Peri-implant Disease: Pathogenesis, Risk Factors,

Diagnosis, Prevention and Treatment

Leena Palomo, DDS, MSD; Géza T. Terézhalmy, DDS, MA
Continuing Education Units: 1 hour

Online Course: www.dentalcare.com/en-US/dental-education/continuing-education/ce457/ce457.aspx

Disclaimer: Participants must always be aware of the hazards of using limited knowledge in integrating new techniques or
procedures into their practice. Only sound evidence-based dentistry should be used in patient therapy.

Participants in this course will be introduced to evidence-based information related to (1) the pathogenesis,
(2) risk factors, (3) diagnosis, and (4) prevention and treatment of peri-implant mucositis and peri-implantitis.

Conflict of Interest Disclosure Statement

• Dr. Palomo reports no conflicts of interest associated with this work.
• Dr. Terézhalmy has done consulting work for Procter & Gamble and is a member of the dentalcare.com
Advisory Board.

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ADA CERP is a service of the American Dental Association to assist dental professionals in identifying
quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses
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Concerns or complaints about a CE provider may be directed to the

provider or to ADA CERP at: http://www.ada.org/cerp

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The Procter & Gamble Company is designated as an Approved PACE Program Provider
by the Academy of General Dentistry. The formal continuing education programs of this
program provider are accepted by AGD for Fellowship, Mastership, and Membership
Maintenance Credit. Approval does not imply acceptance by a state or provincial board
of dentistry or AGD endorsement. The current term of approval extends from 8/1/2013 to
7/31/2017. Provider ID# 211886

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 Overview
Participants in this course will be introduced to evidence-based information related to (1) the pathogenesis,
(2) risk factors, (3) diagnosis, and (4) prevention and treatment of peri-implant mucositis and peri-implantitis.

Learning Objectives
Upon completion of this course, the dental professional should be able to:
• Discuss the pathogenesis and risk factors associated with peri-implant disease.
• Diagnose peri-implant mucositis and peri-implantitis.
• Develop and initiate strategies for the prevention of peri-implant disease.
• Implement appropriate non-surgical and surgical intervention for peri-implantitis.

Course Contents categories: peri-implant mucositis and peri-

• Introduction implantitis. Peri-implant mucositis is soft tissue
• Pathogenesis inflammation surrounding dental implants without
• Risk Factors evidence of bone loss. Peri-implantitis reflects
Plaque progression of peri-implant mucositis and has both
Previous Periodontal Disease soft- and hard-tissue components.
6-8

Occlusal Overload
Prosthesis-related Factors Pathogenesis
Diabetes Mellitus Although the term mucositis is used to describe
Smoking soft tissue inflammation, there is disagreement in
Genetic Factors the literature whether histologically the soft tissue
• Diagnosis around a dental implant more closely resembles
Clinical Appearance, Probing, Bleeding, and/ mucosa or gingiva. Nevertheless, the obvious
or Suppuration pathogenic comparison of peri-implant mucositis is
Radiographs to gingivitis, where only the surrounding soft tissue
Mobility shows inflammation and the alveolar crestal bone
Other Diagnostics is intact. Predictably, like gingivitis, peri-implant
• Preventive Strategies mucositis is reversible.
• Treatment Strategies
• Conclusion Peri-implantitis mirrors the pathogenesis of
• Course Test Preview periodontitis. Exposed titanium surfaces
• References accumulate glycoproteins forming a salivary
• About the Authors pellicle and as bacteria move onto a surface,
the dynamic process of biofilm formation
Introduction begins. Implant-associated biofilm resembles
Dental implants have a very high survival rate.1 that of chronic periodontitis, i.e., mixed, non-
However, the use of survival rate as a metric specific microbes, dominated by gram-negative
for success does not address infection-induced anaerobes.9-11 A notable difference between the
inflammation and its consequences in surviving two conditions is the association of S. aureus with
implants. As the link between oral health and peri-implantitis.12,13
systemic health is elucidated, and infection and
inflammation are emerging as primary links, the In peri-implantitis, as in periodontitis, the biofilm
issue is paramount.2 This is especially poignant in triggers an inflammatory response. Blood vessels
light of reports that up to 48% of dental implants adjacent to the gingivae/mucosal tissue enlarge
show soft tissue inflammation.3-5 and become permeable, allowing the migration of
neutrophils (PMNs) into the pocket space around
Peri-implant disease is an infection-induced the implant. As inflammation progresses, collagen
inflammatory process associated with dental around the blood vessels is lost and lymphocytes,
implants. Since the condition can affect both which subsequently transform into plasma cells
soft and hard tissues, it can be classified into two and macrophages accumulate in the area.

