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Peri-Implant

Complications
A Clinical Guide to
Diagnosis and Treatment

Anastasia Kelekis-Cholakis
Reem Atout
Nader Hamdan
Ioannis John Tsourounakis

123
Peri-Implant Complications
Anastasia Kelekis-Cholakis • Reem Atout
Nader Hamdan • Ioannis Tsourounakis

Peri-Implant Complications
A Clinical Guide to Diagnosis
and Treatment
Anastasia Kelekis-Cholakis Reem Atout
University of Manitoba College of Dentistry University of Manitoba College of Dentistry
Winnipeg Winnipeg
Manitoba Manitoba
Canada Canada

Nader Hamdan Ioannis Tsourounakis
Faculty of Dentistry Southwest Specialty Group
Dalhousie University Winnipeg
Halifax Manitoba
Nova Scotia Canada
Canada

ISBN 978-3-319-63717-4    ISBN 978-3-319-63719-8 (eBook)


https://doi.org/10.1007/978-3-319-63719-8

Library of Congress Control Number: 2018935192

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Preface

With the ever increasing use of dental implants aimed at restoring function and
esthetics, it is anticipated that the oral healthcare team will encounter peri-implant
diseases more frequently.
In addition, given the increasing life spans of treated populations and the parallel
advances in biomaterials and implant designs, dental implants are expected to func-
tion for longer periods of time. It is therefore incumbent on the oral healthcare team
to diagnose, treat, and prevent peri-implant diseases.
This clinical guide has endeavored to address biologic soft and hard tissue com-
plications that occur after loading of dental implants. The etiology, diagnosis, and
treatment options for each condition are discussed in each chapter. Possible risk
indicators for the development of these conditions are reviewed based on current
scientific evidence.
This book is recommended for any member of the oral healthcare team that
maintains dental implants.
It provides a comprehensive, yet simple, review of peri-implant diseases that will
guide the practitioner in the long-term maintenance of dental implants.

Winnipeg, MB, Canada Anastasia Kelekis-Cholakis


Winnipeg, MB, Canada Reem Atout
Halifax, NS, Canada Nader Hamdan
Winnipeg, MB, Canada Ioannis John Tsourounakis

v
Contents

1 An Introduction to Understanding the Basics of Teeth vs. Dental


Implants: Similarities and Differences��������������������������������������������������    1
1.1 Definitions������������������������������������������������������������������������������������������   1
1.2 Epidemiology��������������������������������������������������������������������������������������   2
1.3 Classification of Peri-Implant Diseases����������������������������������������������   2
1.4 Peri-Implant Mucositis vs. Peri-Implantitis����������������������������������������   5
1.4.1 Peri-Implant Mucositis�����������������������������������������������������������   5
1.4.2 Peri-Implantitis ����������������������������������������������������������������������   5
1.5 Teeth vs. Dental Implants ������������������������������������������������������������������   6
1.5.1 Soft Tissues around Implants and Teeth ��������������������������������   6
1.5.2 Fiber Arrangement������������������������������������������������������������������   9
1.5.3 Periodontal Probing����������������������������������������������������������������  10
1.5.4 Inflammatory Response����������������������������������������������������������  11
1.5.5 Biofilm������������������������������������������������������������������������������������  13
1.5.6 Microflora around Dental Implants����������������������������������������  14
1.5.7 Healing������������������������������������������������������������������������������������  14
1.6 Summary of Important Concepts��������������������������������������������������������  16
References��������������������������������������������������������������������������������������������������   16
2 Peri-implant Soft Tissue Deficiencies ����������������������������������������������������   21
2.1 Introduction����������������������������������������������������������������������������������������  21
2.1.1 Etiology����������������������������������������������������������������������������������  21
2.2 Diagnosis��������������������������������������������������������������������������������������������  33
2.3 Management/Treatment Options��������������������������������������������������������  40
2.3.1 Improving Peri-implant Soft Tissue Volume��������������������������  43
2.3.2 Improving the Width of Keratinized Mucosa ������������������������  48
2.4 Summary ��������������������������������������������������������������������������������������������  53
References��������������������������������������������������������������������������������������������������   53
3 Peri-implant Mucositis����������������������������������������������������������������������������   59
3.1 Introduction����������������������������������������������������������������������������������������  59
3.2 Etiology����������������������������������������������������������������������������������������������  59
3.2.1 Risk Indicators������������������������������������������������������������������������  59
3.3 Diagnosis��������������������������������������������������������������������������������������������  61
3.3.1 Bleeding on Probing ��������������������������������������������������������������  61

vii
viii Contents

3.3.2 Probing Depths/Radiographic Evaluation������������������������������  61


3.3.3 Prevalence ������������������������������������������������������������������������������  62
3.4 Management/Treatment Options��������������������������������������������������������  62
3.4.1 Patient Education��������������������������������������������������������������������  64
3.4.2 Systemic and Local Factors����������������������������������������������������  64
3.4.3 Patient-Administered Plaque Control ������������������������������������  69
3.4.4 Mechanical Plaque Control����������������������������������������������������  69
3.4.5 Chemical Plaque Control��������������������������������������������������������  71
3.4.6 Professional Debridement������������������������������������������������������  72
3.5 Summary ��������������������������������������������������������������������������������������������  74
References��������������������������������������������������������������������������������������������������   75
4 Hard Tissue Complications/ Peri-implantitis����������������������������������������   79
4.1 Introduction����������������������������������������������������������������������������������������  79
4.2 Etiology����������������������������������������������������������������������������������������������  80
4.2.1 History of Periodontal Disease ����������������������������������������������  81
4.2.2 Smoking����������������������������������������������������������������������������������  84
4.2.3 Poor Oral Hygiene/Lack of Maintenance ������������������������������  84
4.2.4 Diabetes, Alcohol Consumption, and Genetic Factors IL-1
Polymorphisms ����������������������������������������������������������������������  85
4.2.5 Dental Implant Surface ����������������������������������������������������������  86
4.2.6 Occlusal Overload������������������������������������������������������������������  86
4.2.7 Lack of Keratinized Tissue ����������������������������������������������������  88
4.2.8 Iatrogenic Factors��������������������������������������������������������������������  88
4.3 Diagnosis��������������������������������������������������������������������������������������������  91
4.3.1 Bleeding on Probing ��������������������������������������������������������������  91
4.3.2 Probing Depths and Radiographic Evaluation������������������������  92
4.3.3 Suppuration ����������������������������������������������������������������������������  92
4.3.4 Mobility����������������������������������������������������������������������������������  94
4.3.5 Prevalence ������������������������������������������������������������������������������  94
4.3.6 Disease Progression����������������������������������������������������������������  95
4.4 Management/Treatment Options��������������������������������������������������������  95
4.4.1 Removal of Etiologic Factors�������������������������������������������������  96
4.4.2 Nonsurgical Treatment of Peri-implantitis������������������������������  96
4.4.3 Surgical Treatment of Peri-implantitis������������������������������������  96
4.5 Summary �������������������������������������������������������������������������������������������� 113
References��������������������������������������������������������������������������������������������������  114
An Introduction to Understanding
the Basics of Teeth vs. Dental Implants: 1
Similarities and Differences

1.1 Definitions

Throughout the next sections of this book, the reader will encounter a host of terms.
For purposes of clarity, this is a list of some important definitions taken from the
American Academy of Periodontology (AAP) Glossary of Periodontal Terms [1]:

• Peri-implant mucositis: A disease in which the presence of inflammation is con-


fined to the mucosa surrounding a dental implant with no signs of loss of sup-
porting bone.
• Peri-implantitis: An inflammatory process around a dental implant which includes
both soft tissue inflammation and loss of supporting bone.
• Biotype: The thickness or dimension of the soft and hard tissue surrounding
natural teeth or dental implants.
• Osseointegration: A direct contact, on the light microscopic level, between living
bone tissue and a dental implant.
• Fibro-osseous integration: The interposition of healthy dense collagenous tissue
between a dental implant and bone. Also known as fibro-osteal integration.
• Implant, oral: Endosseous root-form implant – an implant placed into the alveo-
lar process and/or basal bone that derives its support from a vertical length of
bone and supports a prosthesis or other devices. Most commonly made of tita-
nium, it can be cylindrical, tapered, etc.
• Implant fixture: A synonym for a dental implant, especially an endosseous
implant.
• Implant abutment: That part of an implant system that connects the dental
implant with a prosthesis or other devices.
• Overdenture: Complete or partial removable denture supported by soft tissue and
retained roots or implants to provide support, retention, and stability and reduce
ridge resorption.
• Recession: The migration of the marginal soft tissue to a point apical to the
cementoenamel junction of a tooth or the platform of a dental implant.

© Springer International Publishing AG, part of Springer Nature 2018 1


A. Kelekis-Cholakis et al., Peri-Implant Complications,
https://doi.org/10.1007/978-3-319-63719-8_1
2 1  An Introduction to Understanding the Basics of Teeth vs. Dental Implants

• Biologic width: The dimension of soft tissue composed of a connective tissue


and epithelial attachment extending from the crest of bone to the most apical
extent of the pocket or sulcus.
• Occlusal trauma: Injury resulting in tissue changes within the attachment apparatus
due to physiologic or parafunctional forces which may exceed its adaptive capacity.
• Piezoelectric surgery: A surgery performed using an instrument which generates
micro-vibrating motion via the application of electromagnetic forces on a poly-
crystal; the micro-vibration of the metallic tip results in ostectomy and osteo-
plasty of the bone in contact with the tip.

• Peri-implant mucositis is a disease confined to the mucosa and is


reversible.
• Peri-implantitis includes both soft tissue inflammation and loss of support-
ing bone and is irreversible.

1.2 Epidemiology

The prevalence of peri-implant diseases has been reported to range from 5 to 63.4%
according to different reports [2]. This variability is due to various studies reporting
different findings depending on the study design, the definitions (threshold of bone
loss) adopted for peri-implant diseases, population size, and other factors.
A better understanding of peri-implant diseases and a consensus on the diagnos-
tic criteria will eventually help in reducing some of this variability in the prevalence
of peri-implant mucositis and peri-implantitis.

1.3 Classification of Peri-Implant Diseases

A classification system for peri-implant diseases is highly desirable. This will assist
healthcare professionals in determining accurate prevalence estimates, providing
clear diagnoses, and assigning prognoses. It will also improve the communication
between health professionals and researchers, as well as the evaluation of treatment
outcomes. However, to date, there is no consensus on a certain classification system
as far as the authors know. This is consistent with the lack of clarity on established
diagnostic criteria, as well as management protocols of peri-implant diseases.
In this section, two proposed classification systems will be provided as
examples:

• The first was proposed by Froum and Rosen in [3]. This classification for peri-­
implantitis is based on the severity of the disease. A combination of bleeding on
probing and/or suppuration, probing depth, and extent of radiographic bone loss
around the dental implant is used to classify the severity of peri-implantitis into
early, moderate, and advanced categories (Table 1.1, Figs. 1.1, 1.2 and 1.3).
1.3  Classification of Peri-Implant Diseases 3

Table 1.1  Classification of peri-implantitis as proposed by Froum and Rosen [3]


Staging Definition
Early PD ≥ 4 mm (bleeding and/or suppuration on probinga)
Bone loss <25% of the implant lengthb
Moderate PD ≥ 6 mm (bleeding and/or suppuration on probinga)
Bone loss 25% to 50% of the implant lengthb
Advanced PD ≥ 8 mm (bleeding and/or suppuration on probinga)
Bone loss >50% of the implant lengthb
a
Noted on two or more aspects of the implant
b
Measured on radiographs from time of definitive prosthesis loading to current radiograph. If not
available, the earliest available radiograph following loading should be used

a b

Fig. 1.1  Early peri-implantitis as proposed by Froum and Rosen [3]. (a) (left) Clinical photograph
of early peri-implantitis at an implant at the maxillary left lateral incisor position. Note the inflamed
tissue and exudate. (Froum and Rosen [3]). (b) (right) Radiograph of maxillary left lateral incisor
with bone loss <25% of the implant length, depicting early peri-implantitis (Froum and Rosen [3])

a b

Fig. 1.2  Moderate peri-implantitis as proposed by Froum and Rosen [3]. (a) (left) Clinical view
of an implant in the mandibular left first molar site. Note the exudate (Froum and Rosen [3]). (b)
(right) Radiograph depicting moderate peri-implantitis, with bone loss of 25–50% of the implant
length on the mesial and distal aspects of the implant (Froum and Rosen [3])
4 1  An Introduction to Understanding the Basics of Teeth vs. Dental Implants

• The second classification system was proposed by Ata-Ali et al. in [4]. In their
article Ata-Ali et  al. proposed a classification for peri-implant mucositis and
peri-implantitis based on the severity of the disease, using a combination of peri-­
implant clinical and radiological parameters to classify severity into several
stages (stage 0A and 0B  =  peri-implant mucositis and stage 1 to 4  =  peri-­
implantitis) (Tables 1.2 and 1.3).

Currently, there is no consensus on a classification system for peri-implant


diseases.

a b c

Fig. 1.3  Advanced peri-implantitis as proposed by Froum and Rosen [3]. (a) (left) Clinical prob-
ing distal to the implant at the maxillary left canine site measured 8 mm (Froum and Rosen [3]).
(b) (middle) Bleeding on probing was noted 15 seconds following removal of the probe (Froum
and Rosen [3]). (c) (right) Radiograph depicting moderate peri-implantitis with bone loss <50% of
the implant length (Froum and Rosen [3])

Table 1.2  Classification of peri-implant mucositis as proposed by Ata-Ali [4]


Staging Definition
Stage 0A PPD ≤ 4 mm and BoP and/or SUP, with no signs of loss of supporting bone
following initial bone remodeling during healing
Stage 0B PPD > 4 mm and BoP and/or SUP, with no signs of loss of supporting bone
following initial bone remodeling during healing
PPD probing pocket depth, BoP bleeding on probing, SUP suppuration

Table 1.3  Classification of peri-implantitis as proposed by Ata-Ali [4]


Staging Definition
Stage I BoP and/or SUP and bone loss ≤3 mm beyond biological bone remodeling
Stage II BoP and/or SUP and bone loss >3 mm and <5 mm beyond biological bone
remodeling
Stage III BoP and/or SUP and bone loss ≥5 mm beyond biological bone remodeling
Stage IV BoP and/or SUP and bone loss ≥50% of the implant lengtha beyond biological
bone remodeling
BoP bleeding on probing, SUP suppuration
a
Depending on implant length, if peri-implantitis can be classified as simultaneously correspond-
ing to more than one stage, the most advanced stage should be chosen
1.4  Peri-Implant Mucositis vs. Peri-Implantitis 5

1.4 Peri-Implant Mucositis vs. Peri-Implantitis

1.4.1 Peri-Implant Mucositis

• It has been proven that the disease process around dental implants is similar to
that which occurs around teeth. Peri-implant mucositis around dental implants is
seen as the equivalent of gingivitis around natural teeth. Peri-implant mucositis
may or may not progress to peri-implantitis as gingivitis may or may not prog-
ress to periodontitis [5, 6].
• Plaque accumulation on the titanium surface and the formation of a biofilm seem
to be essential for the initiation and progression of peri-implant diseases in a way
similar to that found around natural teeth [7–9].
• Peri-implant diseases are linked to similar gram-negative bacteria associated
with severe chronic periodontitis [5, 6, 10, 11].
• When effectively treated, peri-implant mucositis can be reversed back to health
[5, 6].
• The relatively weak epithelial seal around dental implants is similar in function
to that around natural teeth [12].
• The structural difference between teeth and dental implants does not seem to
influence the host response to the bacterial insult [13, 14].

The removal of the biofilm from the dental implant surface is the primary
objective when treating peri-implant mucositis and will lead to the reversal of
disease to a state of health the majority of the time if adequately performed.

1.4.2 Peri-Implantitis

• Peri-implantitis is seen as the equivalent of periodontitis around natural teeth and


similarly occurs when the overwhelming bacterial insult leads to a destructive
host immune response.
• Studies have shown that peri-implantitis and periodontitis lesions from human
biopsies have many features in common [13, 15].
• Bacterial species associated with periodontitis and peri-implantitis are similar.
Moreover, Staphylococcus aureus may also be an important pathogen in the ini-
tiation of peri-implantitis [13, 16, 17].
• The connective tissue adjacent to the pocket epithelium is infiltrated by inflam-
matory cells, with B-lymphocytes and plasma cells being the most dominant cell
types. Similar markers are upregulated between peri-implantitis and periodonti-
tis, including proinflammatory cytokines such as interleukin (IL)-1, IL-6, IL-8,
IL-12, and tumor necrosis factor (TNF)-alpha [18, 19].
• Despite those many similarities between teeth and dental implants, the severity
and rate of disease progression may differ significantly in peri-implantitis when
compared to periodontitis. Experiments that allowed undisturbed dental plaque
6 1  An Introduction to Understanding the Basics of Teeth vs. Dental Implants

formation on dental implants and teeth in humans and in dogs demonstrated a


more advanced inflammatory cell infiltrate in the peri-implant mucosa. Features
of experimentally created peri-implantitis and periodontitis have also been com-
pared. The results suggested that clinical and radiographic signs of tissue destruc-
tion were more pronounced in peri-implantitis cases. Furthermore, the size of the
inflammatory cell infiltrate in the connective tissue was larger, approaching the
crestal bone around implants [13, 20–23]. This could be attributed to the differ-
ences in the orientation and insertion of collagen fibers around teeth compared to
those around dental implants [22].
• All implants appear to be susceptible to peri-implantitis [24, 25].

Despite the similarities in both the bacterial etiology and the immune host
response components between periodontitis and peri-implantitis, peri-­
implantitis progresses at a faster rate with more pronounced bone loss. This
could be attributed to the differences in orientation and insertion of collagen
fibers around teeth compared to those around dental implants.

Early diagnosis and intervention by the elimination of the bacterial biofilm


and correction of other possible contributory factors is the most effective way
in preventing peri-implant diseases.

1.5 Teeth vs. Dental Implants

There are many differences between dental implants and teeth at both the micro-
scopic and the macroscopic level. Some of those differences are best summarized in
Table 1.4 and Fig. 1.4.
Many articles and book chapters have reported on the similarities and differences
that exist between tissues around teeth and those around dental implants. The reader
is encouraged to consult the published literature on this topic including a recent
review entitled “Peri-Implant and Periodontal Tissues: A Review of Differences and
Similarities” [26]. Part of this section was adapted from this publication.

1.5.1 Soft Tissues around Implants and Teeth

• The anatomy and histology of soft tissues surrounding dental implants and teeth
is structurally similar. Those are made up of keratinized oral epithelium, non-­
keratinized sulcular epithelium, and the underlying connective tissue.

Similar to teeth, the junctional epithelium connects to the dental implant/abutment


surface via hemidesmosomes and basal lamina [27]. The combined height of the
1.5  Teeth vs. Dental Implants 7

Table 1.4  Teeth are different from dental implants on both the micro- and the macroscopic
levels
Teeth Dental Implants
Periodontal fibers Insert into cementum on the root Extend parallel to the surface
surfaces of natural teeth of the implant and/or abutment
13 groups 2 groups
Connection Periodontal ligaments Osseointegration
Connective tissue Lower percentage of collagen fibers Higher percentage of collagen
Higher percentage of cells fibers
More vascular Lower percentage of
fibroblasts. Looks very similar
to a scar tissue
Less vascular
Blood supply to Three different sources (the Two different sources (the
surrounding gingivae periodontal ligament space, the supraperiosteal vessels and a
interdental bone, and the few vessels from the bone)
supraperiosteal region)
Periodontal ligament Present Absent
space
Resistance to More resistant Less resistant
mechanical and
microbiological insults
Biological width (BW) JE: 0.97–1.14 mm JE: 1.88 mm
CT: 0.77–1.07 mm CT: 1.05 mm
BW: 2.04–2.91 mm BW: 3.08 mm
Sulcus depth ≤ 3 mm when healthy Could be >3 mm depending on
multiple factors
Proprioception Periodontal mechanoreceptors Osseoperception
Tactile sensitivity High Low
Axial mobility 25–100 μm 3–5 μm
Fulcrum when lateral Apical third of the root Crestal bone
force applied
Possible relief Pressure absorption, distribution Pressure concentration on the
crestal bone
Adapted from different sources, mainly Tokmakidis et al. [85] and Ramoglu et al. [86].

junctional epithelium and connective tissue attachment is usually referred to as the


“biologic width.” Early work by Gargiulo et  al. [28] estimated this to be about
2.04 mm around teeth. However, a recent systematic review concluded that there is
no universal dimension for biologic width around teeth with large intra- and interin-
dividual variances (subject sample range, 0.2–6.73 mm) [87].

