Continuing Education 2

The Clinical Significance

of Keratinized Gingiva
around Dental Implants
Gary Greenstein, DDS, MS; and John Cavallaro, DDS

Learning Objectives

abstract

differentiate anecdotal
information versus data with
respect to the need to augment
keratinized gingiva around dental
implants

Whether or not keratinized tissue is needed around dental

implants to maintain peri-implant health is a controversial
subject. To clarify this issue a search was conducted for
clinical trials that appraised the significance of keratinized
gingiva (KG) around teeth and dental implants. A critical
assessment of the data revealed that the literature is replete with studies that contradict one another with respect
to the need for KG as it relates to survivability of implants,
gingival response to plaque, inflammation, probing depths,
recession, and loss of bone. When groups of patients with
and without KG were compared with respect to various
clinical parameters, a statistically significant better result
in the presence of KG could be interpreted to indicate that
having KG is advantageous. However, quantitative differences between groups with and without KG were usually
very small. Overall, the data was interpreted to indicate
that some patients may need augmentation of keratinized tissue to maintain peri-implant health. Ultimately,
the decision to augment KG is a judgment call that needs
to be made by the treating clinician, because there are not
enough data to facilitate development of definitive guidelines relevant to this subject. Apparently, the need for KG
is patient specific, and at present there is no method to reliably predict who would benefit from tissue augmentation.

discuss the need for keratinized

tissue around teeth and describe
anatomical differences between
teeth and dental implants
list possible scenarios
that suggest the need to augment
keratinized tissue around implants

24

compendium

October 2011

Volume 32, Number 8

or many years there has been controversy as

all surfaces with < 2 mm of KG manifested signs of clinical inflamto whether keratinized gingiva (KG) is necesmation. It was concluded that 2 mm of KG was needed to mainsary to maintain health around teeth,1,2 and
tain gingival health (1 mm attached gingiva and 1 mm unattached).
Subsequently, numerous investigations were conducted to verify
this debate persists with respect to the role
if keratinized tissue was needed to maintain periodontal health.
of keratinized tissue adjacent to dental im3-5
plants. Historically, an increased zone of
Clinical trials indicated that sites with a minimal amount of KG9
keratinized tissue was presumed desirable
or attached gingiva14-17 could remain healthy and that increasing
the zone of keratinized tissue did not influence periodontal stafor the following reasons: provides a resistant barrier to plaque6
induced inflammation ; replaces unkeratinized margins to pretus.15-17 Furthermore, investigators demonstrated17,18 that reducing
vent recession7; deepens vestibules to provide better access for
inflammation was sufficient to maintain clinical attachment levels
toothbrushing8; dissipates functional and masticatory stress
regardless of the keratinized tissues width. Histologic confirmation that the size of the attached gingiva was noncontributory to
placed on the gingival margin of a restoration9; and improves
4,10,11
maintaining health or avoiding recession was provided in a dog
esthetics, patient comfort, and ease of hygiene.
In response to perceived needs for KG, surgical techniques
model,19 a finding that was confirmed in a study among humans.20
were devised to augment gingiva around teeth and implants.12
Long-term data with respect to the stability of margins with
a lack of KG has been documented. In a group of students with
These procedures continue to be performed because of the
a high degree of oral hygiene, areas with inadequate zones of atpersistent disagreement concerning the requirement for ketached gingiva were maintained (4 to 18 years) without further
ratinized tissue to maintain health. The objective of this parecession.21-23 In contrast, Agudio et al24 reported 10- to 27-year
per is to appraise the data and provide a perspective as to why
generalized conclusions can or cannot be made regarding the
data (means 15.3 years) with respect to two groups of patients
need for KG to sustain health around dental implants. First,
and noted that sites with a lack of attached gingiva manifested a
mean recession of 0.7 mm and 1 mm, respectively.
data related to the relationship between keratinized tissue and
Concerning restorations with subgingival margins, Stetler and
teeth are reviewed. Then anatomic differences in tissues surBissada25 found that teeth with narrow zones (< 2 mm) of keratinrounding teeth and implants are addressed. These data serve
as background information for the discussion concerning the
ized mucosa demonstrated a significantly higher gingival index
relevance of KG in maintaining peri-implant health. To avoid
(GI) than teeth with wide zones of KG (> 2 mm). Similarly, in beagle
confusion about anatomic and histological terminology, definidogs, Ericsson and Lindhe26 reported that subgingival crown martions of terms used in this review are provided in Table 1. The
gins placed in areas with no KG that were allowed to accumulate
specific type of tissue referred to in studies will be stated. Note
plaque over months were prone to develop larger cellular infiltrates
that the terms keratinized mucosa and kethan sites with KG. These data conflict with
table 1
ratinized gingiva represent the same type
the histological report by Wennstrm et
of tissue and may include attached and
al19 that indicated there was no difference
Definition
of
Terms
unattached gingiva.
in the inflammatory response with respect
to the amount of attached gingiva present.
Alveolar mucosa: unkeratinized
In summary, the preponderance of
oral epithelium
Keratinized Tissue around Teeth
evidence indicates that augmenting KG
Gingiva: oral mucosa that is keraaround teeth should be approached cauNumerous authors suggested that a lack
tinized, described as attached or
tiously. The patients dental history and
of keratinized tissue predisposed the periunattached
odontium around teeth to deterioration, bechronicity of problems should be assessed
Attached gingiva: gingiva that is
before performing gingival augmentation.
cause they believed KG was more resistant
tightly bound down around teeth
to periodontal destruction than alveolar
Measurements should periodically be taken
or implants and continuous with
mucosa.6-8 To assess the validity of this asfrom the cemento-enamel junction (CEJ)
the unattached gingiva
sumption, clinical trials were performed to
to the free gingival margin (FGM) to deUnattached gingiva: gingiva
evaluate whether a band of KG was necestermine if recession occurred, or from the
that is not bound down (eg, free
gingival margin, soft-tissue wall
sary to maintain health. In 1972, Lang and
CEJ to the base of the pocket to determine
of the sulcus or pocket)
Le13 published the first controlled clinical
if loss of clinical attachment occurred.27
Ultimately, the status of tissues should
trial that examined the relationship beWidth of attached gingiva:
distance
from
the
mucogingival
tween the width of KG and gingival health.
be the critical determinant as to whether
junction to the free gingival marThey reported that 80% of tooth surfaces
KG should be augmented; this decision
gin minus the probing depth
with > 2 mm of KG were healthy. However,
should not be based upon an assumption
www.dentalaegis.com/cced