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 Figure 1. Pocket formation in the peri-implant Figure 2. At low magnification, the start of
space characterized by a “pot-hole”-like defect. osteoclastic action around teeth affected with
periodontitis.
Fibroblast- and PMN-derived collagenases
catalyze collagen loss apical to the pocket
epithelium. The underlying connective tissue
exhibits increasing lymphocytic infiltrates. Pocket
formation is enhanced in the peri-implant space
characterized by “pot-hole”-like defects (Figure 1),
creating an environment that favors microbial
proliferation. The products of these pathogens
further challenge host immune defenses and
degenerative changes progress apically into the
underlying connective tissue.

At this point, the analogy between periodontitis

and peri-implantitis briefly diverges. Inflammatory
activity around implants is more pronounced
than that observed around natural teeth and
the tissues are more susceptible to the spread
of plaque-associated infection into alveolar
bone.14,15 When cases of peri-implantitis were
systematically compared to cases of periodontitis,
the results revealed that tissue destruction is
more severe in association with peri-implantitis.16,17
One explanation for the apparent greater
severity and increased rate of progression of
tissue destruction is the structural differences
between periodontal and peri-implant tissues.
Unlike natural teeth, dental implants do not
have cementum or Sharpey’s fibers, they are
not bounded by periodontal ligament, and,
consequently, there is direct contact between
Figure 3. At high magnification, note connective
tissue inflammatory infiltrate, which is common to
inflammation around natural teeth and dental implants.
bone and implant surface. It is axiomatic that
infection can progress without impediments from
soft to hard tissue.
Ultimately, as the inflammatory process reaches
the crest of alveolar bone, both in peri-implantitis
and periodontitis, osteoclastic bone resorption
begins (Figures 2 & 3). The inflammatory cells
release cytokines such as interleukin-1 (IL-1),
tumor necrosis factor-α (TNF-α) and interleukin-6
(IL-6). Bone destruction occurs though
osteoclastic action which is triggered by cytokines
and other inflammatory mediators, including IL-1β
and PGE2.

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Risk Factors
While dental implants have a very high survival
rate, a number of factors (e.g., plaque control,
previous periodontal disease, restorative issues,
concomitant systemic diseases, and smoking)
have been identified as prerequisites to the
initiation and progression of peri-implant disease.
Plaque
The most notable risk factor for peri-implant
disease is poor plaque control. This may reflect
a patient’s inability or unwillingness to maintain
optimal oral hygiene. Other impediments may
include prosthesis design, adjacent restoration
contour and margins, and/or loose or broken
restorative components, which interfere with
oral hygiene. Some of these problems may be
avoided by designing removable superstructures,
such as screw retained crowns.
It has also been shown that maxillary soft tissues
adjacent to implants are at increased risk for
plaque-induced inflammation when compared
to the gingivae of natural dentition.18 Biofilm
associated with peri-implant disease is also more
complex than that with periodontitis. Common
periopathogenic bacteria show low prevalence,
and several bacteria, such as S. aureus,
Fusobacterium, and Streptococcus species, have
been identified as candidate pathogens in peri-
implantitis.19
Previous Periodontal Disease
Prospective studies have shown that patients with
history of generalized aggressive periodontitis are
more susceptible to peri-implantitis.20 Subgingival
tissues around implants show higher levels of
periopathogenic and superinfecting bacteria
compared to sites from non-periodontal disease
patients.21 Other studies have found that while
implants are a viable treatment option in sockets
affected by chronic periapical pathoses, the
risk of implant failure is increased when placed
adjacent to teeth with periapical radiolucencies.22
Occlusal Overload
Finite element studies have shown that occlusal
load is concentrated at the implant-marginal bone
interface.23,24 Consequently, occlusal loading
is an important aspect of prosthetic design,
since dental implants do not have a periodontal
ligament to adjust to varying loads and they are
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less resistant to load variations than natural
teeth. A systematic review of the literature
concluded that in the presence of poor oral
hygiene, occlusal overload leads to peri-implant
bone loss.25
Prosthesis-related Factors
Although there are no published randomized
clinical trials which directly prove crown design
is linked to peri-implantitis, it has long been
established that inadequate subgingival margins
of crowns change the microflora and lead to
inflammation around natural teeth. It is intuitive
that the same principles should apply when
considering crown design on dental implants to
minimize the likelihood of peri-implant disease
(Figure 4A, 4B, and 4C).26,27
Cone Beam CT prior to implant placement
facilitates optimal placement of the soft tissue
component of the fixture, i.e., the coronal most
portion of the dental implant with a 1.8 mm
polished collar, so that the implant shoulder and
crown margin are located close to the mucosal
surface. Non-submerged implant fixtures with
passive fits to the other components, should
minimize irritation to adjacent soft tissue.
Residual cement associated with temporary
or permanent crown placement on a dental
implant may irritate the surrounding soft tissues,
contribute to poor plaque control directly or by
creating a rough surface, and promote bacterial
plaque formation.28 Accumulation of biofilm, in
turn, triggers soft tissue inflammation, which if
unchecked progresses to peri-implantitis.
Figure 4A. Poorly contoured temporary restoration with
plaque retentive surfaces covered with biofilm.