• In a human histologic study, the length of the peri- implant seal was found to
be about 4–4.5 mm [88]. When compared to the “biologic width” around teeth,
the same attachment around dental implants was longer nearly by the factor of
1.5 mm [89].
• This protective distance that exists between the alveolar crest of bone and the
base of the gingival pocket should always be kept constant and respected in order
to avoid bone loss around teeth. If for any reason, e.g., deeply placed restorative
margin, this biologic distance is not maintained, then bone around the affected
tooth will resorb in what seems like an adaptive mechanism, to mitigate the
8 1  An Introduction to Understanding the Basics of Teeth vs. Dental Implants

a Enamel b Titanium implant


Sulcus

Sulcular
(crevicular) Sulcular
epithelium epithelium
Junctional
epithelium Junctional
epithelium
Connective
tissue Connective
tissue
Cementum

Bone
Bone

Fig. 1.4  Schematic illustration of hard and soft tissue around a tooth and an implant. (a) Hard and
soft tissue anatomy around a natural tooth demonstrates bone support with a periodontal ligament,
a connective tissue zone above the crest of bone with connective tissue fibers (Sharpey’s) inserting
into dentin, a long junctional epithelial attachment, a gingival sulcus lined with sulcular epithe-
lium, and oral gingival epithelium (outer surface of gingiva). (b) Hard and soft tissue anatomy
around an implant demonstrates some similarities and some distinct differences. There is support-
ing bone in direct approximation to the implant surface without any intervening soft tissues (i.e.,
no periodontal ligament). A connective tissue zone is present above the level of bone with fibers
running parallel to the implant surface and no inserting fibers. There is a long junctional epithelial
attachment, a gingival or mucosal sulcus lined with sulcular epithelium, and oral gingival or muco-
sal epithelium (outer surface of soft tissue) (From Rose LF, Mealey BL: Periodontics: Medicine,
surgery, and implants, St. Louis, 2004, Mosby)

effects of those noxious stimuli. A similar principle applies to dental implants


where changes in the soft tissue to bone relationship may be one of the reasons
for the early crestal bone loss seen around dental implants [29].
• Upon dental implant placement, the fast-moving epithelial cells will migrate api-
cally until they reach the dental implant surface where they attach themselves
rapidly through the basal lamina and the hemidesmosomes [30]. Another possi-
ble attachment modality hypothesized is an indirect epithelium-to-implant con-
tact [31]. This is very similar to what happens around teeth following soft tissue
flap reflection and healing.
• Human studies have demonstrated that epithelium surrounding dental
implants possess similar patterns of differentiation and function to gingival
tissues [32]. However, what stops the epithelium from migrating further api-
cally on the implant surface? The presence of granulation tissue adhering to
the surface of the transmucosal components is considered the principal factor
1.5  Teeth vs. Dental Implants 9

that prevents the apical migration of epithelium [33]. Berglundh speculated


that this most likely occurs due to the interaction of the titanium surface with
the soft tissue [34].
• The following sequence of events occur once an dental implant is inserted into bone:
–– Formation and adhesion of the fibrin clot to the dental implant surface
–– Adsorption of the fibrin clot to the dental implant surface and adsorption of
the extracellular matrix (ECM) proteins and connective tissue cells to the den-
tal implant surface
–– Transformation of the clot into granulation tissue and migration of epithelial
cells on top of the fibrin clot/granulation tissue [35]
• The connective tissue zone next to the dental implant surface is primarily divided
into two segments.
–– The first part is a 50 μm inner zone that is rich in fibers, resembling scar tissue
and containing several scattered fibroblasts in close contact with the titanium
surface. This zone maintains the seal between the peri-implant bone and the
oral environment [36, 37].
–– The remaining part of the connective tissue is comprised of fibers running in
different directions, along with cellular elements and blood vessels [37].
Connective tissue cells and collagen fiber bundles are separated from the
TiO2 surface with a 20-nm-wide proteoglycan layer [38].

The “biologic width” should always be respected and maintained around the
dental implant to decrease early bone loss.

1.5.2 Fiber Arrangement

• In natural teeth, the non-keratinized junctional epithelium attaches to the


enamel surface via the internal basal lamina and hemidesmosomes along the
entire length of the junctional epithelium. In contrast, the attachment of the
peri-implant epithelium to the implant surface is confined to the coronal region
only.
• In human subjects, fibers have been described as running a parallel course to the
dental implant surface [39]. Several other authors, however, have found fibers
oriented in different directions. A perpendicular direction was also found with
dental implants harboring porous surfaces [40, 41]. The orientation of fibers
seems to be dependent on the quality of the mucosa: fibers tend to be parallel in
alveolar mucosa and perpendicular in keratinized mucosa. In teeth, fibers insert
perpendicularly into the cementum.
• Apart from the orientation of the fibers, there exists a significant difference
between the connective tissue around the tooth and abutment. The dentogingival
collagen fibers are firmly inserted into the cementum and the bone, in a
10 1  An Introduction to Understanding the Basics of Teeth vs. Dental Implants

perpendicular or oblique direction, thus serving as a barrier to the epithelial


migration and the impending bacterial invasion [42]. The connective tissue adhe-
sion with dental implants has poor mechanical resistance when compared to the
one on natural teeth [43]. This in part explains the higher rate of disease progres-
sion around dental implants compared to the more resistant cell-rich environ-
ment that typically exists around natural teeth.
• Due to the reduced vascularization and parallel orientation of the collagen
fibers, peri-implant tissues are more susceptible to inflammatory disease than
periodontal tissues. This phenomenon can be verified immunohistochemically
through increased formation of inflammatory infiltrate, nitric oxide 1/3,
VEGF, lymphocytes, leukocytes, and Ki-67 [44]. Besides, in analogy to peri-
odontitis, the level of matrix metalloproteinases (MMP), such as MMP-8, is
increased up to 97.1% in peri-implant lesions. The latter can be used for diag-
nostic purposes [45–47].
• There appears to be a resilient connection between bone, periodontal ligament,
and cementum around a tooth. However, a rigid connection appears in the form
of functional ankylosis/osseointegration, due to the lack of periodontal ligament,
around the dental implant. Absence of resiliency somewhat leads to the direct
transmission of the loads to the bone-implant interface, and no compensatory
tooth movements can accommodate the occlusal disharmony.
• The lack of periodontal ligament also precludes the use of dental implants in
growing individuals.
• The adaptive capacity of the periodontal ligament allows orthodontic tooth
movements; however, such movements cannot be undertaken with dental
implants.
• The highly sensitive receptors present within the periodontal ligament are
responsible for the proprioceptive and tactile sensitivity around the tooth.
Absence of the periodontal ligament leads to reduced tactile sensation and reflex
function around dental implants [48].

Due to the reduced vascularization and parallel orientation of the collagen


fibers, peri-implant tissues are more susceptible for inflammatory disease than
periodontal tissues.

1.5.3 Periodontal Probing

• Periodontal probing is one of the basic diagnostic tools used to measure clinical
attachment level (CAL), pocket depth, and width of the attached gingiva [1].
• The probing depth is the distance between the gingival margin and the depth of
the probe tip penetration into the pocket [49].
• Increased probing depth with concurrent loss of clinical attachment is pathogno-
monic of periodontal disease [50].
1.5  Teeth vs. Dental Implants 11

• Peri-implant probing provides an assessment of different parameters such as


bleeding on probing, suppuration, and exudation from the sulcus and peri-­
implant tissues [40].
• Studies have shown that, when used, probe pressure of 0.5 N penetrates an aver-
age of 0.7  mm deeper at implant sites [51]. Clinical probing depth is greater
around dental implants versus teeth, as the probe tip ends apically to the junc-
tional epithelium into the connective tissue close to the bone crest [52]. This
explains why bleeding on probing is a more reliable sign of inflammation around
a tooth but is less reliable around dental implants.

Gentle probing around dental implants during routine clinical examinations is


necessary to diagnose early peri-implant disease.

1.5.4 Inflammatory Response

• Diagnostic criteria for detection of peri-implant health and for monitoring the
progression of disease are similar to that of periodontal disease. The gingival/
mucosal tissues constitute the primary defense mechanism against microbial
infections. The conversion of the junctional epithelium to the pocket epithelium
is considered to be the key to the progression of gingivitis/peri-implant mucositis
to periodontitis/peri-implantitis.
• When performing visual inspection of peri-implant soft tissues signs of disease
include color alteration, swelling, thickness, and bleeding on probing, all clinical
indices used for the evaluation of gingival disease. Inflammatory lesions may be
present in the absence of visual signs of inflammation.
• The peri-implant crevice is surgically created and is not developed as it is for
natural teeth. Pocket depth is determined by many factors such as abutment
height, depth of fixture countersinking at stage 1 surgery, and the amount of tis-
sue thinning during stage 2 surgery [37]. Structural differences between the peri-­
implant and periodontal tissues, dictate the probing pattern around dental
implants as well.
• As stated previously, the parallel disposition of the collagen fibers to the implant
surface and the absence of the connective tissue insertion cause the probe to go
beyond the epithelial seal, which results in injury to the underlying connective
tissue [53].
• Sulcular exudate from gingiva is called gingival crevicular fluid (GCF), and
that from dental implants is known as peri-implant sulcular (crevicular) fluid
(PISF/PICF). Gingival crevicular fluid is a healthy serum transudate in a
healthy free gingiva, and during inflammation GCF is converted into an
inflammatory exudate originating from the vessels of the gingival plexus.
GCF is recognized as a part of the gingival defense system. GCF is rich in
leucocytes, especially polymorphonuclear leukocytes (PMN), and is attracted
12 1  An Introduction to Understanding the Basics of Teeth vs. Dental Implants

by a chemotactic gradient of bacterial or host origin. It is also rich in host-


derived molecules from blood, as well as substances from microorganisms of
dental plaque. The GCF flow requires permeability-­ induced initiators of
inflammation. About 65 different infection-­induced enzymes and their inhibi-
tors and regulators have been found [26].
• PISF is an inflammatory exudate originating from the vessels of the gingival
plexus and is similar to GCF.  It contains the host-derived enzymes and their
inhibitors, host response modifiers, and tissue breakdown products. PISF vol-
ume, along with increased enzymatic activity, has been suggested to be elevated
during inflammation, which confirms the diagnostic potential of PISF in peri-
implant inflammation.
• GCF functions to continuously flush the dentogingival crevice and release anti-
microbial components of serum such as antibodies and complement enzymes. In
disease, the crevicular fluid flow increases 30 times more than in health.
• The biologic inflammatory response of the tissues around teeth and dental
implants depends largely on their histologic framework. Dental implants are
surrounded by a dense network of collagen fibers that originate from the alveo-
lar bone crest, and extend to the peri-implant mucosal margin in a parallel
fashion, in contrast to teeth, where collagen fibers are perpendicular to the root
surface. The fibers in peri-implant tissues appear very large and follow a circu-
lar arrangement around the dental implant neck. Fiber-to-metal surface contact
has generally not been observed. There are studies, however, that have observed
direct fibrous attachment to the titanium surface [43]. The length of the supra-
alveolar connective tissue in dental implants is also significantly larger than
that of teeth. Teeth have multiple collagen bundle fibers that run in various
directions to various adjacent structures. Studies based on the response of teeth
and dental implants to experimental breakdown, have revealed the differences
in the nature of tissue loss. Ligature-induced periodontal and peri-implant
lesions, in beagle dogs, revealed more pronounced tissue destruction around
dental implants than around teeth. Furthermore, the size of the soft tissue lesion
was found to be larger around dental implants and extended into the bone mar-
row [21]. Another study described the host response results of long-standing
plaque and gingivitis. This study revealed an inflammatory cell infiltrate that
extended more apical into the peri-implant mucosa (~ 1.5 mm) than the gingi-
val tissues (~ 0.9 mm) [55].
• Histomorphometric studies have revealed that dental implants and teeth have
a comparable ratio of collagen, vessels, and plasma cells, whereas peri-
implant tissues have lower proportions of lymphocytes, macrophages, and
PMNs. Hence, peri-implant tissues form a weaker biologic barrier to the api-
cal migration of inflammatory cell infiltrate [20]. Another study measured the
levels of myeloperoxidase (MPO) and nitrite as 2 molecular measures of
inflammation between teeth and dental implants. Although MPO was found to
be stable in healthy and diseased sites, in both GCF and PISF, nitrite levels
were found to be significantly elevated in the PISF of diseased sites compared
to healthy sites [56].
1.5  Teeth vs. Dental Implants 13

1.5.5 Biofilm

• When exposed in the oral cavity the transmucosal abutment of an osseointegrated


dental implant provides a favorable surface for bacterial colonization. This further
leads to the selective adsorption of salivary proteins, peptides, etc., and the rapid
formation of pellicle [55]. Biofilm formation around dental implants is similar to
that formed around teeth [57]. The composition of the pellicle around dental
implants lacks the low molecular mucins commonly found on the enamel in natu-
ral teeth. This may explain the qualitative and quantitative differences of plaque
formation around dental implants, when compared to natural teeth [58]. However,
these differences do not seem to influence the bacterial composition of the early
biofilms formed on the dental implant surface. Biofilm formation on dental
implants is influenced by the properties of the surface to be colonized, including
chemical composition, surface roughness, and surface free energy [59].
• Many studies have pointed out the comparative rates and the composition of the
microbiota associated with health and disease in teeth and dental implants [5, 60,
61]. Classic differences in the microbial profile of the peri-implant flora in cer-
tain in vitro studies reveal an affinity of Staphylococcus aureus for the titanium
surface; however, it is not commony found in the microflora around teeth [62].
This bacterium has, according to the results of Salvi et al. a high positive (80%)
and negative (90%) predictive value for the development of peri-implantitis [63].
A host response to the bacterial challenge is known to develop irrespective of the
dental implant system [64], while the initial host response to the bacterial chal-
lenge in the peri-implant mucosa is similar to that found in gingiva. However, the
long-standing inflammation does have a more pronounced response in the peri-­
implant tissues than in gingival tissues. This leads to the significant apical exten-
sion of the inflammatory infiltrate in the peri-implant mucosa and the increased
size of the lesion as compared to the gingival tissues [57].
• Histopathologic data of human case series have described the dominance of B
cells and plasma cells in the inflammatory lesion, suggesting that peri-implantitis
and periodontitis lesions are similar [65, 66]. Despite the fact that peri-­implantitis
and periodontitis develop similarly, the dynamics of this process could be differ-
ent. Because the periodontitis lesion is walled off by the intact supracrestal con-
nective tissue fiber compartment, the penetration of the infiltrate into the bone
marrow is generally not evident. However, because of the absence of the supra-
crestal connective tissue fibers, the peri-implantitis lesion often progresses rap-
idly into the bone marrow [56, 67].
• Periodontitis and peri-implantitis share common risk factors, such as poor oral
hygiene, tobacco consumption, and diabetes mellitus. Cross-sectional analyses
have evaluated the risk indicators for peri-implantitis to be poor oral hygiene,
history of periodontal disease tobacco consumption, diabetes mellitus, alcohol
consumption, and genetic traits [68].

Periodontitis and peri-implantitis share common risk factors.


14 1  An Introduction to Understanding the Basics of Teeth vs. Dental Implants

1.5.6 Microflora around Dental Implants

• The microbiota on dental implants in edentulous and partially edentulous patients


and in patients with a history of periodontal disease varies. Studies have stated
that the microbiota obtained from colonizing clinically healthy dental implant
fixtures in fully edentulous subjects are similar to the microbiota associated with
healthy periodontal sites in periodontally healthy subjects [69]. It was suggested
that extraction of all teeth results in elimination of the Porphyromonas gingivalis
and Aggregatibacter actinomycetemcomitans from the oral microbiota [70].
• In partially edentulous subjects the developing microbiota around dental implants
is similar to that of natural teeth [71]. This microflora – 85% of which is identi-
fied as gram-positive cocci—colonize the dental implant surface, immediately
after the installation of the fixture. Microbial colonization and the ensuing
inflammatory reaction in the peri-implant tissues might be analogous to the key
events in the pathogenesis of periodontitis. The literature comparing the micro-
biota around dental implants in fully edentulous and partially edentulous mouths,
reports a higher percentage and frequency of black-pigmented bacteroides, fewer
coccoids and motile rods, and a higher frequency of the P. gingivalis and P. inter-
media on implant surfaces in partially edentulous subjects [72, 73]. The micro-
biota of the remaining teeth serve as the primary source of the putative pathogens.
This reveals that the microbial state of the remaining teeth influences the fate of
the newly incorporated dental implants [74]. The microbiota on dental implants
in subjects with a history of periodontal disease is similar in nature to those
found in the periodontal pockets around teeth [75]. It would seem likely that
susceptibility to periodontitis may translate to higher risk for peri-implantitis.
Several reviews have reported a history of treated periodontitis as a risk indicator
for implant outcomes with statistically significant results [17, 76, 77]. Zitzmann
et al. quantified the incidence of the development of peri-implantitis in patients
with a history of periodontitis almost six times higher than in patients with no
history of periodontal inflammation [2].

Active periodontal disease should be controlled before placement of dental


implants.
Microbial biofilms on dental implants, in subjects with a history of periodon-
tal disease, are similar to those found in periodontal pockets around teeth.

1.5.7 Healing

• The healing response of tissues around dental implants varies from that of natu-
ral teeth [78]. Dental implants exhibit a poor vascular supply compared to teeth.
Following dental implant insertion, tissue repair requires development of the
vasculature at the site of injury. The delivery of oxygen and nutrients, as well as
the removal of cell debris is essential for a complete healing process [79].
1.5  Teeth vs. Dental Implants 15

• Berglundh reported that dental implants placed following flap elevation resulted in
poor vascular supply between the junctional epithelium and marginal bone [34].
Ericcson explained that the poor vascular supply in the peri-implant mucosa may
be the reason for the extensive progression of plaque-associated inflammation [55].
• In the presence of teeth, blood supply to the bone comes from 3 different sources:
the periodontal ligament space, the connective tissue above the periosteum, and
from within the bone. However, when a tooth is lost, periodontal ligament blood
supply is also lost. Cortical bone by nature is poorly vascularized and has very
few blood vessels running through it, in contrast to marrow bone. So, when soft
tissue flaps are reflected for implant placement, the third and last source of blood
supply from the soft tissue to the bone (supraperiosteal blood supply) is removed
leaving poorly vascularized cortical bone with minimal or no vascular supply,
thus prompting bone resorption during the initial healing phase [54, 80, 82]. With
a flapless approach, the periosteum and blood vessels remain intact with clinically
insignificant crestal bone loss for up to 4 years [90]. In an experimental study in
pigs, Vlahović et al. concluded that when compared to conventional flap proce-
dures, flapless techniques minimized postoperative bone inflammatory reactions
[91]. Furthermore, flapless implant placement results in the reduction of surgery
duration, pain intensity, related analgesic consumption and most other complica-
tions typical in the postimplant surgery period, accelerating the postsurgical heal-
ing as the amount of tissue injury is known to influence the speed and quality of
healing [81, 92, 93]. In spite of these evident advantages, the major drawback of
flapless approach is that it is a “blind” surgical technique. Nevertheless, the devel-
opment of three-dimensional imaging technology and computer-guided implanto-
logy and its recent widespread adoption in the field of dental implantology have
improved the accuracy in the preparation of dental implant sites [91, 94–96]
• Due to similar etiologies of periodontal and peri-implant infections, the thera-
peutic approaches also appear to be similar – i.e., anti-infective. Evidence sug-
gests that the long-term results of periodontal treatment are promising [83].
Since existing periodontal lesions can become a reservoir of pathogens to colo-
nize the dental implant surface, it is imperative to successfully treat and control
periodontal disease prior to dental implant placement. Periodontal treatment
involves the debridement of the contaminated root surfaces, whereas the treat-
ment of peri-­implantitis focuses on the decontamination of the dental implant
surface. Despite the surface roughness and configuration, decontamination of the
titanium surface poses inherent problems and can likely not be achieved by
debridement alone. Animal studies have concluded that no method of dental
implant surface decontamination is superior to another [84].