October 2011

compendium

25

Continuing Education 2

the cementum. Surrounding implants, the connective tissue fibers are parallel or oblique30 and do not insert into the implant
surface. In addition, the blood supply around implants is less
than around teeth, because the periodontal ligament is absent.31

Animal Models: Histological Response to

Plaque Accumulation

Due to anatomical differences, peri-implant and periodontal

tissues may differ in their response to bacterial infections.26,32
Ericsson et al26 reported that after cessation of hygiene in a dog
model the apical extent of the inflammatory infiltrate was larger
in peri-implant mucosa. Similarly, in a dog model when ligatures
were placed to induce destruction, there was greater bone loss
around implants than teeth.32 It was suggested that peri-implant
mucosa might be more susceptible to destruction than tissues
around teeth. In this regard, when Warrer et al33 placed ligatures
around implants (in monkeys) at sites with and without adjacent
keratinized mucosa, they noted that locations without keratinized
tissue demonstrated more recession and attachment loss than
sites with keratinized tissue. In contrast, Strub et al34, in a dog
model, failed to find differences in peri-implant soft-tissue recession or bone loss between sites with and without attached gingiva.

Fig 1.

Fig 2.
Fig 1. When there is a lack of attached gingiva, the typical finding is
a keratinized margin with mucosa (site Nos. 23 and 26). Fig 2. Site
No. 10 has a mucosal margin.

that augmenting KG is essential to maintaining periodontal health.

These conclusions are in accord with the European Workshop on
Periodontology.1 The participants reached the consensus that treatment for the sole purpose of increasing the apicocoronal width of
the gingiva to maintain periodontal health and prevent the development of soft-tissue recession around teeth cannot be justified.1
Subsequent to this report there have been no data that challenged
the conclusions of the workshop with respect to teeth.
Keratinized Tissue around Implants

Differences in Periodontal Tissues

Surrounding Teeth and Implants

Teeth and dental implants have either gingiva or mucosa adjacent to them as they emerge into the oral cavity. Within the
crevice around these structures the oral sulcular epithelium is
connected to the junctional epithelium (JE). The JE on average is
1-mm long28 and is attached to teeth and dental implants by hemidesmosones.29 Subjacent to the JE around teeth is a connective
tissue layer about 1-mm long. Around teeth, this layer contains
fibers that are perpendicular to the root surfaces and insert into

26

compendium

October 2011

Clinical Trial Results in Humans:

Importance of KG

Concerning the effect of a dearth of KG, there is conflicting information in the literature regarding six issues: implant survivability,
plaque accumulation, tissue inflammation, recession, probing
depths, and bone loss. These issues are discussed separately, because within a given study a lack of KG may negatively affect only
one parameter listed above and not others. Furthermore, it is
recognized that numerous variables that have not been accounted
for in many investigations (eg, biotype, smoking, surgical management of implant area, occlusal forces, etc.) can affect study results.
There are several other issues that should be noted with respect to studies that addressed the role of KG around implants.
Researchers did not differentiate between attached and unattached gingiva. This is probably due to the fact that probing
depths are usually deeper around implants than healthy teeth because of differences in the anatomy. In addition, there is difficulty
in detecting the coronal level of the biologic width, because the
probe penetrates into the JE and this results in underestimating
the amount of attached gingiva present.35 Furthermore, measurements are usually taken on the buccal aspect, and studies have not
related clinical parameters to interproximal tissues. It should also
be noted that when all of the gingiva is excised in a dog model, the
marginal tissue that reforms usually has a keratinized margin that
is not attached.19 Therefore, when there is a lack of KG, the typical
finding is a keratinized margin with mucosa (Figure 1), and only
rarely is a pure mucosal margin found (Figure 2).
Volume 32, Number 8

Long-Term Implant Survivability

Fig 3.

