergence profile of the crowns on implants. Addi- expected as a result of the biologic width establishing its
tionally, proximal sites fequently show deeper probing minimal dimension. However, there are no clinical stud-
depths due to position of the bone crest. However, the ies to support this hypothesis.
mid-facial measurement was recorded to be 3.63 mm, It was suggested that healing abutment discon-
which is very close to the width observed in animal and nection as a part of prosthetic treatment results in dis-
human histology studies. ruption of the epithelial seal, causing bleeding and ul-
The proceedings of the 3rd European Workshop on ceration of the site. This mechanical disruption may
Periodontology and Implant Dentistry state that the func- be considered as an open wound or exposure of con-
tion of the peri-implant seal is “to maintain homeostasis of nective tissue which may result in inflammatory re-
the internal environment in response to challenges from sponses and epithelial migration. The reestablishment
external environment” [84]. Animal and human histology of biological width in more apical position may be the
studies show that there is an increase of inflammatory explanation for crestal bone loss. However, this hy-
cell migration through junctional epithelium, in response pothesis is based on animal study [77]. Moreover, an-
to bacterial presence [45, 54, 71, 71, 73]. These findings other animal study did not confirm that abutment dis-
support the idea that junctional epithelium of biologic width connection may be deleterious to the stability of peri-
around implants serves as a protective mechanism against implant tissues. Such conclusion is in agreement with
bacterial invasion. This is in agreement with studies around the retrospective clinical trial outcome which suggested
teeth [85]. Studies which experimentally induced peri- that abutment manipulation did not cause any evident
implantitis may be another argument that junctional epi- bone loss or mucosal health impairment around im-
thelium attachment protects bone. Mechanical damage plants. However, control group and randomization were
of junctional epithelium by means of subgingival ligature not used in this study; therefore, the results should be
placement resulted in the loss of protective abilities and evaluated with caution.
constant bone loss around implants [55, 56, 57, 58, 59, 60,
61, 62, 63, 64, 65, 66]. In contrast, a number of articles CONCLUSION
show that the stable bone level around osseointegrated
implant can be maintained even under the onset of plaque- Within the limitations of this analysis and currently
induced inflammation if components of biologic width are available evidence, it can be concluded that the struc-
not mechanically damaged [54, 67, 68, 69, 70]. ture and function of biologic width around implants are
One of the functions of the connective tissue zone well documented in animal and human histological stud-
is to support epithelial tissues and limit its migration ies. However, it is not clear what influence abutment
apically. The dominance of Type I collagen fibers (strong disconnection may have on peri-implant tissues, as
and inelastic) in connective tissues confirms their sup- animal experiments provide contrary findings. There is
portive role. However, it must be pointed out that in enough evidence to acknowledge that thin tissues can
Chavier and Coubles’ study, biopsies were taken from cause crestal bone loss in the process of biologic width
keratinized mucosa and may differ from that of non- formation, at least on the level of animal studies. On
keratinized peri-implant mucosa. the other hand, clinical evidence is weak or absent.
It can be summarized that there is enough evidence Data from animal studies should be very carefully
from animal and human histology studies to state that interpreted, when applied to clinical cases, if reliable
the function of biologic width around implants is to pro- clinical evidence is. Therefore, it can be recommended
tect underlying bone. However, clinical controlled to perform randomised controlled clinical trials to test
randomised trials would be desirable, but difficult due to abutment disconnection and tissue thickness influence
ethical reasons. on biologic width around implants.



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