Despite the surface roughness and configuration, decontamination of the tita-


nium surface poses inherent problems and can likely not be achieved by
debridement alone. Animal studies have concluded that no method of dental
implant surface decontamination is superior to another.
16 1  An Introduction to Understanding the Basics of Teeth vs. Dental Implants

1.6 Summary of Important Concepts

• Peri-implant mucositis is a disease confined to the mucosa and is reversible.


• Peri-implantitis includes both soft tissue inflammation and loss of supporting
bone and is irreversible.
• Currently, there is no consensus on a classification system for peri-implant
diseases.
• The removal of the biofilm from the implant surface is the primary objective in
the treatment peri-implant mucositis and will lead to the reversal of disease, in
most cases, if properly performed.
• Despite the similarities in both the bacterial etiology and the immune host response,
between periodontitis and peri-implantitis, peri-implantitis progresses at a faster
rate with more pronounced bone loss. This can be attributed to the differences in
orientation and insertion of collagen fibers around teeth vs. dental implants.
• Early diagnosis and intervention, by eliminating the bacterial biofilm and con-
trolling other possible contributing factors, is the most effective way in prevent-
ing peri-implant diseases.
• The “biologic width” should always be respected and maintained around dental
implants to avoid early bone loss.
• Due to the reduced vascularization and parallel orientation of the collagen fibers,
peri-implant tissues are more prone to inflammatory breakdown than periodontal
tissues.
• Gentle probing around dental implants during routine clinical examinations is
necessary to diagnose early peri-implant disease.
• Periodontitis and peri-implantitis share common risk factors.
• Active periodontal disease should be controlled before placement of dental implants.
• Microbiota on dental implants in subjects with a history of periodontal disease
are similar in nature to those found in the periodontal pockets around teeth.
• Despite the surface roughness and configuration, decontamination of the tita-
nium surface poses inherent problems and can likely not be achieved by debride-
ment alone. Animal studies have concluded that no method of dental implant
surface decontamination is superior to another.

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Peri-implant Soft Tissue Deficiencies
2

2.1 Introduction

The definition of a “successful implant” has evolved over the years to include,
beyond functional utility, high esthetic outcomes. Nowadays, a definition of a suc-
cessful dental implant includes, among others, the patient’s and clinician’s esthetic
satisfaction, which is achieved by a restoration that is in harmony with the surround-
ing teeth and tissues [1]. The final restoration should match the size, form, and color
of the adjacent teeth and be framed by soft tissues consistent in color, shape, and
texture [2] (Fig. 2.1).
The harmonization of peri-implant structures may depend on several clinical
parameters such as bone and soft tissue volume, precise implant placement, and the
quality of the prosthetic restoration. Appropriate diagnosis and treatment planning
is imperative to achieve a successful outcome.
Lack of keratinized mucosa, inadequate soft tissue volume, and peri-implant tis-
sue recession may all result from inappropriate treatment planning and execution.
Peri-implant soft tissue plastic surgery has been used to prevent and correct such
tissue deficiencies. In this chapter both preventive and treatment strategies will be
reviewed.

2.1.1 Etiology

Multiple factors may predispose to peri-implant soft tissue deficiencies. These fac-
tors may have a synergistic effect on dental implant esthetics, stability of the peri-­
implant tissues, and peri-implant tissue health [3] (Table 2.1).

2.1.1.1 Inadequate Keratinized Tissue


The need for keratinized mucosa around dental implants has been controversial.
While some systematic reviews have shown no significant difference in long-term

© Springer International Publishing AG, part of Springer Nature 2018 21


A. Kelekis-Cholakis et al., Peri-Implant Complications,
https://doi.org/10.1007/978-3-319-63719-8_2
22 2  Peri-implant Soft Tissue Deficiencies

Fig. 2.1  Excellent hard


and soft tissue outcome
with a dental implant
present in the maxillary
right central incisor
position

Table 2.1  Factors predis- Inadequate keratinized mucosa


posing to peri-implant Soft tissue volume
recession Periodontal biotype
Dental implant position
Peri-implant bone volume
Persistent inflammation
Timing of implant placement
Prosthesis design and contour
Adapted from Jia-Hui Fu et al. “Esthetic soft tissue management for
teeth and implants”. J Evid Based Dent Pract. 2012;12 (3 Suppl):
129–42

peri-implant health and stability, others have disputed this conclusion. Wennström
et al. examined the importance of keratinized tissue in maintaining peri-implant
health and tissue stability. They concluded that there was limited evidence that
keratinized tissue was necessary if plaque control was adequate. Appropriate
width of keratinized tissue was defined as >2 mm [4]. However, recent evidence
has shown a stronger correlation between the lack of keratinized tissue around
dental implants and worse peri-implant parameters, including more pronounced
gingival recession [5] (Fig. 2.2). Despite the controversy existing in the literature,
on the need for keratinized tissue around dental implants, soft tissue augmentation
may be advantageous for the maintenance of peri-implant soft tissue health [6].
Furthermore, an increased width of keratinized tissue may facilitate more effec-
tive oral hygiene and improve peri-implant soft tissue health, as well as long-term
soft tissue stability [7].

2.1.1.2 Soft Tissue Volume/Mucosal Thickness


There is no general consensus on the amount of soft tissue needed around dental
implants in order to maintain soft tissue architecture. Zigdon and Machtei found
that thin mucosa (<1  mm) was associated with two times greater recession than
thick (>1 mm) [8]. In addition, a narrow mucosal band (<1 mm) was associated with
three times greater mucosal recession and more peri-implant attachment loss.
2.1 Introduction 23

Fig. 2.2  Thin keratinized


mucosa with high frenulum
attachment on the
mandibular first premolar
implant, resulting in
peri-implant tissue
recession

Fig. 2.3 Sub-optimal
soft tissue volume allowing
the titanium abutment to
show through the tissue
creating a gray shadow, at the
maxillary right first premolar
implant

It has been recommended that the optimal thickness of the peri-implant tissue be
around 2 mm [9, 10]. Evidence suggests that when the tissue volume is less than
2 mm, the restorative material may affect the esthetic outcome [11, 12]. Thus, all
ceramic abutments/restorations should be used in order to achieve optimal esthetics.
On the other hand, when the soft tissue volume is more than 2 mm, more options for
the restorative materials are available, as the esthetic outcome does not seem to be
compromised [13, 14] (Fig. 2.3).
There is evidence that soft tissue volume may facilitate hard tissue stability. A
prospective controlled clinical trial found that significantly less bone loss occurred
around bone-level implants placed in naturally thick buccal mucosa when compared
to ones surrounded by thin soft tissue [15]. However, at this point in time, Akcali
et al., in a systematic review, found that there is insufficient evidence that soft tissue
thickness impacts crestal bone loss [16]. Unfortunately, a critical soft tissue dimen-
sion that would offer long-term peri-implant soft tissue stability has not yet been
universally accepted [17].
24 2  Peri-implant Soft Tissue Deficiencies

2.1.1.3 Periodontal Biotype


Periodontal biotype plays a critical role in the predictability of the outcome and
long-term stability of peri-implant soft tissues. Multiple studies have subdivided
periodontal tissues into thin, scalloped, and thick, flat periodontium [18, 19].
Each periodontal biotype responds differently and has its own characteristics that
may affect the final surgical outcome [20, 21] (Table 2.2). One of the difficulties
in evaluating the data that attempts to link peri-implant biotype to mucosal reces-
sion is that current studies have limited sample size and lack of consensus as to
what is considered a thin or thick biotype. In some studies thin biotype is defined
as “probe seen through the labial tissue,” while in others 1mm or less soft tissue
thickness is used as a criterion. There are, however, some studies that have shown
an increased risk of mucosal recession around dental implants, in patients with
thin soft tissue biotype [22–24]. In general, periodontal biotype should be taken
into consideration during treatment planning, keeping in mind that a thick peri-
odontal biotype is typically more predictable in preserving the gingival architec-
ture when compared to a thin biotype. In patients with a thin biotype, a more
sophisticated treatment protocol should be selected in order to achieve the desired
outcome (Figs. 2.4 and 2.5).

2.1.1.4 Dental Implant Position


Implant position in relation to the buccolingual, apico-coronal, and mesiodistal
dimensions of the alveolar ridge is a factor that influences the degree of bone

Table 2.2  Characteristics of tissue biotypes, their association to tooth morphology, and the reac-
tion of each biotype to inflammation, surgery, and tooth extraction
Periodontal biotypes Thin, scalloped biotype Thick, flat biotype
Anatomy and Scalloped gingiva Flat soft tissue
anatomical variations Scalloped bone Flat bony architecture
Pointed papillae Short papillae
Thin buccal plate Thick buccal plate
Increased prevalence of fenestration Dehiscence and fenestration
and dehiscence defects defects are rare
Tooth morphology Narrow teeth (tapered) Wide teeth (square)
Tooth proportions of 50–60% Tooth proportions of 80–90%
Inflammation Responds to inflammation by Responds to insult by pocket
recession and loss of the thin alveolar formation, and infra-bony
bone defects
Surgery Delicate tissues, unpredictable Predictable hard and soft tissue
healing (recession, tissue dehiscence) healing
Tooth extraction Extensive ridge resorption Minimal ridge resorption
Sourced from: Olsson M and Lindhe J: Periodontal characteristics in individuals with varying form
of the upper central incisors. J Clin Periodontol 1991; 18: 78-82, Becker W, Ochsenbein C, Tibbetts
L, Becker BE. Alveolar bone anatomic profiles as measured from dry skulls. J Clin Periodontol
24:727-731,1997 Kao, R. T., Fagan, M. C. & Conte, G. J. (2008) Thick vs. thin gingival biotypes:
a key determinant in treatment planning for dental implants. Journal of the California Dental
Association 36, 193–198. De Rouck T, Eghbali R, Collys K, De Bruyn H, Cosyn J. The gingival
biotype revisited: transparency of the periodontal probe through the gingival margin as a method
to discriminate thin from thick gingiva. J Clin Periodontol 2009; 36: 428–433
2.1 Introduction 25

Fig. 2.4  Thick biotype,


short papillae, flat tissue
architecture

Fig. 2.5  Thin biotype,


pointed papilla, scalloped
gingiva

remodeling following implant placement [25]. Bone remodeling may have a nega-
tive impact on the soft tissue position around dental implants and could lead to
unfavorable esthetic outcomes.

Buccolingual
A recent systematic review identified buccal implant positioning as one of the fac-
tors that can lead to resorption of the buccal plate and mucosal recession [26]. This
finding was supported by another systematic review that reported that immediately
placed implants that were buccally malpositioned in extraction sockets had a three
times greater chance of recession when compared to more palatally placed implants
[27] (Fig. 2.6).

Apico-coronal
Some clinical guidelines have been proposed regarding the ideal dental implant
positioning. Funato et  al. described the ideal position as a restoration-driven 3D
implant placement [28]. The author also suggested that the platform of the implant
should be placed 2–4 mm below the mid-buccal aspect of the future gingival mar-
gin. Buser described the concept of “comfort zone and danger zone,” when dental
implants are placed in the esthetic zone, where the position of the dental implant
26 2  Peri-implant Soft Tissue Deficiencies

Fig. 2.6  Peri-implant mucosal recession is obvious at the right maxillary central incisor due to the
buccal position of the dental implant

shoulder should be at the ideal point of emergence [29]. He also suggested that the
implant shoulder should be placed as shallow as possible and as deep as necessary,
as a compromise between biological principles and esthetics.

Mesiodistal
The distance between an implant and a tooth or among two implants can affect pap-
illary height.
When considering implant placement adjacent to a tooth, the papilla fill depends
mostly on the clinical attachment level of the adjacent tooth and more specifically
on the apico-coronal distance from the alveolar bone crest to the contact point.
Choquet et al. reported that when the distance from the alveolar crest to the contact
point is 5 mm or less, the papilla was present in almost 100% of the cases, whereas
when the distance increased to 6 mm or more, the papilla was present in only 50%
or less of the cases [30]. The greater the distance from the bone crest to the contact
point, the higher the risk for incomplete papilla fill. There is no current agreement
in the literature on an absolute number that will result in a predictable papilla fill [9].
Buser et  al. suggested that the mesiodistal distance between a tooth and an
implant should not be less than 1.5 mm and between two implants should be 3 mm
or more [29]. Therefore if this distance is not respected, there is a risk of bone loss
resulting in loss of interproximal papilla.
When two implants are placed adjacent to each other, there appears to be an addi-
tive osseous remodeling effect. A study with adjacent implants found that when
implants were placed within 3  mm from each other, they developed 1.04  mm of
interproximal bone loss compared to implants placed at a greater than 3.0 mm dis-
tance, which lost only 0.45 mm of bone [31]. However a recent systematic review
concluded that based on the current level of evidence, it is not possible to determine
an absolute number for an optimal inter-implant distance. However, a tendency
existed for incomplete papilla fill when adjacent implants were placed closer than
3 mm [32] (Fig. 2.7).

2.1.1.5 Peri-implant Bone Volume


A critical component of treatment planning in dental implant therapy is the amount
of available bone. It has been postulated that to maintain stable peri-implant soft
2.1 Introduction 27

Fig. 2.7  Loss of inter-


implant soft tissue due to
inadequate inter-implant
distance

tissue levels on the buccal aspect of dental implants, a minimum amount of 1–2 mm
of buccal bone needs to be present [33, 34]. While some studies support the con-
cept that a thick buccal plate will support peri-implant soft tissues and prevent
recession, others have disputed this claim [35]. Given the fact that no consensus
currently exists in the literature, it would seem prudent for the clinician to aim at
obtaining a buccal plate thickness of 1–2 mm. This can be accomplished by various
ridge augmentation methods. Buser et  al. in a 10-year follow-up of 41 implant
cases placed in conjunction with GBR found that this technique achieved good
dimensional stability over several years [36]. This has been supported by a recent
consensus report that stated that “lateral bone augmentation procedures are associ-
ated with peri-­implant soft tissue stability based on bleeding on probing (BOP),
probing depth (PD), and marginal bone levels (mBI) ranging from 1- to 10-year
follow-up” [37].

2.1.1.6 Persistent Inflammation


Peri-implant diseases are defined as inflammatory lesions of the surrounding peri-­
implant tissues and include peri-implant mucositis and peri-implantitis. Both of
these peri-implant diseases are infectious in nature and are caused by bacterial bio-
films [38].

2.1.1.7 Timing of Implant Placement


Timing of implant placement may critically influence the final esthetic outcome [9].
The timing of dental implant placement is dependent on specific hard and soft tissue
characteristics of the extraction socket. Hammerle et al. introduced a classification
for implant placement in extraction sites outlining the advantages and disadvantages
of each [39]. Chen and Buser amended this classification and used the terms imme-
diate, early, and late implant placement [22] (Table 2.3).

2.1.1.8 Immediate Implant Placement


Even though the survival rate of immediately placed dental implants is comparable
to early or late placements, the risk of mucosal recession is also elevated [40].
28 2  Peri-implant Soft Tissue Deficiencies

Table 2.3  Timing of dental implant placement, following tooth extraction


Immediate implant Late implant
placement Early implant placement placement
Same day as Soft tissue healing Partial bone healing Complete bone
extraction 4–8 weeks following 12–16 weeks following healing
tooth extraction tooth extraction More than 16
weeks
Adopted from Buser D, Chappuis V, Belser UC, Chen S.  Implant placement post extraction in
esthetic single tooth sites: when immediate, when early, when late? Periodontology 2000.
2017;73(1):84–102

In a long-term follow-up study, the placement of immediate dental implants


resulted in an average buccal mucosal recession of 1.13 mm [41]. This might be
related to the dimensional changes of the alveolar bone and soft tissue following
tooth extraction. Immediate implant placement does not reduce bone remodeling
[42]. A history of periodontal disease, trauma, or pathology may also result in hard
and soft tissue loss. In a recent systematic review, it was shown that immediate
implant placement is associated with greater variability in outcomes and a higher
frequency of recession of >1 mm of the mid-buccal mucosa in 9–41% of sites, 1–3
years postoperatively. In comparison, early implant placement exhibited no sites
with recession >1 mm [27] (Fig. 2.8). Immediate implant placement is a surgically
demanding procedure and requires an experienced skill set. Proper case selection is
crucial to achieve the desired outcome.
Selection criteria to increase outcome predictability include:

1. Gingival levels of the failing tooth are at the same level as the adjacent and/or
contralateral teeth.
2. The extraction socket has a fully intact buccal plate.
3. There is a thick gingival biotype.
4. The sagittal root position is favorable.
5. There is sufficient bone volume apical and palatal to the extraction socket to
allow for ideal three-dimensional implant placement with adequate primary sta-
bility [40, 43].

In a review by Chen and Buser, it was noted that the majority of studies pub-
lished after 2008 involving immediate implant placement imposed inclusion criteria
that included a thick biotype and an intact buccal plate in an effort to reduce muco-
sal recession [27]. Multiple treatment modalities have been utilized to minimize soft
and hard tissue changes following immediate implant placement. Those include
flapless surgery, simultaneous placement of connective tissue grafts, the use of bone
grafts in the residual socket gap, and immediate provisionalization.
Another recent study demonstrated that the least amount of soft tissue changes
occurred when a bone graft was placed in the residual socket gap after immediate
implant placement followed by either a custom healing abutment or a provisional
restoration [44]. In the same study, sites that received no bone graft or a stock heal-
ing abutment showed significant tissue collapse.
2.1 Introduction 29

Fig. 2.8  Following tooth extraction, a dental implant was immediately placed to replace the right
maxillary lateral incisor. The residual socket gap was grafted with bovine xenograft, and a custom
healing abutment was fabricated to maintain the gingival architecture. Following adequate healing,
the final restoration was placed. The peri-implant soft tissue architecture was maintained, and no
buccal contour collapse was noted
30 2  Peri-implant Soft Tissue Deficiencies

2.1.1.9 Early Implant Placement


The concept of a 4–8-week healing period post extraction, to allow for soft tissue
healing, is utilized in cases where additional height and thickness of soft tissue are
required (Fig. 2.9). In a 3D analysis of alveolar bone changes at 8 weeks post extrac-
tion, Chappuis et al. found that most osseous remodeling occurred in the center of

Fig. 2.9  The maxillary left central incisor was diagnosed with a root fracture and was deemed
hopeless. Due to the buccal recession, the early implant placement protocol was selected to restore
the edentulous site. Following 6 weeks of healing, a dental implant was placed at a favorable three-
dimensional position. Contour augmentation was done with freeze-dried bone allograft and bovine
xenograft. The graft was covered with an absorbable collagen membrane, which was secured with
absorbable periodontal sutures. The implant was exposed, 6 months following placement.
Significant buccal bone width was noted. An autogenous, vascularized, pedicle connective tissue
graft was used to increase the soft tissue thickness. The peri-implant soft tissue was further devel-
oped with a temporary implant-supported crown, to create satisfactory buccal tissue contour,
mucosal margin level, and interproximal papillae
2.1 Introduction 31

Fig. 2.9 (continued)

the facial plate with minimal changes in the proximal areas [45]. Consequently a
two-wall morphology was present at 8 weeks post extraction facilitating osseous
grafting and implant placement. Low risk for mucosal recession, good esthetic out-
comes, and adequate facial bone thickness have been reported [43].
Early implant placement with partial bone healing is another dental implant
placement protocol in the esthetic zone. This placement protocol has been advo-
cated when a periapical bone lesion is present and hard tissue healing is desired to
assist in appropriate implant position and primary stability [43].