Fig 4.

Fig 5.

Fig 3. Some sites without keratinized gingiva, such as Nos. 7 and 10,
manifest an increased amount of inflammation in response to plaque
compared to other locations with keratinized gingiva (eg, site Nos. 5
and 12). Fig 4. In the absence of attached gingiva, tissue adjacent to
an implant can remain healthy (site No. 12). Fig 5. Absence of attached
gingiva predisposes some patients to progressive recession (site No.
4). Fig 6 and Fig 7. Absence of keratinized tissue often does not result
in additional recession. Site No. 24 demonstrates recession at time of
crown insertion (Fig 6). Fig 7 demonstrates that the tissue level has
remained stable after 1 year. This patient had good oral hygiene.

Based on long-term implant studies, numerous investigators concluded that there was little or no difference in the survival rate for
implants surrounded by oral mucosa or KG.36-40 These data pertain
to smooth-surfaced implants and screw-retained prostheses. On
the other hand, two investigations demonstrated there was a lower
implant survival rate when keratinized tissue was absent around
textured-surfaced implants. This occurred around hydroxyapatite (HA)-coated implants41 and IMZ plasma-sprayed implants.42
However, confounding variables include the fact that HA-coated
implants may manifest a lower long-term survival rate than noncoated implants43-45 and plasma-sprayed implants have been replaced with sandblasted/acid-etched (SLA)-surfaced implants.46,47
Currently, textured-surfaced implants are employed. In this
regard, Abrahamsson et al48 reported that the histological attachment of the tissue (JE and connective tissue) adjacent to an implant was consistent irrespective of the type of implant or surface
roughness.49 However, they also indicated that plaque control was
easier on smooth-surfaced implants compared to textured surfaces.48 Therefore, the following question arises: If it is harder to
cleanse textured surfaces than smooth surfaces and most of the
above survival data pertains to smooth surfaces, is it appropriate to
extrapolate the above findings to textured surfaces? To definitively
answer that question, additional long-term studies are needed
to assess whether textured-surfaced implants will manifest high
survival rates over a long period of time despite a dearth of KG.

Plaque Index

Three studies reported a higher plaque index (PI) around implants associated with < 2 mm of KG compared to > 2 mm KG (Table 2).4,10,50 Ostensibly, this was due to the tissues being movable or
they were more tender to brush, so sites were avoided during oral
hygiene. Others did not corroborate these findings.28,50-52 Schrott
et al50 reported higher plaque readings on the lingual but not the
buccal when both sides manifested a dearth of keratinized tissue.

Inflammation
Fig 6.

It was suggested that KG tissue is more protective than mucosa

and inhibits an inflammatory alteration in the connective tissue
around implants.48 In this regard, when there was a dearth of keratinized tissue (< 2 mm), several investigators reported there was
a statistically significant increase in the amount of inflammation
(GI or percentage of sites manifesting bleeding upon probing)
compared to sites with > 2 mm KG (Figure 3) (Table 2).4,11,53 Others reported the amount of inflammation was not increased when
there was a lack of KG (Figure 4).28,51,52

Recession
Fig 7.

www.dentalaegis.com/cced

Some researchers found that the absence of KG was associated

with a statistically significant increased amount of recession
October 2011

compendium

27

Continuing Education 2

around implants in humans (Figure 5) (Table 2),50,51,53 but this

finding conflicted with data of others (Figure 6 and Figure 7).28,54
Brgger et al52 found a weak correlation between the amount
of KG and recession. In addition, it should be noted that in the
study by Schrott et al50 the standard deviation around the means
was greater than the mean data, which raises questions as to the
accuracy of these findings regarding recession (for < 2 mm vs. >
2 mm KG, recession was, respectively, 0.69 +/- 1.11 mm vs. 0.08
+/- 0.86 mm). Furthermore, it needs to be noted that a lack of
attached gingiva may not be the precipitating factor for ongoing
deterioration of a site, but rather a consequence of recession.