Figure 4B. Mucositis, associated with temporary in the
mouth. Note color change and rolled gingival margin
versus gingival color and contour of the adjacent
natural tooth.
Figure 4C. Note thickened gingival margins after
removal of temporary.
Diabetes Mellitus
Just as periodontitis is more common in persons
with diabetes, poor glycemic control is also
associated with peri-implant disease.29 Although
the role of distinct phlogistic (inflammatory)
mediators in its pathogenesis is not fully
elucidated, evidence suggests proinflammatory
gene expression at peri-implantitis sites is affected
by glycemic control.30 Indeed, the prognosis
with dental implants is improved in patients with
glycosylated hemoglobin levels below 7 (normal
range: 4 to 5.7%).31
Smoking
The incidence of peri-implantitis is increased
in smokers with an odds ratio of 3.6 to 4.6.32‑34
A meta-analysis across 13 studies found that
smoking increased the annual rate of bone loss
around dental implants by 0.164mm/year.35 In
smokers, even apparently healthy peri-implant
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sites have increased levels of IL-1β, TNF-α, and
prostaglandin E2 levels in peri-implant crevicular
fluid when compared to non-smokers.36
Genetic Factors
A genetic disorder characterized by IL-1 gene
polymorphism has been suggested as a risk
factor for peri-implantitis.37 However, based
on a systematic review of 27 relevant articles,
no definitive conclusion can be drawn.38 In
contradistinction, chronic inflammatory diseases,
such as rheumatoid arthritis, do appear to increase
the risk of peri-implantitis. A determination of the
odds ratios through meta-analytic studies and
systematic reviews is currently under way.39
Diagnosis
A combination of diagnostic tools is needed to
evaluate the health status of dental implants.6,7
Presence or absence of a single sign or symptom
is generally not sufficient to establish a diagnosis
of peri-implantitis or to distinguish between peri-
implant mucositis and frank peri-implantitis.
Clinical Appearance, Probing, Bleeding, and/or
Suppuration
Signs of peri-implant mucositis are similar to those
of gingival disease. In mucositis, soft tissue color
changes from pale pink to more red, or may even
appear bluish or cyanotic (Figure 5A). Edema
of the gingival margin may present as rolled
or thickened instead of knife-edged (Figure 5B
Interdental papilla may look blunted (Figure 5C).
Spontaneous bleeding or bleeding upon probing
and/or suppuration may be noted.
Probing with traditional light force (0.25N) protects
adjacent soft tissues. Using a plastic probe
protects the implant surface from scratches.
Increasing probing depths, especially with
bleeding and or suppuration, when compared
to baseline probing (when the final restoration
was placed) can be helpful in early diagnosis.
However, increasing probing depths and the
presence of bleeding and/or suppuration do not
distinguish between peri-implant mucositis and
peri-implantitis.8
Radiographs
Either conventional or digital periapical
radiographs are useful in evaluating interproximal
bone levels (Figure 6). These radiographs
Figure 5A. Note cyanotic gingiva.
Figure 5B. Note thickened rolled margin around
implant.
Figure 5C. Note bulbous, red, papilla with spontaneous
bleeding, distal to #8 implant.
should be compared to baseline radiographs
obtained when the final restoration was placed.
Radiographic comparison with baseline values is
particularly useful. Subtraction programs are also
available to further define radiographic changes.
In the absence of such a program, however,
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Figure 6. Note bone loss around the coronal-