2.1.1.10 Late Implant Placement


Late implant placement is advocated more than 16 weeks following osseous heal-
ing. A randomized clinical trial compared soft tissue stability following immediate
and delayed dental implant placement at 3 and 6 months. This study found no
32 2  Peri-implant Soft Tissue Deficiencies

Fig. 2.10  The maxillary right central incisor was deemed hopeless due to severe loss of attach-
ment. Following tooth extraction the site was developed through guided bone regeneration. After
6 months of healing, adequate ridge volume was noted. A dental implant was placed and, subse-
quently, restored with a screw-retained prosthesis

significant differences in the soft tissue changes. Authors agree that both immediate
and delayed implant placement approaches are appropriate and that the preferred
treatment approach should be based on other factors such as bone dimension, dehis-
cence, and fenestrations [46]. In another multicenter randomized controlled clinical
trial, the esthetic outcome for both immediately and delayed single implants in the
anterior maxilla was compared 1-year postoperatively. The authors reported that
patients of both groups were equally satisfied at 4 months and 1 year after loading
[47] (Fig. 2.10).
2.2 Diagnosis 33

2.1.1.11 Prosthesis Design and Contour


In order to enhance the esthetic outcomes and healing around dental implants
placed in an ideal position, it is critical to have a proper emergence profile of the
restoration. A transition from the circumferential design of the dental implant plat-
form to the correct cervical tooth anatomy is required for an appropriate restoration
contour. The facial contour of the dental implant restorations could be flat, con-
cave, or convex. Each contour has a different effect on the facial soft tissue healing
and stability [48].
A recent study attempted to determine the effect of abutment contour on the peri-­
implant soft tissue around restored dental implants. This paper identified two dis-
tinct zones within the implant abutment and crown, defined as critical and subcritical
contours. The critical contour is located immediately apical to the mucosal margin
(1.5 mm); it could be on the crown, abutment, or both, whereas the subcritical con-
tour is the area located apical to the critical contour from the dental implant neck to
the gingival margin [48]. Changes in the critical contour have a major influence on
the stability of the mucosal margin around dental implants, while alterations in the
subcritical contour have a minor effect. The concave or flat contour is often pre-
ferred in order to avoid pressure on the buccal tissue, while over-contoured restora-
tions may cause contraction of the buccal tissue and recession [48] (Fig. 2.11).
The type of abutment used could also influence the stability of the mucosal mar-
gin around dental implants. In a 2-year prospective multicenter cohort study, 72
patients with single dental implants in the anterior area were examined [49]. In this
study the authors concluded that zirconia and titanium cad-cam abutments had bet-
ter mucosal margin stability when compared to the stock counterparts.

2.2 Diagnosis

Peri-implant tissue deficiencies may have an impact on the esthetic appearance


of implant-supported restorations, as well as on the health status of the peri-
implant tissues. Such deficiencies may refer to lack of keratinized tissue, and/or
insufficient tissue volume, which includes thin peri-implant tissue and/or peri-
implant tissue recession (Figs. 2.12, 2.13). To date, widely accepted definitions
on peri-implant tissue deficiencies do not exist. No threshold has been defined, in
regard to the lack of peri-implant keratinized tissue. Most studies, though, have
identified that a band of peri-implant keratinized tissue of 1.5–2.0 mm may be
advantageous for the maintenance of peri-implant health and stability of the peri-
implant tissues. Furthermore, the term peri-implant tissue recession is unclear
and confusing. Based on the glossary of periodontal terms, peri-implant tissue
recession is the migration of the peri-­implant mucosa, apical to the implant plat-
form [50]. Although this definition may address the lack of tissue quantity, it
does not address the presence or absence of keratinized tissue or the esthetic
appearance of the implant restoration.
Multiple indices have been proposed in the literature for the objective assessment
of the peri-implant tissues, surrounding implant-supported restorations. In 1997,
34 2  Peri-implant Soft Tissue Deficiencies

Fig. 2.11  Gradual modification of the prosthesis contour and shape may alter the peri-implant
soft tissue architecture. The temporary restoration of the implant at the left maxillary central inci-
sor was modified to achieve favorable tissue architecture that would create symmetry and harmony,
of the implant-supported crowns and the peri-implant tissues, with the adjacent teeth. (Courtesy of
Dr. Jose D. Viquez)

Fig. 2.12  Lack of keratin-


ized tissue, in conjunction
with inadequate peri-implant
tissue volume, may predis-
pose to peri-implant tissue
recession
2.2 Diagnosis 35

Fig. 2.13  Peri-implant tissue enhancement is often needed before the delivery of the final restora-
tion. The lack of attached and or keratinized peri-implant mucosa may hinder adequate oral
hygiene and jeopardize the long-term outcomes

Table 2.4  Proximal contour papilla index


0 1 2 3 4
Papilla No papilla is Less than half At least half of the The papilla The papillae are
fill present, and of the height height of the papilla fills up the hyperplasic and
there is no of the papilla is present, but not entire cover too much
indication of a is present. A all the way up to the proximal of the single-­
curvature of convex contact point space and is implant
the soft tissue curvature of between the teeth. in good restoration and/
contour the soft tissue The papilla is not harmony or the adjacent
adjacent to the contour completely in with the tooth. The soft
single-implant adjacent to the harmony with the adjacent tissue contour is
restoration single-implant adjacent papillae papillae. more or less
crown and the between the There is irregular
adjacent tooth permanent teeth. optimal soft
is observed Acceptable soft tissue
tissue contour is in contour
harmony with
adjacent teeth
Sourced from Jemt T.  Regeneration of Gingival Papillae After Single-Implant Treatment Int. J
Periodont Rest Dent 1997:17:327-33

T. Jemt developed the “proximal contour papilla index” [51]. This index objectively
measures the amount of interproximal tissue present, between a tooth and a dental
implant (Table 2.4). The “papilla height classification system” [52] (Table 2.5) and
the “modified Jemt papilla index” [53] (Table 2.6) are other indices that have been
used for the evaluation of the interproximal peri-implant tissues as well.
More recently, a pilot study attempted to validate another index for the objective
esthetic assessment of implant-supported restorations, the implant crown esthetic
index [54]. This index takes into consideration nine parameters, which assess the
color, form, and surface characteristics of the restoration and the peri-implant tis-
sues. The clinician assigns penalty points, on a 5-point or a 3-point rating scale
(depending on the parameter examined). The points are assigned based on the
amount of mismatch or discrepancy that any of those nine parameters may have,
36 2  Peri-implant Soft Tissue Deficiencies

Table 2.5  Papilla height classification system


Normal Class I Class II Class III
Papilla Interdental The tip of the interdental The tip of the The tip of the
level papilla fills papilla lies between the interdental papilla lies interdental
embrasure space interdental contact point at or apical to the papilla lies
to the apical and the most coronal interproximal CEJ, but level with or
extent of the extent of the coronal to the apical apical to the
interdental interproximal CEJ (space extent of the facial CEJ facial CEJ
contact point/ present, but (interproximal CEJ
area interproximal CEJ is not visible)
visible)
Sourced from Nordland & Tarnow. A Classification System for Loss of Papillary Height. J
Periodontol 1998; 69:1124–1126

Table 2.6  Modified Jemt papilla index


0 1 2 3
Papilla No papilla or Less than half of the At least half of the Interproximal area
fill a negative height of the proximal height of the proximal completely occupied
papilla area occupied by soft area occupied by soft by soft tissue
tissue tissue
Sourced from Schropp & Isidor. Clinical outcome and patient satisfaction following full-flap ele-
vation for early and delayed placement of single-tooth implants: A 5-year randomized study. Int J
Oral Maxillofac Implants 2008;23:733–743

with the adjacent and contralateral teeth and tissues (Table 2.7). Based on the num-
ber of points accumulated, the esthetic result is deemed “excellent” (0 penalty
points) or “poor” (5 points or more). However, if any major discrepancy or mis-
match is noted, the esthetic result is automatically deemed poor. This study con-
cluded that the implant crown esthetic index is a useful tool to objectively rate the
esthetics of implant-supported single crowns. Nevertheless, its practical use needs
to be determined with larger-scale clinical trials.
The “pink esthetic score” (PES) is another index that was developed, to objec-
tively assess the peri-implant soft tissues, compared to the contralateral tooth [55].
This index evaluates seven variables: mesial papilla, distal papilla, soft tissue level,
soft tissue contour, alveolar process deficiency, soft tissue color, and texture. Each
variable is assessed with a score from 0 to 2, with 2 being the best and 0 the poorest
score that can be achieved (Table 2.8). Hence, the highest score that can be achieved
with PES is 14. This index showed a high level of reproducibility, in regard to the
evaluation of the peri-implant soft tissues, of single-implant-supported
restorations.
A cross-sectional, retrospective study attempted to objectively evaluate the
esthetics of implants placed in the anterior maxilla, using the early implant place-
ment protocol [56]. This study developed a new index to comprehensively assess
outcome parameters, using objective esthetic criteria. This new index included the
existing PES index, further simplified, and complemented by the “white esthetic
score” (WES) index. The PES/WES index includes five parameters to assess the
2.2 Diagnosis 37

Table 2.7  Implant crown esthetic index


5 1 0 1 5
Crown penalty points
    Mesiodistal Grossly Slightly No Slightly Grossly
dimension undercontoured undercontoured mismatch overcontoured overcontoured
    Position of Grossly Slightly No Slightly Grossly
incisal edge undercontoured undercontoured mismatch overcontoured overcontoured
    Labial Grossly Slightly No Slightly Grossly
convexity undercontoured undercontoured mismatch overcontoured overcontoured
    Color and Gross mismatch Slight No
translucency mismatch mismatch
    Surface Gross mismatch Slight No
mismatch mismatch
Mucosa penalty points
    Position of Deviation of ≥ Deviation of < No
labial margin 1.5 mm 1.5 mm deviation
of peri-
implant
mucosa
    Position of Deviation of ≥ Deviation of < No
mucosa in 1.5 mm 1.5 mm deviation
the
approximal
embrasures
    Contour of Grossly Slightly No Slightly Grossly
the labial undercontoured undercontoured deviation overcontoured overcontoured
surface of
the mucosa
    Color and Gross mismatch Slight No
surface of mismatch deviation
the labial
mucosa
Total penalty
points
Penalty points are assigned to each of the above items if not matching to the desired situation: one
penalty point for minor (slight) deviations and five penalty points for major (gross) deviations. The
total score leads to a final esthetic score:
0 penalty points: excellent esthetics
1 or 2 points: satisfactory esthetics
3 or 4 points: moderate esthetics
5 or more points: poor esthetics
A major deviation automatically leads to a poor esthetic result and can never be accepted as moder-
ate or satisfactory
Sourced from Meijer et al. A new index for rating aesthetics of implant-supported single crowns
and adjacent soft tissues – the Implant Crown Aesthetic Index. A pilot study on validation of a new
index. Clin. Oral Impl. Res. 16, 2005; 645–649

peri-implant soft tissues and five parameters for the implant-supported restoration
(Table 2.9). These parameters are scored at a scale from 0 to 2 based on their har-
mony and symmetry with the adjacent and contralateral teeth. The maximum score
that can be attained with the PES/WES index is 20.
38 2  Peri-implant Soft Tissue Deficiencies

Table 2.8  The pink esthetic score


Variables 0 1 2
Mesial papilla Shape vs reference Absent Incomplete Complete
tooth
Distal papilla Shape vs reference Absent Incomplete Complete
tooth
Level of tissue Level vs reference Major Minor No discrepancy
margin tooth discrepancy > discrepancy < 1 mm
2 mm 1–2 mm
Soft tissue Natural, matching Unnatural Fairly natural Natural
contour reference tooth
Alveolar Alveolar process Obvious Slight None
process deficiency
Soft tissue Color vs reverence Obvious Moderate No difference
color tooth difference difference
Soft tissue Texture vs reference Obvious Moderate No difference
texture tooth difference difference
Adopted from Furhauser et al. Evaluation of soft tissue around single-tooth implant crowns: the
pink esthetic score. Clin. Oral Impl. Res. 16, 2005; 639–644

Table 2.9  PES/WES index


Pink esthetic score
Parameter Absent Incomplete Complete
    Mesial papilla 0 1 2
    Distal papilla 0 1 2
Major Minor No
discrepancy discrepancy discrepancy
    Curvature of facial mucosa 0 1 2
    Level of facial mucosa 0 1 2
    Root convexity/soft tissue color and 0 1 2
texture
Maximum total PES score
White esthetic score (WES)
Parameter Major Minor No
discrepancy discrepancy discrepancy
    Tooth form 0 1 2
    Tooth volume/outline 0 1 2
    Color (hue/value) 0 1 2
    Surface texture 0 1 2
    Translucency 0 1 2
Maximum total WES score 10
Adopted from Belser et al. Outcome Evaluation of Early Placed Maxillary Anterior Single-Tooth
Implants Using Objective Esthetic Criteria: A Cross-Sectional, Retrospective Study in 45 Patients
With a 2- to 4-Year Follow-Up Using Pink and White Esthetic Scores. J Periodontol
2009;80:140-151

The complex esthetic index (CEI) was proposed as a tool to rate the esthetics of
anterior single-tooth implant-supported restorations [57]. The CEI consists of three
different components. It includes a soft tissue index (S) and an implant-supported
restoration index (R), for the evaluation of the peri-implant soft tissues and implant
restorations. Additionally, the CEI includes a third component, the predictive index
2.2 Diagnosis 39

Table 2.10  Complex esthetic index (CEI)


Rating and evaluation grades of parameter
variations
Adequate Compromised Deficient
Index and parameters (20%) (10%) (0%)
S: Soft tissue index
    1. Soft tissue contour variations No <2 mm ≥ 2 mm
    2. Soft tissue vertical deficiency No 1–2 mm ≥2 mm
    3. Soft tissue color and texture No Moderate Obvious
variations
    4. Mesial papillae appearance Complete fill Partial fill None
    5. Distal papillae appearance Complete fill Partial fill None
General rating and evaluation grade 100% 60–90% <50%
P: Predictive index
1. Mesial interproximal bone height <5 mm 5–7 mm >7 mm
2. Distal interproximal bone height <5 mm 5–7 mm >7 mm
3. Gingival tissue biotype >2 mm 1–2 mm <1 mm
4. Implant pico-coronal position 1.5–3 mm >3-5 mm >5 mm
5. Horizontal contour deficiency No 1–3 mm >3 mm
General rating and evaluation grade 100% 60–90% <50%
R: Implant-supported restoration index
1. Color and translucency No Moderate Obvious
2. Labial convexity in the abutment/ No <1 mm <2 mm
implant junction
3. Implant/crown-incised edge position No ±1 mm ±2 mm
4. Crown width/length ratio <0.85 0.85–1.0 >1.0
5. Surface roughness and ridges No Moderate Obvious
General rating and evaluation grade 100% 60–90% <50%
Each component is rated separately, and all evaluated parameters are graded as adequate (rating
20%), compromised (rating 10%), or deficient (rating 0%)
Adopted from Juodzbalys & Wang. Esthetic Index for Anterior Maxillary Implant-Supported
Restorations. J Periodontol 2010;81:34–42

(P). This component evaluates the mesial and distal bone height, the tissue biotype,
the apico-coronal position of the implant, and the horizontal ridge contour. Each
component of this index assesses five different characteristics that relate to the
esthetic appearance of the peri-implant tissues and the implant-supported restora-
tion. Each characteristic is rated as adequate (20%), compromised (10%), or inad-
equate (0%) (Table 2.10). Each component is rated separately, and the combination
of the three comprises the final CEI score. When all components are deemed ade-
quate, then the CEI has a rating of 100%. If one of the components is compromised
(60%–90%), then the CEI would render a compromised but clinically acceptable
result. A <50% CEI rating is deemed esthetically unacceptable.
Those indices that have been reported in the literature show promising results in
regard to their applicability and reproducibility. However, the present indices are
lacking information that would propose any intervention to enhance peri-implant
soft tissues, to improve esthetics or peri-implant tissue health, based on the index
evaluation outcome. More recently, a classification system was proposed, evaluat-
ing peri-implant tissue deficiencies around loaded dental implants [58]. This system
40 2  Peri-implant Soft Tissue Deficiencies

focuses on the enhancement of peri-implant tissues to improve peri-implant health.


According to this classification, there are four distinct clinical scenarios:

• The width of keratinized tissue at the buccal aspect of the implant measures
≥2 mm.
• The width of keratinized tissue at the buccal aspect of the implant measures
<2 mm (presence or absence of a frenulum, low inserting).
• The width of keratinized tissue at the buccal aspect of the implant measures
<2 mm, and a soft tissue recession can be distinguished (i.e., the rough implant
surface is visible). The peri-implant mucosa is thin, and no frenulum pull is
visible.
• No or minimal width of keratinized tissue at the lingual aspect of the implant in
the mandible.

This classification system proposes a treatment modality for peri-implant tissue


enhancement, based on the type of deficiency.
Due to the great variety of methods, parameters, and measures used, there is still
no commonly accepted index for the evaluation of dental implant restorations and
peri-implant soft tissues. A recent systematic review concluded that “there is a
strong need for a consensus on objective and well-defined parameters to assess aes-
thetics in implant dentistry” [59]. Furthermore, a consensus for the diagnosis of
peri-implant tissue deficiencies is also required, focusing on the need for peri-­
implant tissue enhancement, to improve and maintain peri-implant tissue health.

2.3 Management/Treatment Options

Mucogingival procedures come with a great variety of techniques and materials that
offer treatment flexibility, improved esthetic outcomes [8], and better maintenance
[60]. The esthetic outcome variables usually examined are recession coverage, soft
tissue volume of the peri-implant tissue, gain of keratinized tissue, and interproxi-
mal papillary fill. Recent evidence supports peri-implant tissue enhancement, as
thicker peri-implant soft tissue will result in more favorable peri-implant parameters
and long-term stability of the outcome. Evidence from earlier studies, however, is
controversial on the need for soft tissue augmentation around dental implants.
A recent literature review [58] suggested that the timing of peri-implant mucosal
augmentation is critical to reach the desired outcome. Evidence from this review
indicated that attempting to enhance peri-implant soft tissues, after the delivery of a
restoration, decreases significantly the predictability of the outcome. The authors
advocated soft tissue enhancement during site development (pre-implant surgery)
(Fig. 2.14), implant placement (Fig. 2.15), and/or at second-stage surgery (implant
exposure) (Fig. 2.16), as the predictability of tissue augmentation increases, when
compared to interventions after loading. However, in another systematic review, it
2.3  Management/Treatment Options 41

Fig. 2.14  Adequate site development is important to optimize the final outcome. Following tooth
extraction, freeze-dried bone allograft was used to preserve the ridge dimensions. An autogenous,
pedicle connective tissue graft was also utilized to minimize the volumetric alterations after tooth
extraction and further improve the ridge volume

was shown that similar outcomes of peri-implant soft tissue augmentation could be
achieved regardless of the timing of intervention [61] (Fig. 2.17).
The appropriate treatment modality is selected based on the diagnosis that takes
into consideration all predisposing factors. Bassetti et  al. proposed a treatment
decision tree, based on the pre-existing tissue quality/quantity [58] (Table 2.11). A
coronally advanced flap with a subepithelial connective tissue graft (SCTG) is
42 2  Peri-implant Soft Tissue Deficiencies

Fig. 2.15  Ridge augmentation was performed to replace this congenitally missing lateral incisor.
Although hard tissue volume increased significantly, a ridge deficiency is evident. An autogenous
subepithelial connective tissue graft was utilized to increase the tissue volume at the time of
implant placement. Following the delivery of the final restoration, adequate peri-implant tissue
volume and keratinized tissue were noted, contributing to a pleasing esthetic outcome

proposed for type I deficiencies and a combination of vestibuloplasty with a free


gingival graft (FGG) for type II deficiencies. Type III deficiencies would require a
more extensive intervention as the authors advocated a combination of both the
aforementioned treatment modalities. The same treatment modalities, also, apply
for type IV deficiencies, which may, additionally, require apical repositioning of
the floor of the mouth. Multiple treatment modalities have been advocated with
two common outcomes: the gain of keratinized mucosa and the increase of peri-
implant tissue volume.
2.3  Management/Treatment Options 43

Fig. 2.16  Two dental implants were placed in this severely resorbed alveolar ridge, following
ridge augmentation. The implant sites lack soft tissue volume and keratinized mucosa. At the time
of stage 2 surgery, vestibuloplasty was performed in conjunction with a split-thickness, apically
positioned flap. Two, partially epithelialized, free soft tissue grafts were placed at the buccal aspect
of each dental implants. After 4 weeks of healing, there is a significant increase in peri-implant
tissue volume and keratinized mucosa

2.3.1 Improving Peri-implant Soft Tissue Volume

Subepithelial connective tissue grafts have been advocated for the treatment of
mucosal recession and the increase of peri-implant tissue volume (Fig. 2.18). In a
6-month prospective study, ten patients were treated with a coronally advanced flap,
in conjunction with a free connective tissue graft around restored dental implants.
The flap was advanced to overcompensate the mucosal recession with an average of
44 2  Peri-implant Soft Tissue Deficiencies

Fig. 2.17  Significant peri-implant mucosal recession was noted at the maxillary right central inci-
sor implant. Prior to flap elevation, the buccal contour of the existing crown was altered, to obtain
a more concave abutment surface. A lateral sliding flap in conjunction with a connective tissue
graft was performed to correct the mucosal recession. Significant resolution of the mucosal defect
was observed, after 1 year. Further improvement was noted after 5 years, with a significant increase
in peri-implant soft tissue volume