Probing Depths

Most studies concluded that a lack of KG was not associated with

increased probing depths (Table 2)4,11,51; however, one study reported contradictory data.53

Bone or Clinical Attachment Loss

Several clinical trials concluded that the absence of KG was associated with a statistically significant increase in bone loss (Table
2)4,41,51 or attachment loss53 when sites with and without KG were
compared, but others did not corroborate this finding.11,55 The
study by Chung et al11 also noted that there was no association
between bone loss and absence of KG and these data pertain to
different implant surface configurations (eg, smooth, textured).
Several other factors need to be considered when interpreting
these data. It should be noted that the mean differences between
control and test groups with respect to bone loss reported by Kim
et al51 and Bouri et al4 were only 0.34 mm51 and 0.28 mm,4 respectively. Furthermore, in all of the previous studies, assessments of
bone loss were done on nonstandardized radiographs and the data

by Block et al41 were determined on HA-coated dental implants,

which were prone to bone loss and failure.
The Role of KG around Implants
Supporting Overdentures

Adibrad et al56 reported that when implants supporting an overdenture with < 2 mm KG surrounding them were compared to implants
with > 2 mm KG, sites with < 2 mm of keratinized tissue were associated with higher plaque accumulation, gingival inflammation,
bleeding upon probing, and mucosal recession. It was speculated
that the flange of overdentures may favor plaque accumulation and
mucosal irritation.56 In contrast, Heckman et al57 noted no significant difference was found between bleeding scores at sites with
and without KG under an overdenture. Similarly, Kaptein et al58
reported no difference in probing depth, plaque, or bleeding around
implants with respect to the width of KG under overdentures. Others also found there was no detrimental effect around implants that
supported overdentures if there was a lack of KG.40,59-61
Discussion

It was anticipated that a comprehensive inspection of the literature would provide an unambiguous answer to the question of
whether or not KG around dental implants is necessary to maintain peri-implant health. However, the literature provided contradictions with respect to every facet of this review, which precludes drawing definitive conclusions. In addition, the literature
pertaining to dental implants failed to provide any clarity as to how
much KG is necessary to maintain health. It appears there may
be circumstances where it is beneficial to have keratinized tissue

table 2

Statistically Significant Differences in Humans: Amount of Keratinized Tissue Related to

Clinical Parameters in the Presence of < 2 mm vs. 2 mm of Keratinized Gingiva
Study

N PI GI Pocket BOP Recession Bone

(# implants)
Depth
(%)
(mm)
loss (mm)

Bouri et al4
Kim et al
51

Length

76 (200)

1.8 vs. 1.3*

1.5 vs. 0.91*

ns

89 vs. 71*

100 (276)

ns

ns

ns

0.72 vs. 0.32* 0.65 vs. 0.41* 13 m

NMD

NMD

NMD

NMD

Wennstrm et al 39 (171)
20

1.72 vs. 1.24* 4.1-4.9 yrs.

5 yrs.

Chung et al

69 (339)

1.51 vs. 1.26*

0.94 vs. 0.76* ns

ns

ns

3 yrs.

Bengazzi et al54

40 (158)

ns

ns

2 yrs.

Zigdon et al53

32 (63)

3.2 vs. 2.6* 0.36 vs. 0.23* 0.90 vs. 0.27*

3.3 vs. 2.6*

3.52 m

58 (307)

0.24 vs. 0.25B -

11

< 1 mm vs. 1 mm
Schrott et al50

0.67 vs. 0.40L*

0.05 vs. 0.07B 0.69 vs. 0.08B* -

5 yrs.

0.22 vs. 0.13L*

N = number of patients; PI = plaque index; GI = gingival index; BOP = bleeding upon probing; * = statistically significantly different; ns = not significant; - = not reported; NMD = no
major differences-multiple regression analysis; = bleeding scored 0 for absence and 1 for presence; = attachment loss, bone loss not recorded; B = buccal; L = lingual