most implant threads.
radiographs taken perpendicular to the implant
can show clear thread demarcation, useful for
comparison.
Mobility
Once implant mobility is present, the implant is
considered to have a hopeless prognosis and
removal is the de fault treatment plan. Often, it is
the restoration or a component of the abutment
that is mobile. Such a situation may lead to
future bone loss, but does not significantly affect
immediate implant prognosis. However, loose
restorative components create space for pellicle
adhesion and trigger the start of the inflammatory
cascade leading to peri-implant disease.
Other Diagnostics
Just as with other oral infections, microbial
diagnosis of peri-implantitis may be performed
using direct microscopy, Gram’s Method of
staining, culture, immunoserologic identification
and nucleic acid methods. In certain situations
inflammatory markers and genetic diagnostics may
also be used.
Preventive Strategies
Since one of the marked differences between
peri-implantitis and periodontitis is the more rapid
progression of peri-implantitis and the severity of
associated tissue destruction, treatment success
(outcome, prognosis) relies heavily on prevention,
and early diagnosis and treatment.
Toothbrushes
In general, electro-mechanical toothbrushes
have been shown to be more effective in plaque
removal than manual toothbrushes, especially
in mandibular lingual areas.40,41 While well
controlled prospective studies that demonstrate
the superiority of powered brushes specifically
around dental implants have not been done, it
is intuitive that maintaining good plaque control
around dental implants is beneficial.
Dentifrices
There are no controlled, prospective studies
comparing the efficacy of various toothpaste
formulations around dental implants. However,
there is robust evidence that, dentifrices with
stannous fluoride and those containing triclosan
with a copolymer have statistically significant
antiplaque and antigingivitis activity.42
More recently, in controlled 6-month clinical trials,
a stannous fluoride-sodium hexametaphosphate
containing dentifrice has been shown to have
superior antiplaque and antigingivitis efficacy.43,44
In addition, the stannous fluoride-sodium
hexametaphosphate formulation has been shown
to have antigingivitis activity in subjects previously
found to be non-responsive to a triclosan-
copolymer containing dentifrice.45
Mouthwashes
There are no controlled, prospective studies
comparing the efficacy of various mouthwash
formulations around dental implants. However,
there is robust evidence that mouthwash
formulations containing chlorhexidine and
essential oils have statistically significant
antiplaque and antigingivitis activity.42 The same
meta-analysis also concluded that the anti-plaque
and anti-gingivitis effects of cetylpyridinium
chloride (CPC) mouthwashes are formulation-
dependent.
In a 6-month placebo controlled clinical trial, a
0.07% cetylpyridinium chloride mouthrinse was
found to be statistically superior to placebo in
reducing plaque and gingivitis.46 Another 6-month
study showed no statistically significant difference
in the antiplaque and antigingivitis effects of
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a 0.07% cetylpyridinium chloride mouthrinse
when compared to an essential oil-containing
mouthrinse.47
A recent study evaluated the performance of
four commercially available CPC-containing
mouthrinses versus a negative control (CTR) using
the Disk Retention Assay (DRA) and the Plaque
Glycolysis and Regrowth Method (PGRM).48 The
DRA assessed the percentage of CPC adsorption