0.5  mm (0.2–1.2  mm). These patients had a mean mucosal recession defect of
3 mm, and 99.6% of recession coverage was obtained immediately following the
procedure. Significant shrinkage of the tissue was noted after 1 month, giving a
mean coverage of 75%. Further recession occurred after 6 months, for an average
peri-implant recession coverage of 66% [62]. In a 1-year prospective study, 16
patients with non-submerged dental implants, with a mean buccal recession of
2  mm, were treated with a coronally advanced flap combined with a SCTG,
2.3  Management/Treatment Options 45

Table 2.11  Proposed intervention around loaded dental implants, based on the pre-existing peri-­
implant tissue condition
Soft tissue deficiency Proposed treatment
Type I (buccal) Subepithelial connective tissue graft + Coronally
Width of KM ≥2 mm advanced flap
Type II (buccal) Vestibuloplasty + Free gingival graft
Width of KM < 2 mm (presence or
absence of a frenulum low inserting)
Type III (buccal) Subepithelial connective tissue graft + Coronally
Width of KM <2 mm in combination advanced flap + Vestibuloplasty + Free gingival graft
with a soft tissue dehiscence
Type IV (lingual) Vestibuloplasty + Free gingival graft
Minimal width or lack of keratinized
mucosa at the lingual aspect
    • Adequate vertical distance Tunneling technique + Subepithelial connective tissue
between the floor of the mouth and graft
the alveolar ridge
Type IV (lingual) Lowering of the floor of the mouth + Free gingival
Minimal width or lack of keratinized graft (split-skin graft)
mucosa at the lingual aspect
    • Floor of the mouth is elevated in
relation to the alveolar ridge
Adapted from Bassetti et al. Soft tissue grafting to improve the attached mucosa at dental implants:
A review of the literature and proposal of a decision tree. Quintessence Int 2015;46:499–510

harvested from the maxillary tuberosity. After 1 year the recession defects were
decreased to a mean of 0.3 mm resulting in 89.6% of mean coverage and 56.3% of
complete defect resolution. Furthermore the esthetic evaluation through a visual
analog scale (0–10) improved from 3.5 to 8.5 [63]. Zucchelli et al. evaluated the
efficacy of peri-implant mucosal augmentation, through a surgical-prosthetic
approach, around restored, single dental implants with buccal dehiscences [64]. In
this study the implant crown was removed, and the abutment contour was altered.
Each site was then grafted with a split-thickness, coronally advanced flap in con-
junction with a SCTG.  Following adequate healing, a new final restoration was
placed. After 1 year, the mean soft tissue dehiscence coverage was 96.3%, and com-
plete coverage was achieved in 75% of the treated sites.
Soft tissue substitutes have been suggested as an alternative to autogenous tissue
grafts for the treatment of soft tissue defects around teeth and implants (Fig. 2.19).
The abundance of tissue material, the lack of a second surgical site, as well as the
reduced morbidity following the surgical procedure have made soft tissue allografts
an attractive alternative [65].
Acellular dermal matrices (ADM) are the most studied soft tissue substitutes, as
an alternative to autogenous tissue grafts, for the treatment of recession defects,
around teeth. Although soft tissue allografts seem to have many advantages, SCTGs
still remain the “gold standard.” A systematic review, by Cairo et al., demonstrated
that a combination of a coronally advanced flap with ADM did not improve the
clinical results, compared to the coronally advanced flap alone, when used to treat
gingival recession defects [66]. Furthermore, in the same review, it was shown that
46 2  Peri-implant Soft Tissue Deficiencies

Fig. 2.18  Progressive recession was noted at this implant during the first 2 years in function. The
peri-implant tissue is lacking keratinization and volume, and peri-implant tissue recession is evi-
dent. Following the preparation of a split-thickness flap, a partially epithelialized connective tissue
graft was used. The epithelialized part was placed toward the coronal aspect of the implant. The
flap was advanced to cover only the de-epithelialized part of the tissue graft. Following 3 months
of healing, complete coverage of the exposed rough surface is noted, along with a significant
increase in peri-implant tissue volume and keratinized mucosa

a SCTG offered superior results, compared to ADM, when both grafts were com-
bined with a coronally advanced flap. When it comes to dental implants, a system-
atic review (Thoma et  al.) concluded that the addition of various soft tissue
allografts offers no benefit, in regard to the increase of keratinized mucosa and soft
tissue volume, around dental implants, when compared with autogenous soft tissue
grafts [67].
2.3  Management/Treatment Options 47

Fig. 2.19  The maxillary left central incisor was lost due to trauma. Following extraction, 6 weeks
were allowed for soft tissue healing. A dental implant was placed with the early implant placement
protocol. Following implant placement, contour augmentation was performed using freeze-dried
bone allograft, layered with a bovine xenograft and covered with an absorbable collagen mem-
brane. A soft tissue allograft was used to increase the peri-implant soft tissue volume. Increased
ridge volume is noted after 3 months of healing. Two weeks after the second-stage exposure, there
is a significant increase in peri-implant tissue volume and presence of adequate keratinized tissue
48 2  Peri-implant Soft Tissue Deficiencies

Fig. 2.19 (continued)

2.3.2 Improving the Width of Keratinized Mucosa

A wider zone of keratinized tissue is proven to improve periodontal parameters and


promote gingival health [5, 68]. The treatments described for the increase of kera-
tinized mucosa include vestibuloplasty, apically positioned flap/vestibuloplasty
(APF/V) in combination with autogenous tissue grafts (FGG or SCTG) (Fig. 2.20),
or soft tissue substitutes (ADM or collagen matrices). The use of FGGs is a predict-
able choice for the augmentation of the keratinized case around dental implants
[69]. In a prospective study, vestibuloplasty alone was performed around 131 dental
implants, placed at sites with a mean of 2.23 mm of keratinized mucosa [70]. The
vestibuloplasty procedure was performed at the time of implant placement. This
technique allowed for a mean of 5 mm increase in keratinized mucosa, compared to
baseline. Furthermore, the result of this study indicated that the gain in keratinized
tissue remained stable for a period of 4 years.
In a randomized controlled trial, vestibuloplasty alone was compared to vestibu-
loplasty combined with FGG, in regard to the increase of keratinized tissue around
dental implants [71]. The increase in keratinized tissue was significantly greater in
the FGG group compared to vestibuloplasty alone (2.36 vs 1.15 mm). A similarly
designed study compared APF/V in conjunction with ADM or FGG, in regard to the
increase of peri-implant keratinized tissue [72]. This study demonstrated that the
autogenous FGG was superior to ADM, with an increase in keratinized tissue of
2.3  Management/Treatment Options 49

Fig. 2.20  Lack of keratinized tissue and limited peri-implant tissue volume are noted around
these two implants, along with high frenum attachments. Vestibuloplasty was performed and the
split-thickness flap was apically positioned. A free, partially epithelialized, soft tissue graft was
placed at the buccal aspect of the implants, with the epithelialized portion facing apically. The graft
was immobilized with periosteal sutures. Following 4 weeks of healing, there is a significant gain
in peri-implant tissue volume, in both height and thickness. The frenum attachments were elimi-
nated, and there is also significant increase in peri-implant keratinized mucosa

2.57 vs 1.58 mm. Another study evaluated the effect of APF/V, APF/V combined
with FGG, or APF/V combined with a collagen matrix (Collatape®, Zimmer Dental,
Carlsbad, USA) [73]. This comparison revealed a significant increase of keratinized
tissue in the FGG group, compared to the other treatment modalities, which showed
only a mild to moderate effect.
50 2  Peri-implant Soft Tissue Deficiencies

Recently, a porcine-derived collagen matrix (Mucograft®) has been introduced


for the increase of keratinized tissue around teeth and implants (Fig. 2.21). In an
experimental study, a prototype, porcine-derived collagen matrix (CM), was com-
pared to SCTGs for large volume, soft tissue, ridge augmentations [74]. A volumet-
ric analysis of digitized master casts revealed no significant differences between the
two groups. This study concluded that this substitute may be a good alternative of
SCTGs, for the augmentation of localized soft tissue ridge deficiencies. The efficacy

Fig. 2.21  Lack of keratinized tissue noted at the posterior maxillary right. Ridge augmentation
was performed due to a severe ridge deficiency, which resulted in displacement of the mucogingi-
val junction. Eight weeks following implant placement, vestibuloplasty was performed and the
split-thickness flap was apically positioned. A soft tissue substitute was placed at the recipient bed
and immobilized with periosteal sutures. After delivery of the final restoration, an increase of
2–3mm in keratinized tissue was noted
2.3  Management/Treatment Options 51

of this new CM has been assessed in multiple studies. In a randomized controlled


trial, teeth or implant abutments of partial fixed restorations, with ≤1 mm of keratin-
ized tissue, were treated with either SCTG or CM [75]. A significant increase in
keratinized tissue, of 2.5 and 2.6 mm, was noted for the test and control groups,
respectively. No significant differences were noted between groups, in terms of
keratinized tissue gain. In a similarly designed study, the same collagen matrix was
compared to SCTGs, regarding the increase of keratinized tissue around dental
implants, only [76]. This study demonstrated a significant increase in keratinized
tissue for both groups, with no significant difference between test and control (2.75
vs. 2.8 mm). Both of the abovementioned studies concluded that this CM is a suit-
able substitute to SCTG, for increase of keratinized tissue around teeth and implants.
Furthermore, both studies reported significantly lower patient morbidity and less
surgical time, for the test group.
A Cochrane systematic review attempted to answer the question “what is the
best approach to manage soft tissue recession around dental implants” [77]. The
authors concluded that there is insufficient reliable evidence to provide a recom-
mendation on which is the most effective soft tissue augmentation technique
around dental implants. Another systematic review analyzed the efficacy of soft
tissue grafting around dental implants in partially edentulous patients, in regard to
the gain of keratinized tissue and the increase of peri-implant tissue volume [67].
This review concluded that better outcomes were observed, in terms of peri-implant
tissue volume, when a coronally positioned flap combined with a SCTG was used,
compared to a coronally advanced flap alone. Vestibuloplasty combined with a free
gingival graft offered superior results in terms of increase in keratinized tissue
compared to vestibuloplasty alone or no treatment. Soft tissue allografts (ADM)
demonstrated very high shrinkage rates, with a histological picture that resembled
scar tissue. The increase in keratinized tissue was similar for autogenous grafts
(2.2–2.5 mm) and CMs (1.8–2.3 mm). However, CMs demonstrated better esthet-
ics and less patient morbidity.
More recently, another systematic review assessed the influence of peri-implant
tissue augmentation, on peri-implant health or disease, in partially or fully eden-
tulous patients [78]. This review evaluated the increase of keratinized tissue width
or increase in mucosal thickness, on various peri-implant parameters related to
peri-implant disease (Fig. 2.22). The increase of keratinized tissue did not signifi-
cantly affect BOP, when comparing augmented and non-augmented sites.
However, there was a tendency for decreased BOP in augmented sites when com-
pared to maintenance with mucosa alone. On the other hand, gingival index (GI)
scores were significantly better for the augmented sites, compared to controls that
had <2  mm width of keratinized tissue. Furthermore, augmented sites demon-
strated significantly lower plaque scores (PI), compared to controls. Peri-implant
probing depths (PD) and marginal bone levels were also superior to sites aug-
mented with autogenous grafts, compared to all control treatments, with a statisti-
cally significant difference. This meta-analysis favored APF combined with
autogenous gingival grafts, over any other treatment modality, for the increase of
peri-implant keratinized tissue.
52 2  Peri-implant Soft Tissue Deficiencies

Fig. 2.22  These two implants are part of a full-arch, implant supported prosthesis, that was never
completed. There is poor oral hygiene, lack of keratinized and attached mucosa, and mucosal
recession. Vestibuloplasty and an apically positioned flap were performed, in conjunction with an
autogenous free gingival graft. The graft was stabilized with periosteal and sling sutures. Following
adequate healing, there is a significant increase in keratinized tissue and soft tissue volume. Oral
hygiene has dramatically improved, however, the exposed rough dental implant surface will always
be susceptible to plaque accumulation

Augmentation procedures for the increase of peri-implant mucosal thickness


were predominantly recommended to improve implant esthetics. Only recent stud-
ies have attempted to investigate the effect of mucosal thickness on peri-implant
health [78]. Due to the lack of clinical data, this systematic review did not detect any
influence of increased mucosal thickness on BOP, GI, or PI. Although limited data
were also available regarding the effect of mucosal thickness on PDs and marginal
References 53

bone levels, this data favored augmented sites, with increased mucosal thickness,
compared to controls.

2.4 Summary

Peri-implant tissue deficiencies may compromise dental implant esthetics as well as


peri-implant health. Inadequate peri-implant tissue volume and lack of keratinized
tissue are the most common peri-implant tissue deficiencies that may predispose to
peri-implant tissue recession. Tissue biotype, implant malposition, and poor pros-
thesis design are also a few other factors that may contribute to peri-implant tissue
recession. Unfortunately, to date, no uniform criteria exist for the diagnosis of peri-­
implant soft tissue deficiencies, and consequently no specific treatment modalities
can be recommended for their management. Peri-implant soft tissue augmentation
procedures may compensate for ridge volume deficiencies and improve peri-implant
esthetics. Multiple techniques and materials have been described for the enhance-
ment of peri-implant keratinized tissue and soft tissue volume. Based on the avail-
able evidence, autogenous tissue grafts are the treatment of choice, and collagen
matrices may be a good alternative. Peri-implant tissue augmentation with autoge-
nous tissue grafts improved peri-implant parameters (BOP, GI, PI, PD) and demon-
strated more stable marginal bone levels. Thus, improvements in quality and
quantity of peri-implant soft tissues may play a critical role in the long-term survival
and success of dental implants.

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Peri-implant Mucositis
3

3.1 Introduction

The definition of peri-implant mucositis has been revised over the years. It was
originally described as “a reversible inflammatory change of the peri-implant soft
tissue without bone loss” [1] and eventually was included in a collective term of
“peri-implant diseases,” which were deemed to be infectious in nature [2]. According
to the Glossary of Terms of the American Academy of Periodontology [3], peri-­
implant mucositis is “a disease in which the presence of inflammation is confined to
the mucosa surrounding a dental implant with no signs of loss of supporting bone.”

3.2 Etiology

The primary etiology of peri-implant mucositis is microbial biofilm accumulation


on the implant fixture [4, 5]. Shortly after placement, bacterial plaque colonizes
dental implant surfaces [6, 7]. This biofilm is similar to the one identified around the
natural dentition, and the inflammatory process seems to mimic that of gingivitis
around natural teeth [8]. In an animal study Ericsson et al. [9] demonstrated that
prolonged plaque accumulation on implant abutments resulted in inflammation of
the peri-implant mucosa due to the establishment of an inflammatory cell infiltrate.
This finding was supported by further human studies where it was demonstrated that
the accumulation of plaque initiates peri-implant inflammation [8, 10, 11].

3.2.1 Risk Indicators

There are several risk indicators that may contribute to the development of peri-­
implant inflammation. To date there is some evidence to support the following as
risk indicators for the development of peri-implant mucositis: poor oral hygiene,
smoking, radiation therapy, and residual cement [12].

© Springer International Publishing AG, part of Springer Nature 2018 59


A. Kelekis-Cholakis et al., Peri-Implant Complications,
https://doi.org/10.1007/978-3-319-63719-8_3
60 3  Peri-implant Mucositis

3.2.1.1 Poor Oral Hygiene


A clinical study performed by Pontoriero et al. [13] proved that there was a cause and
effect relationship between the absence of oral hygiene and plaque accumulation and the
development of peri-implant mucositis. Furthermore experimental peri-­implant mucosi-
tis was reversed when oral hygiene measures were instituted [14]. A recent cross-sec-
tional study supported the importance of good oral hygiene by multilevel analysis which
determined that a high plaque score was a risk indicator for peri-implant mucositis [15].

3.2.1.2 Smoking and Radiation Therapy


Karbach et al. [16] examined 100 patients with a 1–19-year follow-up and showed
that smoking was a significant risk indicator for the development of peri-implant
mucositis. Similarly Roos Janseker et al. [17] and Rinke et al. [18] determined that
smoking was a possible indicator for peri-implant mucositis.
In the same study that assessed smoking as a risk indicator for peri-implant
mucositis, Karbach et al. [18] indicated that radiation therapy was also an “explana-
tory variable” for the presence of peri-implant inflammation.

3.2.1.3 Residual Cement and Poor Restoration Design


There is increasing evidence that the presence of residual cement in the subgingival
tissues contributes to peri-implant tissue inflammation [19]. In a prospective study
evaluating the influence of the restorative margin position and the amount of unde-
tected cement, Linkevicius et al. concluded that the more apical the restorative margin,
the greater the probability of undetected cement being present. The greatest amount of
cement was detected when the restorative margin was placed 2–3 mm subgingivally.
Furthermore if an undercut >2 mm is present on the implant restoration, the chance of
residual cement increases significantly even if the restorative margin is shallow [20].
A current literature review investigated the role of cement as a risk indicator in
peri-implant diseases. It concluded that there is an association with a tendency to
higher disease prevalence with cemented, compared to screw-retained, implant res-
torations [21]. The authors advocated the collection of baseline data 2 weeks follow-
ing the placement of the implant prosthesis with regular follow-up intervals for early
detection of peri-implant mucositis and cement excess. A retrospective case analysis
compared screw-retained restorations to cement-retained restorations in patients
with and without a history of chronic periodontitis. This study demonstrated, that
patients with a history of chronic periodontitis and residual cement tended to develop
peri-implant diseases more rapidly (23.4 months compared to 40.8 months). Patients
with a history of periodontal disease and screw-retained prostheses had a lower
incidence of peri-implant disease. It was therefore recommended to consider screw-
retained restorations in patients with a history of periodontal disease [22].

3.2.1.4 Potential Emerging Risk Indicators


There is weak evidence for diabetes, abutment surface characteristics, absence of
keratinized tissue, genetics, gender, time function, alcohol consumption, and rheu-
matoid arthritis as risk indicators for peri-implant mucositis [12, 23]. However,
these factors should always be considered when developing a treatment plan for
future implant patients, or an individualized maintenance protocol for patient with
existing implants.
3.3 Diagnosis 61

3.3 Diagnosis

There is heterogeneity in the diagnostic criteria used in studies to define peri-implant


mucositis [24]. In one study, peri-implant mucositis was defined as bleeding on
probing around implants with no bone loss [25]. In another study, however, the case
definition was identified as plaque, probing depth ≤ 5 mm, and evidence of inflam-
mation by modified bleeding index [26]. More recently Felo et al. defined peri-
implant mucositis [27] as bleeding on probing, modified gingival index >1.5,
modified plaque index >1.5, and probing depth ≤ 3 mm.
Out of all the diagnostic parameters, bleeding upon probing has been consis-
tently used in all studies as a tool for the diagnosis of peri-implant mucositis.

3.3.1 Bleeding on Probing

The clinical tool in the diagnosis of peri-implant mucositis is bleeding on gentle


probing (<0.25 N) [28]. In an experimental animal study, healthy peri-implant sites
showed an absence of bleeding on probing, while peri-implant mucositis sites
showed an increase of bleeding on probing [29].
The presence of inflammatory signs such as edema, redness, and hyperplasia as
well as bleeding upon probing is pathognomonic of peri-implant mucositis (see
Figs. 3.1 and 3.2a–c).

3.3.2 Probing Depths/Radiographic Evaluation

Periodontal probing using a light force (0.2–0.3 N) has been deemed a reliable tool
for diagnosing peri-implant diseases [30].
To confirm the diagnosis of peri-implant mucositis, stable probing depths,
recorded from the time of prosthetic component connection, are of importance in
conjunction with the establishment of baseline radiographs [31].

Fig. 3.1 Localized
inflammation of the lingual
mucosa of peri-implant
tissues
62 3  Peri-implant Mucositis

a b

Fig. 3.2 (a) Visual signs of redness of marginal peri-implant tissues; (b) clinical probing depth
less than 4 mm; (c) bleeding upon probing

3.3.3 Prevalence

There are significant limitations in the present literature as to the prevalence of peri-­
implant diseases. Those relate more to issues of study design such as small sample
sizes, randomization bias, cross-sectional nature, and short follow-up. Moreover,
the variations applied to thresholds for bone loss also affect the disease classifica-
tion and perceived prevalence. In a recent systematic review, the subject level preva-
lence of peri-implant mucositis was reported to range from 19 to 65% [32]. Further
meta-analyses estimated the weighted mean prevalence of peri-implant mucositis to
be 43% (CI: 32–54%) [33].