and others where it is unnecessary, and this may vary in different

between clinical parameters and absence/presence of KG, a pospatients and sites within the same mouth. However, defining spesible explanation for inconsistency in the literature is that with
cific situations adjacent to implants (eg, clefting of gingiva, recesgood oral hygiene, peri-implant soft-tissue health can usually be
sion, shallow vestibule, frenum pull) or for particular patients (eg,
maintained if keratinized tissue surrounding implant/restoration
thick or thin biotypes) that may benefit from gingival augmentais absent.5 However, if there is less than good oral hygiene, it may
be advantageous to have KG.5 Use of the good hygiene criterion
tion has never been investigated. Instead, studies consistently
is
complicated by the fact that defining a threshold that would be
employed test and control groups with respect to either a dearth
considered less than good hygiene is problematic.
or an adequate band of KG. To provide a perspective as to what
information can be derived from studies and clinical experience,
After reviewing the literature, Yeung5 suggested that a case
the impact of a lack of keratinized tissue on peri-implant health
could be made for augmenting keratinized tissue around implants
is discussed from several points of view: periodontal response to
to facilitate plaque control by reducing mobile mucosal tissue. To
plaque adjacent to crown margins on teeth and implants, overall
bolster this contention, he referred to a consensus of opinions exstatistical significance of study findings, and interpretation and
pressed by authors who participated in a debate as to whether KG
practical application of data to patient management.
was needed around implants. The authors supported the practice
In general, subgingival crown margins on teeth predispose paof augmenting keratinized tissue around implant restorations
tients to increased plaque accumulation and greater amounts of ginwhen practical to minimize complications.71 In contrast, Esposito
25,62-65
gival inflammation than teeth without crowns.
Hypothetically,
et al72 concluded in a systematic review that there was insufficient
the inflammatory reaction around implant restorations may be
evidence to recommend increasing KG to maintain peri-implant
worse than around teeth, because tissues surrounding dental imhealth. Since publication of that systematic review several clinical
plants may be more susceptible to inflammation due to the altered
trials were published.4,11,50,51,53 They provided mixed results with
structure of connective around an implant.1,26,30 However, this hyrespect to the necessity of augmenting keratinized tissue when
pothesis is based upon animal studies that assessed the peri-implant
comparing studies, and within the same investigation the absence
response when hygiene is ceased for months or if ligatures were
of KG may or may not have an effect on certain clinical parameters. Perplexingly, the data can be interpreted opposite ways. It
placed. These artificially created situations can provide some proof
could be concluded that a strong case cannot be made for routine
of principle concepts, but these data cannot be directly extrapolated
to patient management. Furthermore, it needs to be noted that indiaugmentation of keratinized tissue around dental implants when
vidual thresholds of plaque necessary to trigger signs of disease may
there is dearth of KG, because there is inconsistency between
vary between patients.66 Most importantly, investigators reported
studies to indicate that it is detrimental to restore implants when
that the response of tissues to plaque in patients was similar around
there is a lack of KG. Furthermore, when there were differences
teeth and implants,67,68 and tissue response around implants was not
in the response of clinical parameters at sites with or without KG,
problematic even when there was dearth of KG.20,51,52 Based on these
the mean differences were usually small. In contrast, it could be
studies and the above clinical trials relating the level of plaque to
contended that recent investigations indicated additional bone4,51
the amount of KG, it cannot be concluded that all patients are more
or attachment loss53 was associated with a dearth of keratinized
prone to plaque accumulation due to a lack of KG.
tissue. While the increased mean bone loss was usually small
Assessment of the clinical trials relating clinical parameters to
(Table 2), there may be sites where bone loss was substantial.
the amount of KG can provide a perspective concerning trends that
However, frequency distributions were not provided; therefore,
it is not possible to distinguish how often and to what extent this
have been observed. Inspection of data in Table 2 suggests that in
some studies there is a tendency to find increased inflammation,
occurred or if the data was skewed by a few sites that had extensive
recession, and bone loss associated with diminished amounts of
bone loss. It could also be asserted that short-term data (Table 2)
keratinized tissue. However, it is important to note that statistimay not reflect the possibility that an inflamed site may continue
to deteriorate and compromise a restoration.
cally significant findings only indicate that the event did not occur by chance. It does not mean that the outcome was large or
Apparently, for some patients a lack of KG may be a risk factor
important.69 Therefore, clinicians need to decide
for one or more issues: plaque accumulation,
whether findings in Table 2 are clinically signifitissue soreness while brushing, increased gincant. Unfortunately, the definition of clinical
gival inflammation, recession, and bone loss.
significance varies depending on the following
In this regard, studies are needed to provide
factors: specific clinical field being addressed,
predictive values with respect to how often speRelated content:
size of the effect, measurement used to evaluate
cific types of biological problems occur when
Learn more about implants at
a therapy, and, ultimately, the clinical importance
KG is lacking. Ultimately, when there is a lack
dentalaegis.com/go/cced27
of the findings.70 With respect to the relationship
of keratinized tissue, clinicians need to make
www.dentalaegis.com/cced

October 2011

compendium

29

Continuing Education 2

a decision to augment or not to increase the band of KG at a site

for that particular individual based on data in the literature, the
patients dental history, the unique characteristics of the site
being treated, and the clinicians experiences.
The literature does not clearly define a patients susceptibility to
deterioration in the absence of KG; however, there are situations
where it seems logical that augmentation of KG would be beneficial:
Chronically inflamed sites, despite oral hygiene instruction
and periodontal therapy. Sometimes it is necessary to alter
the gingival topography to make hygiene easier.
Locations with ongoing recession or continued loss of clinical
attachment or bone, regardless of periodontal therapy and
good oral hygiene.
Sites where the patient complains of soreness when brushing,
despite the appearance of gingival health.
Dental history suggesting predisposition to periodontitis or
recession.
Patients noncompliant with periodic professional maintenance.
To improve esthetics.