onto anionic cellulose discs and provided a
measure of the substantivity and bioavailability
of CPC mouthrinses. The PGRM test examined
the effects of CPC on the metabolism and growth
properties of sampled in vivo plaque following
treatment.
Products tested were Crest Pro Health (CPH700
ppm); Colgate Total US (CT750 ppm); Scope
Mouthwash (SCP450 ppm); and Colgate Total
Puerto Rico (CT450). Comparison of DRA
to PGRM showed a linear relation between
CPC bioavailability and its clinical antimicrobial
performance with rank ordered efficacy, i.e.,
CPH700>CT750>SCP450>CT450>CTR.
The study concluded that the antiplaque
and antigingivitis activity of CPC-containing
mouthrinses is predicated on optimal CPC
substantivity and bioavailability.
Treatment Strategies
Just as mechanically disrupting the causative
biofilm from the surface of a tooth can reverse
the effects of gingivitis and prevent progression
to periodontitis, so too is the case for peri-implant
mucositis.9 Therefore, the treatment of peri-
implant mucositis and initial therapy for frank peri-
implantitis aims to eliminate the biofilm from the
surface of the dental implant.
Non-surgical Treatment
Conventional non-surgical therapy appears to
successfully reverse peri-implant mucositis. Laser
therapy alone or as an adjunct to conventional
therapy has been evaluated, however, the
superiority of laser treatment has not be
established.49 Adjunctive antibiotic therapy (both
locally applied and systemic) in association with
mechanical removal of plaque had only limited
success.51,52 Failure may be related to the frequent
presence of bacteria resistant to clindamycin,
amoxicillin, doxycycline, or metronidazole.53
Surgical Treatment
Non-surgical therapy reduces local inflammation
and infection, but it does not resolve the
underlying osseous defect.54-56 Reversing frank
peri-implantitis successfully hinges on bone
regeneration.57,58 The process, however, is
complicated by the fact that there is no cementum
on the surface of dental implants and the
periodontal ligament, which communicates with
marrow spaces in bone, is also absent.
The first step in successful regeneration of bone,
as with bone regeneration around natural teeth,
is predicated on effective decontamination of the
affected site, i.e., establishment of surgical access
followed by removal of granulation tissue, calculus,
and biofilm. Air powder abrasive treatment of
the implant surface offers no advantage over
traditional decontamination.59 Similarly, Er:Yag
laser decontamination was also found to be less
effective than traditional decontamination.60
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Implantoplasty, removal of the micro- and
macro-roughened implant surface has also
been evaluated as a means to attain absolute
decontamination of the implant surface.61,62
However, procedure-related complications, e.g.,
heat production, deposits of implant material into
the surgical field, damage to the implant surface,
and weakening of the implant structure appear to
negatively affect prognosis.
Conclusion
The challenges of diagnosing and treating
peri-implant disease will become much more
widespread as the popularity of dental implants
continues to rise. The paucity of well controlled
scientific evidence against the backdrop of
increasing prevalence of peri-implant mucositis
and peri-implantitis, and a lack of robust
evidence-based treatment options make the
prevention of peri-implant disease a priority.
Course Test Preview
To receive Continuing Education credit for this course, you must complete the online test. Please go to:
www.dentalcare.com/en-US/dental-education/continuing-education/ce457/ce457-test.aspx