3.4 Management/Treatment Options

Removal of plaque from the abutment/implant surface is the main goal of treatment
of peri-implant mucositis. This goal can be achieved with patient education, oral
hygiene instruction, professional debridement, and ensuring that there is adequate
access to the area in question.
There is currently evidence in the literature to support that peri-implant mucosi-
tis is reversible, similarly to gingivitis, when treated effectively with recommended
therapeutic modalities [13, 14]. One study however did report that full resolution of
experimentally induced peri-implant mucositis in humans was not fully reversed at
3 weeks when oral hygiene measures were reinstituted [14]. Another more recent
3.4  Management/Treatment Options 63

study countered these results by observing that in an elderly population, reinstituted


oral hygiene measures resulted in complete resolution of peri-implant mucositis
[34]. It is important to note, however, that a return to baseline of inflammatory cre-
vicular fluid biomarkers was noted in both studies (Figs. 3.3 and 3.4).

a b

Fig. 3.3 (a–c) 3–5 mm clinical probing depths with bleeding on probing

a b c

Fig. 3.4 (a) Baseline radiograph, (b) radiograph 1-year post-implant loading, (c) radiograph
6 years later exhibiting no evidence of bone loss beyond physiologic remodeling
64 3  Peri-implant Mucositis

Table 3.1  Peri-implant mucositis management


Patient education
Peri-implant
Systemic factors Local factors debridement Maintenance
Smoking Prosthesis design (poor Patient administered Individualized protocol
access for oral hygiene)
Inability to perform Cement Professionally
oral hygiene administered

Treatment of peri-implant mucositis is essential, as there appears to be evi-


dence that the lack of periodic supportive peri-implant maintenance may result,
for some patients, in the development of peri-implantitis. After 5 years of regular
peri-implant maintenance, 18% of patients developed peri-implant disease
as opposed to those with no maintenance where 43.9% developed peri-
implantitis [35].
The primary goal of treatment of peri-implant mucositis is to prevent plaque
accumulation. This is achieved by eliminating biofilms at the mucosal abutment
interface and around implant-supported restorations. Challenges in achieving this
goal for both the patient and the treating clinician are the design and surface tex-
ture of the implant abutment, the design of the prosthesis or superstructure, and
the patient’s ability and compliance to perform adequate oral hygiene.
Upon initial diagnosis of peri-implant mucositis, the clinician will use a two-­
pronged approach for treatment (Table 3.1).
The first approach aims at controlling or modifying local or systemic etiological
factors such as smoking cessation counseling, prosthesis design modification,
patient education, and oral hygiene instruction.
The second approach aims at maintaining peri-implant tissue health such as the
establishment of a professional, patient-centered peri-implant debridement proto-
col, and a maintenance plan.

3.4.1 Patient Education

Prior to initiation of implant treatment, it is crucial to educate each patient on the


importance of adequate plaque control and the need for appropriate maintenance of
the implant prosthesis. This is of particular necessity in patients with a past history
of chronic or aggressive periodontitis and associated tooth loss as a result of these
diseases.

3.4.2 Systemic and Local Factors

3.4.2.1 Systemic Factors

Smoking
A discussion with the patient about the impact of smoking on peri-implant tissue
health is very important. In a recent microbiological study, smoking seemed to
3.4  Management/Treatment Options 65

affect the peri-implant microbiome, creating a high-risk bacterial community for


peri-implant disease [36]. Smoking has now been identified in the literature as an
independent risk indicator for peri-implant mucositis [37].

Systemic Factors Influencing the Ability to Perform Adequate


Oral Hygiene
Inability to perform oral hygiene can be due to systemic factors, such as the devel-
opment of conditions that affect the cognitive or physical abilities of an individual
to perform adequate oral hygiene. Conditions such as Alzheimer’s, senile demen-
tia, or Parkinson’s may place the onus of oral hygiene delivery on loved ones or
healthcare staff. A thorough individualized assessment is paramount. Possible con-
version of a fixed restoration to a removable prosthesis may be needed, in patient
with full-arch implant supported restorations to assist in daily homecare
maintenance.

3.4.2.2 Local Factors

Prosthesis Modification
An assessment will be made of the area to be treated, and an evaluation of the
prosthesis will be performed, to ensure adequate access for plaque control.
Adjusting restorations to allow for appropriate access to the peri-implant tissues
as well as patient education is of paramount importance in the long-term mainte-
nance of dental implants (Figs. 3.5 and 3.6).
Ridge lap restorations, closed embrasure spaces, and flanges on fixed implant-­
supported prostheses are all examples of prosthetic barriers to adequate oral
hygiene. A study demonstrated that 48% of implants that presented with peri-
implantitis had no accessibility/capability for proper oral hygiene. Furthermore, the
authors stated that inadequate plaque control was found in around 74% of implants
studied [38].
It is important to note, however, that it may not be advisable to simply adjust the
prosthesis or superstructure but it may be necessary to fabricate a new prosthesis
altogether after obtaining adequate tissue health (Figs. 3.7 and 3.8). Such may be
the case of pink porcelain restorations with buccal flanges (Fig. 3.9).

Cement
The diagnosis of residual cement as a contributing factor to peri-implant mucositis
is not easy to establish, as a certain percentage of peri-implant mucositis cases do
not respond to conventional treatment [25]. In addition many times cement is
not radiographically detectable and has been found around implant restorations
and peri-implant tissues despite concentrated attempts at removal [20] (Figs. 3.10
and 3.11).
Removal of cement remnants should be attempted initially nonsurgically, with
careful monitoring of soft and hard tissues, for resolution of the peri-implant inflam-
mation. If persistence of the inflammation is noted and/or signs of peri-implant bone
loss develop, removal of the superstructure or elevation of the peri-implant tissues
to gain better access is recommended.
66 3  Peri-implant Mucositis

a b

c d

Fig. 3.5 (a) Closed embrasure space. (b) Radiographic evidence of poorly seated restorations and
presence of cement. (c) Radiographic evidence of stable bone levels over a 5-year period. (d)
Opening of embrasure space
3.4  Management/Treatment Options 67

a b

c d

Fig. 3.6 (a) Over-contoured buccal restoration due to nonideal (palatal and coronal) implant
placement. (b) Recontouring of restoration and placement of a soft tissue graft. (c) Suturing of soft
tissue graft in place. (d) 5-year follow-up of healthy peri-implant tissues

Fig. 3.7  Before and after prosthesis flange adjustment to facilitate oral hygiene measures.
Disclosing paste on the intaglio aspect of the prosthesis assists in ensuring appropriate contours for
the performance of adequate oral hygiene (Courtesy of Dr. J. Viquez)
68 3  Peri-implant Mucositis

Fig. 3.8  Prosthesis adjustment, oral hygiene instructions, and patient compliance result in a sig-
nificant decrease in peri-implant inflammation (Courtesy of Dr. J. Viquez)

Fig. 3.9  Pink porcelain ridge lap flanges making plaque removal very difficult for the patient and
healthcare provider

Fig. 3.10  Presence of cement not detectable on radiograph


3.4  Management/Treatment Options 69

Fig. 3.11  Persistent inflammation and purulence that went untreated resulted in the loss of this
implant fixture due to the presence of cement on the implant threads

3.4.3 Patient-Administered Plaque Control

3.4.3.1 Oral Hygiene Instructions


Oral hygiene instructions given to patients with dental implants are modeled after
those given to patients with periodontal diseases. An individualized protocol should
be established, and the clinician should evaluate the patient’s ability to perform
adequate plaque control. A plaque index is recommended as a guide on proper oral
hygiene maintenance [39] (Renvert S and Giovannoli JL 2012 textbook).
One challenge when faced with reviewing current literature on patient-­
administered plaque control is that there are, frequently, no definitions provided of
peri-implant mucositis at baseline and often resolution outcomes are not reported
[40]. Thus, the delivery of oral hygiene instructions is often performed on an empir-
ical basis.

3.4.4 Mechanical Plaque Control

3.4.4.1 Electric vs. Manual Toothbrushes


Both manual and electric toothbrushes can be used in a self-administered oral
hygiene program. Four comparative studies were conducted on the outcomes of
patient-administered plaque control with manual or powered toothbrushes. No dif-
ference between powered versus manual toothbrushes was evident [40].
70 3  Peri-implant Mucositis

In a Cochrane systematic review, there appeared to be superior patient preference


and ease of maintenance with electric toothbrushes; however the correlation was
weak [41].

3.4.4.2 Flossing vs. Interdental Brushes


The use of toothbrushing alone has been shown to be ineffective at removing all inter-
proximal plaque around teeth [42]. Various tools have been used in the performance
of interdental cleaning such as dental floss, interdental brushes, and toothpicks.
A recent randomized clinical trial compared the efficacy of dental floss to inter-
dental brushes in controlling bleeding on probing and reducing implant plaque
scores [43]. No significant differences in plaque or bleeding indices were noted in
the 6-month follow-up (Fig. 3.12).
When a qualitative pain questionnaire, was given to the same cohort, patients
expressed a slight preference in terms of the ease of use of interdental brushes
(Fig. 3.13).
Recently there has been a case report on the presence of floss remnants subgin-
givally around dental implants with exposed rough surfaces [44]. Another case
series pointed to a potential allergic response of certain individuals to coated or
flavored dental floss [45]. Consequently in this instance as well, clinicians should

LS-Means for Group*TIME


with 95% confidence Limits

Group 0 1

0.6
BOP_average LS-Mean

0.4

0.2

0 months 3 months
TIME

Fig. 3.12  Comparison of mean peri-implant bleeding on probing in patients using floss (blue) vs.
interdental brushes (red) at 6 months showed no statistical differences
3.4  Management/Treatment Options 71

Fig. 3.13  In a recent


clinical trial, patients found
interdental brushes easier
to use than dental floss

take into account individual patient needs and circumstances when recommending
oral hygiene aids.

3.4.5 Chemical Plaque Control

3.4.5.1 Toothpastes
Two studies have compared the efficacy of a triclosan-containing toothpaste to a
sodium fluoride toothpaste when using a manual toothbrush [46, 47]. Both studies
reported greater reduction of the triclosan group on bleeding on probing at 6 months,
when compared to the sodium fluoride group. This finding can be explained by tak-
ing into account the anti-inflammatory effect of triclosan as reported in Trombelli
and Farina [48]. However, these results should be interpreted with caution, as nei-
ther study reported on the number of patients with resolution of peri-­implant muco-
sitis [40].

3.4.5.2 Gel
In a double-blind randomized clinical trial, the use of a 0.5% chlorhexidine gel in
conjunction with manual toothbrushing was compared to the use of a placebo gel.
All patients received professionally administered mechanical debridement. Both
groups experienced a reduction in the mean number of probing depths and bleed-
ing on probing, but there were no statistically significant differences between
groups [25].

3.4.5.3 Mouthwashes
The use of various antiseptic mouthwashes has been proposed as an adjunct to
patient-administered mechanical therapy. Essential oil and chlorhexidine mouth-
washes have been used in clinical trials.
72 3  Peri-implant Mucositis

Different methods of delivery have been investigated, namely, rinsing and


self-irrigation.

Rinsing
Ciancio et al. [49] demonstrated a beneficial effect of rinsing with an essential oil
mouthwash (Listerine®) in patients that had not received mechanical professional
therapy. A reduction in plaque and gingival inflammation was observed in the con-
trol group when compared to the placebo group. In another study comparing rinsing
with 0.2% chlorhexidine to self-administration of 1% chlorhexidine gel, De Siena
et al. [50] reported a reduction in bleeding scores at the 3-month examination period
when compared to baseline. Both methods were equivalent in their effect, but due to
the lack of a control group, the efficacy of the chlorhexidine products alone could
not be evaluated.

Self-Irrigation
In a study comparing self-irrigation of 0.06% chlorhexidine to rinsing with a 0.12%
chlorhexidine solution, self-irrigation was shown to be more effective in reducing
peri-implant mucositis than rinsing alone. There was less staining and calculus for-
mation in the self-irrigation group [27].

3.4.6 Professional Debridement

Even though professional debridement is paramount to successful peri-implant


therapy, it is insufficient by itself in the long term. Adequate patient-­administered
plaque control is also crucial, in maintaining peri-implant health [51].

3.4.6.1 Curettes, Ultrasonic, and Sonic Instrumentation


A recent randomized controlled clinical trial compared the outcomes of hand instru-
mentation with unfilled resin-tipped curettes (Hu–Friedy Implacare II) to a piezo
ultrasonic scaler (Tigon W&H), in a group of peri-implant maintenance patients.
After 1 year of follow-up, no differences in bleeding indices, plaque, or probing
depths were noted. Cytokine testing did not reveal any differences between the
treatment modalities, neither did patient preference [52]. In a multicenter study
comparing the effect of sonic scalers with plastic tips, rubber cup with polishing
paste, titanium curettes, and airflow with glycine powder, all treatment modalities
were effective in reducing peri-implant mucositis, with no statistically significant
differences between the two methods [53].

3.4.6.2 Air Polishing


Glycine powder seems to be the instrument of choice in air polishing devices, as it
appears to be less abrasive to titanium surfaces than sodium bicarbonate [54]. Two
randomized controlled clinical trials have failed to show a greater decrease in bleed-
ing on probing or a resolution of peri-implant mucositis with the use of an air pol-
ishing device as compared to mechanical debridement [55, 56]. A recent systematic
3.4  Management/Treatment Options 73

review and meta-analysis concluded that “glycine air powder polishing is as effec-
tive as the control treatments at mucositis sites” [57].

3.4.6.3 Adjunctive Local Antibacterials


Professionally administered 0.12% chlorhexidine irrigation and chlorhexidine gel
application did not show any superior benefits to mechanical debridement alone [26].
These results were supported by a more recent clinical trial that compared 0.12% sub-
gingival chlorhexidine irrigation, home rinsing, and mechanical therapy, to mechanical
therapy with placebo solutions. While both treatment modalities were effective in
reducing inflammation and peri-implant mucositis, the authors noted that complete
resolution of inflammation was not achieved in all sites with either modality [58].
The use of a full mouth decontamination protocol used to treat peri-implant
mucositis patients was investigated by Thone-Muhling et  al. [59] The bacterial
reduction after full mouth decontamination was noted to be temporary with a ten-
dency towards recolonization.
In a double-blind randomized clinical trial, patients were instructed to brush
daily with a manual toothbrush with either 0.5% chlorhexidine or placebo gel.
While, in both groups, there were statistically significant reductions in the mean
number of sites with bleeding on probing and a decrease in the mean probing
depths between 1 and 3 months, no differences were noted between test and control
groups [25].

3.4.6.4 Adjunctive Local and Systemic Antibiotics


A study by Renvert et al. [60] compared minocycline to chlorhexidine gel application
following mechanical debridement. At the 1-year follow-up, no differences were
observed between the two groups in terms of clinical probing depths and plaque levels
(Fig. 3.14). A similar outcome was noted when tetracycline fibers were used in the
treatment of peri-implant mucositis and hyperplasia. This was also true when sys-
temic antibiotics were studied. Another clinical trial compared the use of systemic
azithromycin and mechanical debridement vs. debridement alone in the treatment of

Fig. 3.14  Administration of local antibiotic


74 3  Peri-implant Mucositis

peri-implant mucositis. This study did not report any difference on bacterial counts
between the two groups [61].

3.5 Summary

The primary approach for treating peri-implant mucositis is patient education and
patient-administered plaque control. Appropriate design of implant restorations and
the provision of adequate oral hygiene aids as well as demonstration of their use are
of paramount importance. The provision of peri-implant professional evaluation
and therapy is a cornerstone of implant treatment.
Although clinical improvements of peri-implant mucositis lesions with profes-
sional debridement and adequate oral hygiene are well documented, it is important
to note that not all lesions are responsive to the above treatments. Consequently,
adjunctive methods of therapy such as patient- or professionally administered
chemical plaque control may have some additional benefits. It is up to the treating
clinician to select and prescribe appropriate treatment combinations based on indi-
vidual patient needs.

Recommendations for Dental Professionals [37] (Adapted from Jepsen et al.)

• An individual risk assessment should be performed prior to implant ther-


apy; factors such as presence of periodontal disease, poor oral hygiene
practices, or smoking should be addressed prior to initiation of implant
therapy.
• Patients should be informed prior to initiation of treatment of the risks of
biological complications and the need for appropriate oral hygiene mea-
sures and peri-­implant maintenance.
• Professional, individualized, supportive peri-implant maintenance should
be established, based on baseline clinical and radiographic records
(Fig. 3.15).

Fig. 3.15 Healthy
peri-implant tissue in an
area that is difficult to
reach due to patient’s
excellent oral hygiene
efforts and good
professional support
References 75

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34. Meyer S, Giannopoulou C, Courvoisier D, Schimmel M, Müller F, Mombelli A. Experimental
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Hard Tissue Complications/
Peri-­implantitis 4

4.1 Introduction

Dental implants have been proven to be a very predictable treatment modality to


replace missing teeth. Since the introduction of dental implants in dentistry, their
popularity and range of applications have exponentially increased. A similar
increase has been noted in the range and incidence of biological complications
around dental implants. Due to inconsistencies in the terminology used in the litera-
ture, the reported data can not be interpreted properly. This makes an estimation of
the prevalence of biological complications impossible. The terms peri-implant
mucositis and peri-implantitis were clearly defined at the First European Workshop
on Periodontology in 1993 (Figs. 4.1 and 4.2). Peri-implantitis was defined as an
inflammatory process around a dental implant, which includes both soft tissue
inflammation and loss of supporting bone [1]. It is the result of a disturbance of the
equilibrium between the load of the bacterial plaque and the host immune response.

Fig. 4.1  The presence of peri-implant soft tissue inflammation is evident, especially around
the middle implant. The respective radiograph, however, shows no signs of any loss of supporting
bone

© Springer International Publishing AG, part of Springer Nature 2018 79


A. Kelekis-Cholakis et al., Peri-Implant Complications,
https://doi.org/10.1007/978-3-319-63719-8_4
80 4  Hard Tissue Complications/Peri-implantitis

Fig. 4.2  The deep probing depth, along with the bleeding and suppuration upon probing, rendered
the diagnosis of peri-implantitis. Significant bone loss was seen radiographically, and a circumfer-
ential, infra-bony defect was identified clinically, upon flap reflection

The clinical signs of peri-implantitis are characterized by soft tissue inflammation,


manifesting as redness, swelling and bleeding on probing, which may be accompa-
nied by suppuration. However, progressive radiographic bone loss is the main diag-
nostic parameter. Peri-implantitis is a very common entity among biologic
complications that occur around dental implants.