ABOUT THE AUTHORS

Gary Greenstein, DDS, MS

Clinical Professor, Department of Periodontology, School of Dental Medicine,

Columbia University, New York, New York; Private Practice, Surgical
Implantology and Periodontics, Freehold, New Jersey

John Cavallaro, DDS

Clinical Director of Dental Implant Fellowship, Clinical Associate Professor, Department

of Prosthodontics, School of Dental Medicine, Columbia University, New York, New
York; Private Practice, Surgical Implantology and Prosthodontics, Brooklyn, New York

References
1. Lindhe J, Echeverria J. Consensus report of session II. In: Lang NP,
Karring T, eds. Proceedings of the 1st European Workshop on Periodontology. Berlin, Germany: Quintessence Publishing; 1994:210-214.
2. Marquez IC. The role of keratinized tissue and attached gingiva in
maintaining periodontal/peri-implant health. Gen Dent. 2004;52(1):74-78.
3. Cairo F, Pagliaro U, Nieri M. Soft tissue management at implant
sites. J Clin Periodontol. 2008;35(8 suppl):163-167.
4. Bouri A Jr, Bissada N, Al-Zahrani MS, et al. Width of keratinized
gingiva and the health status of the supporting tissues around dental
implants. Int J Oral Maxillofac Implants. 2008;23(2):323-326.
5. Yeung SC. Biological basis for soft tissue management in implant
dentistry. Aust Dent J. 2008;53(suppl 1):S39-S42.
6. Maynard JG Jr, Ochsenbein C. Mucogingival problems, prevalence
and therapy in children. J Periodontol. 1975;46(9):543-552.
7. Sullivan HC, Atkins JH. Free autogenous gingival grafts. 3. Utilization of grafts in the treatment of gingival recession. Periodontics.
1968;6(4):152-160.
8. Nabers JM. Extension of the vestibular fornix utilizing a gingival
graftcase history. Periodontics. 1966;4(2):77-79.
9. Miyasato M, Crigger M, Egelberg J. Gingival condition in areas of

30

compendium

October 2011

minimal and appreciable width of keratinized gingiva. J Clin Periodontol. 1977;4(3):200-209.

10. Chang M, Odman PA, Wennstrm JL, Andersson B. Esthetic outcome of implant-supported single-tooth replacements assessed by the
patient and by prosthodontists. Int J Prosthodont. 1999;12(4):335-341.
11. Chung DM, Oh TJ, Shotwell JL, et al. Significance of keratinized
mucosa in maintenance of dental implants with different surfaces. J
Periodontol. 2006;77(8):1410-1420.
12. Thoma DS, Beni GI, Zwahlen M, et al. A systematic review assessing soft tissue augmentation techniques. Clin Oral Implants Res.
2009;20(suppl 4):146-165.
13. Lang NP, Le H. The relationship between the width of keratinized
gingiva and gingival health. J Periodontol. 1972;43(10):623-627.
14. Tenenbaum H. A clinical study comparing the width of attached
gingiva and the prevalence of gingival recessions. J Clin Periodontol.
1982;9(1):86-92.
15. Hangorsky U, Bissada NF. Clinical assessment of free gingival graft
effectiveness on the maintenance of periodontal health. J Periodontol. 1980;51(5):274-278.
16. de Trey E, Bernimoulin JP. Influence of free gingival grafts on the
health of the marginal gingiva. J Clin Periodontol. 1980;7(5):381-393.
17. Dorfman HS, Kennedy JE, Bird WC. Longitudinal evaluation of
free autogenous gingival grafts. A four year report. J Periodontol.
1982;53(6):349-352.
18. Kennedy JE, Bird WC, Palcanis KG, Dorfman HS. A longitudinal
evaluation of varying widths of attached gingiva. J Clin Periodontol.
1985;12(8):667-675.
19. Wennstrm J, Lindhe J. Role of attached gingiva for maintenance
of periodontal health. Healing following excisional and grafting procedures in dogs. J Clin Periodontol. 1983;10(2):206-221.
20. Wennstrm JL. Lack of association between width of attached
gingiva and development of soft tissue recession. A 5-year longitudinal study. J Clin Periodontol. 1987;14(3):181-184.
21. Salkin LM, Freedman AL, Stein MD, Bassiouny MA. A longitudinal study of untreated mucogingival defects. J Periodontol.
1987;58(3):164-166.
22. Freedman AL, Green K, Salkin LM, et al. An 18-year longitudinal study of untreated mucogingival defects. J Periodontol.
1999;70(10):1174-1176.
23. Freedman AL, Salkin LM, Stein MD, Green K. A 10-year longitudinal
study of untreated mucogingival defects. J Periodontol. 1992;63(2):71-72.
24. Agudio G, Nieri M, Rotundo R, et al. Periodontal conditions
of sites treated with gingival-augmentation surgery compared to
untreated contralateral homologous sites: a 10- to 27-year long-term
study. J Periodontol. 2009;80(9):1399-1405.
25. Stetler KJ, Bissada NF. Significance of the width of keratinized
gingiva on the periodontal status of teeth with submarginal restorations. J Periodontol. 1987;58(10):696-700.
26. Ericsson I, Berglundh T, Marinello C, et al. Long-standing plaque
and gingivitis at implants and teeth in the dog. Clin Oral Implants
Res. 1992;3(3):99-103.
27. Greenstein G. Advances in periodontal disease diagnosis. Int J
Periodontics Restorative Dent. 1990:10(5):350-375.
28. Gargiulo AW, Wentz FM, Orban B. Dimensions and relations of
the dentogingival junction in humans. J Periodontol. 1961;32:261-267.
28. Wennstrm JL, Bengazi F, Lekholm U. The influence of the masticatory mucosa on the peri-implant soft tissue condition. Clin Oral
Implants Res. 1994;5(1):1-8.
29. Shimono M, Ishikawa T, Enokiya Y, et al. Biological characteristics
of the junctional epithelium. J Electron Microsc (Tokyo). 2003;52
(6):627-639.
30. Berglundh T, Lindhe J, Ericsson I, et al. The soft tissue barrier at
implants and teeth. Clin Oral Implants Res. 1991;2(2):81-90.