1. ______________ is defined as soft tissue inflammation surrounding dental implants without

evidence of bone loss.
a. Peri-implantitis
b. Peri-implant mucositis
c. Peri-implant disease
d. None of the above.

2. All of the following statements are correct with respect to the pathogenesis of peri-implantitis
except which one?
a. The obvious pathogenic comparison of peri-implantitis is to gingivitis.
b. Peri-implantitis mirrors the pathogenesis of periodontitis.
c. Implant-associated biofilm resembles that of chronic periodontitis.
d. In peri-implantitis, as in periodontitis, the biofilm triggers an inflammatory response.

3. Which of the following statements is correct with respect to peri-implantitis?

a. Inflammatory activity around implants is more pronounced than that observed around natural teeth.
b. When cases of peri-implantitis were systematically compared to cases of periodontitis, the results
revealed that tissue destruction is more severe in association with peri-implantitis.
c. As the inflammatory process reaches the crest of alveolar bone, both in peri-implantitis and
periodontitis, osteoclastic bone resorption begins.
d. All of the above.

4. All of the following statements are correct with respect to peri-implantitis except which one?
a. The most notable risk factor for peri-implant disease is poor plaque control.
b. Maxillary soft tissues adjacent to implants are at reduced risk for plaque-induced inflammation when
compared to the gingivae of natural teeth.
d. Biofilm associated with peri-implant disease is more complex than that with periodontitis.
e. S. aureus, Fusobacterium, and Streptococcal species have been identified as candidate pathogens
in peri-implantitis.

5. Which of the following statements is correct with respect to peri-implantitis?

a. Prospective studies have shown that patients with a history of chronic and/or aggressive periodontitis
are more susceptible to peri-implantitis.
b. Studies have shown that while implants are a viable treatment option in sockets affected by chronic
periapical pathoses, the risk of implant failure is increased when placed adjacent to teeth with
periapical radiolucencies.
c. A systematic review of the literature concluded that in the presence of poor oral hygiene, occlusal
overload leads to peri-implant bone loss.
d. All of the above.

6. Which of the following statements is correct with respect to prosthesis-related factors and
the likelihood of peri-implant disease?
a. It is intuitive that crown design, i.e., gingival margins of crowns, on dental implants can affect the
likelihood of peri-implant disease.
b. Non-submerged implant fixtures should have passive fits to the other prosthetic components, so as
not to impinge on adjacent sift tissue.
c. Residual cement associated temporary or permanent crown placement on a dental implant promotes
bacterial plaque formation and triggers inflammation.
d. All of the above.

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7. All of the following statements are correct with respect to peri-implantitis except which
one?
a. The prognosis with dental implants is improved in patients with diabetes mellitus when their
glycosylated hemoglobin levels are below 7%.
b. The incidence of peri-implantitis increases in smokers with an odds ratio of 3.6 to 4.6.
c. It has been concluded that a genetic disorder characterized by IL-1 gene polymorphism is a
definitive risk factor for peri-implantitis.
d. Chronic inflammatory diseases, such as rheumatoid arthritis, appear to increase the risk of peri-
implantitis.

8. Signs of peri-implant mucositis may include _______________.

a. soft tissue color changes from pale pink to more red
b. bluish or cyanotic soft tissue
c. edema of the gingival margin rolled margin around the implant
d. All of the above.

9. Which of the following diagnostic criteria must be met to distinguish between peri-implant
mucositis and peri-implantitis?
a. Spontaneous bleeding or bleeding upon probing and/or suppuration.
b. Increased probing depth.
c. Evidence of radiographic bone loss over time in comparison to baseline values.
d. Mobility

10. In general, all of the following statements are correct with respect to the plaque removal
efficacy of toothbrushes except which one?
a. Electro-mechanical toothbrushes have been shown to be more effective in plaque removal than
manual toothbrushes.
b. Manual toothbrushes have been shown to be more effective in plaque removal than
electromechanical toothbrushes in mandibular lingual areas.
c. Well controlled prospective studies that demonstrate the superiority of powered brushes specifically
around dental implants have not been done.
d. It is intuitive that maintaining good plaque control around dental implants is beneficial.

11. In general, which of the following statements is correct with respect to the antiplaque and
antigingivitis efficacy of dentifrices?
a. There are no controlled, prospective studies comparing the efficacy of various toothpaste
formulations around dental implants.
b. There is robust evidence that in general, dentifrices with stannous fluoride or triclosan with a
copolymer have significant antiplaque and antigingivitis activity.
c. Stannous fluoride-sodium hexametaphosphate has been shown to have activity in subjects non-
responsive to a triclosan-copolymer containing dentifrice.
d. All of the above.

12. In general, which of the following statements is correct with respect to the antiplaque and
antigingivitis efficacy of mouthwashes?
a. There are no controlled, prospective studies comparing the efficacy of various mouthwash
formulations around dental implants.
b. There is robust evidence that mouthwash formulations containing chlorhexidine and essential oils
have significant antiplaque and antigingivitis activity.
c. Recent studies have concluded that a 0.07% cetylpyridinium chloride mouthrinse formulation is as
effective as essential oil-containing mouthrinses and has superior substantivity and bioavailability
compared to other CPC formulations.
d. All of the above.

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13. Which of the following statements is correct with respect to non-surgical treatment of peri-
implant mucositis?
a. Conventional non-surgical therapy appears to successfully reverse peri-implant mucositis.
b. Laser therapy alone or as an adjunct to conventional therapy has been evaluated, however, the
superiority of laser treatment has not be established.
c. Adjunctive antibiotic therapy in association with mechanical removal of plaque had only limited
success.
d. All of the above.