4.2 Etiology

Bacterial biofilms have been proven to be the primary etiological factor for the ini-
tiation of the inflammatory lesion of the periodontal tissues. Several animal studies
have demonstrated the mechanisms of the development of the inflammatory lesion
around dental implants [2, 3]. Evidence supports that the initiation and progression
of peri-implantitis follows the same series of events as periodontal disease.
The response of the peri-implant tissues to the bacterial insult (biofilm forma-
tion) follows a similar pattern to the one noted around natural teeth, both in magni-
tude and intensity. This will ultimately lead to complete loss of osseointegration and
implant failure (Fig. 4.3a, b). A similar response was also noted, to established bio-
films in both implants and teeth, with an increase in the inflammatory infiltrate and
substantial loss of collagen. The peri-implant lesion was considerably larger and
with greater apical extension for peri-implant mucosa than teeth [4].
Multiple other variables can influence the progression of peri-implant disease
(Table 4.1). A variable can be characterized as a true risk factor, for the progression
of peri-implant disease, once it has been studied in longitudinal studies and its nega-
tive impact has been established. Variables with an impact on the progression of
peri-implant disease, that have been identified in retrospective and cross-sectional
studies, can only be identified as risk indicators.
4.2 Etiology 81

Table 4.1  Etiological factors associated with the prevalence and progression of peri-implantitis
History of periodontal disease
History of smoking
Poor oral hygiene
Diabetes
Genetic factors—IL-1 polymorphism
Alcohol consumption
Implant surface
Occlusal overload
Presence of keratinized tissue
Iatrogenic factors
Adapted from Heitz-Mayfield LJA.  Peri-implant diseases: diagnosis and risk indicators. J Clin
Periodontol 2008; 35 (Suppl. 8): 292–304

Fig. 4.3  Significant plaque and calculus deposits are noted around the body of this implant. The
implant was entirely encapsulated in soft tissue and was removed as it presented with significant
mobility. Established biofilm formations are noted on the rough surface of a failed dental implant

4.2.1 History of Periodontal Disease

The progression of periodontal disease may ultimately lead to tooth loss, and reha-
bilitation of the lost dentition with dental implants (Fig. 4.4). As defined by Heitz-
Mayfield and Huynh-Ba [5], implant survival refers to the presence of an integrated
implant with or without complications and implant success to the presence of an
implant without any complications. A multitude of studies have been conducted to
determine the effect of the history of periodontal disease on the survival and suc-
cess of dental implants [7–15]. Evidence suggests that patients with a history of
periodontal disease are more susceptible to peri-implant bone loss, compared to
healthy controls [6].
In a systematic review by Van der Weijden [7], it was concluded that implant
survival rates and peri-implant bone loss, of dental implants placed in individuals
with a history of treated periodontal disease, might be different from those in peri-
odontally healthy individuals, in the long-term. In another meta-analysis [8], it was
also concluded that dental implants placed in patients with a history of treated peri-
odontitis exhibited a higher incidence of peri-implantitis and marginal peri-­implant
bone loss.
82 4  Hard Tissue Complications/Peri-implantitis

Fig. 4.4  A patient with a failing dentition, as a result of chronic periodontitis, received full mouth
reconstruction with implant-supported prostheses. Compliance with a strict maintenance schedule
was established prior to implant treatment. Peri-implant tissues appear healthy, and radiographic
bone levels appear stable, 1 year following treatment

Karoussis et al. [9] evaluated the short- (<5 years) and long-term (>5 years)
survival and success rates of dental implants placed in patients with a history of
periodontitis. This review demonstrated that implants placed in patients with pre-
viously treated periodontal disease have similar survival rates with implants
placed in periodontally healthy patients. However, individuals with a history of
periodontal disease experienced a significantly higher incidence of peri-implanti-
tis, deeper probing depths, and increased peri-implant bone loss. Late implant loss
and peri-implant bone loss was also demonstrated in another systematic review by
Quirynen et al. [10]. This was true, especially for implants with a very rough sur-
face, and for patients that were not on a regular maintenance schedule. The rate of
late implant loss was three times higher for subjects that did not receive regular
maintenance therapy.
Klokkevold and Han [11] concluded that there is no significant difference on
survival rates of implants placed in patients with a history of treated periodontitis
4.2 Etiology 83

(95%) compared to patients with no previous history of periodontal disease (97.1%).


However, this study indicated that patients with a history of treated periodontal
disease experienced significantly lower implant success rates (11.05% better for
periodontally healthy patients), as defined by adverse outcomes of peri-implant
tissues.
More recently two systematic reviews assessed the survival and success of
implants placed in patients with a history of periodontal disease. Zangrando et al.
[12] analyzed, the long-term (>5 years) survival and success rates of dental implants
placed in patients with a history of periodontal disease. The authors concluded that
dental implant therapy can be successful in patients with a history of periodontal
disease, as long as the periodontal disease had been properly treated, and the patients
were enrolled in a regular maintenance program. The study demonstrated an implant
survival rate of 92.1% after 10 years of follow-up. However, increased prevalence
of bleeding on probing and residual pocket depths were directly associated with
occurrence of peri-implantitis. Furthermore, non-­ compliance with periodontal
maintenance and tobacco smoking had a negative influence on implant outcomes.
Another systematic review, reported that implants placed in patients with a history
of treated periodontitis had a higher incidence of biological complications and
implant loss [13]. Moreover, smoking and lack of periodontal maintenance nega-
tively affected the success of dental implants. Evidence from this review suggested
that patients with sites of persistent periodontitis were four times more likely to
develop biological complications compared to successfully treated individuals.
Moreover, when aggressive periodontitis subjects are treated with implants, a trend
for lower implant survival and success rates was noted, when compared to chronic
periodontitis individuals or healthy individuals.
A recent study systematically assessed the literature to identify the effect of a
history of aggressive periodontitis on implant therapy [14]. The results of this
review indicated that the effect of aggressive periodontitis depends on the “end
outcome” reported. No significant difference was found when “implant survival”
was used as the end outcome, for patients with aggressive periodontitis com-
pared to healthy or chronic periodontitis patients. However, when “implant fail-
ure” was considered as the end outcome, a risk ratio for implant loss of 4.00 and
3.97 was identified, when comparing the aggressive periodontitis group with the
healthy and the chronic periodontitis groups, respectively. The authors con-
cluded that due to the small sample of failed implants in aggressive periodontitis
patients, these numbers should be interpreted with great caution. This review
also demonstrated that implants in patients with a history of aggressive peri-
odontitis experienced more marginal bone loss, compared to implants in patients
with a history of chronic periodontitis (0.28  mm vs. 0.43  mm). The authors
advised caution in the interpretation of this fact, as it might not be clinically
significant.
The survival rates of supra-structures and implants are high in individuals with a
history of periodontitis-associated tooth loss. However, the higher incidence of peri-­
implantitis may jeopardize the longevity of the implant treatment. Therefore,
implant treatment in periodontitis-susceptible patients is not contraindicated,
84 4  Hard Tissue Complications/Peri-implantitis

provided that there is adequate plaque control and that an individualized mainte-
nance program is implemented [15].

4.2.2 Smoking

Cigarette smoking should be considered a risk factor for the long-term survival and
maintenance of dental implants. In a systematic review and meta-analysis [16], it
was shown that smoking may significantly affect the survival of dental implants,
with an implant-related and patient-related OR of 2.25 and 2.69, respectively, when
smokers were compared to non-smokers. Previously augmented implant sites
showed a significantly higher risk for implant failure when smokers (OR 3.61) were
compared to non-smokers (OR 2.15). Furthermore, biological complications, such
as peri-implant tissue inflammation and marginal peri-implant bone loss, were
found to occur with higher frequency in smoking compared to non-smoking
individuals.
In contrast, studies reporting on implants with recently introduced micro-­
roughened surfaces show a significantly lower risk of implant failure in smokers
with an OR of 1.49 [17, 18]. Thus, implant surface treatment may play a role in the
survival of implant fixtures in smokers. Smoking was found to have a negative influ-
ence on the occurrence of biologic complications on machined, Titanium Plasma
Sprayed (TPS) and Hydroxy-apatite (HA) coated implants [19]. However, when
comparing implants with particle-blasted and acid-etched (SLA), anodized (TiUnite)
and dual acid-etched (Osseotite) surfaces no significant influence of smoking on
marginal bone loss was noted around those implants [20].
Patients undergoing implant treatment should be thoroughly informed regarding
the potentially negative influence of cigarette smoking on dental implants and their
overall health. The positive influence of the newer micro-roughened surfaces on
implant survival and peri-implant marginal bone levels should be further investi-
gated, with more studies, and further reinforced with more adequately powered,
long-­term evidence in large sample sizes.

4.2.3 Poor Oral Hygiene/Lack of Maintenance

There is substantial evidence that poor oral hygiene is associated with an increase in
peri-implant marginal bone loss (Fig. 4.5). In an epidemiologic study of Brazilian
subjects, individuals with high plaque scores (>2) were 14.3 times more likely to
experience peri-implant marginal bone loss when compared to individuals with low
plaque scores [21]. In another prospective study, it was noted that 48% of implants
referred for treatment of peri-implantitis, had restorations that did not allow enough
access for adequate oral hygiene [22].
Lack of regular peri-implant maintenance care has also been associated with an
increased incidence of marginal peri-implant bone loss.
4.2 Etiology 85

Fig. 4.5  Poor oral hygiene, due to limited access, and complete lack of maintenance, resulted in
severe peri-implant inflammation and loss of peri-implant soft and hard tissues. Upon peri-implant
therapy, two of the implants were replaced, and the fixed prosthesis was converted to a removable
one in order to facilitate maximum access for proper oral hygiene and implant maintenance

4.2.4 D
 iabetes, Alcohol Consumption, and Genetic Factors IL-1
Polymorphisms

There is limited evidence to suggest that diabetes, alcohol consumption, or gene


polymorphisms can negatively affect peri-implant tissue health and lead to
86 4  Hard Tissue Complications/Peri-implantitis

peri-­implant bone loss. Although diabetic subjects may be at increased risk for den-
tal implant failure [23], only one study has shown that patients with poor metabolic
control may be at increased risk of peri-implantitis [21]. Similarly, there is only one
study indicating that individuals consuming >10  g of alcohol daily, may be at
increased risk of peri-implant bone loss.
A systematic review by Huyhn-Ba et al. [24] could not reach a conclusion on
whether or not IL-1 genotype status is associated with peri-implantitis. The identi-
fication of IL-1 gene polymorphisms as risk factors for peri-implant disease cannot
be justified at this time.

4.2.5 Dental Implant Surface

The dental implant surface quality may determine the tissue reactions to the implant
fixture [25]. Dental implant surface characteristics, such as roughness and chemical
treatment, have been shown to play a role in the progression of peri-implant bone
loss. The initial Branemark implant carried a machined surface with a roughness
(Sa) of 0.5–1.0  μm, and is the most widely researched implant. Rough-surface
implants (Sa >2.0 μm TPS and HA coated) were shown to have a favorable bone
response which led to faster osseointegration. However, rough-surface implants
demonstrated a higher incidence of peri-implantitis and a more rapid progression of
marginal bone loss. On the other hand, moderately rough-surface implants (Sa 1.0–
2.0 μm most of the implants used today, TiO Blast, SLA, TiUnite, Frialit-2) have
shown no increase in the incidence of peri-implantitis and maintenance of the mar-
ginal bone levels for a follow-up of 5 years [26]. Nevertheless, in an animal study
by Berglundh et al. [27], it was shown that the progression of peri-implantitis, in
moderately rough-­surface implants (SLA surface), was more pronounced than in
smooth-surface implants, if left untreated. In another comparative animal study, it
was shown that progression of experimentally induced peri-implantitis occurred in
implants with different geometry and surface treatment [28]. Peri-implant marginal
bone loss was more pronounced on implants with an anodized surface (TiUnite). In
a randomized controlled clinical trial by Wenstromm et  al. [29], patients were
treated with implant-supported fixed partial dentures and followed up for a period
of 5 years. This study demonstrated that implants with a moderately rough surface
(TiO Blast Sa 1,5  μ) had similar marginal bone levels with machined surface
implants after 5  years in function. In the same study, moderately rough-surface
implants demonstrated a similar response to peri-implant bone loss, when compared
to implants with a machined surface.

4.2.6 Occlusal Overload

The effect of occlusal overload on peri-implant bone loss is reported in the literature
with great controversy. Early reports on animal models, by Isidor [30, 31], showed
that loss of osseointegration and implant mobility could be observed 4.5–15.5 months
4.2 Etiology 87

Fig. 4.6  This implant lost bone integration completely, 3 months following the installation of the
final restoration. The implant was placed in a grafted site (ridge preservation, first radiograph, top
left), 5  months following graft placement. Four months following implant placement (second
radiograph, top right), the implant appeared stable at a torque of 35 N/cm, and the bone levels
appeared normal at the stage 2 appointment. Three months following the placement of the restora-
tion, the implant became mobile and was removed. A radiograph at his time showed significant
bone loss and a peripheral radiolucency

following implant placement, when excessive load was applied (Fig. 4.6). Implants
in the control group, which were allowed to accumulate plaque, showed a mean
marginal bone loss of 1.8 mm. However, the models of occlusal overload applied in
these studies do not reflect real clinical scenarios.
More recent histological observations though, demonstrated that occlusal over-
load does not affect the peri-implant bone levels or bone to implant contact of
88 4  Hard Tissue Complications/Peri-implantitis

Table 4.2  Effect of occlusal overload on peri-implant parameters


Bone loss
48 implants Probing depths (mm) Shoulder crest (mm) Bone to implant contact (%)
Not loaded 2.5 ± 0.3 3.6 ± 0.4 73
Overloaded 2.6 ± 0.3 3.7 ± 0.2 75
Adapted from Heitz-Mayfield LJ, Schmid B, Weigel C, Gerber S, Bosshardt DD, Jönsson J, Lang
NP, Jönsson J. Clin Oral Implants Res. 2004 Jun;15 [3]:259–68.

osseointegrated dental implants, in the absence of peri-implant inflammation [32].


In this study the occlusal overload model applied was more relevant to clinical prac-
tice, utilizing implant-supported crowns in supraocclusion in order to create over-
load of the dental implants (Table  4.2). However, occlusal overload can be
detrimental on the peri-implant marginal bone levels, when applied to dental
implants surrounded by inflamed peri-­implant tissues. In another dog study, utiliz-
ing the same model of occlusal overload, it was demonstrated that overloading may
aggravate the peri-implant bone resorption, only in the presence of peri-implant
inflammation [33]. Peri-implant bone loss is noted when a load in excess of 3000
micro strain is applied. According to the third EAO concensus conference, none of
the studies conducted to evaluate the effect of overload on peri-implant bone, have
measured the amount of micro strain on the bone-implant interface [34].

4.2.7 Lack of Keratinized Tissue

The amount of keratinized mucosa (KM) around dental implants has been discussed
in the literature with great controversy. Evidence suggests that KM may not be nec-
essary to maintain peri-implant health [35] and may not be associated with peri-
implant bone loss [36]. However, despite its presence, peri-implantitis may still
occur [37]. Earlier studies had failed to show any correlation between keratinized
and attached mucosal width, and increased implant success [35]. Soft tissue grafting
increased the width of keratinized tissue: however, no improvement in implant suc-
cess rates was noted [38].
Recent studies suggest otherwise (Fig. 4.7). Wider KM will better preserve hard
and soft tissue [39] and may be more favorable for the long-term maintenance of
implants [40]. Furthermore, lack of KM may result in greater soft tissue recession
and inadequate plaque control [41]. This resulted in a clinical recommendation of
2 mm of KM around implants [42].

4.2.8 Iatrogenic Factors

Hard tissue changes around dental implants may also be provoked by non-bacterial
causes. Traumatic surgical techniques, implant design, implant malposition, loose
prosthesis, or abutment are only a few of the parameters that can lead to peri-implant
bone loss [43]. The most widely researched iatrogenic factor contributing to
4.2 Etiology 89

Fig. 4.7  Deep peri-implant probing depth was noted on the buccal aspect of this implant, along
with a lack of keratinized tissue. Upon flap reflection, significant bone loss was noted. Open flap
debridement with implantoplasty and guided bone regeneration of the infra-bony components of
the defect was done. Following adequate healing time, soft tissue augmentation was performed,
to increase the quantity (volume) and improve the quality (keratinized mucosa) of the peri-
implant tissue

peri-­implant bone loss is the residual cement that remains in the peri-implant tissue,
following delivery of the final restoration (Fig.  4.8). The positive relationship
between residual cement and peri-implant disease was demonstrated in a prospec-
tive study with the use of an endoscope [44]. This study showed that 81% of cases
with peri-implant disease were associated with residual cement, as detected with the
use of an endoscope. Furthermore, 74% of these cases showed no signs of
90 4  Hard Tissue Complications/Peri-implantitis

Fig. 4.8  Significant plaque accumulation was noted around these two implants in the posterior
mandible, upon prosthesis removal. The implants were placed at a supra-crestal position leaving
the rough surface exposed. This along with an unhygienic prosthesis design provoked significant
plaque accumulation and hindered optimal oral hygiene. Upon flap reflection significant bone loss
was noted around both implants. The implants were removed along with the adjacent first premo-
lar, which was deemed hopeless. Excess cement was noted along the open margin of the tooth
supported crown as well as on the rough surface of the dental implants

peri-­implant disease 30 days following the removal of the cement remnants. The
high prevalence of residual cement in cases of peri-implantitis may be explained by
the fact that most of the commercially available cements are non-detectable by
radiographic means [45]. Another study confirmed the capacity of residual cement
to elicit peri-implant inflammation, leading to peri-implant bone loss [46]. This
inflammatory response can be exaggerated in patients with a previous history of
periodontal disease. Furthermore, the amount of residual cement is directly
4.3 Diagnosis 91

proportional to the depth of the margin of the restoration [47]. Thus, restorations
with subgingival margins are more likely to retain cement material following the
final delivery of the restoration. Different methods of crown cementation have been
proposed in order to reduce the prevalence of residual cement during delivery of the
final restoration. Alternatively, screw-retained restorations may be selected.

4.3 Diagnosis

Peri-implantitis is defined as an inflammatory process around a dental implant,


which includes both soft tissue inflammation and loss of supporting bone [48, 49].
Due to the similarities, in the pathogenesis, of periodontitis with peri-implantitis,
similar criteria have to be used in order to diagnose peri-implantitis [50].

4.3.1 Bleeding on Probing

The absence of bleeding on probing (BOP) is considered an excellent predictor of


health and periodontal stability [51]. The presence of BOP has shown limited posi-
tive predictive value, and it is considered a weak marker for future periodontal dis-
ease progression. BOP around dental implants (Fig.  4.9), however, has shown a
significantly higher positive predictive value compared to teeth. In a study by
Luterbacher et al. [52], it was demonstrated that implants with a positive BOP in
≥50% of the recall appointments showed 100% chance for disease progression.
Disease progression was defined as a 2.5 mm of attachment loss or −3.7 in Computer
Assisted Densitometric Image Analysis (CADIA) values, over a period of 5 years.
These values were further reinforced when paired with microbiological tests that
showed the presence of certain pathogenic bacteria [52]. Hence, the presence of
BOP around dental implants may be a valuable diagnostic parameter to monitor the
stability of peri-implant tissue health.

Fig. 4.9  Deep clinical probing depths were noted around this implant. Shortly after the probe was
removed, bleeding was noted across the mucosal margin around the implant-supported
restoration
92 4  Hard Tissue Complications/Peri-implantitis

4.3.2 Probing Depths and Radiographic Evaluation

Clinical assessment of peri-implant tissue health is imperative in order to establish


the long-term success of implant treatment. Probing of the peri-implant tissue (25 N
probing force) is a safe diagnostic means to identify any deviation from peri-­implant
tissue health. Any disruption of the soft tissue attachment with the implant surface,
by a periodontal probe, will be restored fully by 5 days [53]. Lang et al. [54] have
demonstrated that the peri-implant mucosa has the capacity to provide the underly-
ing bone with an excellent seal in the presence of peri-implant mucosal health and
peri-implant mucositis. In the presence of peri-implantitis, however, the probe tip
will penetrate further to the underlying bone. Hence, probing around dental implants
is a valuable tool to monitor peri-implant tissue health and diagnose peri-implant
diseases.
Multiple studies have suggested a specific probing depth threshold that can be
associated with peri-implant tissue health. However, it is important to note that a
sub-crestal position of the implant may often be necessary in order to achieve an
optimal outcome, especially in the esthetic zone. This will ultimately result in
deeper probing depths, which alone are not considered a sign of peri-implant dis-
ease. Thus, it is important to establish a health-related baseline at the time of the
connection of the prosthetic components. Comparison of future measurements to
baseline is essential to identify the presence of health or pathology [43].
Establishing a baseline is also critical for the radiographic records in order to
detect any future bone loss around the implant fixture. Baseline radiographs should
be taken at implant placement and after the connection of the restorative component
[43], as bone loss prior to this time point may be due to iatrogenic factors or normal
bone turnover during the healing phase. Every effort should be made to standardize
these radiographs by taking them perpendicular to the implant body, with a clear
demarcation of the restorative platform and the implant threads. The implant threads
will serve as points of reference to diagnose peri-implant bone loss in future
radiographs.
Anytime there is bleeding on probing with increasing probing depths; a new
radiograph is recommended, in order to confirm the progression of further bone
loss, if any, in comparison to baseline measurements (Figs. 4.10 and 4.11).