Volume 32, Number 8

31. Berglundh T, Lindhe J, Jonsson K, Ericsson I. The topography of

the vascular systems in the periodontal and peri-implant tissues in
the dog. J Clin Periodontol. 1994;21(3):189-193.
32. Lindhe J, Berglundh T, Ericsson I, et al. Experimental breakdown
of peri-implant and periodontal tissues. A study in the beagle dog.
Clin Oral Implants Res. 1992;3(1):9-16.
33. Warrer K, Buser D, Lang NP, Karring T. Plaque-induced peri-implantitis in the presence or absence of keratinized mucosa. An experimental study in monkeys. Clin Oral Implants Res. 1995;6(3):131-138.
34. Strub JR, Gaberthuel TW, Grunder U. The role of attached gingiva
in the health of peri-implant tissue in dogs. 1. Clinical findings. Int J
Periodontics Restorative Dent. 1991;11(4):317-333.
35. Polson AM, Caton JG, Yeaple RN, Zander HA. Histological determination of probe tip penetration into the gingival sulcus of humans using an
electronic pressure-sensitive probe. J Clin Periodontol. 1980;7(6):479-488.
36. Brnemark PI, Svensson B, van Steenberghe D. Ten-year survival
rates of fixed prostheses on four or six implants ad modum Brnemark in full edentulism. Clin Oral Implants Res. 1995;6(4):227-231.
37. Buser D, Mericske-Stern R, Bernard JP, et al. Long-term evaluation
of non-submerged ITI implants. Part 1: 8-year life table analysis of a
prospective multi-center study with 2359 implants. Clin Oral Implants
Res. 1997;8(3):161-172.
38. Jemt T, Chai J, Harnett J, et al. A 5-year prospective multicenter
follow-up report on overdentures supported by osseointegrated
implants. Int J Oral Maxillofac Implants. 1996;11(3):291-298.
39. Lindquist LW, Carlsson GE, Jemt T. A prospective 15-year followup study of mandibular fixed prostheses supported by osseointegrated implants. Clinical results and marginal bone loss. Clin Oral
Implants Res. 1996;7(4):329-336.
40. Mericske-Stern R. Clinical evaluation of overdenture restorations
supported by osseointegrated titanium implants: a retrospective
study. Int J Oral Maxillofac Implants. 1990;5(4):375-383.
41. Block MS, Gardiner D, Kent JN, et al. Hydroxyapatite-coated cylindrical implants in the posterior mandible: 10-year observations. Int J
Oral Maxillofac Implants. 1996;11(5):626-633.
42. Kirsch A, Ackermann KL. The IMZ osteointegrated implant system. Dent Clin North Am. 1989;33(4):733-791.
43. Binahmed A, Stoykewych A, Hussain A, et al. Long-term followup of hydroxyapatite-coated dental implantsa clinical trial. Int J
Oral Maxillofac Implants. 2007;22(6):963-968.
44. Biesbrock AR, Edgerton M. Evaluation of the clinical predictability of hydroxyapatite-coated endosseous dental implants: a review of
the literature. Int J Oral Maxillofac Implants. 1995:10(6):712-720.
45. Albrektsson T, Sennerby L. State of the art in oral implants. J Clin
Periodontol. 1991;18(6):474-481.
46. De Boever AL, Quirynen M, Coucke W, et al. Clinical and radiographic study of implant treatment outcome in periodontally susceptible and non-susceptible patients: a prospective long-term study.
Clin Oral Implants Res. 2009;20(12):1341-1350.
47. Esposito M, Hirsch JM, Lekholm U, Thomsen P. Failure patterns
of four osseointegrated oral implant systems. J Mater Sci Mater Med.
1997;8(12):843-847.
48. Abrahamsson I, Berglundh T, Wennstrm J, Lindhe J. The peri-implant hard and soft tissues at different implant systems. A comparative study in the dog. Clin Oral Implants Res. 1996;7(3):212-219.
49. Abrahamsson I, Zitzmann NU, Berglundh T, et al. The mucosal attachment to titanium implants with different surface characteristics: an
experimental study in dogs. J Clin Periodontol. 2002;29(5):448-455.
50. Schrott AR, Jimenez M, Hwang JW, et al. Five-year evaluation of
the influence of keratinized mucosa on peri-implant soft-tissue health
and stability around implants supporting full-arch mandibular fixed
prostheses. Clin Oral Implants Res. 2009;20(10):1170-1177.
51. Kim BS, Kim YK, Yun PY, et al. Evaluation of peri-implant tissue
www.dentalaegis.com/cced