14. Which of the following statements is correct with respect to surgical treatment of peri-
implantitis?
a. Reversing frank peri-implantitis successfully hinges on bone regeneration.
b. Surgical treatment of peri-implantitis is complicated by the fact that there is no cementum on the
surface of dental implants and the periodontal ligament, which communicates with marrow spaces in
bone, is also absent.
c. The first step in successful surgical treatment hinges on effective decontamination of the affected
site, i.e., establishment of surgical access followed by removal of granulation tissue, calculus, and
biofilm.
d. All of the above.

15. All of the following statements are correct with respect to surgical treatment of peri-
implantitis except which one?
a. Air powder abrasive treatment of the implant surface in association with surgical treatment offers no
advantage over traditional decontamination.
b. Er:Yag laser decontamination in association with surgical treatment was found to be less effective
than traditional decontamination.
c. Implantoplasty, removal of the micro- and macro-roughened implant surface, has been shown to
attain absolute decontamination of the implant surface.
d. All of the above.

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References
1. Albrektsson T, Dahl E, et al. Osseointegrated oral implants. A Swedish multicenter study of 8139
consecutively inserted Nobelpharma implants. J Periodontol. 1988;59(5):287-296.
2. Van Dyke TE, van Winkelhoff AJ. Infection and inflammatory mechanisms. J Periodontol. 2013Apr;
84 (4 Suppl):S1-7.
3. Berglundh T, Persson L, Kloinge B. A Systemic review of the incidence of biological and technical
complications in implant dentistry reported in prospective longitudinal studies of at least 5 years.
J Clin Periodontol. 2002;29 Suppl 3:197-212.
4. Fransson C, Lekholm U, Jemt T, Berglundh T. Prevalence of subjects with progressive bone loss at
implants. Clin Oral Implants Res. 2005;16:440-446.
5. Roos-Jansåker AM, Lindahl C, Renvert H, Renvert S. Nine- to fourteen-year follow-up of implant
treatment. Part II: Presence of peri-implant lesions. J Clin Periodontol. 2006;33:290-295.
6. Zitzmann NU, Berglundh T. Definition and prevalence of peri-implant diseases. J Clin Periodontol.
2008;35:286-291.
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About the Author

Leena Palomo, DDS, MSD

Dr. Palomo is Associate Professor of Periodontics and director of the undergraduate
(DMD) program in periodontics at School of Dental Medicine, Case Western Reserve
University, Cleveland, Ohio. Dr. Palomo earned her undergraduate as well as her
DDS (1996) and MSD (2004) degrees from Case Western Reserve University.
Dr. Palomo is certified of the American Board of Periodontology. Dr. Palomo has
published several articles in refereed medical and dental journals and has been
invited as a featured speaker by many local, state, national, and international
professional societies.

Email: lvb3@case.edu

Géza T. Terézhalmy, DDS, MA

Professor and Dean Emeritus
School of Dental Medicine
Case Western Reserve University

Dr. Terézhalmy is Professor and Dean Emeritus, School of Dental Medicine, Case
Western Reserve University, Cleveland, Ohio; and a Consultant, Naval Postgraduate
Dental School, Navy Medicine Manpower, Personnel, Training & Education
Command, Bethesda, Maryland. Dr. Terézhalmy received a B.S. from John Carroll University, University
Heights, Ohio; a D.D.S. from School of Dental Medicine, Case Western Reserve University, Cleveland,
Ohio; a Certificate of Oral Medicine Residency from the National Naval Dental Center, Bethesda,
Maryland; and a M.A. from The George Washington University, Washington, D.C. Dr. Terézhalmy is
certified by the American Board of Oral Medicine and the American Board of Oral and Maxillofacial
Radiology (Life). Over the past 40 years, he has held more than 30 positions in professional societies;
served as editor or contributing editor for several publications; co-authored or contributed chapters
for several books; published over 225 abstracts and articles in peer reviewed journals; and accepted
invitations to lecture before many local, state, national, and international professional societies.

Email: gtt2@case.edu

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