4.3.3 Suppuration

Suppuration with or without probing represents a pathognomonic sign of peri-­


implant disease (Fig. 4.12). The presence of suppuration denotes the presence of
active infection and pathological changes. Therefore, further evaluation and treat-
ment is indicated.
4.3 Diagnosis 93

Fig. 4.10  Deep clinical probing depths with profuse bleeding upon probing were noted around these
implants. Significant bone loss is noted on the corresponding radiograph, along with a radiopaque
finding at the mesial of implant #13. Upon flap reflection the clinical and radiographic findings were
confirmed. Significant bone loss can be seen in the intraoperative picture. Circumferential bone loss
is noted around both implants, along with an infra-bony defect around the most distal implant

Fig. 4.11  This patient received two dental implants to replace his central incisors. The implants pre-
sented with mobility, severe inflammation of the peri-implant soft tissues, and spontaneous suppuration
94 4  Hard Tissue Complications/Peri-implantitis

2008 2011 2012

Fig. 4.12  Progressive bone loss can be seen around these three implants. The bone loss follows a
different pattern around each implant, with a non-linear progression in time

4.3.4 Mobility

The ultimate result of untreated peri-implantitis is the loss of supporting bone


around the dental implant fixture. As this infection develops due to plaque accumu-
lation around the gingival margin of the implant restoration, bone loss occurs at the
coronal aspect and progressively extends apically. Therefore, mobility of the implant
denotes complete loss of integration and ultimately implant failure.

4.3.5 Prevalence

It is widely accepted that all of the abovementioned diagnostic parameters are use-
ful for the diagnosis of peri-implant diseases. However, there is inconsistent evi-
dence when reporting prevalence rates. These differences can be explained by the
lack of uniform guidelines in the diagnosis of peri-implantitis and the wide range of
threshold values of diagnostic measurements. Furthermore, the level of data report-
ing (patient level vs. implant level) contributes to that variation. In an epidemiologic
study, Koldsland et al. [55] demonstrated that different diagnostic thresholds would
yield different rates of prevalence of peri-implant diseases. The most significant
parameter affecting the prevalence of peri-impant disease, is the threshold of pathol-
ogy as it relates to probing depths. The most significant change in prevalence occurs
when the probing depth threshold increases from ≥4 mm to ≥6 mm.
In a systematic review by Tomasi et al. [56], the authors agreed that the preva-
lence of peri-implant diseases depends on the diagnostic threshold and that no set
criteria for diagnosis exist. In a meta-analysis of five studies, it was cautiously esti-
mated that the prevalence of peri-implant diseases is approximately 10% when
reported on the patient level and 20% when reported on the implant level [57].
However, the lack of uniform diagnostic criteria was also pointed out in this
meta-analysis.
4.4  Management/Treatment Options 95

In an effort to create consistency in the diagnosis of peri-implantitis, different


classification systems have been proposed, [58] classifying peri-­implantitis, based
on the severity of the defect (See Sect. 1.3).
Unfortunately, to date, no uniform diagnostic criteria are widely accepted for the
diagnosis of peri-implantitis. The potential intervention depends on the stability of
the case over the long-term based on the clinical and radiographic measurements
taken at baseline.

4.3.6 Disease Progression

The progression of peri-implant disease has been extensively researched. Most


studies have implemented the model of ligature-induced peri-implantitis [3], in
order to induce peri-implant bone loss. The most distinct difference between the
periodontal lesion and the peri-implantitis lesion is that the first has a self-limit-
ing capacity due to the configuration of the gingival collagen fibers around the
teeth, a characteristic that is not found in the latter [59]. Furthermore, following
ligature removal, there was spontaneous bone loss around the implant fixtures.
Different studies have assessed the progression of bone loss (Fig. 4.12), on dif-
ferent implant surfaces during a period of plaque accumulation, following a
period of ligature-­induced peri-implantitis [27, 60, 61]. In general, all studies are
in agreement that peri-implantitis progresses in a faster rate on rough implant
surfaces, compared to smooth-surface implants. When different rough surfaces
were compared [60], no statistically significant differences were found between
the different rough implant surfaces. However, in the analysis there was a consis-
tent finding that indicated a more pronounced severity of peri-implantitis on
anodized surface implants.
The pattern on peri-implant bone loss was reported in a cohort study of 487 peri-­
implantitis-­affected implants [62]. The peri-implant bone loss showed a nonlinear
pattern and the rate of bone loss increased over time. In this study the pattern of
peri-implantitis-associated bone loss showed a variation among individuals and a
similar pattern of progression within the same subject.

4.4 Management/Treatment Options

As there are many common features on the pathogeneses and the diagnoses of peri-
odontal and peri-implant diseases, similar strategies and treatment modalities are
applied toward their treatment [63]. The ultimate goal of peri-implantitis treatment
is to establish inflammation-free peri-implant soft tissues, eliminate all plaque
retentive factors, prevent any further bone loss [64]. Furthermore, treatment aims to
allow adequate access for proper oral hygiene for long-term peri-implant tissue
health.
96 4  Hard Tissue Complications/Peri-implantitis

4.4.1 Removal of Etiologic Factors

Once the diagnosis of peri-implantitis has been rendered, a thorough assessment of


the peri-implant tissues, as well as the corresponding prostheses, should be per-
formed in order to identify all local causative factors. Systemic and environmental
factors that may provoke the occurrence and progression of peri-implantitis should,
also, be identified. The control and/or elimination of these factors is crucial for the
success of the treatment and the maintenance of the desired outcome.

4.4.2 Nonsurgical Treatment of Peri-implantitis

Although nonsurgical debridement has been proven effective for the treatment of
peri-implant mucositis, it shows limited efficacy when used alone for the treatment
of peri-implantitis. It has been demonstrated that the addition of local antimicrobi-
als to mechanical debridement offers marginal improvement of peri-implant tissue
parameters [65]. A recent systematic review evaluated the success of treatment pro-
tocols on inflammation resolution in patients with peri-implantitis-­affected implants
[64]. Although most protocols showed improvement on peri-­implant tissue param-
eters, 18–89% of implants still bled on probing following nonsurgical therapy of
peri-implantitis. This type of treatment may be more suitable for esthetic areas
where a surgical approach would result in implant thread exposure and compro-
mised esthetics [66]. Laser treatment or photodynamic therapy were proven effec-
tive in reducing inflammation for a period of at least 6 months. Their effect though
on probing depths and attachment levels was negligible [67]. Once the nonsurgical
treatment has been completed, a close follow-up of 1–2 months is necessary in order
to re-evaluate peri-implant parameters [68].

4.4.3 Surgical Treatment of Peri-implantitis

4.4.3.1 Surface Decontamination


Since the nonsurgical treatment modalities have limited efficacy, surgical interven-
tion is usually needed. The surgical treatment of peri-implantitis aims on the arrest
of peri-implant bone loss and often times on the regeneration of the resorbed bone.
The main determinant of success of surgical intervention is the decontamination
of the exposed implant surface. This task is carried out through mechanical debride-
ment, often combined with chemical disinfection and implant surface modification
(Fig. 4.13). A systematic review of the literature revealed that no specific chemical
agent (Table 4.3) was superior for implant surface decontamination [69]. Another
systematic review addressed the effect of various instruments on roughness altera-
tions of the surface of dental implants, as well as their prosthetic components [70]
(Table 4.4). According to this analysis, smooth-surface implants and implant pros-
thetic components should be treated with nonmetal instruments (nonmetal curettes
and nonmetal power-driven tips), as it was shown that these leave smooth surfaces
4.4  Management/Treatment Options 97

Fig. 4.13 (a) Peri-implant inflammation and radiographic bone loss are evident around this
implant. Upon flap reflection significant peri-implant bone loss was noted, and the implant was
planned for removal. A titanium micro-brush was used to clean the distal half of the exposed
implant surface. Upon removal the implant was submitted for microscopic examination. (b) The
microscopic examination revealed established bacterial biofilms on the contaminated implant sur-
face. The area of the implant treated with the titanium micro-brush presents with a clean rough
surface, free of bacterial biofilms

unaltered or may produce the least increase in surface roughness. On the other hand,
treatment of the exposed rough surface of dental implants with metal instruments
(power-driven and curettes) showed a decrease in roughness. This occured by either
tearing or scrapping off parts of the TPS surface, or decreasing the height of eleva-
tions of the SLA surface.
98 4  Hard Tissue Complications/Peri-implantitis

Table 4.3  Agents used for implant surface decontamination


Abrasive pumice
Air powder (sodium bicarbonate, glycine, etc.)
Chlorhexidine
Citric acid
Delmopinol
EDTA
Hydrogen peroxide
Laser therapy
Photosensitization
Saline
Adapted from Claffey N, Clarke E, Polyzois I, Renvert S: Surgical treatment of peri-­implantitis. J
Clin Periodontol 2008; 35 (Suppl. 8): 316–332

Table 4.4  Instruments used for mechanical debridement of the implant surface
Nonmetal instruments Metal instruments
Curettes/ultra-sonic Curettes/ultra-sonic
 • Plastic  • Stainless steel
 • Carbon  •  Titanium
 • Resin reinforced,  • Gold coated
 • Non-resin reinforced
Air abrasion Burs: carbide/diamond
Rubber cup with/without abrasive paste Diamond polishers
Adapted from Louropoulou A, Slot DE, Van der Weijden F. Titanium surface alterations following
the use of different mechanical instruments: a systematic review. Clin. Oral Impl. Res. 23, 2012;
643–658

A recent review analyzed the literature for different implant surface decontami-
nation protocols and their correlation with the treatment outcome [71]. Due to the
heterogeneity of the data, no method was proven to be superior. Interestingly the
factors that mainly influenced the surgical outcome were: adequate access for proper
decontamination, defect configuration, the use of a bone replacement graft, as well
as the use of a membrane.
Laser therapy has also been used as an aid for the decontamination of the exposed
implant surface and the regeneration of the peri-implant bone. Multiple laser
devices, with various wavelengths, have been used, with the Er:YAG laser being the
one most extensively researched. A recent systematic review of the literature indi-
cated that the improvements noted from the use of lasers in the treatment of peri-­
implantitis are not substantial in order to indicate a major change in the
peri-implantitis treatment protocols [72]. Another systematic review and meta-­
analysis concluded that due to limited data, the use of lasers in the treatment of
peri-implantitis, was not found superior when compared to conventional treatment
modalities [67]. Existing evidence is in agreement, that more well designed clinical
trials, with longer follow-up periods, are necessary to validate the use of lasers for
the treatment of peri-implant diseases.
4.4  Management/Treatment Options 99

4.4.3.2 Surgical Intervention Modalities


Multiple surgical procedures have been advocated for the surgical treatment of peri-­
implantitis, and the choice of intervention may greatly depend on the configuration
of the peri-implant defect [73, 74] (Table 4.5).
The main goal of surgical intervention is to gain access to the contaminated den-
tal implant surface (Fig.  4.14). Access flap surgery, however, has shown limited
efficacy on the treatment of peri-implantitis. In a prospective study, dental implants
diagnosed with peri-implantitis were treated with access flap surgery and bone
recontouring. After a 2-year follow-up period, 50% of the implants appeared dis-
ease-free. However, 42% of the implants in this study showed signs of peri-implant
disease despite treatment, with seven implants removed due to excessive bone loss
[75]. In a different study, implants presenting with peri-­implantitis were treated with
access flap surgery, bone recontouring, and implantoplasty. Although implanto-
plasty appears to be a more radical method of implant surface decontamination, it is
likely to have a positive effect on the final outcome [76, 77].
A recent meta-analysis assessed the efficacy of surgical interventions on the
treatment of peri-implantitis [78]. The results of this review indicated that surgical
intervention would yield an average probing depth reduction of 2–3 mm. The addi-
tion of implantoplasty seemed to yield superior results, compared to access surgery
alone (Fig. 4.15). A mean radiographic bone fill of approximately 2 mm was noted
for defects treated with bone grafts or guided bone regeneration (Fig. 4.16). This
review concluded that the best results in the literature are reported in studies with
very sophisticated implant surface decontamination protocols and those that used a
combination of bone replacement grafts with bone morphogenetic proteins. The use
of barrier membranes, however, may not offer significant advantages, as the risk of
membrane exposure is substantial and may compromise the final result.

Table 4.5  Armamentarium of surgical procedures


Diagnosis Surgical intervention
Mucogingival defect with bony Mucogingival therapy (see Chap. 2)
fenestration or dehiscence
Horizontal bone loss mild/moderate Apically positioned flap with osseous respective
surgery with or without implantoplasty
Vertical bone loss Bone grafts with or without resorbable membrane
Contained infra-bony defect, funnel-­ Guided bone regeneration (non-resorbable membrane
shaped three-wall and autogenous bone)
Non-contained one- to two-wall defect
Combined vertical and horizontal bone Guided bone regeneration (non-resorbable membrane
loss and autogenous bone)
Loss of osseointegration or bone loss Explantation, regeneration, and implant restoration
>50% of the implant
Adopted from Parma-Benfenati S, Roncati M, Tinti C.  Int. J Periodontics Restorative Dent
2013;33:627–633
100 4  Hard Tissue Complications/Peri-implantitis

Fig. 4.14  The implant at site 4.6 presented with deep probing depths, bleeding on probing, and
suppuration. The screw-retained restoration was removed, and significantly inflamed peri-implant
tissues were noted. Upon flap reflection a circumferential bone defect was identified. Osteoplasty
and implantoplasty were performed. The modified implant surface was disinfected with the use of
clindamycin slurry, followed by a hydrogen peroxide rinse. A healing abutment was placed, and
the flaps were apically repositioned. Following a healing period of 4 months, clinical probing
depths of 2 and 4 mm were noted at the buccal/lingual and mesial/distal aspects, respectively.
Inflammation-free peri-implant soft tissues were noted after removing the healing abutment. The
initial screw-retained restoration was replaced. Slight mucosal recession was noted at the time of
restoration replacement. At 1-year follow-up (last two pictures), a probing depth of 3 mm, a­ bscense
of mucosal recession, and inflammation free tissues were noted
4.4  Management/Treatment Options 101

Fig. 4.14 (continued) 
102 4  Hard Tissue Complications/Peri-implantitis

Fig. 4.14 (continued) 
4.4  Management/Treatment Options 103

Fig. 4.15  This implant presented with pain and significant tissue edema around the restoration.
Upon removal of the restoration, severe inflammation was evident at the peri-implant soft tissue,
with clinical probing depths of 9–10 mm. Plaque and calculus deposits were noted on the implant
restoration. Upon flap elevation, significant amounts of granulation tissue were noted, around the
implant. Following removal of granulation tissue, bone loss of about 4 mm was noted around the
implant, as well as at the proximal surfaces of the adjacent teeth. Implantoplasty, and osteoplasty
were performed, and the implant surface was decontaminated with hydrogen peroxide. A stock
healing abutment was placed, and the flaps were repositioned apically. After a healing period of 4
months, the healing abutment was removed, and the peri-implant soft tissues were re-evaluated.
The peri-implant soft tissues appeared healthy, with no bleeding upon probing. Clinical probing
depths of 3 mm were noted at all aspects of the dental implant. A new implant-supported restora-
tion was installed, following sufficient healing time. At the 1-year follow-up, the peri-implant tis-
sues appear healthy with no bleeding upon probing and normal probing depths. The radiographic
examination revealed stable bone levels over the healing period
104 4  Hard Tissue Complications/Peri-implantitis

Fig. 4.15 (continued)
4.4  Management/Treatment Options 105

Fig. 4.15 (continued)
106 4  Hard Tissue Complications/Peri-implantitis

Fig. 4.15 (continued)

In a recent systematic review, it was noted that most studies, reporting on the
surgical treatment of peri-implantitis, were considered at high risk of bias [64].
Even though, favorable outcomes were reported in the majority of clinical trials,
13–53% of dental implants still bled on probing following surgical intervention.
Successful treatment outcomes need to be more consistently defined. Thus, a com-
posite criterion of PD <5 mm with no concomitant BOP, and no progressing bone
loss, was proposed as the threshold for the need of further treatment [64].
To date, existing evidence on the prevention and treatment of peri-implant dis-
eases is subject to a high level of bias, inadequate quality of reporting, and outcome
measures [79]. Both clinical and preclinical studies provide inadequate or missing
information [79, 80]. Surrogate outcomes, such as probing depths, attachment lev-
els, and recession, are often adopted as endpoints, as they have been extensively
researched in periodontal disease. However, these endpoints may not represent out-
comes appropriate for treatment comparisons. Literature on quality reporting is in
agreement that future research must adhere to more strict guidelines.
The choice of surgical treatment modality is largely dependent on defect configu-
ration, as well as local and systemic factors. The amount of the remaining bone sup-
port will dictate whether treatment should be rendered or the dental implant needs to
be removed. Dental implant removal should be considered for those fixtures that have
lost more than 2/3 of their total bone support (Fig. 4.17). Furthermore, when signifi-
cant peri-implant bone loss is noted prior to the connection of the implant restoration,
implant removal should also be considered. Reconstruction of the deficient site is
necessary prior to proceeding with dental implant replacement (Fig. 4.18).
4.4  Management/Treatment Options 107

Fig. 4.16  This implant presented with evidence of peri-implantitis. Clinical and radiographic data
confirmed peri-implant bone loss. Upon flap elevation the granulation tissue was removed, and the
exposed rough implant surface was mechanically debrided with a titanium micro brush. Following
defect debridement and implant surface decontamination, a circumferential bone defect was noted.
The infra-bony defect was grafted with a combination of autogenous bone chips with freeze-dried
bone allograft. The flaps were repositioned and sutured firmly around the implant restoration
108 4  Hard Tissue Complications/Peri-implantitis

Fig. 4.17  Significant radiographic bone loss along with deep probing depths were noted around
this implant prior to the initiation of the restorative phase. Following flap reflection significant
bone loss was identified around the dental implant, accounting for more than 50% of its total
length. Thus, dental implant removal was planned, with subsequent site development for future
implant replacement. An dental implant removal tool was used, and the implant was reversed
torqued and removed. Upon implant removal, a significant bone defect was noted, with total anni-
hilation of the palatal wall. Significant bone loss was observed at the adjacent lateral incisor due to
the peri-implant infection. Peri-implant bone loss may often affect the prognosis of the adjacent
teeth, if it is not dealt within a timely manner. Enamel matrix derivative (Emdogain Straumann®)
was used on the denuded root surface, and the residual ridge defect was reconstructed with freeze-
dried bone allograft (MTF Dentsply) and a non-absorbable Ti-reinforced d-PTFE membrane
(Cytoplast®). After 8 weeks the membrane was removed and the site healed uneventfully. Following
healing, adequate ridge width was observed clinically and radiographically. The defect at the
mesial aspect of the lateral incisor was fully healed. A regular platform implant (Straumann 4.1 ×
10 mm) was placed and was subsequently loaded with a provisional restoration to develop the soft
tissue profile. The final restoration was delivered 4 months following implant placement
4.4  Management/Treatment Options 109

Fig. 4.17 (continued)
110 4  Hard Tissue Complications/Peri-implantitis

Fig. 4.17 (continued)
4.4  Management/Treatment Options 111

Fig. 4.17 (continued)
112 4  Hard Tissue Complications/Peri-implantitis

Fig. 4.18  Significant inflammation was noted around these implants, with deep probing depths
and bleeding upon probing. A peri-apical radiograph revealed significant bone loss around implants
at sites 1.1 and 1.3. Upon flap elevation a significant amount of granulation tissue was noted. The
defect was thoroughly debrided, and the exposed rough implant surface was decontaminated via
mechanical (diamond burs) and chemical (tetracycline slurry and hydrogen peroxide) means. The
defect was grafted with freeze-dried bone allograft, following implant surface decontamination. A
collagen membrane was used to contain the bone graft, and the flap was repositioned and sutured
around the implant restorations. Significant reduction of the inflammation was noted during the
initial healing period. Healthy peri-implant tissues were noted at the 5-year follow-up
4.5 Summary 113

Fig. 4.18 (continued)

4.5 Summary

The incidence of peri-implant complications will continue to increase as the use of


dental implants, as a treatment modality, becomes more popular. All patients receiv-
ing dental implants should be informed of the possibility of peri-implant complica-
tions. Good oral hygiene is of paramount importance as it is the main limiting factor
for most complications. A radiograph should be taken when an increasing
114 4  Hard Tissue Complications/Peri-implantitis

peri-­implant probing depth is identified. When a diagnosis of peri-implantitis has


been rendered, all etiological factors should be controlled or eliminated, when pos-
sible. The choice of the surgical treatment modality should depend on the amount of
peri-implant bone loss, as well as the configuration of the peri-implant bony defect.
Optimal oral hygiene is very important to maintain peri-implant tissue health, fol-
lowing the surgical intervention. A personalized maintenance recall protocol should
be implemented until all peri-implant parameters are stable and compatible with
health.

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