response according to the presence of keratinized mucosa. Oral Surg

Oral Med Oral Pathol Oral Radiol Endod. 2009;107(3):e24-e28.
52. Brgger U, Brgin WB, Hmmerle CH, Lang NP. Associations between clinical parameters assessed around implants and teeth. Clin
Oral Implants Res. 1997;8(5):412-421.
53. Zigdon H, Machtei EE. The dimensions of keratinized mucosa
around implants affect clinical and immunological parameters. Clin
Oral Implants Res. 2008;19(4):387-392.
54. Bengazi F, Wennstrm JL, Lekholm U. Recession of the soft tissue
margin at oral implants. A 2-year longitudinal prospective study. Clin
Oral Implants Res. 1996;7(4):303-310.
55. Roos-Jansaker AM, Renvert H, Lindahl C, Renvert S. Nine- to
fourteen-year follow-up of implant treatment. Part III: factors associated with peri-implant lesions. J Clin Periodontol. 2006;33(4):296-301.
56. Adibrad M, Shahabuei M, Sahabi M. Significance of the width of
keratinized mucosa on the health status of the supporting tissue around
implants supporting overdentures. J Oral Implantol. 2009;35(5):232-237.
57. Heckmann SM, Schrott A, Graef F, et al. Mandibular two-implant
telescopic overdentures. Clin Oral Implants Res. 2004;15(5):560-569.
58. Kaptein ML, De Lange GL, Blijdorp PA. Peri-implant tissue health
in reconstructed atrophic maxillaereport of 88 patients and 470
implants. J Oral Rehabil 1999;26(6):464-474.
59. Adell R, Lekholm U, Rockler B, Brnemark PI. A 15-year study of
osseointegrated implants in the treatment of the edentulous jaw. Int
J Oral Surg. 1981;10(6):387-416.
60. Lekholm U, Adell R, Lindhe J, et al. Marginal tissue reactions at
osseointegrated titanium fixtures. (II) A cross-sectional retrospective
study. Int J Oral Maxillofac Surg. 1986;15(1):53-61.
61. Apse P, Zarb GA, Schmitt A, Lewis DW. The longitudinal effectiveness of osseointegrated dental implants. The Toronto Study: peri-implant
mucosal response. Int J Periodontics Restorative Dent. 1991;11(2):94-111.
62. Lang NP, Kiel RA, Anderhalden K. Clinical and microbiological
effects of subgingival restorations with overhanging or clinically
perfect margins. J Clin Periodontol. 1983;10(6):563-578.
63. Silness JA. Periodontal conditions in patients treated with dental
bridges. 3. The relationship between the location of the crown margin and
the periodontal condition. J Periodontal Res. 1970;5(3):225-229.
64. Silness J. Periodontal conditions in patients treated with dental
bridges. 2. The influence of full and partial crowns on plaque accumulation, development of gingivitis and pocket formation. J Periodontal
Res. 1970;5(3):219-224.
65. Marcum JS. The effect of crown marginal depth upon gingival tissue. J Prosthet Dent. 1967;17(5):479-487.
66. Cobb CM. Clinical significance of non-surgical periodontal therapy:
an evidence-based perspective of scaling and root planing. J Clin
Periodontol. 2002;29(suppl 2):6-16.
67. Zitzmann NU, Berglundh T, Marinello CP, Lindhe J. Experimental
peri-implant mucositis in man. J Clin Periodontol. 2001;28(6):517-523.
68. Pontoriero R, Tonelli MP, Carnevale G, et al. Experimentally induced
peri-implant mucositis. A clinical study in humans. Clin Oral Implants
Res. 1994;5(4):254-259.
69. Greenstein G. Clinical versus statistical significance as they
relate to the efficacy of periodontal therapy. J Am Dent Assoc.
2003;134(5):583-591.
70. Lindgren BR, Wielinski CL, Finkelstein SM, Warwick WJ. Contrasting clinical and statistical significance within the research setting.
Pediatr Pulmonol. 1993;16(6):336-340.
71. Krygier G, Glick PL, Versman KJ, et al. To minimize complications,
is it essential that implant abutments be surrounded by keratinized
tissue? Int J Oral Maxillofac Implants. 1997;12(1):127-131.
72. Esposito M, Grusovin MG, Maghaireh H, et al. Interventions for replacing missing teeth: management of soft tissues for dental implants.
Cochrane Database Syst Rev. 2007;18;(3):CD006697.
October 2011

compendium

31